Editorials

Using shared care to tackle the complexity of optimal patient management Globally, the burden of disease has shifted from acute to chronic illnesses and the management of multiple comorbidities. To address the challenges this creates, integrated care has received growing attention as a means of improving health care delivery and outcomes.1 Integrated care (frequently equated with “disease management” and “shared care”) is defined by the World Health Organization as a concept bringing together inputs, delivery, management and organization of services related to diagnosis, treatment, care, rehabilitation and health promotion. Integration is a means to improve services in relation to access, quality, user satisfaction and efficiency.2 For the first time, Australia has a shared care model for the management of a chronic condition — namely, glaucoma — launched under the Pharmaceutical Benefits Scheme (PBS) in January 2008. Under the new PBS guidelines (Box),3 authorised optometrists can co-manage patients with glaucoma in a shared care arrangement with an ophthalmologist. Also, similarly to optometrists in the United Kingdom, Canada, and the United States, authorised optometrists in Australia may now prescribe therapeutic agents for certain eye conditions under the PBS. In January 2008, prescribing rights for topical ophthalmic medications were extended to certified optometrists as a result of a legislative change (National Health Amendment [Pharmaceutical Benefits] Act 2007 [Cwlth]).4 The range of medications that authorised optometrists may prescribe under the PBS includes lubricants and therapeutic agents for treating allergies, infection, inflammation, and glaucoma. Glaucoma is a heterogeneous group of diseases leading to a progressive optic neuropathy. It is the most common cause of preventable blindness in developed countries.5 Commonly, glaucoma is managed with topical hypotensive medications that include prostaglandin analogues, carbonic anhydrase inhibitors, selective α-adrenoceptor agonists and topical β-blockers. Under the shared care model, the patient’s ophthalmologist and optometrist together develop a written management plan that specifies the treatment goals and the roles and responsibilities of the two practitioners, create a review schedule, and communicate clinical information to the patient’s general practitioner to promote an integrated approach. The PBS guidelines also recommend that a pharmacist be involved in providing medicines information, such as advice related to administration and techniques to limit systemic absorption and side effects of ophthalmic medications, as well as potential interactions with concomitant systemic medications for comorbidities.3 Quality integrated care practices require effective communication and coordination among the involved health care providers and with patients. Decision making in relation to medicines for optimal patient management is increasingly complex because of more pharmacotherapeutic options for more conditions, increasing exposure and age at exposure of older patients to a wider range of medications, and rising numbers of affected patients as the population ages. Ophthalmic medications are often overlooked in medical history taking. Almost half the medical records kept by GPs have been reported to have no record of eye drops being used by patients with glaucoma.6 Ophthalmologists, GPs, optometrists and pharmacists need to consider a patient’s comorbidities and concurrent treatments to be able to provide a holistic approach to patient care. Topical ophthalmic medications may have effects on other diseases and their management: topical β-blockers may cause bronchospasm in those with reactive pulmonary disease,7 and their prescription may warrant an additional bronchodilator. Topical ophthalmic medications may interact with systemic medications. Polypharmacy, especially in the older population, may have serious consequences.8 For example, cimetidine, an over-the-counter H2-receptor antagonist for gastrointestinal irritation, may increase the effect of β-blockade when used in conjunction with β-blockers and should be used with caution in patients with underlying cardiac conditions.9 Australia’s new integrated care model promises to increase patient access to eye health care services, particularly in rural areas, and thereby enhance continuity and quality of care in these regions.2 Involvement of optometrists offers the opportunity for increased detection of glaucoma and patient access to subsidised ocular therapeutic agents. However, the processes and clinical outcomes of this new model of care need to be evaluated rigorously to determine its quality, feasibility and durability. Are anticipated improvements being realised? Are there unintended consequences? Important measures will include the rate of medication-related problems among glaucoma patients before and after the introduction of this shared care arrangement; patient adherence to and persistence with therapy; detection of undiagnosed glaucoma (prevalence of which has been reported to be high10); patient satisfaction; rates of visual field deterioration; and intraocular pressure levels. Some of these outcomes, such as medication use outcomes recorded in computerised health care datasets, will be easier to measure than others. Commitments by government and public agencies to rigorous research and funding to allow prospective studies and direct measures of health outcomes would seem a sound investment. This would provide valuable information not only for Australia but also for other countries that develop and implement integrated care models. Guidelines for the shared care of glaucoma patients under Australia’s Pharmaceutical Benefits Scheme (PBS)3 Confirmation of diagnosis and development of a management plan An authorised optometrist who makes a provisional diagnosis of glaucoma is to refer the patient to an ophthalmologist for confirmation of the diagnosis. With the consent of the patient, the optometrist and the ophthalmologist are to develop a management plan together, including the sharing of care between the two practitioners, and the communication of clinical information to the patient’s nominated general practitioner. Patients being considered for anti-glaucoma therapy with a β-blocking agent should be assessed for any potential cardiovascular or respiratory risk by a medical practitioner (eg, the patient’s GP) before initiating therapy. This assessment should be repeated if a change in dose of the β-blocker is proposed. Once a treatment plan is established with the ophthalmologist, the optometrist can prescribe topical medications under the PBS and perform ongoing reviews to monitor the patient. Changes to the management plan are only made following consultation between treating practitioners. A written patient management plan must specify: all the agreed components of treatment, including any pharmacotherapy; target intraocular pressures and actions to be taken if these are not achieved within a specified time frame; an agreed approach to monitoring visual fields and optic disc imaging and actions to be taken following changes in visual fields; triggers for referral for immediate ophthalmological and GP review; likely side effects from agreed treatment and the action to be taken to address these; an agreed schedule for patient review by both practitioners; who is responsible for performing each of the required tests and the required frequency for performing them; an agreed method for timely communication of clinical findings and patient management between the two practitioners and the patient’s nominated GP.

Christine Y Lu BPharm, MSc, PhD · Vicky H Lu MB BS, MPH · Ivan Goldberg MB BS, FRANZCO, FRACS · Richard O Day MD, FRACP

Blood lead levels in children in Mount Isa are substantially elevated, and a purported lack of knowledge of the lead source is no longer tenable Environmental lead levels and blood lead concentrations in children at Mount Isa, in north-western Queensland, are substantially elevated compared with background values1-3 and, as a consequence, there is a public health risk. This problem is exacerbated by the reluctance of stakeholders, including Xstrata Mount Isa Mines Ltd, operator of Mount Isa Mines (MIM), and Queensland environmental and health authorities to acknowledge and respond effectively to the fact that the main environmental lead source is mining and smelting activity.1,2 It is frequently claimed that the lead source is natural surface mineralisation;4-6 this is not the case. Mount Isa city, located immediately adjacent to MIM, is a major lead, zinc and copper producer, and Australia’s largest atmospheric emitter of sulfur dioxide, lead and other metals.7 The emissions are likely to have had an impact on the blood lead level (BLL) of a significant proportion of the city’s population of about 21 000. The causal link between smelter lead emissions and an increased risk of adverse health effects has been convincingly documented elsewhere,8 and responded to, albeit with varying degrees of urgency, at smelting sites around Australia (Box).9 In Mount Isa, the link has been routinely questioned and remedial action delayed. In recent decades, considerable evidence has emerged showing lifelong negative health, intellectual and sociobehavioural effects associated with childhood BLLs above 10 μg/dL, the level widely regarded as the threshold above which intervention is necessary. However, there is emerging evidence of adverse effects occurring at 5–10 μg/dL, and even at levels as low as 2 μg/dL.8-11 In 2008, Queensland Health reported that Mount Isa children aged 1–4 years had a mean BLL of 5 μg/dL, with 37% having levels > 6 μg/dL and 11.3% having levels > 10 μg/dL.3 Recent data from Fremantle, Western Australia, an urban centre with no major industrial lead source, showed a mean BLL in children of 1.8 μg/dL, with no individual readings exceeding 10 μg/dL.12 This is similar to the mean BLL of 1.9 μg/dL (with only 1.6% of readings ≥ 10 μg/dL) for children aged 1–5 years in the United States in 1999–2002.10 Compared with these figures, BLLs remain substantially elevated in many of Mount Isa’s children and, as shown by numerous studies elsewhere, the level of lead exposure is likely to correlate with neurocognitive impairments.8-11 Lead exposure places children on an abnormal developmental trajectory that may result in reduced social and educational achievement and unmet life potential. Assuming that the Mount Isa BLL data are representative of all 1–4 -year-olds in the city (of whom 27% were sampled),3 then, on average, every nine days a child will exceed the BLL threshhold of > 10 μg/dL. Research commissioned during a Queensland government-led inquiry a decade ago,1 as well as subsequent peer-reviewed studies,2 have unequivocally demonstrated widespread contamination of soil and airborne dust in and around Mount Isa, as a result of both historic and ongoing mining and smelting activity by MIM. Contaminants include lead, copper and other metals and metalloids. Frequent claims that natural mineralisation of soils is the main cause of increased lead levels4-6 are incorrect, and have stymied an appropriate response to the Mount Isa lead problem. The “gossans” (ridges of lead-bearing surface rocks) initially discovered west of Mount Isa are now largely covered by mining operations, and cannot be a major source of environmental lead. Furthermore, there is no substantial natural exposure of copper ore, which was discovered “accidentally” during deep drilling. These observations are supported by data published by several of MIM’s own geologists over the past 60 years.13 Numerous soil profiles in and around Mount Isa show that it is usually only the surface layers that are contaminated with lead and copper.1,2 Concentrations of these metals correlate significantly with each other and are up to 20 times higher at 0–2 cm depth than at 10–20 cm depth. This shows that (1) soil contamination with both lead and copper can only have come from particles emitted into the atmosphere from MIM, as there is no other common source for both metals, and (2) that the surface soil metal enrichment can only have come from aerial deposition of contaminated particles. Lead isotope fingerprinting, used as a tracer, shows that surface soil — but in most cases not deeper soil — contains lead from the Mount Isa lead ore body due to aerial deposition.1 The capture by MIM of smelter fumes (sulfur dioxide and associated metal-bearing particles) is inefficient, as shown by the ongoing high emission levels that, for some compounds, have been rising in recent years.7 The Queensland Government’s air quality data for Mount Isa14 show 10 breaches of the guideline level for sulfur dioxide between September 2009 and February 2010, and that lead concentrations in air increased substantially during these breaches. However, the current legal standard for lead concentrations in air in Mount Isa is higher than the Australian national lead-in-air standard of 0.5 μg/m3, and therefore was not breached.15,16 More importantly, the current Mount Isa standard is an order of magnitude greater than the recently revised US lead-in-air standard,8 which was lowered by the US Environmental Protection Agency after assessing about 6000 studies related to the health impacts of lead exposure.8 The lower standard was deemed necessary to properly protect the health and wellbeing of children.8 The evidence is clear. There is a single primary source of environmental lead in Mount Isa: the historic and ongoing mining and smelting activity. Acceptance of this patent fact by all stakeholders will lead to a more targeted remedy to the lead problem, and better health and environmental outcomes for the community of Mount Isa. A purported lack of knowledge of the lead source is no longer a tenable response and provides no long-term resolution for Xstrata, the government or the children of Mount Isa whose futures are at risk. Australian mining- and smelting-related blood lead levels and government and industry responses9 Port Pirie, South Australia Early 1980s: high blood lead levels (BLLs) confirmed 1984 onwards: decontamination and demolition of residences, slag dumps covered, emissions controlled 2004: BLLs decreased but remain elevated Broken Hill, New South Wales Early 1990s: high BLLs confirmed 1994 onwards: land and home evaluation and remediation 2006: BLLs decreased but remain elevated Boolaroo, NSW Early 1990s: high BLLs confirmed 1991 onwards: emissions controlled 1997: lead abatement of homes 2003: smelting operations ceased 2005: BLLs decreased substantially after smelter closure Mount Isa Mines, Queensland 1994: high BLLs confirmed 1997: Mount Isa lead emission limits set above Australian national limits (national limits written into law in 2009, to apply in Mount Isa from 2012) 2000: partial emission capture 2007: Xstrata Mount Isa Mines “lead pathways” study initiated (not completed June 2010) 2008: BLLs lower than in 1994 but remain elevated 2009: Queensland government lead management report 2010: highest lead emissions in Australia

