Editorials

Indigenous and non-Indigenous Australians need to work together to restore balance Healing is part of life and continues through death and into life again. It occurs throughout a person’s life journey as well as across generations. It can be experienced in many forms such as mending a wound or recovery from illness. Mostly, however, it is about renewal. Leaving behind those things that have wounded us and caused us pain. Moving forward in our journey with hope for the future, with renewed energy, strength and enthusiasm for life. Healing gives us back to ourselves. Not to hide or fight anymore. But to sit still, calm our minds, listen to the universe and allow our spirits to dance on the wind. It lets us enjoy the sunshine and be bathed by the golden glow of the moon as we drift into our dreamtime. Healing ultimately gives us back to our country. To stand once again in our rightful place, eternal and generational. Healing is not just about recovering what has been lost or repairing what has been broken. It is about embracing our life force to create a new and vibrant fabric that keeps us grounded and connected, wraps us in warmth and love and gives us the joy of seeing what we have created. Healing keeps us strong and gentle at the same time. It gives us balance and harmony, a place of triumph and sanctuary for evermore. Associate Professor Helen Milroy, Aboriginal Child Psychiatrist and Australia’s first Aboriginal doctor, 2009. The Apology by the Prime Minister to Aboriginal and Torres Strait Islander peoples of Australia in February 2008 was the first step in a significant healing journey. Importantly, it was the commencement of a healing process rather than an end in itself. The Apology created a climate of hope and a sense that the government may be open to taking a different approach to Indigenous health and Indigenous affairs generally. This year, the Prime Minister marked the first anniversary of the Apology by announcing the establishment of a Healing Foundation to address trauma and healing in Indigenous communities.1 It is therefore timely to generate wide-ranging discourse about healing and what it means for Aboriginal and Torres Strait Islander health. A healing journey will not only deliver better lives for Aboriginal and Torres Strait Islander peoples, but is essential for the wellbeing of Australia as a nation. Healing means different things to different people. Within medical science, healing has specific meanings related to the pathophysiology of wound closure, organ repair and system function. The process of cell turnover occurs in the body to ensure health through the renewing of red blood cells, the sloughing and replacement of various epithelia, and bone remodelling. Throughout our daily work as doctors, we see the body’s “enthusiasm for life”. For Aboriginal and Torres Strait Islander doctors, healing goes beyond treating the disease. It is about working towards reclaiming a sense of balance and harmony in the physical, psychological, social, cultural and spiritual lives of our people, and practising our profession in a manner that upholds these multiple dimensions of Indigenous health. In essence, it is “Moving forward in our journey with hope for the future, with renewed energy, strength and enthusiasm for life”. Specific and holistic concepts of healing are not dissimilar, however, particularly if the foundational concept is that of “renewal”. Healing needs to occur at various levels — from cells, organs and systems to individuals, families and communities. A number of different modalities may be used to ensure healing is meaningful to different people and different communities. For example, this could mean Western-trained doctors working alongside Ngangkaris (traditional healers from Central Australia) to deliver an optimal health service that facilitates physical repair, psychological buffering, social nurturing, cultural reclamation and spiritual maintenance. Indigenous healing services need to be culturally meaningful and must focus on why people are at risk of succumbing to physical disease and to using drugs and alcohol, as well as the ways in which restoring cultural norms and repairing the social fabric can mitigate these negative disruptions. Health professionals must be culturally competent and need to understand the cultural and spiritual elements of health. The national effort to improve the health of Indigenous Australians is vital and must continue apace, with the driving principle of a holistic view of Indigenous health as being: Not just the physical well-being of the individual but the social, emotional, and cultural well-being of the whole community. This is a whole-of-life view and it also includes the cyclical concept of life–death–life.2 Having a state of health (however defined) assumes an individual has access to all levels of health care services and is able to negotiate the health system successfully. It also assumes access to nutritious food; the ability to have a good night’s sleep and feel safe; the capacity for motivation and the facility to undertake regular exercise or recreation; and the presence of sound relationships with family, community and society. It assumes that an individual is protected by reasonable health infrastructure. Many of these issues have been tackled in recent health reviews and initiatives, Council of Australian Governments announcements, and the national effort to “close the gap” in life expectancy. These initiatives are to be applauded, although they are well overdue. If implemented effectively, they can go some way towards healing. These efforts need to occur in parallel with a national discussion on the issues that are a little more confronting and yet are known to have an impact on health, such as the effects of cultural dislocation, dispossession,3 loss of autonomy,4 social exclusion, racism, and marginalisation.5 Unless Aboriginal and Torres Strait Islander peoples are able to take action to restore balance to their lives and to experience the strength that comes from regaining that balance — and unless the rest of society facilitates, supports and nurtures this action — we will be forever addressing the symptoms rather than the root causes. Until these issues can be resolved, healing cannot occur at a community level or at a national level. How can the medical profession further contribute to Australia becoming a healed nation? As a collective, we can promote understanding of the multiple determinants of Indigenous health — the physical, psychological, social, cultural and spiritual aspects of wellbeing; ensure this understanding informs clinical interactions as well as policy and resource allocation; advocate for and practise culturally appropriate health service provision across the care spectrum; encourage sectors such as housing, education and justice to work with the health sector to create reform; and advance an appreciation of the healing strengths of reconnecting with family, culture and Country. Clearly healing is a complex issue, and I hope this article raises questions and possibilities as to how healing might occur, and helps to explore the frameworks within which it can occur. The fundamental aim of healing is to provide a better future for our children and to create a world in which Aboriginal and Torres Strait Islander peoples and culture thrive. As a profession working towards this end, we can truly show leadership in guiding change and generating a sustainable vision of health for all Australians into the future.

Tamara Mackean BSc(Med), MB BS

Challenging the assumption that higher rates of intervention provide no benefits for babies Hardly a week seems to pass in Australia without an article in national newspapers drawing attention to the differences in obstetric intervention rates between private patients cared for by obstetricians and public patients who receive various models of care.1 The reported assumption has consistently been that the higher intervention rates observed in private patients are of no benefit to women or their babies, and possibly cause harm. This opinion has inevitably led to suggestions that federal support for private obstetric care be scaled back and redirected to models of care with lower intervention rates.2 An article by Robson and colleagues in this issue of the Journal reporting the results of a review of births in Australia (Adverse outcomes of labour in public and private hospitals in Australia: a population-based descriptive study)3 thus achieves increased significance by being published at a time when the federal Health Minister has received and is preparing her response to the report of the Maternity Services Review.4 Robson and colleagues report a retrospective analysis of the 789 240 singleton births occurring between 37 and 41 weeks’ gestation in Australia during 2001–2004, excluding about 15% of pregnant women for methodological reasons.3 Outcomes reported in the National Perinatal Data Collection (NPDC) were adjusted for recorded risk factors. Their study confirms increased intervention rates in private patients. A previous study by Roberts and colleagues reporting higher instrumental delivery rates for low-risk private patients found a higher risk of low Apgar scores in babies of public patients,5 which might have implied a possibility of poorer outcomes for these babies, but perinatal mortality and morbidity data were otherwise lacking. Robson et al’s study demonstrated a twofold increase in risk of perinatal death for babies delivered in public hospitals, as well as significant increases in risk of low Apgar scores, need for high-level resuscitation, and admission to a special care or neonatal intensive care nursery. Of the two maternal outcomes available in the NPDC, only perineal trauma was reported, and, somewhat unexpectedly given the higher rate of instrumental deliveries in private patients, the rate of third- and fourth-degree lacerations was lower in private patients (also confirming the findings of Roberts et al’s study5). Unfortunately, incomplete data precluded reporting of maternal blood loss, and the NPDC does not report other maternal complications. This situation should hopefully be addressed in the future by the Royal Australian and New Zealand College of Obstetricians and Gynaecologists’ planned maternal morbidity audit. So what can we learn from this study? It is always more difficult to rely on retrospective data, especially when gathered from populations with different sociodemographic factors, even when adjusting as far as possible for known risk factors. However, unless we are to conduct randomised controlled trials of private versus public models of maternity care (unlikely) or planned caesarean versus planned normal delivery (even more unlikely), the quality of these data is as good as any we are likely to obtain. It is worth noting that in restricting their analysis to women with singleton pregnancies delivered between 37 and 41 completed weeks’ gestation, Robson et al minimise the bias that follows from the fact that women with preterm deliveries, which are at highest risk of perinatal morbidity, are generally transferred when possible to tertiary referral centres in the public system. However, failure to similarly exclude outcomes for predictably high-risk pregnancies delivered at term at these centres (eg, babies with antenatally diagnosed major congenital abnormalities) introduces a numerically small but possibly significant bias towards a relatively higher risk of adverse outcomes in the public patient group. Adjusting for other known risk factors also minimises to the extent possible the differences in outcomes attributable to different prevalences of these risk factors in populations of differing socioeconomic background, but cannot eliminate them altogether. Notably, some of these socioeconomic differences would be expected to increase the risk for babies of private patients (higher proportions of primigravidae, maternal age of 40 years or older, and history of previous caesarean delivery). In addition, the exclusion of babies delivered after 41 completed weeks’ gestation is likely to reduce the rate of adverse outcomes in the public patient group, as allowing pregnancies past 41 weeks — when perinatal mortality is 70% higher than for babies delivered at 40 weeks6 — is virtually unknown in private patients, but does occur in the public system. This study has inevitably generated some media controversy7 because for the first time there are national data, albeit with methodological limitations, to suggest that private obstetric care and its associated higher rates of intervention might actually be benefiting babies, if not their mothers. The study is silent on major maternal problems other than severe perineal trauma, which might be associated with the increased obstetric intervention rates associated with private care and especially with caesarean delivery (haemorrhage, hysterectomy, wound complications and venous thromboembolism). Is it possible to extrapolate the findings of this study to conclude that private care provided by obstetricians, with its increased intervention rates, prevents perinatal mortality and morbidity in Australia? No, but it must make us at least consider the possibility, and challenge the tacit assumption that continuity of care with a private obstetrician and/or higher intervention rates do not prevent perinatal morbidity and mortality. Historically, it was always assumed that a decision in favour of intervention (especially caesarean delivery) presented a balance of risks — babies benefited, but this benefit was bought at the cost of increased maternal risk. More recently, some studies have been published which suggest that babies born by caesarean delivery are actually at higher risk of adverse outcomes, including perinatal death.8 Robson et al’s study supports a return to the previous understanding that, in choosing obstetric intervention, clinicians and their patients need to balance the potential benefits for the baby with the risks borne by the mother.

Andrew F Pesce MB BS, FRANZCOG

Guidance for clinicians on how to interpret conflicting evidence from recent studies Patients with advanced chronic obstructive pulmonary disease (COPD) have profound functional impairment and increased mortality.1 Inhaled bronchodilators, including the anticholinergic agents tiotropium bromide and ipratropium bromide, relieve symptoms and improve lung function and quality of life. Tiotropium also reduces COPD exacerbations and hospitalisations.2 Recently, the safety of anticholinergics in patients with COPD has been questioned. Based on a pooled analysis provided by the manufacturers, the United States Food and Drug Administration (FDA) alerted clinicians to an increased risk of stroke with tiotropium.3 Furthermore, a meta-analysis by Singh and colleagues4 and a nested case–control study by Lee and colleagues5 have reported an increased risk of cardiovascular events and death in patients taking inhaled anticholinergics. Two background issues are relevant. First, with once-daily tiotropium, an improvement in lung function is maintained over time, whereas the respiratory effects of ipratropium wear off within 6 hours of each dose. It is therefore likely that their physiological effects outside the respiratory system are different. Also, the potential for overuse is greater with ipratropium, when taken as needed for symptom relief. Second, the presence of COPD is itself associated with an increased risk of cardiovascular death.6 Reasons for this are incompletely understood and controversial. Furthermore, except for long-term oxygen, no medications for treating COPD clearly improve survival. A recent study suggesting improved survival with inhaler treatment was not designed to answer this question and its results require confirmation.7 The meta-analysis by Singh et al (some results of which have recently been revised in a published correction4) studied 17 randomised controlled trials in which cardiovascular events were reported and that involved 13 645 patients in whom either anticholinergics (ipratropium or tiotropium) or control therapies were used for at least 30 days.4 It included data not available in previous meta-analyses. The primary outcome was a composite of cardiovascular death, myocardial infarction or stroke. This was more prevalent in the anticholinergic group, with a relative risk of 1.60 (95% CI, 1.22–2.10) and a risk difference of 0.007 (95% CI, 0.003–0.013). The secondary outcome was all-cause mortality, which was not statistically different between the two groups (the revised value given in the correction to the original study [P = 0.05] approaches, but does not reach, statistical significance). The nested case–control study by Lee et al used national databases to identify 32 130 cases (patients with COPD who died) and 10 times that number of controls (surviving patients with COPD) in the US.5 It showed an association of ipratropium use with both all-cause mortality (odds ratio [OR], 1.11; 95% CI, 1.08–1.15) and cardiovascular death (OR, 1.34; 95% CI, 1.22–1.47). Tiotropium was not examined in this study. Coincidentally, results of the largest and longest-running randomised controlled trial of tiotropium use — the UPLIFT trial — have also recently been published.8 This was a 4-year study investigating the clinical benefit of tiotropium and decline in lung function in 5993 patients with COPD. It found that in patients treated with tiotropium, there was no increase in cardiovascular death or stroke, myocardial infarction was less frequent, and there was a non-significant trend to lower all-cause mortality. These findings are in keeping with a meta-analysis conducted in 20062 and a large population study in 2007,9 but the prospective nature of the UPLIFT study gives it greater validity. How can these very different results be explained? Methodological weaknesses and differences in study design are probably a major factor. First, cardiovascular events and strokes were not defined a priori in any of the studies, raising the possibility of inaccurate data collection. In this setting, all-cause mortality is likely to be more reliable. Second, both the UPLIFT trial and Singh et al reported very high discontinuation rates. A third methodological weakness is the presence of confounders; for example, Lee et al’s study was not able to eliminate or adjust for the crucial confounders of COPD severity and smoking status. Finally, study populations differed. In the UPLIFT study, the rate of ongoing smoking was low and the use of other concurrent COPD medication probably higher than in most of the studies analysed by Singh et al — both these factors may be cardioprotective. How does one act on this conflicting and partially flawed safety data? Regarding tiotropium specifically, no study has shown an increase in all-cause mortality. In the studies performed so far, all-cause mortality is likely to be a more robust outcome than death due to cardiovascular or respiratory causes. Even if the increase in cardiovascular events with tiotropium reported by Singh et al is correct, the size of the effect is small, and the unchanged all-cause mortality suggests that another specific cause of death has decreased. Singh et al did not report respiratory deaths, but some other studies have shown a decrease in these with tiotropium use,9 consistent with its beneficial effects on exacerbations and hospital admissions.8 The safety of ipratropium is less clear. The concerns raised by Singh et al are reinforced by Lee et al’s finding of increased all-cause and cardiovascular mortality with ipratropium use. No guidelines have yet incorporated these recent studies into their recommendations, and the FDA’s response based on its ongoing safety review is pending. In the interim, the use of tiotropium in patients with COPD is likely to be safe and beneficial. If a short-acting bronchodilator is desired, the cardiac risk profile of the patient must be considered because of the uncertain safety of both ipratropium and short-acting β2 agonists.10 Finally, the uncertainty about the safety of anticholinergics needs to be placed in the context of managing patients whose COPD presents major challenges related to their severe respiratory impairment and the increased risk of comorbidities such as lung cancer, depression and osteoporosis, as well as cardiovascular disease.