Niels C Munksgaard PhD · Mark P Taylor BSc(Hons), PhD · Alana Mackay BEnvMgt

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

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

Evidence concerning the safety of rosiglitazone continues to evolve In February 2010, the United States Senate Committee on Finance released a report on the safety of rosiglitazone.1 The report concluded that there were possible cardiac risks associated with rosiglitazone and that the manufacturer, GlaxoSmithKline (GSK), was aware of this well before it became public. The authors further stated that, rather than warn patients and regulatory authorities promptly, GSK executives chose to intimidate independent physicians who publicised the possible risks, minimise the impact of adverse findings, and downplay the possibly beneficial cardiovascular effects of the other available drug in the class, pioglitazone.1 A week before the Finance Committee report was released, an editorial by Steve Nissen, lead author of the meta-analysis that first raised cardiovascular concerns regarding rosiglitazone in 2007,2 was published online.3 The editorial related to an article on the increased risk of heart failure, a recognised adverse effect of glitazones, found in the Rosiglitazone Evaluated for Cardiac Outcomes and Regulation of Glycaemia in Diabetes (RECORD) trial.4 However, it was more a detailed account of the sequence of events surrounding rosiglitazone’s possible adverse cardiovascular effects, starting with its US approval in 1999. The editorial viewed the RECORD trial (the main results of which were published mid 20095 but not considered in the Finance Committee report) as underpowered, despite demonstrating that rosiglitazone was non-inferior to metformin or sulfonylurea for the primary endpoint of cardiovascular hospitalisation or death. Although there were no new safety concerns or efficacy data in either the Finance Committee report or Nissen’s editorial, there was a prompt media response. The New York Times, for example, highlighted a suggestion by the Finance Committee that if every diabetic patient in the US taking rosiglitazone was given pioglitazone instead, 500 heart attacks and 300 cases of heart failure would be averted every month.6 There was also a quick response from GSK, which categorically rejected the findings of the Finance Committee and the assertions of the New York Times in separate media statements, and published a point-by-point response to Nissen’s editorial.7 More recently, the results of a retrospective analysis of US Medicare data for older patients8 and an expanded meta-analysis from Nissen’s group,9 both suggesting adverse cardiovascular effects of rosiglitazone, have contrasted with a post-hoc analysis of data from the Bypass Angioplasty Revascularization Investigation in Type 2 Diabetes study, in which rosiglitazone was found to be of significant benefit in patients with established coronary artery disease.10 At present, rosiglitazone remains approved for use in Australia as monotherapy or as part of dual oral combination therapy with metformin or a sulfonylurea,11 although only the combination therapy is subsidised by the Pharmaceutical Benefits Scheme. The product information contains a boxed warning for patients with known ischaemic heart disease, particularly those taking nitrates, and highlights the increased risk of myocardial ischaemia found in pooled short-term clinical studies.11 In the US and Europe, rosiglitazone remains available despite the recent media reports. The US product information has similar warnings to those of the Australian version, while the European version has the general recommendation that the drug not be used by patients with ischaemic heart disease and/or peripheral arterial disease. One possible reason why rosiglitazone was not withdrawn in 2007 is that the statistical methods used in the original meta-analysis2 were questionable. Alternative reasonable approaches can yield increased or decreased risks that are either statistically significant or not significant for both myocardial infarction and cardiovascular death.12 As there are no trials with cardiovascular events as the primary endpoint showing benefit of pioglitazone over other therapies, the most compelling evidence for its apparently better cardiovascular profile comes from a similar meta-analysis to that for rosiglitazone.3 A cardiovascular disease outcome study of rosiglitazone versus pioglitazone is, therefore, justifiable and in progress (Thiazolidinedione Intervention with Vitamin D Evaluation [TIDE]; ClinicalTrials.gov NCT00879970). Nevertheless, TIDE might become a casualty of the recently reactivated controversy before it reports in 2015, as the Endocrinologic and Metabolic Drugs Advisory Committee of the US Food and Drug Administration (FDA) continues to review the ethical and clinical implications of the available rosiglitazone safety data. Although the debate about the safety of rosiglitazone has centred on cardiovascular risk, a further potential concern is fracture.13 The deleterious effects of glitazones on bone emerged in animal studies dating back to 1996. Unfortunately, despite knowledge of these data, neither glitazone manufacturer included prespecified bone loss parameters and endpoints in any clinical trial. However, retrospective analyses of data from blood glucose-lowering efficacy trials involving rosiglitazone and pioglitazone, reported in 2006 and 2007, respectively, confirmed an increased fracture risk in humans.13 Given that these drugs have been available in Australia and most other countries for only 10 years, their long-term effect on fracture rates is worrying, especially in postmenopausal women. Glitazone therapy can improve glycaemic control in patients with type 2 diabetes, but patients should be selected according to drug-specific contraindications and warnings, the glycaemic effect should be reviewed after at least 3 months to confirm response, and adverse effects including weight gain, fluid retention and reduced bone density should be monitored during continued use. The recent adverse publicity regarding rosiglitazone highlights issues that can arise when drugs are approved and marketed without definitive efficacy and safety data. There is a need for pharmaceutical companies, academia and regulatory authorities to use preclinical and early phase clinical data to identify, through careful phenotyping, the patient population with the most potential for benefit and the least potential for harm when new drugs are being evaluated for registration. One important consequence of the rosiglitazone controversy is that adequately powered Phase IV cardiovascular safety studies are now required by the FDA when new therapies for diabetes are registered.3 The promise of the glitazones was that they targeted one of the central pathophysiological defects in type 2 diabetes, namely insulin resistance, and improved markers of cardiovascular risk including serum C-reactive protein and microalbuminuria. Unfortunately, based on a variety of clinical trials and observational studies, they do not appear to have a consistent cardiovascular advantage over established blood glucose-lowering agents, including metformin and sulfonylureas.

Timothy M E Davis MB BS, DPhil, FRACP · Johannes B Prins MB BS, PhD, FRACP

It may be time to invest more in primary care research, including research on clinical conditions Here is a simple exercise: in the PubMed website (http://www.ncbi.nlm.nih.gov/pubmed), type “The New England Journal of Medicine[Jour] AND Australia[All Fields]”, and you will see that the journal has published about 90 Australian articles since 2000. Scanning through them, you will find that just one includes an Australian general practitioner as an author (Professor John Marley, in 10th author position), for an article describing the large blood pressure trial ANBP2.1 Repeating this exercise for JAMA (the journal of the American Medical Association) yields one Australian GP author in one of 79 Australian papers (Professor Chris Silagy as first author), in an analysis of protocols of published systematic reviews and reports.2 But what should we expect in the way of research from just one discipline — general practice — in one country? Should we conclude that general practice is not a glittering performer among the medical and health disciplines in Australia, or that it is holding its own? On one hand, it could be argued that general practice is not likely to be the area for such revolutionary discoveries as will command attention from the two most-cited medical journals. We could, instead, think of general practice as the final common pathway for best practice, honed in specialty clinical practice and research. On the other hand, general practice could be described as not only an obvious but perhaps even an indispensable place for research in the areas of health services (ways of delivering care better) and clinical research into diseases encountered in primary care. It may even be a place for basic science research. General practice is where about three-quarters of all medical consultations in Australia take place. The gaps between practice and the best evidence are as wide there as anywhere, and our need for information is urgent.3 On the basis of the numbers of clinicians in the discipline who need information, primary care research output should be the highest compared with the other (smaller) disciplines. But this was not the case a decade ago and is still not the case today, although the situation has improved. A 2001 study, using clinician numbers in the discipline as a denominator, showed that research in the area of internal medicine and surgery in Australia was 60–100 times more productive than that of general practice.4 In addition, general practice research is usually published in journals that are considerably less cited than specialty journals (although a citation index is an imperfect way of measuring research quality).5 The stimulus for a surge in Australian primary care research came from an unexpected quarter. In 1989, the proposal to form a register of GPs, championed by the Royal Australian College of General Practitioners (RACGP), was met with opposition from some non-RACGP-aligned GPs and the Australian Medical Association. The Australian Government referred this political hot potato to the Senate Select Committee on Health Legislation and Health Insurance, which took submissions around the country.6 The Committee noted that little information was available about Australian general practice, and made two recommendations. One recommendation approved the proposed GP register (registration then requiring vocational GP training); the other was for a program of evaluative research to be established, the General Practice Evaluation Program (GPEP).7 This was the predecessor of the current Primary Health Care Research Evaluation and Development (PHCRED) program and, between them, these programs have since been the major sources of funding for Australian general practice research.8,9 Early general practice research was over-reliant on surveys and descriptive studies.7 Intervention studies started soon afterwards, although they were bemoaned as still too few and insufficiently rigorous.10 The subject matter for research has been heavily biased towards health services research at the expense of clinical illnesses, as might be expected from the historical origins of the funding.11 The investment has certainly paid off, lifting the average from one to three publications per 1000 Australian GPs per year over the past decade, with physicians now being “only” 50 times more productive than GPs.12 Primary care research has been criticised for being too “soft” (using qualitative rather than quantitative methods), and it may be true that too many nascent researchers think that qualitative research, or even survey research, will be easier than quantitative research; neither is. However, this is to confuse the mode of research with its purpose, that is, to answer the type of question that is being asked. One must use the right tools for the job. For example, questions about interventions need randomised trials; questions about diagnosis need consecutively enrolled cohort studies; and questions about aetiology need case–control studies. But sometimes a question, particularly in relation to implementation of multistranded interventions, can only be answered by using several methods — “mixed methods” research — to allow for some of the complexities of primary care.13 More important is the question of what to research. It may be time to invest more in primary care research on clinical conditions (Box). There is more uncertainty about clinical conditions managed in primary care than about many conditions managed by specialists, and there is much research to conduct. A useful leaf that we, as GP researchers, should take from the specialists’ book is to work more collaboratively with basic science researchers. A good example of a successful collaboration of this sort is a study about the prevalence of whooping cough in children, which has changed the way we think about persistent cough after apparently trivial acute respiratory infections — might it be due to pertussis? In this study, bench-top scientists worked with GP researchers to generate a rapid and reliable diagnostic test for infection with Bordetella pertussis.15 Now is the time for more investment in primary care research — of any kind. Australian primary care research funding 2000–2010: clinical research items compared with total items14 Funding body Total items funded Clinical research items funded Primary Health Care Research Evaluation and Development* 46 0 National Health and Medical Research Council 166 27 Pharmacy Guild 82 0 Total 294 27 * Since 2003.

Christopher B Del Mar MB BChir, FRACGP, MD · Mieke L van Driel MD, PhD

Will it bring about real behavioural change in general practice? Achieving high-quality and cost-effective care for those with chronic disease requires changes in the behaviour of both doctors and patients. In the past, fragmented policy has led to fragmented management of chronic disease, and there is now an opportunity for change. A new payment scheme for the care of people with diabetes, proposed as part of the federal government’s National Health and Hospitals Network, is centred on patients voluntarily enrolling with a practice and general practitioners being paid in a way that changes their behaviour.1 The proposal is worth $449.2 million over 4 years or up to $10 800 annually per practice, and includes a sign-up payment of $1500 per practice, voluntary patient enrolment, capitation payments ($100 per patient) and annual payments of up to $950 per patient linked to “keeping . . . patients healthy and out of hospital”. Although there is evidence that changing the way doctors are paid can influence their clinical decisions, evidence of how such a change affects patients’ health outcomes and quality of care is scarce. Systematic reviews reveal only a handful of well designed studies that provide reasonable evidence of effects of changes to payment systems on both doctors’ behaviour and clinical outcomes, although recent evaluation of the Service Incentive Payment (SIP) for care of patients with diabetes showed positive outcomes, including an impressive improvement in the appropriate use of glycated haemoglobin (HbA1c) testing.2,3 The first challenge to the supremacy of fee-for-service in general practice remuneration for patient care came with the introduction of the Practice Incentive Program (PIP) in 1998. The PIP has always involved a form of capitation payment and, since 2001, has included “pay for performance” for diabetes and asthma management, cervical screening and (until 2005) mental health care. PIP payments take the form of SIPs and, for treatment of diabetes, are based on completing cycles of care for at least 20% of the practice’s patients with diabetes. So how might these changes in payment affect the way GPs deliver diabetes care and the outcomes achieved? How will the new payments relate to existing programs and will the scheme extend the role of practice nurses? First, patient registration has the potential to strengthen the relationship between doctors and the populations they serve. There is good evidence that continuity of care improves patient outcomes,4 especially for those with diabetes. However, limiting registration to specific groups of patients is a piecemeal approach and inefficient. Voluntary registration for all chronic diseases that require longitudinal care would seem a better way forward. Other questions remain to be resolved. What is in it for patients? Will they appreciate the benefits of more intensive diabetes care? For GPs, participation is limited to accredited practices. Presumably, those already claiming payment through the cycles of care program for diabetes will participate — but will their behaviour actually change? Will new doctors be drawn into this scheme? A key concern is the role of capitation payment. Payments based on patient counts could induce general practices to include in the scheme only those patients whose diabetes is already well controlled, and practices with disadvantaged populations, where treatment is more difficult, may be less likely to participate. However, given that the scheme’s capitation payment of $100 per patient is provided in addition to existing fee-for-service and pay for performance, then incentives for opportunistic selection of patients may be less (depending on the relative size of the performance payments). Care must be taken to avoid opportunities for gaming and other unintended consequences. Second, the scheme’s authors have not detailed the role of pay for performance. The scheme provides an opportunity to pay for outcomes rather than inputs. Paying for improvements in outcomes, rather than for meeting a specified threshold, should be a key element to encourage participation of practices with currently low outcomes of care for diabetes. But how should performance be measured? The cycles of care programs have the advantage of using Medicare data and not adding to GPs’ burden of data reporting. However, the new scheme, by requiring improvements in HbA1c, blood pressure or serum lipid levels to be measured, will rely on practice-level data. The reporting of data by GPs has proved to be feasible through the Australian Primary Care Collaboratives Program and in standard general practice, but often requires further investment in information technology.5 Third, is the $449.2 million new money or a re-use of the diabetes SIP money? If the latter, and if those currently claiming SIPs move over to the new scheme, then behaviour may not change and quality of care may not improve. There are multiple sources of financing, such as the Enhanced Primary Care items for chronic disease and team-care arrangements. Will these be discontinued and funding redirected into this new scheme? Multiple funding sources create red tape and confusion, further limiting the likelihood of behaviour change. Fourth, team-based care and the role of nurses have been given a boost with $390 million for the direct employment of 4600 practice nurses. Although the numbers of practice nurses have been growing rapidly,6 their roles have been limited to existing Medicare items. Direct salary support will enable practices to use their nurses’ skills flexibly and fully, including skills in diabetes care.7,8 However, nurses should also be given equitable shares of performance pay, if teams are to function effectively.9 Using management of diabetes as a test case for this new model of funding patient care is welcome, but as with all test cases, careful evaluation is required before the model is expanded. Evaluation should be a priority from the time the scheme is introduced. The most important question is whether the new scheme will be able to drive real behavioural change among primary care teams and patients, rather than being just another way of delivering funding to those already doing a good job.

Doris Young MB BS, MD, FRACGP · Anthony Scott BA(Hons), MSc, PhD · James D Best MD, FRACP, FRCPath

Despite significant investment in e-health, practical outcomes are yet to be realised In classical Fabian tradition, the federal Labor government has embarked on a series of reforms that will have an impact on the welfare of “Australian working families”. The rationale for the health reforms1 has been exhaustively detailed in the reports of the National Health and Hospitals Reform Commission2 and the taskforces on the National Preventative Health Strategy3 and National Primary Health Care Strategy.4 A significant and unifying theme in all these blueprints for health reform is the centrality and crucial involvement of general practice in achieving change. Indeed, these reforms would come to nothing without the willing acceptance and widespread cooperation of general practitioners. In this special General Practice issue of the Journal, Kidd summarises the reform schedules for general practice (page 71).5 However, there is mounting evidence that GPs are already experiencing difficulties meeting the constant and ever-changing demands placed on their practices, as illustrated on the cover of this issue. To impose yet another structural reform agenda in an already chaotic environment will be a monumental challenge. Generally speaking, reform is more readily acceptable if it: lessens rather than increases the workload; improves the efficiency and effectiveness of tasks; increases the quality and safety of services; and provides tangible incentives for participants. Without a doubt, a major source of frustration and consternation with the federal government’s reform agenda is the very clear sense that it is essentially a top-down approach, rather than a bottom-up consultative process. In fact, if there were to be a national poll of GPs ranking current health reform initiatives, “e-health” — the use of digital data transmitted, stored and retrieved electronically in support of health care6 — would definitely emerge as a major priority. Such information technology infrastructure is crucial to all health care communication in the 21st century but, to date, all we have achieved in Australia has been to indulge in expensive and time-consuming chatter. We have been talking the talk but not walking the walk! It must be acknowledged that e-health has been on the federal government’s agenda for more than a decade. In 2000–01, the then Health Minister, Michael Wooldridge, announced the planned development of HealthConnect — a national system of e-health records that could be shared over secure networks with strict privacy and consent controls.7,8 The system was trialled in pilot studies across the country and, in March 2004, the government allocated $128 million for national implementation.8 But then, in 2005, Health Minister Tony Abbott (now leader of the federal Opposition) pulled the plug on HealthConnect.7 Around the same time, the federal, state and territory governments established the National E-Health Transition Authority (NEHTA), with a clear purpose: to lead the uptake of e-health systems of national significance; and to coordinate the progression and accelerate the adoption of e-health by delivering urgently needed integration infrastructure and standards for health information.9 Since its inception in July 2005, NEHTA has been spending just under $164 000 a day.7 It is yet to deliver any e-health outcomes beyond a 2009–2012 strategic plan and the development of a national health care identifier system that was recently ratified by the Australian Government.10 In May this year, the federal government allocated NEHTA a further $466.7 million over 2 years, ostensibly to fund development of core national standards and tools that can provide all Australians with access to a personally controlled electronic health record from 2012–13. The federal government will thus spend $639 315 each day on the implementation of personally controlled electronic health records.7 Despite this, vigorous debate is ongoing as to who will actually control the records! Confusion reigns. It must be remembered that the realisation of e-health infrastructure in Australia is underpinned by taxpayers. Whether it will ever produce a functional electronic communication and record system, which actually improves health care delivery, is the million-dollar question.

Martin B Van Der Weyden MD, FRACP, FRCPA

A major change in medical teaching practices is needed to improve patient safety The Lucien Leape Institute, in Boston, USA, was formed in 2007 to provide a strategic vision for improving patient safety, and is composed of national “thought leaders” (http://www.npsf.org/lli/). The Institute has produced a report on the urgent need to reform medical education,1 and states that many believe we are at a transformational moment similar to that which led to the profound changes in medical education following the release of the Flexner report in the United States 100 years ago.2 It is a decade since the release of national reports on patient safety that triggered a wake-up call,3-5 and 15 years since the publication of the Quality in Australian Health Care study.6 However, progress has been much slower than we would have liked. System-based changes, although desirable and necessary, have not done the job of improving patient safety. Although there have been some notable successes and high-profile champions of safety, we are unable to measure progress or to reassure patients that they will receive safe, high-quality care.7,8 It’s time to turn to those who will actually provide the health care to the patients of the future. Health care is characterised by islands of excellence in a sea of mediocrity, and it is into this sea that our new health sciences graduates are launched. By the time of graduation, most will have been exposed to enough facts and figures about health care-associated harm to find them alarming, and most will have sufficient insight into the dysfunctional nature of “the system” to feel apprehensive about their preparedness for the voyage ahead of them.9 The good news is that the actual delivery of health care takes place at the interface between individual health care professionals and patients (and their carers).9 Although this is where the final link in a chain of errors may be forged, it is also where constant vigilance and attention to detail by both individuals and members of multidisciplinary teams can ensure, on a daily basis, that what needs to happen, does in fact happen.10 Much is said about clinical autonomy, and daily interaction is the sphere in which individual medical and nursing clinicians can have a massive impact on “getting it right”.9 But clinical interaction must be from the perspective of the patient, and in line with best practice, not with old habits, new fashions or outdated dictates from an incumbent hierarchy. Structured, evidence-based care plans provide transparency and allow all team members to monitor patient compliance with treatment, and intervene when necessary. James Reason, who has written extensively on error and safety, has exhorted us to celebrate the remarkable capacity of individual team members to continuously turn potential adverse events into “near misses” in high-risk systems.10 Although altruistic, well intentioned young graduates are forced by the system into moulds and practices they may not like, and over which they have little control, the majority will, against considerable odds, manage to provide high-quality, patient-centred care. However, they could and should be better equipped for the formidable tasks they face. Most new graduates are well equipped to deal with the technical aspects of health care, and are well mentored in these by their seniors,1 but transformational change is needed to produce a new generation of clinicians endowed with a proper understanding of what is wrong. They need to be equipped with non-technical skills such as situation awareness, communication techniques, empathy and graded assertiveness,9 and to be imbued with an understanding that real change is urgently needed and must come from them. The 12 recommendations for transformational change made by the Leape report1 are paraphrased here. The first four address the organisational context, recommending that leaders in medical teaching should: place the highest priority on creating learning cultures that emphasise patient safety; launch a broad effort to promote the development and display of the necessary personal attributes, such as professionalism, collaborative behaviour and transparency; provide incentives and resources to support this effort; and place greater emphasis on screening prospective students for the appropriate attributes. The next three recommendations in the report are about strategies for teaching patient safety, recommending that: patient safety be treated as a science; the shaping of the desired skills, attitudes and behaviours becomes an integral part of the core competencies required by accreditation bodies; and patient safety education becomes a life-long process. The final five recommendations deal with strategies to “leverage acceleration of the desired changes” so as to: modify accreditation standards so that these become curricular requirements, with required competencies at graduation; expand program requirements in postgraduate training programs; direct attention to safety-related preparation of graduates entering clinical training; ensure that medical schools are evaluated with respect to their performance in these areas; and establish incentives to achieve these changes. Health sciences students in Australia are now variously exposed to teaching about systems thinking, interprofessional learning, human error, incident reporting and open disclosure. This is a good start, but an evident lack of system-wide progress, and the robust homeostatic mechanisms that tend to maintain the system’s status quo, show that more than this is needed. Patient safety is not just another technical problem to be added to the curriculum. It is a serious, enormously costly, multidimensional problem8 that can only be addressed by transformational change in the attitudes and behaviours of the people who will be in a position to dictate how medicine will be practised1 where it matters: at the interface between them and the patients of the future.9

William B Runciman PhD, FANZCA, FJFICM

PSA testing may lead to overtreatment, but this should not rule out its judicious use as an early predictor of prostate cancer Two recent articles, an opinion piece from Richard Ablin, the discoverer of prostate-specific antigen (PSA) and a self-proclaimed “authority in the field”, published in the New York Times,1 and a subsequent interview with Ablin published in the BMJ,2 contend to inform the public of the “hugely expensive public health disaster” of PSA testing. Yes, PSA testing is not without its flaws, but to malign it in this manner is truly lamentable. Before 1980, there was no diagnostic test for prostate cancer; there was no effective radiation therapy; there was no safe surgery, and the only option for most men with prostate cancer was to have their testes removed — surgical castration. Most men, of course, feel quite attached to their testes, and castration carries myriad physical and psychological side effects. A common emergency department presentation at that time was acute paraplegia due to prostate cancer metastatic lumbar spine cord compression.3 This is a rare presentation in 2010. Since the introduction of PSA testing in the 1980s, we have seen a 25% reduction in mortality from prostate cancer; stage migration means 80% of men now present with localised, either small-volume or advanced, prostate cancer.4 Because the PSA test facilitates early diagnosis, most men with prostate cancer are diagnosed with a lead time of about 9 years before the onset of metastatic disease.5 The contention, however, is that the PSA test is a poor screening tool; and this is reasonable, because we ask far too much of a single blood test. The PSA test will not differentiate between aggressive and indolent prostate cancer. Furthermore, after the onset of benign prostatic hyperplasia (BPH) in men from about 45 years of age, background noise due to BPH reduces the sensitivity of the PSA test at PSA levels below 10 ng/mL, although a PSA level above 10 ng/mL is still very indicative of the presence of prostate cancer. The key problem facing health professionals dealing with prostate cancer can be readily articulated: it is the inability to discriminate between aggressive and indolent prostate cancer. It is acknowledged that, while PSA testing has led to greatly reduced mortality, its widespread use has also led to greatly increased detection of prostate cancers, many of which will not prove to be life-threatening.6 This has led to considerable overtreatment of indolent prostate cancer by surgery and radiation therapy, although increased use of active surveillance has demonstrated that clinicians are being more considered when counselling men about their management options.7 What if we were to use PSA testing in a more judicious and targeted manner so that men could have a single test before the onset of BPH? Swedish researchers have elegantly shown that the effect of benign transition zone-related PSA levels can be eliminated by testing all men at baseline before the development of BPH. In a study of a large cohort of men in Malmö, Sweden, PSA levels in men below the age of 45 years reliably predicted the development of significant prostate cancer up to 25 years later.8 Between 1974 and 1986, 21 000 Swedish men aged under 45 years provided blood samples as part of a cardiovascular study. At the end of 1999, participants who had developed prostate cancer were identified using Swedish Cancer Registry data. PSA level at 45 years of age was found to be a very strong predictor of prostate cancer being diagnosed up to 25 years later, with an area under the receiver operating characteristic curve of 0.76 (signifying high discriminatory ability). PSA levels between 2 and 3 ng/mL (which are often cited as being within the normal range) were associated with a more than 19-fold increased risk of subsequent prostate cancer development. The researchers went on to show that 80% of advanced cancers (stages T3, T4 and metastatic at diagnosis) occurred in men who had had PSA levels above the median when tested at age 44–50 years.9 This study suggests that we could use a single PSA level as a predictor for the long-term risk of prostate cancer in younger men around the age of 45 years. This supports the advice from the Urological Society of Australia and New Zealand and the American Urological Association that men aged 40 years should have the merits of a PSA test discussed with them. Those with a PSA level well below the median for men in their 40s of about 0.6 ng/mL5 (the vast majority at this stage) could be reassured that they are at very low risk of developing prostate cancer and advised to have another test 5 or 10 years later. The nihilistic musings of Ablin do nothing to help inform a rational policy towards the early detection of prostate cancer. Rather than dispense with a test that has contributed significantly to the reduction in mortality from prostate cancer over the past 30 years, and while we wait for better biomarkers in the future, we should instead advocate a more discriminating use of PSA testing.10

Anthony J Costello MB BS, FRACS · Declan G Murphy MB, FRCS Urol

Vaccine scares are inevitable and we need to plan accordingly Twelve years after The Lancet published the study by Wakefield and colleagues1 that suggested a link between measles–mumps–rubella (MMR) vaccination, inflammatory bowel disease and autism, the journal has fully retracted the article. The retraction followed the findings of the Fitness to Practise Panel of the UK General Medical Council, released 28 January 2010, that certain statements in the article were false — namely, that children were “consecutively referred” and that investigations were “approved” by the local ethics committee.2 Wakefield’s theory had a significant impact on MMR vaccination rates in the United Kingdom. Looking at why Australia was relatively unaffected provides insights into how to better manage vaccine scares in the future. After publication of the article, many readers had written without delay to The Lancet regarding methodological deficiencies of the original research.3 Subsequent studies overwhelmingly supported the safety of MMR vaccination, but the accumulation of this evidence took years to achieve, with considerable opportunity costs, including time and resources spent on investigations which could have been better directed elsewhere.4 In the UK, the MMR vaccination rate fell from 91% in 1997–98 to 80% in 2003–04.5 Notably, there has been no decline in coverage for other vaccines for children in the UK. Despite a recovery in the MMR vaccination rate to 85% by 2008–09,5 there was a large upsurge in measles occurrences in the UK, beginning in 2002.6 In 2009, 1144 laboratory-confirmed measles cases were reported in England and Wales.6 The impact was also felt in the United States, where Wakefield’s theory augmented unsubstantiated fears about thiomersal (a mercury-based preservative) in some vaccines leading to autism. A recent survey found that one in four US parents believed that some vaccines cause autism in healthy children.7 Vaccine scares are typically depicted as conflicts between science and dogma; between the informed and the misinformed.8 The publication of Wakefield et al’s article in The Lancet breached the boundary between the two: here was a well credentialled specialist at a highly regarded teaching hospital whose findings were published in a renowned journal. These signifiers of prestige may have overshadowed the relatively poor quality of the science in the original article. Fortunately, in the years since the article was published, Australia’s MMR vaccine uptake has been relatively stable, as measured by the Australian Childhood Immunisation Register9 (Box). However, there were other consequences of Wakefield et al’s article, including the time and resources needed to address parents’ concerns.11 Some health professionals appeared to accept Wakefield’s theory. A 2006 survey of doctor and nurse vaccination providers in regional New South Wales found that 12% believed there was an association between MMR and autism, with a further 29% being unsure.11 Despite this, Australian MMR coverage remained essentially unaffected. The fact that Australian MMR vaccination rates remained stable may be related to some key differences between Australia and the UK: (i) in Wakefield, the UK had a “home-grown champion” for the MMR–autism theory; (ii) the extensive and sustained coverage of this issue in the UK media continually exposed new cohorts of parents of MMR-eligible children to the theory, while Australian television only sporadically reported the story; (iii) there is bipartisan political support for immunisation in Australia, whereas there was grandstanding by a member of the UK Conservative opposition and a refusal by the nation’s Labour Prime Minister to reveal whether his own son was immunised;12 and (iv) a foundation of mistrust in UK government assurances was perpetuated by public perceptions of the management of the Creutzfeldt–Jakob disease issue.13 The child vaccination program is held in high regard by most Australians, and, for this reason, the media have traditionally sidelined our small but vocal antivaccination lobby. This high level of public confidence has been helped by the structural support originating from the first National Immunisation Strategy in 1993, followed in 1997 by the federal Immunise Australia: Seven Point Plan, including financial incentives for parents and providers to adhere to the national vaccination schedule.14 What can the world learn from the Wakefield experience? First, we should accept vaccine scares as inevitable and plan accordingly. There remains the potential for vaccine safety scares to lead to large-scale opting out of vaccination, exacerbated by dwindling familiarity with the severe effects of vaccine-preventable diseases, and a groundswell of dissent from the antivaccination movement. Second, public communication about vaccine risk, particularly regarding responses to adverse events following vaccination in new vaccine programs, needs to be planned, and should involve multiple stakeholders, as new issues can arise with little warning. This occurred as recently as 23 April 2010, when Australia’s Chief Medical Officer advised a temporary suspension of the 2010 trivalent seasonal influenza vaccine to children 5 years of age and under.15 This suspension followed an increase in febrile convulsions among young child vaccine recipients reported in Western Australia. Third, the current level of trust in vaccine programs that we enjoy in Australia is a precious resource and must be continually fostered with good communication. Such communication is more than a didactic one-way process — it requires an interactive engagement between professionals, the public and the media. Clearly, this will be important and challenging after the recent suspension of the trivalent influenza vaccine, because professional and public concern generated by this suspension could spread to concern about influenza vaccination for other age groups.16 Australian federal, state and territory governments are now developing a new national vaccination strategy. Essential considerations in this strategy will be how the postmarketing surveillance of adverse events following vaccination is to be conducted, and authoritative and timely communication about vaccine safety with professionals and the public. MMR, DTP, OPV, Hib and hepatitis B vaccine coverage for Australian children at 24 months of age, 2000 to 2009*10 MMR = measles–mumps–rubella. DTP = diphtheria–tetanus–pertussis. OPV = oral polio vaccine. Hib = Haemophilus influenzae type b. Hep B = hepatitis B. * Figure updated with 2008–2009 data (Brynley Hull, Epidemiologist, National Centre for Immunisation Research and Surveillance, personal communication).