Mark J Hew MB BS, PhD, FRACP · Piersante Sestini MD · Louis B Irving MB BS, FRACP, FRACGP

Do you have patients who could benefit from therapeutic pacing and defibrillator devices? In recent years, management of chronic heart failure has advanced considerably, especially the optimisation of key pharmacological strategies (angiotensin-converting enzyme inhibitors, β-blockers) and multimodal management. In parallel, there has been a quieter revolution: the use of therapeutic pacing and defibrillator devices in patients with heart failure has moved from experimental and clinical research to everyday clinical practice. Milestones include landmark trials establishing the definitive mortality benefit of implantable defibrillators in ischaemic cardiomyopathy,1 the clinical utility of electronically synchronising contraction of both ventricles,2 and mortality benefits of cardiac resynchronisation therapy (CRT).3 Nonetheless, therapeutic pacing and defibrillator devices appear to be underutilised,4 perhaps due to lack of awareness of their clinical benefits and concerns regarding cost. What are the established modalities? Sudden cardiac death is a significant risk in patients with impaired left ventricular function. The use of implantable cardioverter defibrillators (ICDs) is established in primary and secondary prevention of sudden cardiac death in chronic heart failure — large randomised controlled studies have demonstrated a significant mortality benefit.1,5 American6 and Australian7 guidelines for heart failure management state that an ICD may be used after cardiac arrest, ventricular tachycardia or ventricular fibrillation; ≥ 40 days after myocardial infarction in patients with New York Heart Association (NYHA) class I, II or III symptoms and left ventricular ejection fraction (LVEF) ≤ 30%; and in patients with ischaemic or non-ischaemic cardiomyopathy, NYHA class II or III symptoms and LVEF ≤ 35%. Newer “risk stratifiers” are being explored to better identify patients likely to benefit from ICD therapy.8 The implantation procedure for an ICD is identical, in principle, to that of a pacemaker, with some exceptions: the lead is larger (thus stiffer), so care is required during its manipulation within the heart; the battery is larger, so it requires careful positioning to avoid skin erosion; and testing of the device involves inducing ventricular fibrillation to ensure adequate sensing of arrhythmia and an adequate safety margin in terms of the threshold of defibrillation. Also, the sophisticated programming of ICD therapy requires a cardiac electrophysiologist. ICDs can be programmed to treat ventricular arrhythmias with either antitachycardia pacing (which is painless) or shock therapy. After the patient experiences their initial therapy, which unfortunately may involve a potentially distressing shock while the patient is conscious, individualised adjustments may be needed. Despite the survival benefit associated with ICDs, their impact on quality of life is uncertain. In contrast to other heart failure therapies, ICDs do not improve cardiac function. They would not be expected to improve a patient’s exercise capacity or ability to perform activities of daily living. Also, implantation can be associated with various immediate and late complications, including device infection, failure and inappropriate discharge.9 The failing heart is frequently characterised by abnormalities of mechanical synchrony, often reflected by abnormalities of electrical conduction. Based on adverse consequences of ventricular dyssynchrony in heart failure, researchers have sought to resynchronise the failing myocardium. One approach, CRT, involves pacing both ventricles in a coordinated manner to restore the normal physiological chronology of left- and right-sided contraction. Ventricular dyssynchrony can be crudely detected on an electrocardiogram by QRS prolongation.10 Epidemiologically, QRS prolongation has been associated with worsening of clinical outcomes in patients with heart failure. Echocardiography has been proposed as a better tool for evaluating mechanical dyssynchrony.11 The implantation of a CRT device extends the standard pacemaker or ICD implantation procedure by placement of a left ventricular pacing lead. This requires specialised sheaths to access the coronary sinus, angiographic identification of an appropriate lateral branch, and careful positioning of the lead. Several factors determine the ideal position for the lead, including proximity to the lateral wall at a position furthest from the right ventricular lead, stability of lead placement, presence of viable myocardium that can be captured by pacing at the site, and avoidance of diaphragmatic pacing. The procedure requires an experienced operator and a service that can optimise programming. CRT has undergone considerable evaluation and, according to American and Australian guidelines, it is indicated in patients with NYHA class III or IV symptoms, LVEF ≤ 35% and QRS duration on electrocardiogram > 120 ms.6,7 More than 4000 patients have been evaluated in randomised single- or double-blind controlled trials of CRT in heart failure and, in systolic heart failure, CRT has consistently been associated with improved patient wellbeing and ventricular systolic function, and reduced recurrent hospitalisation for heart failure. Meta-analyses and a stand-alone study have shown reduced all-cause mortality with CRT.3,12 These benefits add to those of standard drug therapies for systolic heart failure, and may be further enhanced by use of a defibrillator. Indeed, most CRT devices used in Australia include a defibrillator function. Ideally, patients should be in sinus rhythm for maximum benefits from this therapy. Some evidence suggests that CRT is also beneficial in patients with atrial fibrillation, and that this cohort may be better optimised with atrioventricular node ablation.13 However, current Australian Government Department of Health and Ageing guidelines do not support the use of these devices in patients with atrial fibrillation.14 In addition, not all patients who meet the criteria for CRT benefit from the therapy. There is a 20%–30% “non-response rate”, in that patients do not feel better or ventricular function does not improve.14 The reason for this is elusive, but improved evaluation of dyssynchrony, using measures more sophisticated than QRS duration (eg, echocardiography, magnetic resonance imaging), may reduce the non-response rate, and CRT trials that base entry criteria on results of imaging alone are underway. Nonetheless, CRT has gained popularity in recent years, particularly for patients who remain severely symptomatic despite drug therapy. What other modalities are being evaluated? Cardiac contractility modulation (a new form of electrical therapy) is currently being evaluated in patients with heart failure. A recent clinical study demonstrated improved exercise tolerance and quality of life,15 but these data need to be confirmed in large, randomised controlled studies. Ventricular pacing alone has also been trialled, but can result in deleterious mechanical effects. In patients with impaired left ventricular function, right ventricular pacing can cause further deterioration.16 Adverse effects may be minimised by pacing the right ventricular outflow tract or high septum rather than the apex.17 Perhaps more importantly, atrioventricular synchrony can be maintained, and many pacemakers allow minimisation of ventricular pacing by various programmable algorithms. What is needed now? Over the past decade, many pacing therapies have been rigorously evaluated in patients with chronic heart failure, and there are now proven indications for their application in clinical practice. The clinical outcomes, potential problems and costs of CRT, ICD and right-sided pacing are summarised in the Box. Doctors should be aware of these therapies and consider referring individual patients who meet the criteria for their use. Comparison of some features of pacing modalities for chronic heart failure and comorbid arrhythmias Cardiac resynchronisation therapy Implantable cardioverter defibrillator Right-sided pacing Clinical outcomes Decreased mortality, morbidity and hospitalisation Improved exercise tolerance, quality of life, NYHA class Decreased mortality Decreased incidence of sudden cardiac death No proven benefit in chronic heart failure Potential problems Relatively high non-response rate Procedural complications (early and late) Uncertain quality-of-life benefits Inappropriate discharge Procedural complications (early and late) Worsening left ventricular function in systolic chronic heart failure in certain modalities Cost14 High: public hospitals, $21 075; private hospitals, $59 100* High: public hospitals, $14 975; private hospitals, $45 100† Relatively low NYHA = New York Heart Association. RA = right atrial. RV = right ventricular. LV = left ventricular. * Costs for cardiac resynchronisation therapy include: (public hospitals) generator, $17 000; RA lead, $475; RV lead, $1500; LV lead, $2100; and (private hospitals) generator, $44 500; RA lead, $1350; RV lead, $8750; LV lead, $4500. † Costs for implantable cardioverter defibrillator include: (public hospitals) generator, $13 000; RA lead, $475; RV lead, $1500; and (private hospitals) generator, $35 000; RA lead, $1350; RV lead, $8750.

Henry Krum MB BS, PhD, FRACP · Prashanthan Sanders MB BS(Hons), PhD

A national study of eating disorders highlights potential underdiagnosis and high rates of complications in 5–13-year-olds In this issue of the Journal, Madden and colleagues report their prospective investigation of eating disorders in children across Australia (Madden et al).1 This study is an important “first” and investigates the putative increasing problem of early-onset eating disorders (EOEDs) in children aged 5–13 years. Over 3 years, detailed data were collected by the Australian Paediatric Surveillance Unit for 101 children who were managed either as outpatients or in hospital for EOEDs — mainly from paediatricians, but also from child psychiatrists. Most children were hospitalised for treatment. The study raises interesting issues and unanswered questions about eating disorders. Although there are no earlier data for comparison (ie, conclusions cannot be drawn about whether or not the incidence of eating disorders in younger children is increasing), the annual incidence rate for EOEDs of 1.4 per 100 000 children aged 5–13 years accords with international figures. This is especially true of the even higher incidence rate in New South Wales, where there may have been more comprehensive reporting. Of particular concern were the high rates of severe, life-threatening medical complications (hypothermia, hypotension and bradycardia) in inpatients, suggesting under-referral or under-recognition of the problem, and thus delays in active specialist care. Further, most of the children received nasogastric feeding, and a third received psychotropic medication — treatments that may not have been required with earlier, more active intervention. Turning to specific issues, there was a relatively high proportion of boys in this study — a quarter of the total. In contrast, men account for about one in 10 adult cases of anorexia nervosa and bulimia nervosa. When broader diagnostic groups, such as binge eating disorder, are considered, rates are higher, particularly in community samples,2 albeit men account for a minority (around 30%) of patients.3 However, the types of eating disorder reported in higher numbers in men (such as binge eating disorder) differ from the EOEDs reported in Madden and colleagues’ study. EOED was characterised by “determined food avoidance plus weight loss or a failure to gain weight during a period of growth, in the absence of any identifiable organic cause”1 — a variant of anorexia nervosa, if not full-spectrum anorexia nervosa. Nevertheless, the finding that one in four EOED cases affected boys is consistent with results of other studies. For example, a Danish study found males to be younger than females at first presentation and more likely to re-present with psychotic disorder.4 In addition, a large recent study of United States high school students found that binge-eating symptoms were reported by 11.0% of girls and 3.3% of boys, and that recurrent serious purging behaviour (eg, vomiting, laxative use or excessive exercise) was reported by 9.4% of girls and 13.5% of boys.5 How EOEDs in children relate to the eating disorders that emerge later, in adolescence and adult years, is unknown. A 10-year follow-up of a community cohort of 1943 Australian 14–15-year-old adolescents found that partial anorexia nervosa and bulimia nervosa occurred in nearly one in 10 girls aged 15–17 years, and that these girls appeared to be psychologically vulnerable, with poorer functional outcomes and psychiatric morbidity. However, there was little evidence of progression to full anorexia nervosa or bulimia nervosa.6 In contrast, prepubertal children with eating disorders are thought to have a particularly poor prognosis, with high levels of physical and psychiatric morbidity.7 Madden and colleagues’ data support a hypothesis that EOEDs may differ in important ways — including sex distribution and course — from eating disorders with onset in adolescence and adulthood. Whether they have a differing outcome is unknown, and follow-up is imperative. It is also important that an evidence base for treatments for prepubertal children is developed, despite the well known challenges of conducting controlled trials in an uncommon disorder in children. Notwithstanding this, the high (71%) rate of response to treatment reported by Madden and colleagues accords with other research that has demonstrated more positive treatment outcomes in older children and adolescents when compared with adults, particularly for anorexia nervosa.7 Madden and colleagues report that comorbidities, particularly anxiety disorders and depression, were common in the patients with EOEDs; they also found that around one in five patients were prescribed antidepressants, and one in 10 were prescribed antipsychotics. Given the concerns about the effects of these medications on the developing brain and the risks of antidepressant prescribing in youth, this level of use seems high. It is likely to reflect the severity of illness (especially anorexia nervosa), and the small evidence base supporting use of second-generation antipsychotics, such as olanzapine, in adults with anorexia nervosa.8 Lastly, these results highlight the dilemma of how to address concerns about the epidemic of obesity, while also avoiding contributing to the problems of the much smaller number of children with EOEDs that involve severe dietary restriction and weight loss. Although there is no similar “epidemic of eating disorders”,9 a recent South Australian study indicated that disordered eating in adults is increasing, mostly in the overweight population.10 This supports closer integration of prevention strategies and treatments for disordered eating and obesity, such as the promotion of healthy eating patterns and foods, rather than severe dietary restriction. Extreme weight control behaviour and weight disorders are both important health problems in young people, and Hippocrates’ aphorism that “a diet brought to the extreme point of attenuation is dangerous; and repletion, when in the extreme, is also dangerous”11 remains relevant today. In conclusion, Madden and colleagues address an important and potentially increasing problem in prepubertal children. It is imperative that research attention is now directed towards understanding why such young children are developing severe eating disorders and how effective identification and treatment can be targeted earlier.