Julie Leask PhD, MPH, DipAppSci · Robert Booy MD, FRACP, FRCPCH · Peter B McIntyre PhD, FRACP, FAFPHM

A simplified revision of the uniform conflict of interest disclosure form is now available The great variability in the processes that different journals use to ask about and report authors’ potential conflicts of interest creates confusion for authors, readers and the public. To help lessen this confusion, the International Committee of Medical Journal Editors (ICMJE) developed an electronic uniform disclosure form and placed it in the public domain in October 2009. The ICMJE member journals piloted the form, encouraged other journals to use it, and invited feedback. We recognised that the reporting of competing interests is complex and nuanced and sometimes contentious, and thus anticipated modifying the form based on feedback received. We are grateful to the many authors, editors and other interested parties who took the time to comment on the form and its implementation. The issues raised ranged from technical problems about the correct deployment of the form (it requires the user to download version 8.0 or higher of the free Adobe Reader software to function) to concerns about the ethics of inquiring about non-financial associations. The Committee considered these valuable comments and revised the form at our most recent meeting. We made several modifications. The major change in the reporting instrument is the removal of the queries about potential competing interests of authors’ spouses and minor children and about non-financial competing interests. We made this change based on the largely negative feedback that we received about these sections. People who commented about this issue made it clear that there is immense difficulty in defining competing interests beyond those that involve the direct exchange of money from an interested party to an individual author or the author’s institution. Because the Committee continues to believe that there are situations in which indirect or non-financial factors could influence (or appear to influence) the conduct or interpretation of work, we replaced the specific questions with a single open-ended query (new Section 4) that asks, “Are there other relationships or activities that readers could perceive to have influenced, or that give the appearance of potentially influencing, what you wrote in the submitted work?” This change places the onus on the person completing the form to identify and report appropriate non-financial competing interests. It has the advantage of being less intrusive than the previous queries, while providing a locus where authors can report non-financial relationships that may be perceived as potential conflicts of interest. In response to comments about the clarity of the form, each field in the form now has a numeric designation. We have modified the language in the instructions and in the individual queries. To make the form more useful to non-native English speakers, we are creating a glossary of terms used in the form and will be posting guidelines for translation of the form’s instructions into multiple languages. The translation of this form is particularly challenging because translations must capture the essence of the queries rather than their literal meaning. The glossary and guidelines will be available at the ICMJE website (http://www.icmje.org) in the next few months; translations will be posted on the ICMJE website as they become available. The new form, in English, is currently available on the ICMJE website and the websites of our member journals. Authors who have completed the older version of the form in conjunction with a journal submission need not complete the new form, but the new form will be the standard for new submissions. We welcome continued input from the user community. Comments can be sent via the “Contact ICMJE” link at the ICMJE website. The Committee will consider comments received before 1 May 2011 when we prepare the next iteration of the uniform conflict of interest disclosure form. The complexity, subjectivity and emotionality of conflict disclosure assures that some will consider this vehicle for reporting to be excessively burdensome, while others will think it falls short in one area or another. We cannot, however, let the perfect be the enemy of the good. We hope that the revised ICMJE form will be another step towards simplifying and standardising reporting of conflicts of interest. A more uniform reporting process will alleviate the confusion that prevails when multiple journals use different reporting formats, and will ease the reporting burden on members of the biomedical research community, so they can pursue the research that will improve the care that we deliver to our patients. With these thoughts in mind, we encourage all journals to adopt the new version of the uniform disclosure form.

Jeffrey M Drazen MD · Peter W de Leeuw MD, PhD · Christine Laine MD, MPH · Cynthia Mulrow MD, MSc · Catherine D DeAngelis MD, MPH · Frank A Frizelle MB ChB · Fiona Godlee MB BChir, BSc · Charlotte Haug MD, PhD, MSc · Paul C Hébert MS, MHSc · Astrid James MB · Sheldon Kotzin MLS · Ana Marusic MD, PhD · Humberto Reyes MD · Jacob Rosenberg MD, DSc · Peush Sahni MS, PhD · Martin B Van Der Weyden MD · Getu Zhaori MD

Family history has a role, but who should be responsible for exploring and recording it? The increasing age, number and comorbidities of hospital inpatients has increased the load on emergency departments and necessitated significant redesign, including the introduction of short-stay and medical assessment units. These units are diverse in their casemix, but common factors include higher acuity of illness and expedited discharge. Obtaining a complete history of a patient’s acute illness and longstanding comorbidities, as well as his or her social and psychological issues, represents the ideal standard of care. Obviously, however, there are tensions between providing holistic care and continuity of care to the patient and achieving the rapid turnover required in such units. Genetic markers and tests are increasingly available for an expanding range of conditions. Genetic counselling has moved from specialised clinics into the mainstream practice of many disciplines. The inheritance of disease is rarely a simple algorithm, and these new genetic tools provide complexity rather than clear direction. Relevant guidelines are uncommon outside cancer medicine. Family history is a frequent criterion for determining further genetic testing. For example, the Amsterdam criteria for diagnosis of hereditary non-polyposis colorectal cancer (HNPCC) include a family history of at least three relatives with HNPCC-associated cancer.1 There can be harm in failing to interpret genetic tests correctly, and the complexity of many conditions demands a high level of knowledge. “Genetic literacy” is a term that has been used to describe competence in this area.2 However, it seems unreasonable to expect all doctors to be skilful at all times in eliciting and interpreting the family history and then appropriately counselling and testing each patient. Family history is an older tool than genetic testing and is poorly defined, applied and understood.3 Even now, there is not enough evidence to gauge its reliability and role.4 The family history can aid stratification of a patient’s risk of heritable conditions, and it has diagnostic utility for disorders with classic Mendelian inheritance, but it may be less useful in disorders with multifactorial inheritance or more complex genetic expression. In this issue of the Journal Langlands and colleagues report that family history is not recorded in the case notes of most medical short-stay patients.5 They argue that a family history offers potential health gains for the patient and relatives and suggest that there should be increased focus on this element of the medical history. However, this seems unrealistic in the context of increased workload and time pressures, particularly in a hospital short-stay unit. The acute admission is not an ideal setting for detailed and accurate history taking; patients are usually unwell and access to their family is compromised. The family history recorded is often inaccurate4 or misleading, not only because the level of health literacy among patients is variable but also because familial clustering is not distinguished from heritable disease. The accuracy of reporting of family history is rarely studied, but it has been shown that it can be poor in patients with cancer4 or cardiovascular disease.6 The primary care setting affords better opportunities to explore and record family history and to make adjustments after clarification with relatives. Certain conditions (eg, malignant hyperthermia, Huntington disease) drive consideration of genetic testing of the affected individual and sometimes lead to testing of family members. The counselling required should form part of an ongoing relationship with the patient and family. As Langlands and colleagues state,5 the family history may be a casualty of increasing numbers of acute hospital admissions. Perhaps it is a justifiable casualty in the acute health care environment, as long as information is elicited accurately afterwards. Ideally, a patient should have his or her acute illness diagnosed and managed within the acute admission, with a clear plan then delineated for follow-up, which includes notification of those who will be responsible for doing so. It is important to have a use for any family history information once it is accurately obtained. In future, the acquisition of a family history must embrace the developments in our understanding of genetic disease. Without diminishing the role of specialised genetic units, primary care clinicians and specialists in chronic care will need to assume greater responsibility for exploring family history. Screening assessments can identify those requiring a more comprehensive review. We would argue that, under present circumstances and with doubt hanging over its sensitivity, specificity and effect on health outcomes,3,4 the family history is a justifiable omission from many acute hospital admissions. The concept of holistic care is a noble one and, if we are to work within a new paradigm of shorter hospital inpatient stays, we will need to develop a strategy for preserving this concept. Certain diseases, such as unprovoked venous thromboembolism, should trigger an immediate focus on family history, but a routine family history is best ascertained when people are not acutely unwell. If we are serious about disease prevention and the role of genetics in modern medical management, more guidance is needed in terms of which patient groups will benefit from genetic testing and how any positive results will be managed. An integrated approach should include guidance for screening that is based on a better defined family history that has been obtained in the non-acute setting. This approach requires protocols for disease-specific genetic testing and specialist referrals for further assessment and management. A recent National Institutes of Health conference offers hope in this regard.3

Josephine S Thomas BM BS, FRACGP, FRACP · Campbell H Thompson DPhil, FRACP, MD

It is time to reconsider the clinical benefits arising from family history and start making better use of it A patient’s family history may aid clinical diagnosis and contribute to disease risk assessment and prediction. It frequently yields valuable social history, including information about family support structures and insights into individual beliefs about illness.1 Although taking family history is traditionally regarded as a routine part of the medical history, it is not used in a systematic way in clinical practice. In this issue of the Journal, Langlands and colleagues report the results of an audit in an Australian teaching hospital, which found that nearly three-quarters of patients admitted to a short-stay medical unit had no documentation of family history having been considered as part of the diagnostic assessment.2 A similar situation exists in primary care. Although there are no published comparable data from Australian general practice, a primary care study in the United States found that only 16% of subjects (n = 362) had any record of their family history in their clinical chart, including 15 individuals at high risk of an inherited cancer syndrome.3 Internationally, there is growing recognition that a family medical history can support tailored disease prevention, which may be more effective than existing approaches.4 This is also reflected in the Australian Medicare-funded adult health assessment for people aged 45–49 years at risk of developing chronic disease, which specifically includes assessment of the family history of chronic diseases such as diabetes and cardiovascular disease. Family history can also inform the formulation and weighting of differential diagnoses in presentations for a range of common conditions. The risk of many serious diseases is increased in the presence of a family history of the disorder, representing not only shared genetic factors but also environmental and behavioural exposures. For example, the relative risk of breast cancer is 1.4 times higher for women aged 60 years or older if they have a first-degree relative diagnosed with the disease after the age of 60 years; this risk is more than five times higher for women younger than 40 years with a first-degree relative diagnosed before the age of 40.5 Eleven per cent of women with breast cancer have a first-degree relative with the disease. The relative risk of colorectal cancer for a 50-year-old is increased from around twofold with one affected first-degree relative to almost fourfold in people with at least two affected first-degree relatives.6 About 15%–20% of people with colorectal cancer have an affected first-degree relative. In a US population-based study, 14% of the population had a family history of ischaemic heart disease, but these people accounted for 72% of early ischaemic heart disease and 48% of all cases of the disease.7 A parental history of type 2 diabetes is associated with a relative risk of 2.2 and a lifetime risk of 40%.8 These familial disease risks should be compared with other traditional risk factors that are routinely screened for in general practice. For instance, isolated hypertension is associated with a relative risk of 1.8 for ischaemic heart disease and is present in 14% of men and 5% of women with a coronary event.9 There are effective interventions for primary and secondary prevention of all these common diseases, ranging from disease surveillance to drug treatments and lifestyle management. There is some evidence that having knowledge of a family history of a specific condition is associated with improved uptake of a range of disease-preventive activities for breast, colorectal and skin cancer.10-12 Therefore, it is possible that identifying people with a family history of disease could act as an additional motivator for them to change their lifestyle or participate in disease screening. Why then do clinicians continue to neglect the family history as part of routine diagnostic assessment and disease prevention? The experienced clinician will know that recording a patient’s family history to assess disease risk ideally requires a three-generation pedigree, but this can take up to 30 minutes, which is unrealistic in most clinical settings. However, not all patients require such a detailed assessment. Simple, self-completed family history screening questionnaires could provide an answer. Several of these already exist, but many are disease-specific and few have been formally tested to determine their screening characteristics.13 Clinicians also cite patients’ uncertainty about their family history as a barrier. However, a systematic review of self-reported family history found high positive predictive values for cancer in first-degree relatives (breast, 93%; prostate, 85%; colon, 81%), although information was less accurate about second-degree relatives (breast, 91%; prostate, 80%; colon, 77%).14 Of course, sometimes the patient’s perception of his or her family history can be just as important as the reality in determining the patient’s risk perception, illness beliefs and likely response to medical advice. Better methods of recording family history are also required, particularly as we move towards an electronic health record in Australia. Tailored clinical software is potentially the most effective tool for recording and updating a patient’s family history, although current clinical software systems do not support the creation of pedigrees. Previous trials have demonstrated the capacity of computerised pedigree tools to improve the assessment of disease risk and identify those individuals who may benefit most from seeing a clinical geneticist.15 However, while clinicians continue to ignore the importance of the family history in diagnosis and risk assessment, software companies have little incentive to integrate family history tools into their systems. Raising awareness among consumers is an alternative approach that may drive clinicians to consider family history more often. A family health history campaign run in New South Wales in 2007 resulted in increased community awareness and discussions about family history within families and between patients and their general practitioners.16 While DNA-based disease risk prediction remains to be proven as an effective clinical tool, family history is a simple but potent tool that is available now for disease prevention. Langlands and colleagues audit findings show that this important element of the clinical history is seldom included in routine patient assessments.2 The family history should not be seen as a relic of medical school teaching; it is time to reconsider the clinical benefits arising from family history and start making better use of it in clinical practice.