Phillipa J Hay MD, DPhil, FRANZCP

An appropriate strategy is to test patients with symptoms and signs attributable to coeliac disease In recent years, knowledge about coeliac disease (CD) has improved significantly, and we now have a better understanding of the diagnosis and pathogenesis of the disease. In this issue of the Journal Chin and colleagues report the largest community study of CD undertaken in Australia.1 The study found a prevalence of CD of between 0.56% and 0.96%,1 similar to prevalences found in European population studies. A recent population-based serological study (without biopsy) in the United States found a prevalence of 0.95%.2 The screening strategy used by Chin and colleagues involved IgA and IgG anti-tissue transglutaminase (anti-tTG) antibody assays, HLA-DQ2 and HLA-DQ8 haplotyping, and, where appropriate, gastroscopy and duodenal biopsy.1 We believe that the data do not justify population-based screening for CD in Australia, but the diagnostic approach developed by Chin et al is appropriate for diagnosing patients in whom CD is suspected. Genetic and environmental factors are important in the genesis of the disease. The role of the HLA-DQ2 and -DQ8 haplotypes is yet to be fully understood. One or other haplotype is present in nearly all CD patients, yet they are also present in 20%–40% of subjects without CD. The “gold standard” for diagnosis has long been histological findings from a duodenal biopsy, despite the discordance between clinical symptoms and these findings. CD is caused by an immune response to antigens in gluten proteins. Wheat, barley and rye, but not corn or rice, contain gluten proteins. Ingested gluten is partially digested to peptides, some of which are absorbed into the lamina propria of the small intestine. The enzyme, tissue transglutaminase, deamidates certain glutamine residues in the peptides to glutamic acid. In patients with CD, this results in enhanced binding to HLA-DQ2 or -DQ8 cells. Within the lamina propria, T cell recognition of the amino acid sequences presented by the DQ2 or DQ8 cells produces a series of inflammatory changes, with the release of cytokines and the activation of lymphocytes. This leads to the characteristic histological findings in the proximal duodenum — lymphocytic infiltration, villous damage or loss, and crypt hyperplasia.3 Increases in transglutaminases in the lamina propria produce several effects: they catalyse the crosslinking of gluten peptide residues to lysine residues in various local proteins, including in transglutaminase itself, creating an immunogenic gluten–peptide–protein complex. This becomes an autoantigen, producing the characteristic IgA/IgG anti-tTG antibody of CD, which is best detected by an enzyme-linked immunosorbent assay. The mainstay of diagnosis of CD remains the anti-tTG assay, followed by duodenal biopsy, with the patient on a gluten-containing diet (equivalent to four slices of wheat bread a day) for several weeks. It is important to recognise that false-negative test results do occur, an underappreciated cause being IgA deficiency, which occurs in one in 40 people and can be identified using a combined IgG/IgA anti-tTG assay. Recent evidence suggests that the IgA/IgG anti-tTG antibody test has superior performance (sensitivity of about 90%, specificity of about 80%) to the anti-endomysial antibody (EMA) test, is less expensive, and overcomes the potential problem of IgA deficiency.4 If doubt persists, HLA haplotyping is useful, and a negative test for both DQ2 and DQ8 effectively excludes the diagnosis.5 Several factors should raise suspicion of the presence of CD and prompt testing: first-degree relatives of CD patients; adult type 1 diabetes mellitus; osteoporosis; ill-defined abdominal symptoms (eg, irritable bowel syndrome); iron or other nutritional deficiency; unexplained transaminase elevations; or Down syndrome. In patients in whom testing points to CD, the benefits of a gluten-free diet should be considered. Given that a gluten-free diet is arduous, we need to be assured that the risk–benefit ratio is appropriate. The benefits in those with florid symptoms are life-transforming (“Doctor, I never knew what it was like to be well before the diet”), but for the symptomless patient the gains in quality or quantity of life are less clear.2 Recent studies show a mild increase in risk of death from malignancy, which appears to diminish with time from diagnosis. Future research needs to quantify the benefits, if any, of lifelong treatment of people with asymptomatic and currently undiagnosed CD. What, then, is the role of screening for CD? To be justified, population screening must be effective, acceptable and cost-effective, and these conditions are not met for CD.6 Focused screening is preferable, as shown by a number of primary care studies. A study from nine surgeries in central England screened 1000 sequential patients with an anti-EMA test and found 30 patients in whom CD was confirmed by small-bowel biopsy. Half of these 30 patients presented with anaemia.7 Another study from five general practices in Yorkshire reported positive serological results in 12 of 1200 subjects, a prevalence of 1%. In patients with irritable bowel syndrome, the figure was 3.3%; in those with iron-deficiency anaemia, 4.7%; and in those complaining of fatigue, it was 3.3%.8 In a more recent US study in primary care, all individuals with symptoms or conditions known to be associated with CD were tested: 30 of 976 patients had positive results of an anti-tTG test and 22 (2.25%) were diagnosed with CD. These studies support our recommendation of a low threshold for serological testing of patients with coeliac-associated conditions. In summary, CD is now recognised as a common disorder, with a population prevalence of nearly one in 100 people. In most people, its manifestations are mild or non-existent. In others, it is associated with symptoms such as fatigue, iron-deficiency anaemia, and vague abdominal complaints. Rarely, CD is associated with more significant problems, such as strange neurological symptoms, hyper- or hypothyroidism and hepatic dysfunction. The most appropriate strategy for general practitioners is to have a high level of suspicion when patients present with symptoms and signs that may be attributable to CD and to test these patients.

John M Duggan AM, MD, FRACP · Anne E Duggan MHP, PhD, FRACP

A key issue is to recognise when a duality of interest has become a conflict of interest In Australia, provision of specialised product information and promotion by the pharmaceutical industry of drugs approved by the Therapeutic Goods Administration is an integral part of the health care environment. The pharmaceutical industry provides information and training to health professionals about new products; funding for conferences; support for professional and social activities secondary to medical education; support for the conduct of research and information about its outcomes; and opportunities to meet with peers. However, the primary goals of the pharmaceutical industry and health professionals differ: the pharmaceutical industry has a financial responsibility to shareholders, while health professionals have a moral responsibility to their patients. The challenge for both is to manage their responsibilities when interacting with one another. The pharmaceutical industry’s code of conduct1 upholds the principles of Australia’s Quality Use of Medicines program and National Medicines Policy. However, an interaction between pharmaceutical representatives and hospital employees will ultimately have a promotional intent. In itself, an indirect promotional activity is not a problem. However, the interaction will often influence prescribing.2 Many health professionals deny that such activity influences their behaviour, although, paradoxically, they believe their peers may be more easily swayed.3 Appropriate provision of patient care requires health professionals to understand these influences and keep them in mind in order to maintain independence of judgement. Ethics relating to promotional activities of pharmaceutical companies and managing conflicts of interest have been recently reviewed.4-10 Some researchers have argued that contact with the pharmaceutical industry should be more restricted and certain activities prohibited. In the United States, steps have been taken to prohibit all gifts (including meals) and to institute central management of product samples.8 A US report commented that “bias, either by appearance or reality, has been woven into the very fabric of continuing education” and called for cessation of commercial support from pharmaceutical and medical device companies.11 In Australia, while the move to state and federal funding and other non-commercial sources for educational and drug information activities is currently being debated, it is unrealistic to prohibit contact between health professionals and the pharmaceutical industry. It may be argued that industry plays an important role in health education — indeed, constructive engagement between industry and health professionals may be in the interests of patients. Severing all contact between industry and health care providers could limit open dialogue, hamper innovation and create a huge gap in educational support for health professionals. Initiatives to bridge the gap have been suggested.4-6 In the meantime, hospital staff must analyse the nature of their current interactions with the pharmaceutical industry and aim to improve it to optimise benefit to the patient. Codes of practice have been developed by professional bodies, societies, hospitals, government and the pharmaceutical industry in an attempt to ensure that interactions between hospital-based health professionals and the pharmaceutical industry are ethical and in the interests of the patient. However, a more practical framework is required to evaluate these interactions and to work towards achieving the highest standards of patient care and quality use of medicines. At the request of its members, the New South Wales Therapeutic Advisory Group (NSW TAG) recently updated its existing position statement on liaison between hospital staff in NSW and the pharmaceutical industry. The position statement provides evidence-based guidelines to help hospital staff recognise the activities that enhance clinical practice and those that potentially damage the relationship between health professionals and patients.12 It suggests steps to minimise potential conflicts of interest and ways to support ethical interaction, including making full use of independent sources of evidence-based medicine. It proposes that all health professionals adopt the approach of the Royal Australasian College of Physicians with regard to identifying and managing dualities and conflicts of interest.13 A duality of interest (where two or more interests coexist) is not unethical, but the key issue is to recognise when one interest is compromising the other (ie, when a conflict of interest is present). It is not enough to voluntarily disclose a duality of interest and then feel justified in proceeding regardless. Members of NSW TAG have discussed establishing a system of review and authorisation, deciding whether steps are necessary to separate or prohibit the conflicting activities and how open communication contributes to the transparency of the process. Our intention has been to ensure that the primary objective of professional interactions with pharmaceutical companies is to advance the health and wellbeing of patients. A recent article called for a set of guidelines for academic medical centres and opinion leaders.4 Extension of practical guidelines to all health professionals is a necessary next step. The pharmaceutical industry has established a system of self-regulation.1 In authorising the Medicines Australia code of conduct, currently under review, the Australian Competition and Consumer Commission requires details to be published of educational events provided or sponsored by member companies. All events have been reviewed by an independent auditor, and the first of these 6-monthly reports is now available.14 The audit had limitations with regard to investigation of high-cost activities and verification of data supplied. Nevertheless, such measures from industry to increase transparency support the intentions of NSW TAG’s position statement.12 The issues discussed in the position statement extend well beyond the pharmaceutical industry. They also include providers of medical devices, chemicals in pathology laboratories, and machines and consumables in radiology departments. Understanding the differences between the role of the health professional and that of the pharmaceutical industry is fundamental to understanding how to handle the interaction between the two groups. This process is evolving and the NSW TAG position statement is considered a “work in progress” to provide guidance within existing codes. The pharmaceutical industry and health professionals need to continue to foster a process of introspective challenge and regulation. Ongoing discussion by all stakeholders to find solutions that benefit patients is paramount.

Diana H Shipp BPharm, MRPharmS · Gordon Mallarkey BSc(Hons), PhD

Transparency and open communication are key to a healthy relationship Medical practice these days is influenced to a large extent by clinical practice guidelines. Usually sponsored by professional bodies, these compendia of advice should be produced by groups of experts with broad representation and credibility. These experts are expected to follow clearly defined processes1 to arrive at recommendations that are based on evidence, and which are unadulterated by other influences, such as commercial considerations. Strict adherence to this framework underpins the authority and acceptability of the guideline. But these standards are sometimes not met, and there have been calls for reform to ensure reliability of guidelines, and thereby offer patients protection from treatment based on guidelines whose content may be affected by extraneous influences.2-4 In this issue of the Journal, Millar5 adds to the disquiet regarding guideline formulation with his critique of the Prevention of venous thromboembolism: best practice guidelines for Australia and New Zealand, fourth edition,6 produced by a Working Party of Australian and New Zealand experts. The Guidelines were published in booklet form by a company part-owned by a member of the Working Party, and were supported by a grant from a pharmaceutical company that manufactures enoxaparin, a low molecular weight heparin recommended in the Guidelines for prophylaxis and treatment of venous thromboembolism. In Australia, the National Health and Medical Research Council (NHMRC) has published criteria for developing guidelines,1 and in doing so has set high standards, including standards for commercial sponsorship. In light of the NHMRC criteria, the overall process involved in the Guidelines can be criticised for the: apparent lack of independent peer review, as best exemplified by publication in a recognised medical journal; lack of comprehensive declarations of conflicts of interests in a setting where at least a perception of pecuniary interest is possible; failure to provide levels of evidence or costing for the recommendations; failure to include a full and readily available list of the references on which the evidence for the recommendations are based; failure to divulge the precise writing process and the details of the relationships between the publisher, the Working Party in general, and individual Working Party members and the sponsoring pharmaceutical company; and publication as a booklet that was initially distributed only by the sponsor, and thus not easily or independently accessible. Millar’s article implicitly raises the question of tolerance by the medical profession in general of the involvement of the pharmaceutical industry with these and other guidelines. At the core of this issue lie the opposing aims and philosophies of the pharmaceutical industry and medicine — namely that, although both groups ostensibly work for the benefit of patients, the industry does so to make a return on capital, whereas doctors generally do so altruistically. As stated in a recent commentary in JAMA: By favoring . . . one therapy over another, guidelines often create commercial winners and losers, who cannot be disinterested in the results and who therefore must be separated from the process.2 Nevertheless, it is natural that the pharmaceutical industry has a keen interest in guideline development. Commenting on the interaction of industry and medicine, Sir Iain Chalmers of the James Lind Initiative in the United Kingdom was recently quoted as saying: I do not blame industry for trying to get away with anything that is normally considered to be its primary purpose, which is to make profits and look after its stakeholders’ interests.7 Sponsorship and marketing behaviour is not unlawful (nor should it be), and indeed is at the centre of company philosophy and statute in a capitalist economy. Therefore, the restraint on unbridled marketing effort that can compromise patient care lies squarely with the medical profession. The profession’s individual members are obliged to maintain a respectful distance from the pharmaceutical industry and show some disdain for the apparent benefits of pharmaceutical sponsorship — to avoid being stabbed, one should not waltz too closely with the porcupines! Two senior editors of JAMA recently wrote: The profession of medicine, in every aspect — clinical, education, and research — has been inundated with profound influence from the pharmaceutical and medical device industries. This has occurred because physicians have allowed it to happen, and it is time to stop.9 In Australia, there is no overarching national policy for interactions of Australian doctors and the pharmaceutical industry. We should consider the lead of our colleagues in the UK, where the Royal College of Physicians of London (RCP) recently published a report entitled Innovating for health: patients, physicians, the pharmaceutical industry and the NHS, which extensively defines a framework for proper interaction.10 The Royal Australasian College of Physicians has also commented on this topic.11 There have also been recent multinational calls for the cessation of industry support for continuous medical education directed to individual doctors and institutions.10,12-14 However, the President of the RCP counsels that there is no need to destroy the bridges between industry and the profession. What is required is that the culture between these sectors should be transparent, and governed by open communication and agreed-upon national policy.15 This is sound wisdom to guide national policy deliberations in Australia.

Martin B Van Der Weyden MD, FRACP, FRCPA

Cycling is an affordable, convenient and achievable form of physical activity for all Australians Cycling, the fourth most popular physical recreation in Australia, is increasingly being used as a means of transport. As a form of regular physical activity, it confers substantial health benefits that are accessible to people of all ages.1 The epidemiological evidence is growing that cycling has health-enhancing effects, independent of other leisure-time physical activity. In a large Danish cohort followed up for 15 years, a 39% reduction in all-cause mortality was observed in those who cycled to work, and this was independent of participation in sport and other physical activity.2 Other large population studies have shown the effects of commuting by bicycle on reducing mortality and cardiovascular risk among Finnish women,3 and similar risk reductions for Chinese adults in Shanghai.4 Ecological observations have noted lower rates of obesity in regions with high rates of cycling.5 The article by Sikic and colleagues in this issue of the Journal describes cycling-related injuries in Victoria, and shows a 5-year increase in emergency department presentations, hospital admissions and major trauma among cyclists.6 This increase is of concern, and the authors reasonably call for preventive approaches. For many years, cycling advocates have called for a greater investment in cycling infrastructure, and studies overseas have demonstrated the potential for this investment to reduce injury outcomes. For example, cycling injuries are between eight and 30 times more common in the United States compared with the Netherlands or Germany.7 Similarly, rates of cycling-related deaths are much lower in Western Europe and declined by 60% between 1975 and 2000, compared with a much smaller decline in the US.5,8 Importantly, as Sikic et al acknowledge, their analyses do not adjust for the population denominator.6 More people are cycling now than 5 years ago — there are about a million new bicycles sold in Australia each year, and more people are cycling to work, with the greatest increases occurring in Victoria where the study by Sikic et al was conducted.1 Although there is a positive correlation between numbers of cyclists and injuries, the association is not simply linear. Known as the “safety in numbers” phenomenon, when more people cycle, collectively it becomes safer, and the injury rate per kilometre cycled decreases.9 Sikic et al suggest that people who ride bicycles should be registered,6 but requiring registration for all cyclists would not provide an accurate measure of cycling “exposure”, such as time spent cycling and distance travelled. It would cost more to administer than it would recoup, and it would likely act as a significant deterrent to casual or occasional cycling. In particular, cyclist registration would make it more difficult to encourage populations to shift to trial spontaneous recreational cycling. Research to calculate cycling times and distances as a population denominator for risk assessment should be a priority. In the Victorian data reported,6 most cycling injuries occurred on streets or highways where bicycles share the road with cars. Even though the absolute risk is still low, these injuries are mostly preventable. Making cycling safer requires better infrastructure and facilities for cycling, especially the provision of separated bicycle paths and cycle lanes.1,7 At the same time, driver attitudes and behaviour must be addressed. Strategies include enforcing lower driving speeds, traffic calming, parking restrictions, and community support for a safer road environment. Further, integrating cycling into public transport schedules and systems, including simple measures such as bicycle parking at train stations, would make cycling easier and give cyclists more options for safe commuting. In London, after the introduction of a “congestion tax” restricting car use into the city centre, combined with new bicycle lanes, cycling education and better public transport, many more cycling trips were made, and yet the overall number of cyclists injured actually declined between 2001 and 2004.10 It is generally understood what needs to be done to increase cycling participation levels. Better urban design, such as higher density development, mixing residential and commercial land use, and shorter trip distances, will facilitate more cycling.1 Other strategies to encourage cycling include behaviour change programs such as TravelSmart, Ride to Work, and Ride to School initiatives, public bicycle events to encourage infrequent and novice riders to cycle in a supportive social environment, and bicycle education programs for both children and adults.1 A dominant car culture and concerns about safety are the main reasons people give for not cycling in Australia.11 Mass media marketing campaigns are needed to help legitimise the value of cycling as transport, and advise drivers about relevant cycling road rules. Despite the perceived risks of cycling, the absolute magnitude of the risk is low, and the benefit-to-risk ratio is overwhelmingly positive; for chronic disease prevention, obesity reduction and mental health, the benefits are substantial.12 Cycling provides an affordable, convenient and achievable form of physical activity for all Australians, including children and youth, through to older adults with chronic conditions. As a physical activity, it also meets transport and traffic management needs, and is eco-friendly. Much more needs to be done in Australia to provide an environment that encourages people to cycle safely. This means giving greater funding and community priority to allocating road space for cycling. It also means physicians recommending that suitable patients consider cycling, and supporting efforts to improve the urban environment for cycling.12

Adrian E Bauman PhD, FAFPHM · Chris Rissel PhD

How can we ensure colonoscopy services are available to those who need them most? Bowel (colorectal) cancer is the most common cancer affecting both men and women in Australia, with 13 076 cases diagnosed and 4164 deaths reported in 2005.1 It is the second commonest cause of cancer-related death, behind lung cancer. The incidence of bowel cancer increases exponentially after 50 years of age, with a lifetime risk of about one in 17 among men and one in 26 among women.1 Bowel cancer satisfies most of the World Health Organization criteria for population cancer screening.2 Specifically, it is a common, serious cancer, and its natural history is reasonably well understood. It arises from precursor adenomas, and removal of these prevents cancer development. Importantly, most adenomas and early cancers are asymptomatic. Detection at early stages confers an excellent prognosis, and there are numerous tests for early detection and intervention, with the potential to reduce the incidence, morbidity and mortality of the disease. Cancer screening aims to identify affected individuals who do not suspect they have the disease. This is in contrast to performing diagnostic investigations for symptomatic patients, or targeting individuals with a significant family history of bowel cancer, a history of inflammatory bowel disease, previous adenomatous polyps or previous bowel cancer. However, bowel cancer screening recommendations can be confusing for medical practitioners. Numerous tests of varying performance levels are available, and it is difficult to separate recommendations for the population from those targeted towards individuals. There are also significant differences between the Australian recommendations endorsed by the National Health and Medical Research Council (NHMRC)3 and two recently published American guidelines, from the United States Preventive Services Task Force (USPSTF)4 and from a collaboration of the American Cancer Society, the US Multi-Society Task Force on Colorectal Cancer (representing the American Gastroenterological Association, American Society for Gastrointestinal Endoscopy, American College of Gastroenterology and American College of Physicians) and the American College of Radiology.5 Interestingly, these guidelines differ due to differing interpretations of essentially the same evidence. It is important to note that the newer American guidelines are less relevant to the Australian health care environment, and should not usurp the existing NHMRC recommendations in Australia. The NHMRC guidelines strongly recommend screening from the age of 50 years, by performing a faecal occult blood test (FOBT) at least every second year. The strength of this recommendation arises from three large, population-based, prospective randomised controlled trials demonstrating a mortality reduction of 15%–33%.3-5 No other cancer screening strategy is based on such strong evidence. Flexible sigmoidoscopy performed 5-yearly receives an equivocal recommendation, whereas colonoscopy and computed tomographic (CT) colonography are not recommended because of insufficient evidence. In contrast, the American guidelines recommend presenting information to patients, who then choose from the options, including high-sensitivity FOBT, flexible sigmoidoscopy or colonoscopy.4,5 The American recommendations diverge on CT colonography: the USPSTF does not recommend it on the basis of unknown long-term harm,4 while the collaborative joint guidelines endorse 5-yearly examinations.5 Unlike the US, Australia has moved beyond making passive recommendations to become one of a few countries actively implementing a nationwide population-based bowel cancer screening program — the National Bowel Cancer Screening Program (NBCSP) — although, currently, only individuals aged 50, 55 or 65 years are invited to participate (http://www.cancerscreening.gov.au/internet/screening/publishing.nsf/Content/bowel-about). The NBCSP, which uses a high-sensitivity immunochemical FOBT, began in 2006 after a pilot program (2002–2004) found that bowel cancer screening would be acceptable, feasible and cost-effective.6 The age restriction for invitees is part of a phasing-in process designed to enable resources to cope with increased downstream demand, especially for colonoscopy, which is the recommended investigation for participants with a positive FOBT result. About 7.5% of NBCSP participants have a positive FOBT result, and 5% of these are found to have cancer.7 Although the federal government has made no commitment to the NBCSP beyond June 2011, it is inconceivable that the program will simply be terminated, given the strong evidence basis for its function. The problem facing Australian medical practitioners is what to do in the face of the various disparate guidelines. A simple approach is to recommend participation in the NBCSP for all invitees. Increased awareness of bowel cancer will also cause some individuals outside the eligible ages to enquire about screening. In these cases, the NHMRC recommendations are most appropriate: for medical practitioners wishing to encourage opportunistic screening, an immunochemical FOBT can be recommended for patients aged between 50 and 75 years. Patients with positive FOBT results will then require follow-up colonoscopy. However, these recommendations ignore the growing tendency, often driven by patients, for screening with colonoscopy. In the absence of symptoms, about 500 colonoscopies need to be performed on 50–75-year-olds to identify one cancer,7 with an associated one in 1000 risk of serious complications.8 This contrasts with one cancer found for every 20 colonoscopies in the NBCSP.7 Of course, many patients will have premalignant adenomas that would be found with colonoscopy screening, which in turn creates a substantial requirement for long-term surveillance colonoscopies. Yet the vast majority of patients with adenomas will never develop bowel cancer, even without future intervention.9 Finally, the imperfections of colonoscopy are becoming increasingly recognised, reducing the ratio of its potential benefits to high cost.10,11 Thus, “indiscriminate” use of colonoscopy diverts availability of this expensive resource away from those most in need of it, especially in the public health system. As a step towards improving colonoscopy access, the Western Australian Department of Health will introduce a Colonoscopy Services Model of Care, scheduled for implementation over the next 2 years in the public hospital system, that prescribes appropriate use and referral processes. This will be supported by trained clinical staff and computerised referral systems to improve the quality and triaging of referrals in the public sector. Patients will also be informed of the priority level of their case, and the appropriate waiting time. Other states in Australia should strongly consider implementing similar strategies. Bowel cancer is common, serious and largely preventable. Medical practitioners should be encouraged to refer individuals for bowel cancer screening in compliance with the current Australian NHMRC recommendations and the NBCSP. Such practice will ensure that colonoscopy resources are available to those most in need in our community.

Hooi C Ee MB BS, FRACP, PhD · John K Olynyk MB BS, FRACP, MD

Victims of previous disasters have helped us learn much that can help those suffering now The horror and tragedy of the recent Victorian bushfires have affected all Australians, evoking both compassionate response and practical support. Alongside other members of their communities, doctors, nurses and other health professionals have all been directly affected, experiencing horrendous threats to life, loss, grief, and dislocation from their homes and way of life. General practitioners, community nurses, social workers and others will be called upon to provide care and to deal with the extensive mental health issues that arise in the aftermath of such incidents. It is important that any response is informed by the most up-to-date research findings in shaping the care provided. Studies, mainly by Australian researchers, have shown that the most important early responses involve protecting and comforting those most directly affected, linking them to loved ones and sources of support, and ensuring assessment and follow-up. A crucial issue is the central role of the GP in the provision of post-disaster services, as shown in a study of all the registered victims of the 1983 Ash Wednesday bushfires in South Australia.1 Local communities have a preference for their GP’s services in the post-disaster period, but they are also likely to need access to community recovery services for practical assistance and resources. Where possible, such services provided after the fires in Victoria should be linked to local clinics to facilitate access to health care. For the GP, assessing patients in terms of the nature of their experience of the disaster will be important — for instance, whether they were directly exposed to the fire, and whether they have lost family members or others close to them, or their home, property or other physical resources. A brief physical health check is important, alongside assessing levels of distress,2 providing guidance about health and wellbeing strategies, and assuring contact and outreach. Formal counselling is most effective after the early weeks, particularly for those with ongoing levels of acute distress related to the horror and life-threatening nature of the experience. Skilled management of bereavement in the early stages requires allowing patients to talk of their loved ones, and assisting them through any disaster victim identification and other formal processes. Follow-up over the months ahead is important for both physical and mental health needs in the post-disaster period. It is important to remember that the affected communities already carry a level of existing morbidity, which needs to be encompassed in planning a response. The magnitude of this problem is reflected in the 2007 National Survey of Mental Health and Wellbeing, which showed that 20% of Australian adults had a psychiatric disorder in the previous 12 months. Post-traumatic stress disorder (PTSD) was the most common disorder, with a 12-month prevalence of 6.4%.3 These findings suggest that the prevalence of traumatic events is much greater than is generally recognised in our community. Those already suffering are particularly at risk, but a further significant proportion may develop problems such as complicated grief, depression and PTSD as a direct consequence of the bushfire disaster.4 A lesson from the Ash Wednesday fires is that victims often delay seeking care for at least 18 months, despite experiencing considerable suffering.5 When they do present to GPs, it is often with physical symptoms,6 and the significance of these is missed. A recent treatment study after the London terrorist bombings that provided help by directly screening the high-risk victims found that many had presented to and requested help from GPs, who had discouraged them from seeking care, underestimating their distress.7 In the aftermath of the Victorian bushfires, one approach that should be considered is the use of screening for depression, PTSD and alcohol misuse in all GP presentations in affected areas. Clinical guidelines demonstrate that this approach leads to better outcomes if the screening is linked to adequate clinical services.8 However, GPs tend to prematurely terminate treatment, with subsequent loss of the demonstrated treatment gains, highlighting a need in fire-affected regions for continuing education programs that address the issues of diagnosis and treatment.9 Members of the emergency services also deserve particular attention because of the prolonged intensity of their exposure, particularly in light of the high number of fatalities.10 The community owes them a special duty of care. Active screening programs linked to occupational health services that are expert in managing traumatic reactions and grief should be instituted, as currently occurs in the Australian Defence Force. The willingness of victims of previous Australian disasters to participate in disaster research has resulted in the capture of many lessons and should be acknowledged. This knowledge needs to be used in the coming months so that the lessons already learned do not have to be rediscovered, as is too often the case after disasters. Future studies should build on what we already know, rather than simply replicating what has been studied before. Research that makes demands on people who are suffering has no role if it is not innovative. Image courtesy: Inspector Ben Shepherd, Rural Fire Service, NSW.