Jon D Emery MB BCH, FRACGP, DPhil · Fiona M Walter MB BCh, FRCGP, MD · David Ravine MB BS, MD, FRCPath

The worldwide availability of preventive genetic health information will benefit millions of families In Australia, it has been estimated that around a million people are affected directly or indirectly by inherited disease. An audit of admissions to a major paediatric hospital in the United States showed that, in 71% of admitted children, their condition had a significant genetic component and, of these, 10% had an inherited disease.1 However, inherited diseases have received little attention in health budgets and research grants. One of the reasons is that each of the thousands of different inherited diseases caused by gene mutations is extremely rare and, as a consequence, affected families and clinicians in the field have little voice. Understanding and developing care for people with inherited disease depends on setting up and maintaining databases with information on the incidence, phenotype, penetrance, treatment strategies, and prognosis of these conditions. Gene mutation databases are labour intensive to develop, populate and maintain, but are essential if we are to realise the benefits of the vast amount of genetic data on individuals and populations, both healthy and unhealthy, embedded in the human genome. At present, there is a lack of funds for critical inherited disease registries or databases in Australia and around the world. Without adequate and sustained funding for database set-up and curation, these databases will inevitably harbour data deficiencies and even inaccuracies, which may have serious health consequences. So, what is being done, and what more can be done, to address this deficiency. Several specific databases already exist: Online Mendelian Inheritance in Man (http://www.ncbi.nlm.nih.gov/omim) is a public database of bibliographic information about human genes and genetic disorders;2 the Human Gene Mutation Database (http://www.hgmd.cf.ac.uk/ac/index.php) collects data on published germline mutations in nuclear genes underlying human inherited disease;3 the National Center for Biotechnology Information (http://www.ncbi.nlm.nih.gov/) provides access to biomedical and genomic information;4 and there are over a thousand genes in locus-specific databases (http://www.hgvs.org/dblist/glsdb.html).5 However, all these excellent activities are insufficient to meet the rapidly emerging need to document all mutations in all genes, which would allow interpretation of the human genomic sequences available from diagnostic, research and, increasingly, commercial sources. At a gathering of experts in human genetics in 2006, the Human Variome Project (www.humanvariomeproject.org) was created to fulfil this need.6-8 This project aims to facilitate “the establishment and maintenance of standards, systems and infrastructure for the worldwide collection and sharing of all genetic variations effecting human disease”. It is working towards the comprehensive collection of genetic information from all sources, ensuring data accuracy, making the information freely available and, at the same time, developing standards to achieve these goals. Critical collaborative projects are underway to define protocols that can be readily extended to all genes and to all countries. The Human Variome Project has initiated two pilot studies that will act as models for global collection of all gene mutations and their effects. The first involves the International Society for Gastrointestinal Hereditary Tumours (InSiGHT; http://www.insight-group.org), the peak international body of health care professionals caring for families with inherited gastrointestinal cancer. InSiGHT maintains a database of mutations in the mismatch repair genes responsible for Lynch syndrome (hereditary non-polyposis colorectal cancer syndrome). InSiGHT has established governance, curation, interpretation, phenotype, functional assay, and histopathology subcommittees to support its database, aiding in ensuring integrity of the data, controlling access for bona fide use, and encouraging submissions of variants from individual laboratories and national data collections. Since engaging with the Human Variome Project, and learning of its experience in locus-specific database management, InSiGHT has increased its variant submissions from 550 to over 11 000, and attracts over 20 000 website “hits” per month, strongly affirming its value to the scientific community. Obtaining funding for this critically important database has been difficult, but full credit needs to go to the Cancer Council Victoria, the Victorian Cancer Agency and, most importantly, to the George Hicks Foundation, for grasping an important leadership opportunity. The second pilot study is being conducted by the Australian Node of the Human Variome Project, which is developing a country-specific system as a model for other countries, where possible using freely available software and data management systems.9 While several countries have collected mutation data for their population, there are no unified collection standards and no links to other international efforts. This project, funded by the Australian Government’s National eResearch Architecture Taskforce (NeAT) (https://www.pfc.org.au/bin/view/Main/NeAT), will address this deficiency. It is in the early- to mid-phase of its work, and trials in two laboratories are expected to take place by the end of 2010. Examples of the potential future uses of a complete list of mutations causing human disease are given in the Box. In brief, the possibilities for preventing or otherwise reducing suffering from disease opened up by the Human Variome Project will benefit individuals, as well as reduce the burden of global health care budgets. The main limitations to achieving the aims of the Human Variome Project are the speed of development and the spread of systems for countries, genes and disease groups; capitalising on these developments is, and will be, dependent on funding. Funding is needed for efforts to collect disease- or gene-specific data and data for individual countries, but the benefits for each country’s health care budget should more than offset the necessary initial outlay. The fact that genetic data are not in a single repository means that expensive professional time is spent “surfing” the web to look for previous examples of a particular mutation, or proper care cannot be given because vital data are buried in hospital files. Funding and recognition of the global Human Variome Project’s key coordinating role has been problematic due to it “falling through the cracks” of existing funding mechanisms. However, this situation is changing, with recognition by the World Health Organization in 2006, and UNESCO in 2010, which hosted the third Human Variome Project meeting at its headquarters in Paris, 10–14 May 2010. The pilot studies and the clear clinical need support the case for funding. It should be remembered that genetics has allowed medical testing to predict outcomes for patients and families contributing to prevention. Past, current and future support will ensure cost-effective, translational and preventive personal genetic health care worldwide, which will benefit millions of families. Future uses of a complete list of mutations causing human disease, as envisaged by the Human Variome Project Individuals (or their advisers) will be able to search their genome sequence for variations. If a variation is found, it can be compared with the complete catalogue of mutations to determine whether it is harmful. Examples include: a variation in a colon cancer gene — if harmful, preventive screening can be instituted; or a variation in the glaucoma gene in a person whose grandfather went blind at age 57 — preventive therapy can be instituted. When two individuals are planning to have children, they will be able to compare their genome sequences with the complete catalogue of mutations and their effects. They might be told that they both have a serious defect in, for example, the gene locus responsible for maple syrup urine disease, and advised to consult a genetic counsellor. This type of use has precedents in the premarital testing for the globin gene causing thalassaemia in the Mediterranean area, particularly in Cyprus. This has resulted in almost complete elimination of this disease through family planning. The ethnic-specific mutations in the Ashkenazi Jewish population are well known. When an individual has a specific disease, defining the mutation in a number of specific genes costs around $50, compared with several thousand dollars when the whole gene in question has to be sequenced. Lists of mutations in genes in all ethnic groups will allow definition of the most common mutations in each group.

Richard G H Cotton AM, BAgSc, PhD, DSc · Finlay A Macrae MB BS(Hons), MD, FRACP

New data bring to a close Australia’s most intensive cancer cluster investigation Though only a small proportion of cancer clusters are reported in the peer-reviewed literature, a consistent picture emerges from those reports. The term “cancer cluster” refers to health authorities being alerted to a perceived increased incidence of cancer, involving 15 cases or fewer in the first instance, within a particular community or group. Aware of the anxiety generated by the prospect of a cancer cluster, cluster investigators focus on local circumstances that might account for increased risk, and if they fail to identify any such factors, the matter rests.1 The report by Sitas and colleagues in this issue 2 is a rare example of the implications of a cluster investigation being rigorously pursued. In this case, the implication was that a cluster among staff of the Australian Broadcasting Corporation (ABC) studios in Toowong, Brisbane, might reflect a higher-than-average risk of breast cancer among female employees of the ABC throughout Australia, due to some common cause.3 In terms of identifying causative agents, notification of an individual cluster can be likened to a case report. Nothing can be immediately proved; everything depends on a subsequent, more broadly based study. Cancer clusters, and their investigation, are distinguished from infectious disease clusters by, among other things, the longer time frame involved and the fact that cancer is the most feared disease in Australia and similar countries. Demands made in respect of cancer cluster investigations centre on whether the cluster is explicable by chance and, if not, what caused it. The Toowong cluster came to national attention via a television program entitled “One in a million”, an epithet derived from the cluster investigators’ initial assessment of the likelihood that the increased incidence of breast cancer might be attributable to chance.4 Calculation of the probability that a cluster is attributable to chance is limited, if not precluded, by a posteriori definition of the study population — often illustrated by reference to the Texas sharpshooter who was in the habit of firing at the side of a barn, locating the bullet hole and painting a target round it.5 But the community wants answers, not technicalities. In the case of Toowong, the difficulty inherent in making such a determination is illustrated by revision of the initial estimate, specified in the summary of the final report as follows: [T]he likelihood of this event occurring by chance is about one in a million. This, however, may oversimplify the situation and, when further analyses are performed, adjustment of the P-value for implied multiple comparisons increased its estimated value to 0.04. That potentially increases the likelihood of the cluster occurring by chance to one in 25.3 Whether cluster investigations have ever revealed a new carcinogen is debated. Though vinyl chloride and diethylstilboestrol are sometimes cited in this context, the carcinogenicity of these compounds was implicated from multiple case reports involving alert physicians rather than from the perceptions of people in the affected group. Indeed, diethylstilboestrol was initially investigated because a lift malfunction in Boston resulted in a gynaecologist and a pathologist exchanging experiences.6 Otherwise, increased numbers of cancer cases within communities located adjacent to point-source pollution may implicate particular carcinogens. However, assessments of lung cancer near steelworks or smelting operations, mesothelioma near asbestos mines, thyroid cancer near a failed reactor, or haematopoietic malignancy in the vicinity of toxic waste dumps7 are readily distinguished from cluster studies, the latter being prompted by increased incidence rather than any attempt to determine whether an increase exists in light of a specific exposure. Novel exposure to carcinogens may also be investigated following spatial aggregation studies, which typically involve hundreds or thousands of cases — for example, the investigation of exposure to pesticides or other agents in relation to increased breast cancer incidence on Long Island, New York.8 Once cluster investigations are distinguished from case reports, point-source pollution investigations and spatial aggregation studies, it is arguable that clusters have rarely, if ever, resulted in the discovery of a specific cause of cancer, much less revealed a new carcinogen. Accordingly, the result of the Toowong cluster investigation was typical. In Toowong, all plausible causes of the cluster, including radiofrequency and extremely low frequency electromagnetic fields, ionising radiation and chemical contamination of the site or its water supply, were excluded.3 The findings of Sitas and colleagues2 are a good outcome for women employed by the ABC, and for those who worked in Toowong specifically. The absence of increased risk of breast cancer among ABC employees Australia-wide, together with a failure to identify any agent that could account for increased risk in Toowong and the 1 in 25 probability that the situation may have arisen by chance,3 mean the case is closed. However frustrating it may be, chance emerges as the most likely explanation. ABC staff at Toowong and elsewhere have no reason to be apprehensive about being at increased risk. There are no reasonable medical or scientific grounds for such women to undergo more rigorous clinical examination or more frequent mammographic screening than is recommended for women in Australia generally. These considerations critically depend on the findings of Sitas et al.2 Likewise, any notion that the building or site at Toowong presents a toxic hazard is now little short of absurd. Hopefully, ABC staff will be so advised. Beyond that, however, this good news might be shouted from the top of Uluru for all the likelihood it has of reaching the wider community, whose perceptions about cancer causation now include the “one in a million” scenario. The media in Australia respond to an insatiable demand for news of unsuspected exposure to carcinogens. Overwhelmingly, reports about possible cancer causation refer to consumer products and food contamination.9 Apart from a correct appreciation of carcinogens in tobacco, perceived causes of cancer range from pesticide residues in food to deodorants, from artificial sweeteners to mobile phones.7 For each such agent, there exists evidence of potential harm — but the relevant risks are either vanishingly small or simply not established. Maintaining speculation about Toowong comes a recent report of another breast cancer case and related matters connected with Toowong (Box). In point of fact, more and more cases of breast cancer will occur among women who once worked at ABC Toowong, in the same way that more and more cases of breast cancer will occur among any cohort of Australian women initially identified as aged 30–50 years. Tragically, one Australian woman in nine will develop breast cancer by the age of 85 years.10 About 60 cases must be anticipated within the Toowong cohort of 550, taking account of no other risk factor than being a woman in Australia. The prospect, however, is that each such case will be reported as involving another Toowong employee, fuelling anxiety about a common cause of harm, with no mention being made of the work of Sitas et al.2 Reference to a lack of risk hardly contributes to the momentum of a great story. But there is a price. People who misunderstand cancer causation are less likely to engage in practices known to reduce the risk of disease.11 Any unwarranted anxiety about insidious exposure to carcinogens seems likely to impede adoption of evidence-based measures to prevent cancer. That, together with any needless burden of anxiety, is bad news. Headlines from the Brisbane Courier Mail, 22 and 26 February 2010