Alexander C McFarlane MB BS(Hons), MD, FRANZCP · Beverley Raphael AM, MB BS, MD, FRANZCP

A stringent, preventive risk-management approach could ensure potable reuse is a safe option As a result of prolonged drought, Australians are increasingly relying on alternative water sources — including rainwater, greywater, and water recycled from stormwater or sewage — for many community and household uses. Health professionals therefore need to be aware of the likelihood, if any, of illness related to water usage. In particular, careful consideration should be given to the safety of water recycling, especially as, at face value, it seems to represent a backward step from John Snow’s mid 19th century discovery of the importance of keeping drinking water and sewage separate.1 The obvious question is: is water recycling safe? There are different types of recycling, and different end uses for recycled water. In Australia, recycled water is currently used for irrigation of parks, golf courses and certain crops, and by various industries. Increasingly, new housing developments are incorporating separate pipes to distribute two grades of water: drinking water, supplied to kitchens and bathrooms; and recycled water for outdoor purposes (garden watering, car washing) and limited indoor use (toilet flushing, sometimes in laundries). As these uses of recycled water should not involve intimate human exposure, they are generally considered to incur negligible health risks. However, plumbing errors or use of recycled water for unendorsed purposes could result in intentional or unintentional ingestion. Fortunately, no recognised disease outbreaks associated with these schemes have so far occurred, and the public seems to be tolerant of these forms of water recycling. The more controversial issue relates to the potential health consequences of using treated recycled water to augment drinking water supplies (also called “potable reuse”). Australian water and health agencies have recognised the need for detailed technical guidance on minimising health risks from reuse schemes, resulting in production of the Australian guidelines for water recycling (AGWR).2,3 Phases 1 and 2 of these guidelines have been endorsed by the Australian Health Ministers’ Conference, and Phase 2 by the National Health and Medical Research Council (NHMRC). The AGWR recognise that the health consequences of system failure in a water recycling scheme could be catastrophic, with the potential for large gastroenteritis outbreaks, and that the greatest threat to public heath is from poor maintenance or poor quality control of water treatment processes. Consequently, the guidelines recommend proactive identification and management of risks, and include a “framework for management of recycled water quality and use”.2,3 One of the framework’s 12 elements involves undertaking a comprehensive risk assessment of each reuse scheme to determine the appropriate type and number of treatment steps required to “clean” the water. Another fundamental aspect of the framework is continuous monitoring of operational characteristics such as disinfection (chlorine concentration) and filtration (turbidity) that indicate water treatment processes are functioning efficiently. In other words, assuring adequate water quality is best achieved by monitoring the performance reliability and integrity of water treatment systems, and not by testing for all possible microbial or chemical contaminants.2,3 This lack of reliance on water quality testing is likely to seem counterintuitive to clinicians; however, the degree of assurance provided by negative test results is constrained by detection limits and the representativeness of small water sample volumes. Water quality testing is thus better suited to providing verification of system performance rather than being used as a routine management tool. There are two main issues raised by opponents of recycling schemes. First, they question whether water treatment processes can be guaranteed to always function effectively. This is a key focus of the AGWR, and it is essential that operators of potable reuse schemes have adequate skills and resources to provide the high level of quality control required to ensure safety. The second issue relates to adequate removal of chemical contaminants, given the large number of substances present in sewage (eg, hormones, pharmaceuticals, personal care products). This is a complex issue, particularly as the health consequences of low-level exposure to many of these substances are currently ill defined by toxicological and health data. The AGWR take a conservative approach to this issue and are consistent with international practices. Moreover, any incremental risks associated with potable reuse are likely to be negligible compared with other sources of direct exposure to these chemicals and with exposure from conventional drinking water supplies. So what is the bottom line? Evidence shows that current public supplies of drinking water in Australian cities do not incur an increased risk of gastroenteritis.4,5 Potable reuse is not yet occurring in Australia, but such water recycling schemes have existed internationally for more than 30 years, with schemes in Europe, the United States and Singapore having no recognised adverse health outcomes.6 Gastroenteritis outbreaks are unlikely when water treatment processes are well managed, so clear guidelines supporting prospective implementation of a preventive risk-management framework are fundamental to ensuring the safety of potable reuse.2,3 Health surveillance, although a relatively insensitive marker, can provide a retrospective indication of health outcomes associated with such schemes. The AGWR acknowledge that safety is not predicated on achieving zero health risk, but that there is an upper limit of tolerable risk (10-6 disability-adjusted life-years per person per year).3 The Australian drinking water guidelines, although now under review, currently contain no health-based target for microbial risk.7 This means that more stringent requirements for water quality are currently applied to potable reuse schemes than to conventional drinking water. While not advocating for or against potable reuse, it is thus paradoxically possible that planned potable reuse could be among the safest approaches to the provision of drinking water.

Karin S Leder MB BS, FRACP, PhD · Joanne E O’Toole BAppSc, MBA · Martha I Sinclair BSc(Hons), PhD

Evidence shows that cost does affect alcohol consumption, and reducing consumption improves public health There is strong evidence that increasing the cost of alcohol reduces the overall amount that is consumed.1 In a range of countries, price increases have been consistently shown to reduce alcohol consumption and related harms in both the general population and at-risk populations such as young people and heavy drinkers. Conversely, price decreases have resulted in an increase in consumption and harm.1-3 In this context, the Australian Government’s April 2008 increase in excise tax (Bill introduced on 11 February 2009) on ready-to-drink (RTD) spirit-based products (RTDs; “alcopops”) is an evidence-based strategy to reduce excessive RTD consumption among young people. The alcoholic content of RTDs is now taxed at a similar rate to that of other spirits (tax increased from $39.36 to $66.67 per litre of pure alcohol). Critics have argued that the RTD tax increase has not reduced alcohol consumption by young people, and will not do so. One claim is that young people will merely switch to other beverages. These arguments have been made by some from the alcohol industry and some researchers. Doran and Shakeshaft, for example, argued that young people “ seem to be price inelastic about their alcohol demand”.4 Citing a national school survey, they claimed that “spirits are by far the beverage of choice for the 45% of 16–17-year-old Australians who drink, despite spirits being the most highly taxed beverage in Australia, and the most expensive per litre of alcohol”. This is not evidence for price inelasticity. They also argued that “overall rates of usual or binge consumption in Australia are unlikely to substantially fall, because spirits hold a smaller market share than beer, and young people will more than likely switch their preference”.4 The weight of scientific evidence suggests otherwise — that overall consumption is likely to decline because young people’s demand for alcohol is elastic.1-3 The survey series on which Doran and Shakeshaft rely shows that beverage preferences vary between boys and girls and over time. In 1999, before reductions in tax and in the retail price of RTDs in 2000, RTDs were the preferred beverage of about 23% of 12–17-year-old female drinkers. By 2005, after the tax decrease, 48% of young females drank RTDs, while the preference for higher-taxed spirits fell from 42% to 30%. For 12–17-year-old males, RTD consumption increased from 6% to 14%, a small share compared with spirits (39%) and beer (33%).5 Although new products and marketing strategies may have contributed to this substantial change, these data suggest that young Australians, like their counterparts in other countries,2 do alter their beverage choices in response to price changes. Definitive statements about the impact of the “alcopops tax” are premature in the absence of independent alcohol sales data. It is regrettable that there are no readily available, official monthly sales data for all alcoholic beverages, like those obtained by the detailed monitoring that we know is conducted by private industry.6 However, available evidence does indicate that the tax has reduced sales of RTDs and the reduction was far from wholly offset by a switch to other beverages. A market research company that regularly compiles reports on sales of alcohol products has estimated national monthly sales of packaged alcohol (sold for off-premises consumption by liquor licensees across the five mainland states of Australia) by beverage type for 2007 and 2008 ().7 These data show that in the 3 months after the April 2008 tax increase, 91 million fewer standard drinks were sold as RTDs than in the same months in the previous year. Standard drinks sold as spirits and beer increased but wine sales decreased. The increase in spirit and beer sales (48 million standard drinks) was only 53% of the 91 million fewer RTD drinks sold. A decline in RTD sales was also reported on the basis of Australian Tax Office data. These showed a 54% reduction in sales of RTDs and a 7% increase in spirit sales from April to June 2008.8 In presenting the Excise Tariff Amendment Bill to Parliament, the Minister for Health and Ageing confirmed that: “Tax office figures drawn from the first nine months of this measure show that alcopops sales have dropped by 35 per cent compared to the previous year”.9 Critics have been hasty in predicting that young people’s drinking would be unresponsive to the RTD tax increase. In keeping with a large body of research evidence, the early indications are that RTD sales declined in the first few months after the tax increase. Previous research suggests that this decline in alcohol sales (a reliable proxy for consumption10) will produce a public health benefit.1-3 Further investigation is needed to determine specifically in which population group(s) the benefit accrues; for example, whether this reduction in RTD purchases occurred primarily among young drinkers (the target of the tax increase), and what other factors may have contributed to the reduction. Informed policy debate requires independent evaluations of short-term and long-term effects of these tax changes on consumption and harm indicators (eg, injuries). Nevertheless, the evidence to date is that the “alcopops” tax is a step in the right direction. Number of standard drinks* consumed in May to July, 2007 and 2008, by beverage type Beverage type Million standard drinks consumed Difference in million standard drinks % Change 2007 2008 RTDs 348 257 − 91 − 26.1 Beer 886 899 13 1.5 Wine 797 776 − 21 − 2.6 Spirits 313 348 35 11.2 Total 2344 2280 − 64 − 2.7 Source: Nielsen Liquor Services Group (NLSG) 2008.7 RTDs = ready-to-drink spirit-based products. * One standard drink = 10 g pure alcohol. To accurately convert beverage volumes to pure alcohol, the NLSG applies alcohol conversion factors at the subsegment level for beer (eg, regular, mid-strength, low-strength beer) and RTDs. Average alcohol contents by beverage type: RTDs 5.0%; beer 4.8%; straight spirits 38.0%; and wine 13%.

Tanya N Chikritzhs BA(Hons), PostGradDip(Epi · Paul M Dietze BSc(Hons), PhD · Steven J Allsop BSc, PhD · Michael M Daube BA(Hons), HonDSci · Wayne D Hall BSc(ApplPsych), PhD · Kypros Kypri BA(Hons), PhD

Clinical software governance and real-world testing involving users are urgently needed In this issue of the Journal, a study from the National Prescribing Service (NPS) examines the quality of drug interaction alerts generated by nine clinical software systems currently used by general practitioners and pharmacists in Australia for prescribing or dispensing medications (Sweidan et al).1 The findings will come as no surprise to those who have repeatedly expressed concern about the shortcomings of clinical decision support software.2,3 Only half of the six prescribing systems examined by the NPS alerted users to all 20 of the major drug–drug interactions tested, which can occur with commonly used drugs and with the potential to trigger serious adverse reactions. The best of the three dispensing systems detected 19 of these drug interactions. Yet Australian GPs are heavily reliant on such software alerts: 88% of respondents to a recent national survey reported relying on their prescribing software to check for drug–drug interactions.4 Any failure of decision support systems to provide adequate drug safety alerts is thus likely to pose risks to patient safety. The NPS study provides a snapshot of software performance in response to artificially generated test cases. Different test cases may have yielded different results. Further, as valuable as they are, such studies cannot provide data on the cause of these failures or the likelihood that they will ultimately result in medication errors. At a fundamental level, we know that the performance of any decision support system will be determined by the completeness and accuracy of its knowledgebase. A second potential cause of missed alerts is the internal procedures and logic used within a decision support system. For example, even though the MIMS DrugAlert Interactions knowledgebase detects all 20 major drug interactions tested in the NPS study, the four prescribing systems based on this knowledgebase failed to uniformly report all of these alerts.1 Anecdotally, we also know that there is variation in the logic used to determine which drug interactions different manufacturers elect to display, and which are treated as low priority. At present, there is scarce information available to indicate which of these different components of decision support systems is most likely to generate safety problems. As a consequence, it is currently not possible to provide guidance to clinicians, policymakers or system manufacturers on the most appropriate safety practices needed to avoid misadventure. Moving beyond laboratory testing of software, there is a critical need to examine the safety of decision support systems in the hands of typical users. There is growing evidence that busy clinicians routinely disable or override computer advice. “Alert fatigue” is a well known consequence of using systems that generate high rates of non-serious or irrelevant alerts.5 The long-term impact of using such systems and their influence on clinicians’ decision making have yet to be systematically investigated. Indeed, the NPS found that the three prescribing systems that alerted users to all the major, clinically significant drug interactions also generated unhelpful alerts for 30%–55% of the clinically unimportant interactions.1 To reduce alert fatigue, software designers could consider smarter decision support systems that can be trained to meet individual practice requirements (akin to an email spam filter that can be gradually trained to recognise and remove irrelevant messages). For instance, GPs could train their prescribing software to provide alerts only for newly prescribed medications and ignore repeat medications where the clinician has previously noted an alert. This lack of clear evidence about the causation of computer-related failures in decision support systems, either on their own or in the hands of typical users, is likely to hamper international efforts to improve the safety governance of clinical software. Among the efforts seeking to address calls to regulate the safety of decision support systems,6 the United States Certification Commission for Healthcare Information Technology is introducing specific requirements for drug interaction alerts in ambulatory care systems.7 In September 2008, the United Kingdom’s National Health Service, which took a lead role in embedding a safety management approach into its procurement processes, published simple developer guidelines for safety features in prescribing systems.8 Future versions are planned to cover drug–drug interaction checking and other decision support functions not included in the initial specification. The International Organization for Standardization, using a risk-management approach, is developing standards for the construction, implementation and use of clinical software. In contrast, even though it is clear that we do need to move to some form of decision support system accreditation in Australia, safety governance of software does not yet seem to be on the agendas of the National E-Health Transition Authority or the Therapeutic Goods Administration. As we approach 5 years since publication of the first study to measure deficiencies in safety features of clinical software,9 research efforts have not translated into changes in clinical software governance in Australia. There is little local support for this research, and examination of the safety of clinical software has not moved beyond the use of artificial test cases. Yet it is clear that the safety of clinical software is as much a product of the human user as it is of the machine. If we are to move from safe design to safe use of clinical software, we must accelerate our efforts to systematically examine the safety of decision support systems in the hands of users. While no one suggests that clinicians should stop using decision support systems, given their clear benefit to patients, we need to understand the “side effects” or unanticipated consequences of the technology,10 and understand in which situations their use might lead to unacceptable clinical risk.

Farah Magrabi BE, PhD · Enrico W Coiera MB BS, PhD, FACMI

The effects of cannabis use on health and social adjustment are profound Substance misuse by Indigenous people has long been recognised as one of the devastating consequences of contact with Western culture. Misuse of tobacco, alcohol and petrol among Indigenous Australians has received much attention. Cannabis, by contrast, has not been viewed as a major problem. But since the 1990s, it has become apparent that heavy cannabis use is common in some remote Indigenous communities.1 The associated health and social burdens are now being recognised.1,2 Indigenous Australians, whether living in urban or rural settings, are more likely than other Australians to report cannabis use.3 Recent reports suggest that cannabis use is also relatively high among Indigenous populations in New Zealand, Canada and North America.4 Limited data are available on patterns of cannabis use among Indigenous Australians.3 However, a recent 5-year study of adolescents and young adults in three remote communities in Arnhem Land in the Northern Territory has found that not only is cannabis use common in remote Indigenous settings, but its effects on health and social adjustment are profound.4-6 These three communities are close to one another but very isolated, being over 550 kilometres from the nearest city. There is one local Indigenous language, and English is a secondary language. Tobacco use was found to be the norm in these communities, with over 90% of adolescents and young adults smoking.7 Because of restricted access to alcohol, problem drinking was uncommon.7 In contrast, cannabis use was endemic, with over 70% of males and 20% of females being current users.5 Cannabis was typically consumed mixed with tobacco and smoked using a locally fashioned “bucket bong” that gives the user a rapid and intense dose with little smoke lost.5 Regular heavy use (≥ 6 “cones” daily) was found in almost 90% of users.7 This is around twice the consumption of regular cannabis users elsewhere in Australia.1 Furthermore, about 90% of the Indigenous users reported symptoms of cannabis dependence.1 This compares with about 20% of users aged 18 or over in the general Australian population.3 Of even greater concern was a suggestion that, for most Indigenous users, cannabis was not a passing adolescent phase. After 5 years of follow-up, the great majority reported continuing heavy use.4 Cannabis use was linked to substantial health problems and social burdens in these communities, which are already disadvantaged by isolation and poverty.2,5,8 Up to 10% of the communities’ total income and between 31% and 62% of a user’s median weekly income was spent on cannabis.5 Cannabis users were less likely than non-users to participate in education or training5 and more likely to report auditory hallucinations, suicidal ideation,6 symptoms of depression,7 and having been imprisoned.6 Community violence increased when cannabis supplies were scarce.1,2 The effects on traditional life were described by one NT Indigenous mental health clinician in the following way: Too many of my people are chained to [cannabis]. They don’t go out hunting or spend time by the river with their family. They just sit and smoke [cannabis], then look for money to buy more [cannabis] and get into fights when they can’t get any (Muriel Jaragba, personal communication). What accounts for the unusual patterns of cannabis misuse in these remote Indigenous communities? There is little evidence that cannabis is grown locally,9 but much anecdotal evidence that market networks supplied by dealers based in urban or regional centres are extensive and resilient, making cannabis readily available (A R C, unpublished observation). Alcohol restrictions have been effective in reducing problem drinking within communities, but may have had the undesirable consequence of encouraging an increase in cannabis use where it could be easily obtained.5 As with risks for other forms of substance misuse in these communities, the social context is important. Limited employment and education opportunities; crowded, poor-quality housing; community-wide feelings of disempowerment; and grief and loss related to high mortality, morbidity and incarceration rates are all likely risk factors for substance misuse. Cannabis misuse is likely to be both a consequence of this type of social disadvantage and a perpetuating influence. Cannabis misuse in remote Indigenous communities has been overlooked for too long. It is now clear that it is yet another major problem for these already disadvantaged communities, with evidence of cannabis misuse across a broad area of northern Australia.1,2,9 As well as in the NT, concerns about the level of cannabis use have recently been noted in Cape York8 and anecdotally in other parts of remote and regional Australia. Further research is needed to investigate the impact of cannabis use on urban Aboriginal and Torres Strait Islander Australians. Effective responses will not be easy. Controls on supply by state- or territory-based police are one of the few available measures.6 In order to be effective, policymakers and service providers would need to work collaboratively with local communities to tie in local prevention and treatment initiatives with existing supply control initiatives. Such programs would need to use Indigenous language and cultural frameworks, build capacity of local Indigenous professionals, and improve understanding of the harms associated with cannabis misuse.10 Ultimately, tackling the misuse of cannabis and other substances in remote settings will depend on creating opportunities for social development and for continuing education, training and employment of adolescents and young adults.

K S Kylie Lee BMus(Hons) · Katherine M Conigrave FAFPHM, FAChAM, PhD · George C Patton MD, FRANZCP · Alan R Clough PhD

Early detection and prevention applies to medical comorbidity as well as psychiatric symptoms Having a psychotic illness has been and remains a barrier to all forms of effective medical care. All serious mental illness is associated with undue medical morbidity and mortality.1,2 Such morbidity stems from a complex web of interactions between the illness itself, various aspects of the patient’s environment, the nature of the antipsychotic medication and, most worryingly, barriers to the acceptance within the wider medical profession of adequate screening and treatment for comorbidity.3 As 70% of patients with persistent psychoses receive some or all of their treatment from non-psychiatric physicians,4 this is an important issue for the broader profession. Severe mental illness is chronic, typically involves progressive neuropsychiatric impairment, and reduces the ability of individuals to independently manage their own care, both medically and socioeconomically. Psychosis lies at the centre of the illness, and its management depends on the use of antipsychotic drugs. These medications are the bedrock on which psychosocial interventions can then be brought into play to aid recovery. Yet, despite the centrality of antipsychotics in treatment, their therapeutic and non-therapeutic effects on the individual patient are by no means predictable. The adage that therapy must be individualised is as true today as it was in the 1950s, when these agents were first introduced. Reported efficacy is moderated by adverse effects, as well as patient-specific factors that influence adherence. These include patients’ own consideration of their susceptibility to the illness, their judgement of its severity, and their personal evaluation of the benefits and risks of treatment.5 The antipsychotic agent clozapine best illustrates the medication issues. Clozapine remains unique in its ability to alleviate the symptoms of patients with refractory illness (30%–40% of patients appear to be “resistant” to other antipsychotics). However, potential toxic side effects of clozapine include agranulocytosis; metabolic disorder (particularly hyperglycaemia, hyperlipidaemia and obesity); seizures; potent sedation; hypotension; hypersialorrhoea; central and peripheral anticholinergia; life-threatening gastric hypomotility; sudden death in elderly patients; and, of recent interest, cardiac complications such as myocarditis, cardiomyopathy and pericarditis.6 Articles by Layland et al 7 and Borovik et al 8 in this issue of the Journal discuss critical adverse effects of clozapine treatment. These reports are timely, as they serve to remind us that uncommon side effects may lead to considerable morbidity and mortality and that vigilance for all potential adverse events is critical in people with mental illness. The metabolic syndrome, along with other cardiometabolic risks such as smoking and inadequate exercise, is more prevalent in people with schizophrenia than in population controls and is a predictor of early coronary heart disease and mortality (with up to 25 years of life lost prematurely).3 Indeed, as the study by John et al 9 demonstrates, the metabolic syndrome appears highly prevalent in several other groups with serious mental illness such as bipolar disorder or schizoaffective disorder. Waterreus and Laugharne 10 propose a data entry form for metabolic risks, based on an earlier algorithm developed as a follow-on to a consensus document on diabetes and antipsychotics.11,12 The items on which their system is based are the five criteria proposed by the International Diabetes Federation to diagnose the metabolic syndrome. However, other factors that contribute to overall cardiometabolic risk should also be considered when monitoring and reviewing patients with enduring psychotic disorders.13 Ageing, family history, ethnicity, obesity, current smoking status, diet, and exercise/lifestyle are all currently being tested for significance in a study being conducted through the Concord Centre for Cardiometabolic Health in Psychosis in Sydney.14 Schizophrenia and bipolar illnesses are also independent risk factors for developing metabolic dysregulation.15 Finally, the issue of non-adherence cannot be ignored. Side effects in general may be important factors leading patients to less than full compliance with medication schedules. When this occurs, the bedrock of their treatment is lost. Thus the causes of the metabolic syndrome, while often laid at the feet of antipsychotic and other orexigenic agents, are more complex. These agents may be seen as forming the tip of the risk iceberg, while a plethora of independent factors associated with psychotic illness form the often unrecognised body of the problem.16 The alarming rates of premature death in this population confirm the need to closely monitor cardiometabolic risks for all patients with psychosis. In particular, although in the short term there may be differences in the incidence of metabolic risk associated with different antipsychotics, limits should not be imposed based on the specific antipsychotic the patient is receiving at any particular time.11 Clearly, the mantra of first-episode psychosis services (“early detection and prevention”) applies to comorbid physical health as well as psychosis itself. The paucity of long-term data in the global literature provided the impetus for a multicentre study currently underway in Australia to examine cardiometabolic risks in first-episode psychosis patients. The study exploits the strong signal of obesity and hyperlipidaemia often seen in clinical settings. Its aim is to determine the time to the development of key cardiometabolic risks from onset of treatment. The relationship between psychotic illness and metabolic illness is not a new one. Maudsley noted in 1895 that “diabetes is a disease which often shows itself in families in which insanity prevails”,17 and Hippocrates observed over two millennia ago that “persons who are naturally fat are apt to die earlier than those who are slender”. Although clinicians acknowledge the need for improved monitoring and management of comorbid and iatrogenic conditions, much needs to be done before outcomes are improved. A clearer understanding of medication side effects, of the metabolic syndrome and of compliance issues is needed. In addition, barriers to screening and management need to be identified and removed.3

Timothy J R Lambert MB BS, FRANZCP, PhD

UK initiatives to increase clinical research capacity hold lessons for Australia The historically unmatched boom in medical science knowledge in the past few decades has steadily increased the opportunities for clinical research. Examples include research into biomarkers and diagnostics, evaluation of potential therapies, and particularly translation of breakthroughs in basic medical science into clinical medicine. Traditionally, it has taken many years to evaluate and validate new treatments, and there is a global need to improve both the capacity and efficiency of clinical research to ensure maximum community benefits in a reasonable timeframe.1 In the United States, several senators have proposed developing a new umbrella organisation that links pharmaceutical and health care industries — a centre for clinical cure.2 A program to support clinical and translational science awards has also been launched. In Canada, there is a proposal to develop a taskforce to review the mission and mandate of the country’s academic hospitals.3 One of the most ambitious responses to the need for increased clinical research capacity has occurred in the United Kingdom. Like Australia, the UK has a splendid tradition in basic medical research, but has been much less successful than the US in translating this work into clinical advances or in building an environment within the National Health Service (NHS) that attracts major clinical trials. The UK Government’s 10-year framework on science and innovation investment includes an ambition to turn the NHS into a world-class collaborative research engine and a preferred host for multicentre trials with and for industry.4 A recent publication, Best Research for Best Health: a new national health research strategy, set out the potential NHS contribution to health research in England.5 The document that largely drove change in the UK was a report by businessman David Cooksey, which looked at the best structure for publicly funded medical research in the UK, with a clear aim of improving translational outcomes and clinical research capacity.6 It is one of the most influential documents in the UK medical research scene to be published in the 60-year history of the NHS, and it led to the transformation of the NHS research and development division into a new National Institute for Health Research (NIHR). Its recommendations, now implemented, include: ring fencing the NHS research budget of almost £1 billion for audited research programs, many of them new; closely aligning the new NIHR (which is responsible for clinical research) with the Medical Research Council (MRC; which is responsible for basic research), and giving both agencies shared responsibility for translational research; and creating a new overseeing office to coordinate publicly funded medical research, focused on outcomes, around major areas of national need — the Office for Strategic Coordination of Health Research, chaired by Professor Sir John Bell, Regius Professor of Medicine at the University of Oxford.7 An early example of this cross-agency collaboration is the development of the new Efficacy and Mechanisms Evaluation Programme, which is funded by the MRC but managed by NIHR. This program has the specific remit of supporting clinical trials that have a major innovative component aimed at gaining new biological insights, elucidating new scientific principles or developing new methodologies.8 A broad series of initiatives has been set in train by NIHR, with major investment in hospital- and community-based clinical research. This includes the establishment of a small number of comprehensive and specialist biomedical research centres, selected after evaluation by an international jury, at which world-class translational and clinical programs are planned or in place. These centres will be the UK equivalents of the Mayo Clinic and Johns Hopkins. A new NHS program is now underway to consolidate some of these centres into university/hospital trust consortia, where research and teaching functions are jointly owned and developed to create academic health science centres, similar to those in North America.9 Although several models are evolving, they have two common principles. First, the university and affiliated hospital sector will jointly own and plan research and teaching. Second, clinical programs will be academically aligned, with the belief that research and teaching excellence will underpin better clinical outcomes for both hospital patients and communities. This might be a good approach for some partnerships between Australian universities and teaching hospitals. Other initiatives developed by NIHR include the development of an extensive clinical research network.10 The aim of this is to ensure that health care professionals and patients throughout England can participate in and benefit from clinical research. Programs established within the clinical research network include an extensive primary care research network; six topic-specific networks, covering cancer, mental health, child health, diabetes, stroke, and dementia and neurodegeneration; and several other comprehensive clinical research networks. Another program is devoted to national technology platforms, the first being centred on imaging technologies.11 In addition, a number of biomedical research units have been established, covering cardiovascular disease, deafness, gastrointestinal and liver disease, musculoskeletal disease, nutrition, and respiratory disease.12 Resourcing to develop or extend similar national networks and centres would be a sensible step for Australia. Total UK funding for basic and clinical research will increase from £1 billion (about A$2.4 billion) in 2006 to £1.7 billion by 2010.13 Basic medical research in the UK was recently given a major boost through the institution of full economic costing for research council funded projects, which meets true infrastructure costs, and the ambitious and well funded programs discussed here are on the way to establishing world-class infrastructure for clinical research. A national structure has been set in place to ensure that the UK takes a leading role in the development of effective new therapies over the next decade. Australia, like the UK, has separate funding streams for clinical care and for research and innovation, and clinical research has been under long-term pressure. The National Health and Medical Research Council (NHMRC) introduced schemes in the early 2000s to fill the gap, such as the Centres of Clinical Research Excellence Scheme, Practitioner Fellowships, and Fellowships for both the early research career stage (eg, the Peter Doherty Australian Biomedical Fellowship and the Neil Hamilton Fairley Overseas Clinical Fellowship) and the more senior postdoctoral years (Career Development Awards) (Professor Warwick Anderson, Chief Executive Officer, NHMRC, Canberra, personal communication). However, what is currently lacking in Australia is a significant new research and development funding stream from the national health budget to fully develop translational clinical research capacity. Such funding would ensure that patients receive the newest treatments, developed in the most beneficial way.