Bernard W Stewart PhD, FRACI, DipLaw

A simple-to-use, inexpensive, low-risk tool that is not about ticking boxes but about keeping patients safe — it encourages surgeons, anaesthetists and perioperative nurses to work as a team, communicate and engage fully in safety processes Following pilot implementation of the World Health Organization’s Surgical Safety Checklist (the Checklist), a 30% reduction in surgery-related death and complications was achieved — a great result from a simple and affordable intervention!1 The Checklist2 was launched in Australia by the Hon Nicola Roxon MP, Federal Minister for Health and Ageing, on 19 August 2009, and a week later in New Zealand by the Hon Tony Ryall MP, Minister of Health. Similar launches have occurred around the world. The Checklist, produced by the WHO’s Second Global Challenge of the World Alliance for Patient Safety, was evaluated in a pilot study involving almost 8000 patients in eight centres, including one in our region, in countries with health systems of varying sophistication.1 This study showed that the Checklist was simple to use, and was associated with a worthwhile improvement in outcomes attributable to improved adherence to a number of predefined safety processes. For example, combined results from the sites showed reductions in: deaths, from 1.5% to 0.8% (P = 0.003); complications, from 11% to 7% (P = 0.001); and unplanned re-operations, from 2.4% to 1.8% (P = 0.047). This was a quality improvement study, not a randomised controlled trial, but the Checklist is a well thought-out, inexpensive, low-risk initiative that makes sense and works. The problem of iatrogenic harm has been characterised and quantified in a number of studies internationally,3,4 including widely cited work in our own region.5,6 These studies show that too many patients are harmed by the health care intended to help them,7 and that this harm is often the result of preventable failures in process.8 The Checklist is a cognitive aid to assist in the processes of caring for patients during anaesthesia and surgery but, more importantly, it is also designed to promote teamwork and communication within the operating room. Therefore, it was appropriate that the launches of the Checklist were collaborative affairs, with wide representation from nursing and medical organisations, including the Royal Australasian College of Surgeons, Australian and New Zealand College of Anaesthetists and Australian College of Operating Room Nurses, among others. The value of checklists in process management has been recognised in high-stakes activities other than medicine since at least the 1930s, and it is now time for surgeons, anaesthetists and perioperative nurses to increase their use of checklists for process control. Various methods of checking have been used by nurses, anaesthetists and surgeons for many years, but unacceptable errors continue to occur. For example, of the serious and sentinel adverse events reported in New Zealand in 2008, 19 cases involved the wrong site, wrong patient or wrong procedure, and six involved retained surgical swabs or other paraphernalia.9 This distressing situation is not far out of line with experiences in similarly sized Australian states or other countries. In New South Wales, in the second half of 2007, there were 10 wrong patient, wrong site or wrong procedure incidents in operating rooms; 61 incidents involving imaging and nuclear medicine; two in radiology services; and 13 in wards and other areas.10 The Checklist is applied in three phases: “Sign In”, when key issues are checked before induction of anaesthesia in the operating room; “Time Out”, which includes introducing all staff in the operating room, a briefing of the team and a final check of key issues before incision; and “Sign Out”, which is a clear handover to postoperative staff of important issues for ongoing patient management. It is relevant that the Checklist was developed through a highly evidence-based process, in which an international interprofessional group of experts reviewed the available literature, identified aspects of the perioperative process which typically fail, and consulted widely in designing a solution. Ticking the boxes is not the objective — getting people to engage in the key processes of perioperative care is. Local modification is encouraged, and an Australian and New Zealand version has been developed and launched,11 which includes prophylaxis of venous thromboembolism as one of the key issues checked during “Time Out”. Change management is hard work and worldwide experience indicates the need for active implementation programs led by clinical champions. The Checklist will not eliminate mistakes, but it has good potential to reduce them. All who practise surgery, anaesthesia and perioperative nursing are asked to adopt the Checklist in an engaged and constructive manner and make it work. The importance of instigating the use of the WHO Surgical Safety Checklist as an operating room routine cannot be overstressed. Preventable iatrogenic harm continues to be a major problem internationally, including in surgery and anaesthesia. The Checklist is an inexpensive, low-risk, adaptable initiative based on commonsense that has been shown to be workable and to significantly reduce harm in surgery and anaesthesia. The Checklist has the support of many local and international medical and nursing organisations.

Alan F Merry MB ChB, FANZCA, FFPMANZCA · Bruce H Barraclough FRACS, DDU, FACS

Patients need to make an informed choice about their pathology referrals In February 2010, despite representations from the Royal College of Pathologists of Australasia (RCPA) and the Royal Australian College of General Practitioners (conveyed via letters, meetings and discussions), the federal government introduced legislation into Parliament to require all pathology request forms to be marked with the advice to patients that they may be taken to any pathology provider.1 Pathology services underpin modern health care, playing a role in 70% of diagnoses and medical decisions.2 The key concern of health professionals is that the “non directed” pathology referral will put patient safety at risk and undermine the quality of information that pathologists provide to patient care. The proposed legislation arose from an interdepartmental review of pathology funding led by the Australian Department of Finance and Deregulation and is touted as creating patient choice.3 However, from the health professional’s perspective, the initiative may seem, at best, disingenuous. Patients have always had the right to take part in choosing their pathology provider — as they do for other medical specialist referrals. Shared decision making between doctor and patient is the strength of the medical specialist referral system, and is of particular importance in making choices about pathology (the “invisible” medical specialty). Amending the request form with a clause advising patients that it may be taken to any pathology provider encourages patients to make the decision on their own, after they have left their doctor’s surgery — thus making this a “patient choice” initiative that threatens fully informed choice. Patients may infer from this government directive that it does not matter which pathology provider they use — that they are all the same. In fact, this is not the case. Although all pathology providers are required to meet a national standard of accreditation, they differ in the range of expertise of their pathologists and laboratory teams, their test catalogue and technologies, the content of reports, their second-opinion networks, their access to pathologists for advice, their turnaround times and notification of urgent results, and their after-hours services. Little of this variability may be apparent to patients, who may instead make their “choice” on the convenience of sample collection and price alone, without due regard to the nature of the pathology consultation their doctor sought or whether the important information will be effectively communicated to their doctor. Patients may choose to shuttle between various pathology providers without understanding the effect this journey may have on the type and usefulness of information provided by pathology testing. For many diseases, a unique diagnostic opportunity arises from testing being carried out in one laboratory over the course of a patient’s acute illness. Pathologists can integrate the findings of a range of tests over time to make a diagnosis and can identify disease progression, remission and recurrence earlier, and with more certainty, from a complete and continuous pathology record. Patients with chronic diseases may understand the importance of serial pathology testing, but may not realise that the tests performed and their reference ranges may vary between laboratories, to the extent that the use of multiple pathology practices could compromise their doctor’s efforts to monitor results and could even affect their treatment. Even laboratories that use the same reference ranges may use their own cumulative or graphical reports of test results to highlight changes in the control of common diseases such as diabetes and cancer and in warfarin therapy. Thus, significant changes in a patient’s disease status may not be recognised if they are presented by a new pathology provider independently of previous data gathered on the patient. Lastly, patients may not understand the effect that their independent choices about pathology providers may have on the communication and traceability of their results. The information required for critical decisions may be delayed or lost because the pathology practice cannot deliver reports to an unknown doctor and the doctor cannot pursue them because he or she does not know which practice the patient chose to attend. A large medical indemnity organisation has indicated that it will need to provide risk management advice to its members should this measure be implemented (David Nathan, Chief Executive Officer, Avant Mutual Group Limited, in a letter dated 3 November 2009 referring to an RCPA letter sent to medical indemnity insurers on 17 September 2009 to acquaint them with this measure). Is this good health policy? Can it be good if it cuts across pre-existing good policy on quality, safety and connectivity (ie, delivery of medical information by information technology systems). The federal government seems intent on proceeding with this legislation, despite the establishment of a Senate inquiry into the risks it poses to patient safety.4 Why is this? Why is the government seeking to interfere in and weaken the doctor’s role in advising patients about their health care? If this is about patient choice, then surely patients would universally choose to be safe? So, if it is not about patient choice, what is it about? By portraying pathology services to the Australian public as being all the same, with no distinction made between the levels of service or expertise offered by different providers, the Department of Finance and Deregulation would be sending a message that pathology is a commodity, to be bought at the lowest price. This premise could be used to justify fee cuts and tendering, both of which are on the federal government’s radar.5 All Australians (including patients and doctors) need to be aware of the risk to patient care once the case has been made that pathology is a commodity rather than a medical service. This risk is not merely theoretical. In Ireland, after a recent government-led tender, all Pap smears from Irish women are now to be reported by a pathology service in the United States — effectively putting an end to training (and the destruction of competency) of Irish pathologists in this area of pathology.6 In New Zealand over the past decade, tendering of pathology in each of the 21 district health boards has disrupted not only patient care but also the pathology workforce.7 There has already been significant government disinvestment in Australian pathology over the past 5 years, with the proportion of the Medicare dollar spent on pathology falling significantly despite a dramatic rise in test numbers over that period (Ed Wilson, Principal, EW Consulting P/L, personal communication). A further government review of pathology funding is underway.5 It is aimed at saving more money and will bring us closer to the line beyond which funding is no longer sufficient to allow pathology practices to maintain the standard expected by Australian doctors and their patients. In recent years, this line has probably already been crossed in Canada, where chronic underfunding has been identified as a major cause of the widespread failure of diagnosis of breast cancer, with resultant government inquiries being conducted.8 The proposed changes to legislation cannot be justified on the spurious grounds that pathology is a commodity and that patients are being offered “choice”, when in fact the choice already existed. If the federal government’s agenda is to reduce funding for pathology services, it needs to take responsibility for its decision and the consequences of that decision for patient care.

Beverley J Rowbotham MD, FRACP, FRCPA

Doctors can best contribute to environmental sustainability by their example and by working actively to change social norms McDermott’s article in this issue of the Journal (The carbon footprints of obesity, chronic disease and population growth: four things doctors can do)1 calls doctors to arms, in the tradition of the famed 19th-century German pathologist Rudolf Virchow and today’s Medical Association for the Prevention of War, to contribute to a better world. Its writer draws attention to profound issues and is to be congratulated. However, her recommendations are not so straightforward. Taken neat, the cure might do more harm than good. Consider obesity. Indeed, a recent article found that an obese population requires substantially more food energy than one with a normal body mass index distribution,2 although it is unclear whether the authors fully considered the shorter life expectancy and lower class-related reduction in other aspects of the ecological footprint of the obese. Elite sportspeople and military recruits also consume disproportionate amounts of food and other resources, but these harder targets were not mentioned. Singling out the obese seems simplistic and discriminatory.3 McDermott also advocates enhanced rights-based family planning, in rich and poor nations, as a means to reduce climate change. She discusses a recent report that found a high climate return for a low cost (that of funding family planning).4 As she mentions,1 the methods used in this thesis can be challenged, as it is obvious that growth in size of wealthy populations fuels far more climate change than does growth in size of poor populations, a distinction that is not clearly made. Criticising the poor for their population growth rate risks becoming another form of victim blaming. However, in the long run, slower population growth everywhere (especially in countries like Australia and the United States) will slow greenhouse gas accumulation. It will also enhance population health in low-income countries. McDermott also correctly advocates social, health and rights-based strategies to complement the largely technical and economic approach to climate change that is now dominant.5 It is easy to list actions that will improve global public health. However, compilers of lists need not only to prioritise their lists’ components, but also to describe how we can realise them. It is true that doctors are powerful role models, and the recent tentative steps by doctors and medical associations to recognise and address the health and other risks of climate change6 are important. However, the virtual absence of health (and the global population) as agenda items for the recent climate change talks in Copenhagen underlines how far there is to go. It is also easy to call for “whole-of-government” approaches, whether to slow climate change, fix the obesogenic environment or to enhance equity. Easy to say, hard to achieve. A well known economic principle is the law of diminishing returns. A second ice-cream is not as tasty as the first. Less well known is the Matthew effect, or the law of increasing returns.7 This principle is a powerful impediment, not only to whole-of-government reforms, but to the transition to sustainability more broadly. Simply put, this principle describes how groups with influence are able to rig public opinion and legislate to benefit powerful minorities rather than the public good.8 The 18th-century philosopher Adam Smith warned against monopolies. The benefits to society and public health, including life expectancy, from reduced inequality are perennially rediscovered.9 Yet progress on reforming coal-fired electricity generation remains stalled both here and in Washington. Advancement of public goods such as public health and climate stability is thwarted by well funded and well organised lobbyists, who far outnumber public-good lobbyists.10 This illustrates an embedded Matthew effect, long operant in the US, and one about which Australia should not be complacent. Our long life expectancy might not always remain so.11 What is it, in this country, that prevents more extreme ideologies from taking root? The answer, in part, lies in our cultural norms and practices, such as our ostensibly “fair go” society, and in a reasonably free press. McDermott’s article1 and its receptive readers help counter the advantages of the powerful. On reflection, it is not hard to see how the attitudes and norms of readers sympathetic to this analysis evolved. We all received a publicly subsidised education. Some of us descend from people who struggled for the opportunities and wealth we may now take for granted. Before our birth, large social movements worked intensely for a fairer world, using organised tactics that reduced the advantages, often hereditary, of those more powerful. Some of this resolution was forged in the trauma of World War II and the preceding Great Depression, helping to deliver the National Health Service in the United Kingdom and diluted copies of it elsewhere. Then, largely in the same English-speaking world, a less vigilant generation was seduced by the “fool’s gold” of neoliberalism, the conceit that marketism would deliver more public goods than would regulation.12 This false remedy has not only generated a decline in equity, but now threatens the whole of civilization.11 What can doctors do? Reflect and act, not just on the four themes proposed by McDermott, but on four hundred more. They can green their clinics, reduce their own footprint and join like-minded groups. There is no single recipe, but the principles of environmental sustainability, justice and commonsense are integral, as are courage and collaboration. Such action may work as a social vaccine against despair. Doctors, with other groups, may long postpone the world’s admission to intensive care.