Edward Byrne MD, FRACP

Australia needs to develop its own guidelines based on local data New guidelines for testing and treating lipid abnormalities in children have recently been published by the American Academy of Pediatrics and the American Heart Association (Box).1,2 These recommendations, made partly in response to the high prevalence of obesity in children in the United States, provoke consideration of whether they should also be adopted in Australia. The previous US recommendations,3 which targeted cholesterol testing to children with a family history of premature cardiovascular disease or high cholesterol levels, had focused on a population-based approach to treatment through a fat- and cholesterol-restricted diet. Drug therapy was reserved for children with more persistent and extreme elevations in cholesterol level. In contrast, the recent guidelines recommend that testing be broadened to include all overweight or obese children, with the first cholesterol assessment to be done between the ages of 2 and 10 years. The new guidelines further recommend that initiation of drug therapy be considered at a younger age (from 8 years) and with a lower low-density lipoprotein cholesterol (LDL-C) level target for children with multiple cardiovascular risk factors. Indirect evidence suggests that childhood lipid abnormalities are important in the development of cardiovascular disease in adults. For example, autopsy studies indicate that atherosclerosis begins in the young and that the extent of lesions correlates with traditional cardiovascular risk factors, including lipid levels.4 However, advanced atherosclerosis rarely occurs in children and adolescents. Arterial wall thickness in adults, as assessed by carotid artery ultrasonography, is associated with childhood lipid levels, and children with lipid abnormalities display altered arterial structure and function.5,6 However, direct evidence for an association between childhood lipid levels and adult cardiovascular outcomes, such as myocardial infarction and stroke, is not available. Why, then, test children and adolescents at all? Would it be equally effective to test young adults? One important potential rationale for cholesterol testing in children is that lipoprotein levels tend to track from childhood into adult life.7,8 Detection of lipid abnormalities in young children could prompt changes in diet and physical activity that would be required through the whole of life. It is important to note, however, that both universal and targeted lipid testing in children result in a high false-positive rate for adult dyslipidaemia.8,9 Moreover, the predictive value of childhood lipid levels depends on the threshold values used to define dyslipidaemia. Threshold values derived from populations of US children may not be sensitive to trends in childhood lipid levels and overweight and obesity in Australia. The prevalence of childhood overweight and obesity is high and increasing in both Australia and the US.10,11 Moreover, in both countries, lipid abnormalities are common in overweight and obese children,12,13 with low high-density lipoprotein cholesterol (HDL-C) and high triglyceride levels particularly prevalent. Importantly, targeting overweight and obese children for LDL-C testing does not improve the specificity for detecting elevated LDL-C levels in adults.8 Although most overweight and obese children with low HDL-C levels become adults with low HDL-C levels, targeting overweight and obese children for HDL-C testing will not identify the majority of adults with low HDL-C levels.8 Overweight and obese children, whether or not they have high triglyceride and low HDL-C levels, require weight management through changes in diet and physical activity levels. But it is uncertain, particularly in the case of young children, whether knowledge of their lipid status will lead to greater motivation to implement such changes. Improved diet and increased physical activity are both safe and effective ways of reducing cardiovascular risk factors in children, and should be promoted across the whole paediatric population.14-17 Most overweight and obese children could be encouraged to adopt these lifestyle changes without testing their lipid status. Testing for lipid abnormalities could be reserved for older, obese children (> 10 years of age) in the context of an overall assessment of their risk for future cardiovascular disease. Screening based on family history may be hampered by inaccurate or incomplete information and the need for adult family members to have their cholesterol levels measured. However, obtaining an accurate family history, combined with testing of adults to detect those with significant elevation in LDL-C levels, may help identify children with inherited dyslipidaemias (eg, familial hypercholesterolaemia). Such children have the highest risk of premature cardiovascular disease and may benefit most from drug therapy at a young age. The new US recommendations also raise questions about which children should be considered for drug therapy for lipid abnormalities. A number of randomised clinical trials have demonstrated the short-term safety and efficacy of HMG-CoA reductase inhibitors (statins) in children.18 Statins are currently the first-line drug treatment for elevated cholesterol levels in children. However, there is a lack of evidence for their long-term safety, and animal studies have shown they may be toxic to the developing fetus.19 Although there have been no controlled epidemiological studies relating gestational exposure to statins with adverse human pregnancy outcomes, case reports of structural anomalies and the biological plausibility of a teratogenic effect mean that statins are contraindicated in pregnancy.20 Thus, a case can be made for reserving statin therapy for older children at high risk of future cardiovascular disease. In girls, it may be appropriate to delay statin therapy until an age when discussions about reproduction and contraception can occur. A strong family history of premature cardiovascular disease or a rapid progression in surrogate measures of atherosclerosis (eg, carotid arterial wall thickness, measured by ultrasound) may lower the age threshold for statin therapy. In Australia, we should be taking action to address the increasing prevalence of childhood cardiovascular risk factors. However, guidelines from the US may not be appropriate for Australian children, and it is imperative that we formulate new local recommendations based on recent local data. Guidelines for lipid assessment and management in Australia should also propose strategies for reducing cardiovascular risk factors in childhood more generally. This will require discussion and collaboration between clinicians, researchers, and governmental and non-governmental organisations, such as Diabetes Australia, the National Heart Foundation, the Paediatric Cardiac Council of the Cardiac Society of Australia and New Zealand, and the Royal Australasian College of Physicians. In the interim, a careful assessment of the risk of future cardiovascular disease is required for all paediatric patients. This will be based on ascertainment of an accurate family history of premature cardiovascular disease, information on diet and physical activity, anthropometric and blood pressure measurements made at routine paediatric health checks, and the targeted assessment of blood lipid levels in older children with a family history of premature cardiovascular disease or hyperlipidaemia and/or multiple other cardiovascular risk factors, including obesity. Summary of recent changes to recommendations in the United States for cholesterol testing and treatment in children1,2 Stronger recommendations for cholesterol testing in children who have cardiovascular risk factors other than lipid abnormalities — particularly overweight and obesity, but also hypertension, cigarette smoking or diabetes. A stronger recommendation on the timing of initial cholesterol testing: between the ages of 2 and 10 years. A recommendation to consider commencing drug therapy in children aged over 8 years (rather than 10 years), with a target low-density lipoprotein cholesterol level of < 3.3 mmol/L (rather than < 4.1 mmol/L).

Julian G Ayer BSc(Med), MB BS, FRACP · David R Sullivan MB BS, FRACP, FRCPA · Gary F Sholler MB BS, FRACP

No drug is completely safe and, while the risks seem small, some side effects can be serious When I went to medical school, the mantra “know thy drugs” was pounded into me repeatedly, and it has served me well. Among the most commonly prescribed drugs in Australia are the proton-pump inhibitors (PPIs). In 2005, one million Australians were dispensed drugs in this class.1 There is no doubt that PPIs are safe relative to most other medications we prescribe, but suppressing gastric acid is not physiological.2 A low level of gastric acid promotes the growth of swallowed and enteric flora in the proximal gut, and these bacteria may be aspirated during episodes of physiological reflux. In this issue of the Journal, Roughead and colleagues assess the risk of pneumonia in Australian veterans taking PPIs (Roughead); they identified a 16% increase in risk, equating to four extra hospitalisations for pneumonia each year for every 1000 people prescribed a PPI.1 A study from Denmark found current use of PPIs was associated with a 1.5-fold (or 50%) increase in the risk of community-acquired pneumonia (95% CI, 1.3–1.7); the attributable proportion (ie, the fraction of pneumonia potentially caused by PPIs) was calculated to be 4%.3 Similarly, a Netherlands study reported an adjusted relative risk for pneumonia among those using PPIs versus those who stopped using the drugs of 1.89 (95% CI, 1.36–2.62).4 There is, therefore, a small increased risk of pneumonia, and this may be further increased in those who have recently begun taking PPIs. However, no preventive strategies are available to reduce this risk, and a causal association has not been established. Indeed, the increase could still be caused by unidentified confounders. For example, many patients in these studies had multiple comorbid conditions that might have given rise to an increased risk of pneumonia in the first place, such as alcoholism, previous stroke, or immune compromise secondary to chronic disease.3,4 A case–control study reported a significantly increased risk of Clostridium difficile infection in those who were exposed to PPIs in the 90 days before the infection, with an odds ratio (OR) of 3.5 (95% CI, 2.3–5.2).5 As expected, previous exposure to antibiotics was also a significant risk factor for C. difficile infection in this study. An association with H2-receptor antagonists, as well as non-steroidal anti-inflammatory drugs (but not aspirin), was also reported.5 An increased risk of other enteric infections has similarly been observed with PPI use (OR, 2.55; 95% CI, 1.53–4.26), although combining data in this meta-analysis was problematic because of significant study heterogeneity.6 Whether other comorbid conditions in patients taking these drugs account for the association remains to be clarified, and any causal link is still speculative. An acid environment is needed for insoluble calcium absorption, but the effects of PPI on dietary calcium absorption are uncertain. Increasing dietary calcium intake and taking calcium citrate as a supplement (which does not require gastric acid for absorption) is not established practice for patients who are prescribed acid-suppressing medications. A large retrospective study from the United Kingdom General Practice Research Database suggested that there was an increased risk of hip fracture in patients taking PPIs, with an adjusted odds ratio of 1.44 (95% CI, 1.30–1.59).7 Importantly, the calculated excess risk was small (about 1263 patients over the age of 50 would need to be treated with PPIs for a year to identify one excess hip fracture). A weaker effect was seen with H2-receptor antagonists. A recent Canadian case–control study in an administrative claims database examined longer-term PPI use and osteoporosis-related fractures; exposure of 7 years or more was modestly associated with an increased fracture risk (OR, 1.92; 95% CI, 1.16–3.18).8 A causal association has not been established, but it may be worth considering increasing calcium intake for prevention and assessing bone mineral density in those requiring a daily PPI for more than 5 years.9 Carpopedal spasm secondary to low serum magnesium and calcium levels that reversed with withdrawal of PPI therapy in two patients has also been reported.10 Iron absorption does not appear to be affected by PPI use, but long-term acid suppression has been linked to malabsorption of vitamin B12, especially in older people.11 Therefore, it may be reasonable to assess vitamin B12 levels annually in older patients requiring maintenance PPI therapy, but this is not routine practice, as the cost versus the benefit is unknown. Patients infected with Helicobacter pylori and who are taking long-term PPI therapy are at increased risk of developing gastric atrophy, but the exact clinical significance remains uncertain.12,13 Gastrin release increases with PPI therapy because of acid suppression, but there is no evidence this leads to neoplastic changes in the stomach. One study reported that 30% of patients taking omeprazole developed gastric atrophy, although this appeared to occur primarily in those concurrently infected with H. pylori.13 However, the development of gastric body intestinal metaplasia is rare, and there is no definite evidence that long-term maintenance PPI therapy in the setting of H. pylori induces dysplasia or gastric cancer. Despite this, some authorities do recommend screening for H. pylori infection if long-term PPI use is contemplated, and offering eradication therapy to those infected, and this is my practice too.14 There appears to be no increased risk of colon cancer in PPI users, which some have speculated could occur secondarily to hypergastrinaemia.15 Finally, an increasing number of cases of acute interstitial nephritis are being reported in association with PPI therapy, and this appears to be an idiosyncratic class effect; sadly, not all patients recover kidney function when they stop taking the drug.16 The bottom line is that no drug is completely safe, and this applies to acid suppression therapy. Fortunately, the risks, if causal, seem small, although preventive strategies are largely unavailable and identifying those at particularly high risk of serious side effects (eg, based on pharmacogenomics to individualise therapy) is not yet an established strategy. However, it is prudent and best practice to warn patients about the potential serious (albeit rare) side effects of PPIs, to prescribe the lowest possible dose of PPI (when indicated) for as short a time as possible, and to consider alternative management options if these are available.

Nicholas J Talley MD, PhD, FRACP

The current review of the Therapeutic Goods Administration is an opportunity to improve the system for updating product and consumer information on drugs Pharmaceutical product information (PI) and consumer medicines information (CMI) are mandatory for prescription products in Australia, and government regulations specify that CMI must be consistent with PI.1 Health professionals and consumers should be able to assume that these sources are up-to-date and consistent with evidence-based best practice. However, this is not necessarily so, particularly for older medications.2,3 There is a wide discrepancy between the high-quality information available for new medications (eg, through series such as NPS RADAR [National Prescribing Service Rational Assessment of Drugs and Research]) and some existing texts2-4 that originate from pharmaceutical sponsors, who pay fees to the Therapeutic Goods Administration (TGA) for review and approval of their submitted material. Officially sanctioned information may appear different from different perspectives: all may seem to be in order when assessed from the top down, and shortcomings may become apparent only when specific end products or outcomes are evaluated. Two examples demonstrate this problem. Current CMI for glucocorticoids fails to distinguish between the dosages for replacement and for anti-inflammatory and immunosuppressive effects, a potential health hazard for several thousand Australians with adrenal insufficiency.3 The CMI in question, presented without professional accountability, remains uncorrected 18 months after attention was drawn to it,4 and is clearly inconsistent with the corresponding PI and advice in the Australian medicines handbook.5 In a second example, review of the PI from four different sponsors for thyroid medications identified erroneous therapeutic recommendations and the omission of well established indications or important side effects, as well as inappropriate advice on dose adjustment.2 Two years after publication of a detailed critique of the PI for these medications,2 11 of 16 salient errors remain uncorrected.6 When medical professionals point out necessary improvements to current PI or CMI, official responses tend to be self-affirming, legalistic and defensive, rather than receptive to evidence and the consensus of clinical expertise. For example, when it was pointed out that the instruction in CMI, “Do not take Cortate if you have an uncontrolled infection”,5 was dangerous for those with adrenal insufficiency, the TGA responded with the unexpected sophistry that this advice meant only “before you commence taking Cortate”, rather than “before you take your continuing medication”.7 A response in the general press from NPS leadership denied any need to differentiate glucocorticoid replacement from other indications.8 What are the systemic weaknesses of Australia’s system of preparing, reviewing and updating PI and CMI? Australian pharmaceutical sponsors may lack the clinical resources and perspective to offer PI that reflects evidence-based best practice. The major publisher of PI and CMI, MIMS Australia, is restricted to publishing the TGA-approved texts.9 PI and CMI are currently presented without professional accountability, a prerequisite for effective review. How can these difficulties be addressed? Some recommend a defined “use by” date for PI.10 However, regular review would not necessarily address clinical concerns, and the cost might be prohibitive. What else can be done? Regulatory authorities must abandon the now familiar response to any critique, “PI is the responsibility of the drug sponsor”, which can be used by these authorities to deny responsibility for deficiencies in that information. Sponsors need stronger clinical support, whether through the TGA or other means, in presenting therapeutic advice. Those who publish and disseminate PI and CMI, such as MIMS Australia, should be able to review, and should be accountable for, those texts. MIMS names a distinguished senior honorary editorial panel,6 who could have a valuable role in endorsing published PI or suggesting necessary revisions. Abundant clinical expertise is available in Australia, often concentrated and coordinated in the clinical and scientific specialty societies, that could be brought together under the auspices of the Royal Australasian College of Physicians. Consensus advice from a specialty society, rather than individuals, would diminish the potential influence of commercial interests or pressure groups. The key to effective updating and improvement of Australian pharmaceutical information is more fluent incorporation of clinical input, as occurs for adverse drug events. A notification process, initiated by vigilant professionals and consumers, should make it possible to eliminate incorrect, misleading, ambiguous or obsolete PI and CMI. The alternative is a progressively widening gap between industry and the consumers and professionals who use or prescribe medications. Both groups have the right to expect reliable, officially sanctioned pharmaceutical information. A revision of structures within the TGA is currently in progress.11 It would be a further setback if this opportunity to incorporate expert professional advice in the preparation and improvement of PI and CMI were overlooked.