Colin D Butler BMed, MSc, PhD

Decisions regarding the use of triple therapy should take into account the balance between thromboembolism and bleeding risk in individual patients The combined use of warfarin and dual antiplatelet therapy (aspirin plus clopidogrel) — so-called triple therapy — is a challenging management problem in patients with a coronary stent who also have an indication for oral anticoagulation. One of the most common clinical scenarios is a patient with atrial fibrillation (AF) who undergoes percutaneous coronary intervention with stenting. Guidelines for antithrombotic therapy recommend that patients with AF who are at high risk of stroke (ie, prior history of stroke or more than one of: age ≥ 75 years, hypertension, diabetes, and congestive cardiac failure) receive warfarin;1 and guidelines for percutaneous coronary intervention management recommend dual antiplatelet therapy in all stent patients to prevent stent thrombosis.2 Both warfarin and clopidogrel increase the risk of bleeding in patients treated with aspirin, and combining all three drugs can be expected to further increase bleeding risk. However, the efficacy and safety of triple therapy have not been evaluated in randomised controlled trials. What is the evidence concerning the efficacy of anticoagulation or antiplatelet therapy in patients with AF who have recently received a coronary artery stent? In patients with AF who are at risk of stroke, warfarin compared with placebo or no treatment reduces the risk of stroke by about two-thirds, whereas aspirin reduces the risk by about one-fifth.3 Adding clopidogrel to aspirin improves the effectiveness of antiplatelet therapy for stroke prevention,4 but warfarin is substantially more effective than dual antiplatelet therapy.5 In patients with a recent coronary artery stent, dual antiplatelet therapy compared with the combination of aspirin and warfarin reduces death or myocardial infarction by half.6 Premature discontinuation of clopidogrel (less than 3 months of treatment for sirolimus-eluting stents; less than 6 months for paclitaxel-eluting stents) is the single most important risk factor for stent thrombosis.7 The efficacy and safety of triple therapy have been examined in multiple observational studies. Meta-analysis of 10 observational studies involving 1349 patients with AF who received triple therapy after stent insertion revealed a weighted mean incidence of major bleeding at 30 days of 2.2% (95% CI, 0.7%–3.7%).8 Increasing the duration of triple therapy to longer than 6 months doubles the risk of major bleeding compared with 1 month of treatment.9 The guidelines recommend at least 4 weeks of dual antiplatelet therapy for patients who receive a bare metal stent and at least 1 year for those who receive a drug-eluting stent.2 What is the optimum antithrombotic management of patients with AF who undergo coronary stent insertion? Decisions regarding the use of triple therapy should take into account the balance between thromboembolism and bleeding risk in individual patients. Dual antiplatelet therapy alone is likely to be adequate for stent patients with AF if they are at low or moderate risk of stroke (CHADS2 stroke risk score [congestive heart failure, hypertension, age ≥ 75 years, diabetes, 1 point each; previous stroke or transient ischaemic attack, 2 points10], 0–1), or if they are at high risk of stroke (CHADS2 stroke risk score, > 1) and deemed to be at unacceptably high risk of bleeding with triple therapy. The most important risk factors for bleeding are older age (eg, > 75 years), severe renal dysfunction (eg, creatinine clearance < 30 mL/min), recent gastrointestinal bleeding (eg, within 6 months), previous stroke, and uncontrolled hypertension (eg, systolic blood pressure > 160 mmHg, diastolic blood pressure > 110 mmHg).11 All other patients with AF who are at high risk of stroke (CHADS2 stroke risk score, > 1) and have recently undergone coronary artery stenting should probably receive warfarin in addition to dual antiplatelet therapy (Box).8 Cardiologists and primary care physicians should communicate closely to optimise antithrombotic therapy and minimise the risk of bleeding in patients who may be candidates for triple therapy. Firstly, the duration of exposure to triple therapy should be limited where possible by selecting a bare metal stent, which requires a shorter duration of antiplatelet therapy than a drug-eluting stent.2 Secondly, aspirin should be used at the lowest proven effective dose of 50–100 mg/day to minimise the risk of gastrointestinal bleeding.12 Thirdly, in patients at high risk of gastrointestinal bleeding, consideration should be given to the use of acid-suppressive therapy, either with a histamine H2-receptor antagonist (eg, ranitidine) or a proton-pump inhibitor.13 Retrospective analyses of administrative databases have suggested that the concomitant use of a proton-pump inhibitor (particularly omeprazole) reduced the efficacy of clopidogrel,14,15 but subsequent analyses of data from randomised controlled trials indicated no loss of benefit of clopidogrel when the two were used in combination.16 If a proton-pump inhibitor is used, it may be reasonable to avoid the use of omeprazole. Finally, warfarin therapy should, ideally, be monitored by an expert anticoagulation clinic to optimise the quality of international normalised ratio (INR) control (target INR, 2–3).11 What are the unresolved issues? Our recommendations for the use of triple antithrombotic therapy in patients with AF and a stent are based on observational studies8 and extrapolations of evidence from randomised controlled trials of antithrombotic therapy for prevention of stent thrombosis and thromboembolism in patients with AF. Dedicated randomised studies are urgently needed to obtain more reliable estimates of the risks and benefits of triple antithrombotic therapy in patients with a coronary artery stent who have AF, as well as in stent patients with other indications for warfarin therapy, such as mechanical heart valves or recent venous thromboembolism. Treatment decision algorithm for patients with atrial fibrillation and a coronary artery stent8 * CHADS2 stroke risk score (congestive heart failure, hypertension, age ≥ 75 years, diabetes, 1 point each; previous stroke or transient ischaemic attack, 2 points).10

Jeremy S Paikin MD · Shamir R Mehta MD, MSc, FRCPC · John W Eikelboom MB BS, MSc

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

Putting to rest the myth that emergency department overcrowding is due to a lack of primary care services Australia’s emergency departments (EDs) are dangerously overcrowded, but a study by Buckley and colleagues in this issue of the Journal1 should be the last nail in the coffin of the long-discredited myth that the root cause is a lack of primary care services. This study used a time series approach to identify a real — but clinically insignificant — change in ED workload after the opening of an after-hours primary care service in the New South Wales inland rural city of Wagga Wagga. The Australian public are entitled to receive high-quality and available care in both primary care and emergency settings, but the overlap between these services is not as important as many have claimed.2,3 In a rural location without pre-existing after-hours primary care services, the introduction of such a service, which treated 14 patients daily on average, was associated with an adjusted daily reduction in ED presentations of seven patients with an Australasian Triage Scale (ATS) category of 4 or 5 (lower urgency). As the authors note, because non-admitted low-urgency patients tend to have low resource needs, this reduction of 8% of total ED presentations would correspond to a lesser reduction in workload. Based on published Wagga Wagga Base Hospital data and accepted casemix measures, this reduction would translate to around 3% of this rural ED’s costs and no more than 4% of its ED medical and nursing staff time. These figures are higher than some other Australian estimates,4,5 mostly from studies in cities with pre-existing after-hours services. However, they remain consistent with the observation from these studies that the overall weekly primary care workload in an ED amounts to no more than one patient per hour. In Wagga Wagga, few general practices open for more than 55 hours per week, and the after-hours service opens for 27 hours, but the ED is always open and is the only source of medical care in this community for more than half the 168 hours in each week. It is no surprise that some patients who could reasonably go elsewhere will present to the ED. Buckley et al’s results show that the after-hours clinic treated an average of 3.7 patients per hour. During the hours the clinic was open, the reduction in ED presentations was 1.8 patients per hour and, when it was closed (ie, the rest of the week), the reduction in ED presentations was 0.2 patients per hour. It is unlikely that extending the clinic’s opening hours would make much difference: opening during office hours would probably reduce presentations to existing general practices, and opening later at night would likely be uneconomical. Although, as the study authors note, general practitioners working in EDs in the United Kingdom have been shown to be more cost-efficient than junior medical staff in the same environment, the actual cost of emergency medicine is dominated by infrastructure and staff expenses 24 hours per day.6 EDs have a high average cost per patient and a low marginal (incremental) cost for additional low-acuity presentations, especially compared with off-site after-hours clinics, where expenses are dominated by medical labour, and the average and marginal costs are much closer together. Even if patients were 100% interchangeable, a new after-hours service would likely represent an increase in total cost to the community, because it would not reduce the need for the “public good” of a 24-hour service available at the hospital. Despite its limitations, this study confirms that “primary care patients” and “ED ATS category 4 and 5 patients” are not interchangeable. It is to be expected that there is some overlap between patients who might want to present to an ED and those who might want to go to a GP — just as there may be overlap between patients going to a GP or a gynaecologist for a Pap smear, or between those going to a thoracic surgeon or a respiratory physician for investigation of a lung mass. However, the finding that 96% of the weekly workload of an ED cannot be substituted by an after-hours service confirms that patients are largely presenting appropriately. By comparison, at least a third of average ED staff workload (and more than half in some places) consists of providing care to those who have completed their emergency treatment and are waiting for an inpatient bed,7 sometimes for days. Australian EDs are dangerously overcrowded with patients, many of whom should not be in EDs because they would be better managed elsewhere. But it is not the so-called primary care patients who are blocking ambulances from offloading8 — it is the “access block” patients waiting for beds on the inpatient wards who are inappropriately occupying ED space and staff time.

Drew B Richardson MB BS(Hons), FACEM, GradCertHE

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

Until the results of several statin trials are available, it is recommended that the current indications and usage of ezetimibe be continued Patients receiving statin therapy to reduce total and low-density lipoprotein cholesterol (LDL-C) levels still have a residual risk of cardiovascular (CV) events. In most statin trials, CV events are reduced by about 30% compared with placebo, leaving about 70% residual risk of CV events that occur in spite of statin therapy. Factors that may contribute to residual risk are listed in Box 1. The Treating to New Targets Study1 showed that residual risk of CV disease increased with low levels of high-density lipoprotein cholesterol (HDL-C), even in patients who had low levels of LDL-C as a result of statin therapy. This suggested that raising HDL-C levels may be beneficial for such patients, a hypothesis investigated in the recent ARBITER 6-HALTS trial (ARBITER [Arterial Biology for the Investigation of the Treatment Effects of Reducing Cholesterol]; HALTS [HDL and LDL Treatment Strategies in Atherosclerosis]). The ARBITER 6-HALTS trial was a study of carotid intima-media thickness (CIMT) in statin-treated patients who had achieved LDL-C goal levels. It compared an HDL-C-raising strategy (additional treatment with extended-release nicotinic acid titrated to 2 g daily) with an LDL-C-lowering strategy (additional treatment with ezetimibe 10 mg daily).2,3 The trial was stopped prematurely at its interim analysis of 180 of the planned 300 patients, on the basis of differences in the primary end point and other secondary analyses.4 The trial included subjects aged 30 years or over with coronary heart disease (CHD), known atherosclerotic vascular disease at other sites, diabetes, a 10-year CHD risk of > 20% (based on Framingham Heart Study criteria), or a coronary calcium score > 400 in men or > 200 in women, who were stabilised on statin therapy equivalent to simvastatin 20 mg/day, with LDL-C levels < 2.5 mmol/L and HDL-C levels < 1.3 mmol/L in men or < 1.4 mmol/L in women.2 Exclusion criteria included raised transaminase levels more than three times the upper limit of normal, current use of or intolerance to ezetimibe or nicotinic acid, a history of chronic liver disease, or the potential for pregnancy. Results of the ARBITER 6-HALTS trial showed that nicotinic acid reduced CIMT more effectively than ezetimibe (Box 2). Importantly, as no control group was included, no comparison can be made between ezetimibe and placebo with regard to their possible effects on CIMT. Atherogenic dyslipidaemia may be an important contributor to residual risk and is typically associated with obesity, the metabolic syndrome and type 2 diabetes. It is accompanied by impaired glycaemic control, hypertension, and procoagulant and inflammatory states, and is characterised by low HDL-C levels, high triglyceride levels, the presence of triglyceride-rich “remnant” lipoproteins, and a preponderance of small, dense, highly-oxidisable LDL particles. Levels of total cholesterol and LDL-C may be close to normal. Patients in the ARBITER 6-HALTS trial had a mean body mass index in the obese range (30.8–31.0 kg/m2) and a waist circumference above normal (mean, 103 cm and 104 cm in the two groups); 32%–40% were diabetic; and 85%–86% were hypertensive.2 Mean glucose levels (5.55–5.77 mmol/L) and triglyceride levels (1.38–1.42 mmol/L) were also in the high-normal range. Patients were selected for inclusion in the trial on the basis of low HDL-C levels. HDL-C levels increased, as expected, in the nicotinic acid treatment group (by about 18%), but unexpectedly decreased in the ezetimibe treatment group (by about 5%).2 The results of the trial may thus be partially explained by the fact that a significant proportion of patients had atherogenic dyslipidaemia, which responds to nicotinic acid therapy but not to ezetimibe therapy. Conclusions from the ARBITER 6-HALTS trial about the LDL-C-lowering effects of ezetimibe and the HDL-C-raising effects of nicotinic acid may be questioned, as ezetimibe and nicotinic acid affect different lipoproteins and metabolic pathways that may influence atherosclerosis. Nicotinic acid lowers levels of triglycerides and triglyceride-rich lipoproteins by reducing free fatty acid flux to the liver; it also lowers lipoprotein (a) and LDL-C levels. Ezetimibe has less pronounced effects on lowering triglyceride levels and raising HDL-C levels. In addition, the protective functions of HDL-C (including reverse cholesterol transport, anti-inflammatory and antioxidant effects) may not necessarily be reflected in HDL-C levels, and functional assessment of HDL-C may assist in assessing the potential benefits of intervention.5 The implication of the ARBITER 6-HALTS trial results is that targeting atherogenic dyslipidaemia with nicotinic acid therapy reduces CIMT and is likely to improve residual risk of CV events because CIMT is a validated surrogate marker for CV events — an important consideration for all patients receiving statins.6 The HATS (HDL-Atherosclerosis Treatment Study) trial demonstrated that CV events could be reduced by treating atherogenic dyslipidaemia with nicotinic acid.7 Previous CIMT studies (ARBITER 2 and 3) showed that a combination of nicotinic acid and statin therapy was superior to statin therapy alone for atherosclerosis stabilisation and regression.8 These results, together with those of the ARBITER 6-HALTS trial, indicate that nicotinic acid may be appropriate supplementary therapy for reducing residual risk in patients taking statins. The results also provide an evidence base for extended-release nicotinic acid to be made available once again under the Pharmaceutical Benefits Scheme. Long-term clinical outcomes trials are already underway to investigate the primary findings of the ARBITER 6-HALTS trial (Box 3).2 Until the results of these trials are available, it is recommended that the current indications and usage of ezetimibe be continued (Box 3). Lifestyle change is an important component of managing residual risk (Box 1). Stopping smoking, controlling weight and increasing physical exercise can all increase HDL-C levels and may contribute independently to reduction in residual risk of CV events. 1 Possible contributors to residual risk in patients receiving statin therapy Cigarette smoking Uncontrolled hypertension Impaired glucose tolerance Reduced physical exercise Central abdominal obesity Inflammation Prothrombotic tendency Proarrhythmic tendency Myocardial ischaemia Left ventricular dysfunction Reduced high-density lipoprotein cholesterol (HDL-C) level Increased low-density lipoprotein cholesterol (LDL-C) level Atherogenic dyslipidaemia: Increased apolipoprotein B and small, dense LDL particles Reduced HDL-C level Increased level of triglycerides and triglyceride-rich lipoproteins 2 Results of the ARBITER 6-HALTS trial2 Treatment group Ezetimibe (n = 111) Nicotinic acid (n = 97) P Baseline Mean CIMT (mm) (SE) 0.8957 (0.1484) 0.9001 (0.1558) 0.93 At 8 months* Mean change in CIMT (mm) (SE) 0.0014 (0.0020) – 0.0102 (0.1650) 0.90 P (change from baseline) 0.48 0.001 At 14 months* Mean change in CIMT (mm) (SE) – 0.0007 (0.0035) – 0.0142 (0.0041) 0.01 P (change from baseline) 0.84 0.001 ARBITER = Arterial Biology for the Investigation of the Treatment Effects of Reducing Cholesterol; HALTS = High-density Lipoprotein and Low-density Lipoprotein Treatment Strategies in Atherosclerosis. CIMT = carotid intima-media thickness. * Change compared with baseline. 3 Summary and future prospects The ARBITER 6-HALTS trial showed that a strategy of raising high-density lipoprotein cholesterol (HDL-C) levels using nicotinic acid therapy was more successful than a strategy of lowering low-density lipoprotein cholesterol (LDL-C) levels further with ezetimibe, at least with regard to reducing carotid intima-media thickness. Results of the trial are relevant to patients receiving statin therapy who have LDL-C levels < 2.5 mmol/L. Many of these patients have atherogenic dyslipidaemia, with low levels of HDL-C and high levels of triglycerides, as well as increased levels of apolipoprotein B and small dense atherogenic LDL particles. Despite having statin therapy, such patients may continue to experience a high rate of cardiovascular disease events — in part because of lack of control of atherogenic dyslipidaemia, which is not targeted by statins or ezetimibe but is alleviated by fibrates and nicotinic acid. The demonstrated superiority of nicotinic acid therapy in the ARBITER 6-HALTS trial is probably the result of improved control of atherogenic dyslipidaemia. Although the results of the trial are potentially important, their relevance to Australian practice is limited because extended-release nicotinic acid, although approved for prescription by the Therapeutic Goods Administration, is not reimbursed by the Pharmaceutical Benefits Scheme. The few patients who can tolerate non-extended-release nicotinic acid at doses of 2 g daily may benefit from this agent when added to statin therapy. An alternative strategy may be to combine statin therapy with fenofibrate therapy (the effectiveness of this approach will be determined by the results of the ACCORD trial, to be presented in early 2010). Other trials are in progress to determine the long-term clinical outcomes of statin therapy combined with ezetimibe (IMPROVE-IT [estimated completion date, 2015]) and with extended-release nicotinic acid (AIM HIGH and HPS2-THRIVE [estimated completion dates, 2011 and 2013, respectively]). Pending the results of these trials, the continued use of ezetimibe is recommended for patients unable to tolerate statins and for those whose LDL-C level is uncontrolled in spite of maximum-tolerated doses of statins. ACCORD = Action to Control Cardiovascular Risk in Diabetes. AIM HIGH = Atherothrombosis Intervention in Metabolic Syndrome with Low HDL/High Triglycerides and Impact on Global Health Outcomes. ARBITER = Arterial Biology for the Investigation of the Treatment Effects of Reducing Cholesterol; HALTS = HDL and LDL Treatment Strategies in Atherosclerosis. HPS2-THRIVE = Heart Protection Study 2 Treatment of HDL to Reduce the Incidence of Vascular Events. IMPROVE-IT = Improved Reduction of Outcomes: Vytorin Efficacy International Trial.

Ian R Hamilton-Craig MB BS, FRACP, PhD

For generic substitution to be safe, consumers and clinicians need to fully understand what is the same or different about various brands of the same medicine A main aim of the National Medicines Policy is to provide Australians with access to safe, high-quality medicines at prices consumers and government can afford.1 As such, generic medicines have an important place in health care. Consumers see generic medicines as an opportunity to access cheaper medicines, while governments see the opportunity to achieve the same health outcomes for patients at a lower cost. Clinicians, on the other hand, have mixed views regarding the role of generic medicines. Many pharmacists see generic medicines as an opportunity to reduce patient costs while maintaining effectiveness, whereas some prescribers express concern that generic medicines are not appropriate or equivalent alternatives in some therapeutic areas (eg, anticonvulsants) and that brand substitution is a challenge to their clinical decision making, with a significant risk of patient confusion. Brand substitution is investigated by Ortiz and colleagues in this issue of the Journal (Ortiz et al).2 This is an important study in many ways, and it provides quantitative information on the extent of brand substitution and switching, a question which is often shrouded in anecdote. As it turns out, these data suggest that the extent of switching between brands of three major classes of medicines on the Pharmaceutical Benefits Scheme is probably less than many clinicians suspect. The study found that about 20% of patients switched brands of selected medicines two or more times during the course of a year. Not surprisingly, medicines that had more brands on the market were generally more likely to be switched. An interesting observation was that brand switching was less likely to be undertaken by older people than younger people. This may be related to a range of factors, including greater caution on the part of the prescriber and pharmacist when dealing with medications for older people. The results of this study, derived from community-dispensing information, need to be considered in the broader context of the health system. Generic (or brand) substitution occurs regularly when patients are admitted to or discharged from a public hospital. Hospitals typically stock only a limited number of brands of a medicine, and these are often generic products. Ortiz et al conclude that generic substitution is occurring and is likely to increase in the future.2 Indeed, their data may underestimate the current brand-switching situation, as the study was conducted before August 2008, when incentives for pharmacists to supply a generic medicine (where one exists) were introduced. The impact of medicine brand switching on health outcomes in the Australian community is unknown. However, a meta-analysis of cardiovascular studies found that different brands of (bioequivalent) medicines were clinically equivalent.3 Ortiz et al speculate on the “potential for patient confusion”.2 Patient confusion about medicines and the risk of double dosing of medicines that contain the same active ingredient are a real concern. There are a number of strategies that can be used in combination to reduce the risk of confusion about medicines, especially in the context of generic substitution. These include: Knowing the drug name. Prescribers and pharmacists should explain the name of each medicine, with the aim of helping consumers know the active ingredient in the medicine they are taking rather than the product’s brand name. Medicines information. Information such as consumer medicine information should be provided (and explained). Knowing what the medicine is for. Consumers should be encouraged to know what each medicine is for. Up-to-date medicines list. Consumers should be supported in keeping a list of their current medicines that includes the name of the active ingredient (sometimes called the generic name), the brand name and the dosage regimen. Clear medicine labels. Labelling of prescription (branded and generic) medicines should be improved so that the active ingredient in the product is displayed with equal or greater prominence to the brand name on the packaging, as recommended by the Therapeutic Goods Administration in the Best practice guideline on prescription medicine labelling.4 Each of these strategies relates to health literacy5 and points to the need for greater “medicines literacy” for consumers and carers. There have been recent attempts to improve “generic medicines literacy” among clinicians in Australia, many of whom still challenge the foundation principle of bioequivalence6 and the quality of generic medicines.7-9 Generic medicines provide an opportunity for consumers and government to offset the rising cost of health care. However, the quality use of generic medicines10 requires careful attention by prescribers and pharmacists to the strategies outlined here to minimise the potential for confusion on the part of the patient. If there is a risk of dose duplication, generic substitution may need to be avoided (independent of the drug involved) unless the patient or carer fully understands both the similarities and the differences between various brands of the same medicine.

Andrew J McLachlan BPharm, PhD

The challenge of convincing governments of the value of a nationally comprehensive data collection Congenital anomalies are worth bothering about — they affect around one in 20 births in Australia.1-3 They are the second most common cause of perinatal and infant mortality and the fourth commonest cause of mortality in 1–14-year-olds in Australia.4,5 They are major contributors to hospital admissions6 and often result in lifetime disability. They are costly to our health system, including the considerable expense of providing programs to screen for, diagnose and terminate pregnancies affected by major congenital anomalies (Down syndrome and neural tube defects in particular). Importantly, some anomalies are preventable, including neural tube defects (70% preventable with adequate periconceptional folic acid7) and anomalies resulting from exposure to teratogens (eg, by avoiding alcohol during pregnancy). For many congenital anomalies, early identification allows interventions to decrease the risk of secondary disabilities. We need good data to monitor trends in congenital anomalies, to identify clusters of cases that may require investigation for possible environmental causes, and to evaluate the effectiveness of interventions for screening, treatment and prevention. Nationally, the Australian Institute of Health and Welfare (AIHW) National Perinatal Statistics Unit (NPSU) collates information on congenital anomalies that is supplied voluntarily by health departments in the states and territories. However, there remains considerable variability between jurisdictions in the scope and quality of the data collected. This variability — which includes the sources of case ascertainment, the upper age limit for inclusion, definitions and classifications used, methods of operation, and resources available for collecting, updating, validating and using the information — limits the utility of the collection. National data published by the NPSU can only be as complete as the data provided by individual states and territories. Lack of completeness is evident in two recent AIHW reports. The first, Congenital anomalies in Australia 2002–2003,8 does not include data from the Northern Territory, because data were not available. This may change, as the NT is reviewing its perinatal data needs. In addition, data were only available from four states on terminations of pregnancy at less than 20 weeks’ gestation for congenital anomalies.8 The absence of information on early terminations is also evident in the second report, Neural tube defects in Australia.9 The prevalence of neural tube defects at birth for the period 1998–2005 was similar for all states included in the report, at around 5 per 10 000 births, but the total prevalence (including early terminations of pregnancy from the four states collecting such information) was more than twice as high, at 10.1 per 10 000 pregnancies. Furthermore, of the four states collecting data on early terminations, the total prevalence in 2005 in South Australia, Victoria and Western Australia was 13.3 per 10 000, double that in New South Wales (6.2 per 10 000), suggesting incomplete ascertainment of terminations in NSW. One of the purposes of the report on neural tube defects9 was to provide baseline data against which to monitor the effect of the introduction of mandatory fortification of bread-making wheat flour with folic acid, in place nationally by 13 September 2009. Because such a high proportion of neural tube defects are diagnosed prenatally and affected pregnancies terminated, post-intervention monitoring in Australia will be restricted to the three states where there is complete ascertainment of such terminations. The inclusion of terminations of pregnancy is essential for a national data collection on congenital anomalies — not only for evaluating interventions such as folic acid fortification, but also for evaluating and monitoring the safety and quality of prenatal screening programs and diagnostic tests, and the associated health and psychosocial impacts. In response to the limitations in national data collection, a program was commenced in 2007 to develop a national minimum dataset on congenital anomalies. Members of a committee representative of the states and territories reached consensus on collecting good data on a limited number of conditions, particularly those with important clinical, social or health care impacts; and on the use of internationally agreed definitions for congenital anomalies. However, because of existing data limitations in some jurisdictions, commitment to a national minimum dataset is not currently possible. In addition, the scope of the proposed national collection has been limited to the perinatal period, which means terminations of pregnancy for congenital anomalies before 20 weeks’ gestation will not be included. These decisions are very disappointing and suggest that Australian policymakers and governments are still to be convinced of the value of monitoring congenital anomalies, which, despite their magnitude and importance as a cause of mortality and morbidity, are clearly not seen as a public health priority. Historically, data collection for congenital anomalies has been unfunded or under-resourced in Australia. Apart from mandatory folic acid fortification, there has been no national policy on the surveillance, prevention and management of congenital anomalies. There has also been no consumer involvement in deliberations on the societal impact of these anomalies, the need to collect national data, and the ways in which these data should be collected and used. The challenge remains to convince governments of the value of a nationally comprehensive collection that can be used to monitor trends, identify clusters that may require investigation, evaluate the effectiveness of screening and interventions for treatment and prevention, and allow research into the prevention of congenital anomalies.

Carol I Bower MB BS, PhD, FAFPHM · David Lester-Smith BM BS, FRACP, MPH · Elizabeth J Elliott MD, MPhil, FRACP