Jim R Stockigt MD, FRACP, FRCPA

Redressing the imbalance between community expectations and the capacity of the hospital system to meet them will require more than recommendations for prescriptive frameworks and practices Should a Martian dispatched to report on the state of Australia’s hospitals happen to land in New South Wales, the nation’s most populous state, his report would be pertinent and predictable: Public hospitals are severely stressed and sick. They are afflicted by bureaucratic inertia, and riven with mistrust, poor communication and bullying. To add to their woes, they are chronically under-resourced and understaffed. To the outsider, they appear to be a collection of islands, with health professionals on one island, and administrators, health boards and bureaucrats on others; all are surrounded by seas of silence. Their political masters are at a loss over what to do or where to turn and, in desperation, they resort to conducting inquiries when media reports of adverse hospital incidents become political millstones. In short, there is a pervasive sense of loss — loss of control, loss of direction, and loss of ownership by the hospitals’ serving health professionals, politicians, and the community they are meant to serve. The Martian is puzzled by this loss and the state of public hospitals. Is this harsh judgement reflective of an extraterrestrial mind, or is it accurate? The tenor of recent hospital-related media headlines or the frequency of high-level hospital inquiries may shed some light on this question. A sample of the former include: Packed hospitals cause 1500 deaths;1 Public hospitals on ‘brink of collapse’;2 Sick opt to walk out of hospitals — long delays in emergency wards;3 Loss of morale driving doctors out;4 Doctors seek cure for bullying;5 Minor cases clog hospitals;6 Longer wait for elective surgery;7 and Westmead doctors seek boss’s removal.8 As to high-level hospital inquiries, there have been no less than three in NSW in the past decade: the Walker Special Commission of Inquiry into Campbelltown and Camden Hospitals in 2003;9 a NSW Parliament Joint Select Committee (chaired by Revd Hon Fred Nile) convened in 2007 to conduct an inquiry into the quality of care of Jana Horska, who had a miscarriage in the emergency department toilets at Sydney’s Royal North Shore Hospital (RNSH);10 and, in 2008, the Special Commission of Inquiry into Acute Care Services in NSW Public Hospitals, led by Peter Garling SC.11,12 This inquiry followed a coronial investigation into the death of Vanessa Anderson, a young patient at RNSH, following a head injury inflicted by a golf ball. In his findings on the Anderson case, NSW Deputy Coroner Carl Milovanovich noted that: There is little doubt that the NSW health system, while certainly staffed by dedicated professionals, is labouring under increased demand and expectations from the general public. Unfortunately, the same issues are invariably identified: not enough doctors, not enough nurses, inexperienced staff, poor communication, poor record keeping and poor management. These are systemic problems that have existed for a number of years and regrettably they all surface in the death of Vanessa Anderson ... it is almost impossible to avoid comment on the unfortunate repetition of the same systemic problems that continue to surface ... the Government of the day has the responsibility to provide adequate resources, training and staff to ensure the delivery of appropriate and timely medical services.13 In short, Coroner Milovanovich poignantly described a system failing because the demands on it exceed its capacity to deliver safe and quality services. On the same day that he delivered his findings, the NSW Labor Government announced the Special Commission of Inquiry into Acute Care Services in NSW Public Hospitals (the Garling inquiry). In this issue of the Journal, Clare Skinner and her colleagues from the Hospital Reform Group provide a synopsis of the main recommendations of this inquiry.14 The Garling report is in desperate need of such a synopsis. In his opening statement, Garling is nothing if not disingenuous, nonchalantly noting that his report is “voluminous and detailed”. My copy of the report weighs nearly 3.5 kg! Leaving aside the 64-page “overview”,12 there are three substantial volumes comprising 1195 pages, accompanied by an incredible 139 recommendations.11 This represents the outcome of reviewing more than 1200 written submissions from more than 900 individuals and organisations, listening to more than 600 citizens in public hearings, making 61 visits to public hospitals, conferring with 27 peak bodies, and holding two conferences — and all in just 10 months.15 Notwithstanding the importance of such activities and the gravity of the resultant report, it provokes issues worth exploring. Inquiries serve multiple complex purposes, including learning, discipline, catharsis and reassurance.16 But an overriding purpose is to establish the truth and to recommend change, seeking to eradicate the shortcomings of the past by creating a more effective and efficient system. In some respects, reports of inquiries are like science. Science seeks the truth, but does not become science unless it is published, widely read, and widely accepted. Important to its reception and wide dissemination are the essential reporting qualities of focus, brevity, clarity and conciseness. These are hardly descriptors of the Garling report! One may well ask who has both the time and the stamina to read a report exceeding 1200 A4 pages. A further complication lies with the very people who are to be instrumental in implementing the recommendations. Hardworking health professionals, including those who have been swept up in the intense scrutiny of the system in which they valiantly try to operate, may be understandably sensitive to criticism and additions to their already burdensome workloads. Furthermore, most health professionals now support the principles of evidence-based medicine, with its taxonomy of levels of evidence. In contrast, the Garling report is based on broad consultation and represents the distillation of a constellation of opinions — the lowest tier in the levels of evidence. As such, it raises the spectre of the ancient Greek philosophical debate as to whether any consensus of opinion is necessarily synonymous with the truth.17 In any event, the report’s lightning rods for change are the 139 recommendations (many with extensive subclauses), and herein lies another problem. The recommendations are presented with no sense of priority and, curiously, are not costed. Finally, while acknowledging that policy formulation is easy and implementation is hard,18 the report is resoundingly silent on the details of implementation, beyond stressing the need for independence and auditing of the process. In this issue of the Journal, Stewart and Dwyer explore some of the conditions that have to be satisfied if the implementation of Garling’s recommendations is to cure the sicknesses of NSW public hospitals and, for that matter, hospitals nationwide.19 The report unearths little that is new in the Australian hospital system that has not been broached by publications in the Medical Journal of Australia over the past decade or so. It aims to increase the efficiency and effectiveness of the current system by way of recommendations directed at optimising health through prescriptive frameworks and practices. It offers little in the way of modifying community and hospital cultures that are trapped in the prevailing imbalance between community demands and expectations and the capacity of the hospital system to satisfy these demands. The Garling recommendations touch ever so briefly on this disconnect; but these cultures can only begin to be addressed more fully by communicating the essence of the report to both the community at large and to all health professionals. Furthermore, we need to move beyond treatment of the symptoms of hospital diseases and determine if there is a commonality of their root causes. This analysis would also inform culture change. For now, Garling’s recommendations need to be prioritised and scrutinised for their ability to actually deliver an improvement in the quality and safety of NSW public hospitals. It is imperative that these recommendations (which are essentially only suggestions) be evidence-based, reality-tested and rigorously debated by health professionals working at the coalface in broad consultative forums, such as the well attended NSW Health Ministerial Forum held in Sydney in December 2008. Will any of this satisfy our observant extraterrestrial Martian? Will the Garling inquiry make a difference to the cultures of health care? We need to know what the state apparatus thinks. As Skinner and colleagues note: “The response from the state government looms as very important, and is eagerly awaited”.14

Martin B Van Der Weyden MD, FRACP, FRCPA

Updated guidelines widen the definition of pre-eclampsia and highlight that hypertension in pregnancy has become a lifelong disorder The “political” enthusiasm for women to have more babies will not come without a downside. Complications such as pre-eclampsia — a major cause of premature delivery — are likely to become more prevalent as increasing numbers of women become pregnant when they are older or obese, and may affect up to 5% of these women. The reason why pre-eclampsia develops is an enigma. Although there have been no recent major advances in the clinical treatment of this diverse disorder, maternal and fetal outcomes in Australia and New Zealand are good.1 The big risk now is that obstetricians, physicians, general practitioners and midwives will become complacent about the management of these high-risk pregnancies. The institution of standardised surveillance guidelines for Canadian women with pre-eclampsia has been associated with a reduction in adverse maternal outcomes (from 5.1% to 0.7%), but not perinatal outcomes.2 For this reason, the updated Australian and New Zealand Guidelines for the management of hypertensive disorders of pregnancy,3 assuming they are adopted, should improve outcomes for women with hypertension in pregnancy. These guidelines, which were produced in 2008 by the Society of Obstetric Medicine of Australia and New Zealand (SOMANZ), highlight key aspects of these complex disorders. First, the traditional definition of pre-eclampsia — as only hypertension with proteinuria — fails to identify women who are at high risk by having other organ involvement (eg, hepatic, haematological or cerebral disease) without proteinuria.4 Second, a spot urine protein : creatinine ratio can be used to detect significant proteinuria, and 24-hourly urine collections are no longer necessary in routine clinical management.5 Third, although all women with pre-eclampsia should initially be admitted to hospital, many hospitals now have a day assessment unit where some patients with pre-eclampsia can be managed as outpatients — providing their initial assessment was as an inpatient. The treatment of these disorders is “supportive”, and does not ameliorate placental abnormalities or alter the pathophysiological sequelae of pre-eclampsia. Treatment of hypertension in pregnancy does not cure pre-eclampsia; it is intended to prevent cerebral haemorrhage and eclampsia (seizures), and may delay proteinuria.6 SOMANZ recommends antihypertensive treatment be commenced promptly in all pregnant women with a systolic blood pressure of 170 mmHg or higher, or a diastolic blood pressure of 110 mmHg or higher. Several rapidly acting agents are suitable for controlling severe hypertension, including oral nifedipine, intravenous labetalol and intravenous hydralazine.7 Treatment of mild to moderate hypertension in the systolic blood pressure range of 140–160 mmHg or diastolic blood pressure range of 90–100 mmHg is more controversial; however, most hospitals in Australia and New Zealand do implement treatment at these levels. At higher levels, treatment is mandatory, and several drug treatments are safe and efficacious: methyldopa, labetalol and oxprenolol are first-line options, and hydralazine, nifedipine and prazosin are second-line options. Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers are contraindicated in pregnancy. The drug of choice for the prevention and treatment of eclampsia is intravenous magnesium sulfate. However, eclampsia complicates only one in 200–300 cases of pre-eclampsia in Australia, and the case for its routine administration in women with pre-eclampsia in countries with low maternal and perinatal mortality rates is not compelling. SOMANZ recommends magnesium prophylaxis only for women considered at high risk of seizures. Some preterm cases are managed expectantly in units that treat patients at high risk, but delivery remains the definitive management. Many women with pre-eclampsia deteriorate for a few days after delivery, and they require close monitoring during this phase. When there is intense pressure to discharge patients quickly, this is an important point to remember. Women want to know their risk of developing recurrent pre-eclampsia or gestational hypertension, which is about 15% for each after pre-eclampsia in the index pregnancy.8 These rates are probably higher after early-onset pre-eclampsia. Low-dose aspirin and calcium supplementation have both been shown to reduce the risk of pre-eclampsia, and should be used in women at high risk of pre-eclampsia, such as those with a history of early-onset pre-eclampsia. It is apparent that women with either pre-eclampsia or gestational hypertension are at increased risk of cardiovascular morbidity in subsequent years, including hypertension, stroke, coronary heart disease, venous thromboembolism and overall mortality.9 These associations could reflect a common cause for pre-eclampsia and cardiovascular disease, or an effect of pre-eclampsia on vascular disease development, or both. A similar risk for later end-stage renal failure has been reported recently, however only 0.08% of women were affected.10 From a practical point of view, it is reasonable to counsel patients who develop hypertension in pregnancy that they will benefit from avoiding smoking, maintaining a healthy bodyweight, exercising regularly and eating a healthy diet. It is recommended that all women with previous pre-eclampsia or hypertension in pregnancy have an annual blood pressure check and regular (at least 5-yearly) assessment of other cardiovascular risk factors, including serum lipids and blood glucose. In other words, hypertension in pregnancy has become a lifelong disorder. Risks and practice recommendations for women with hypertensive disorders of pregnancy are summarised in the Box. Pre-eclampsia and other hypertensive disorders of pregnancy: risks and recommendations Hypertensive disorders of pregnancy are a leading cause of perinatal and maternal morbidity and mortality, even in developed countries. Management according to systematic guidelines3 improves outcomes. Proteinuria is not mandatory for the clinical diagnosis of pre-eclampsia; renal, cerebral, clotting and hepatic dysfunction also indicate severe disease. Prompt treatment of severe hypertension (systolic blood pressure of 170 mmHg or higher, or a diastolic blood pressure of 110 mmHg or higher) or seizures is mandatory; however, debate persists regarding treatment of mild to moderate hypertension in pregnancy and the selection of patients for magnesium sulfate prophylaxis. Several risk factors for pre-eclampsia are recognised, but accurate prediction of women at risk of pre-eclampsia is still developing. Pre-eclampsia is associated with increased risk of recurrence in the next pregnancy and future risk of cardiovascular and renal morbidity. Women who experience hypertension in pregnancy should adopt a healthy lifestyle, even more so than women who have normotensive pregnancies.

Mark A Brown MB BS, FRACP, MD · Sandra A Lowe MB BS, FRACP, MD

For Indigenous Australians, the “health of country” is inextricably linked with human health The impacts of climate change on human health are now being documented in Australia.1 Not surprisingly, these impacts are unequally distributed across our society, as vulnerability depends on a number of factors, including the degree of exposure, sensitivity and adaptive capacity. However, intranational heterogeneity of climate impacts on health has not been adequately documented to date.2 Using this lens, the vulnerability of Australia’s Indigenous people living in remote areas of the country is revealed. Their vulnerability to climate change is intensified by the social and economic disadvantage they already experience — the result of factors that include decades of inadequate housing and public services, and culturally inappropriate medical services. In addition, specific cultural ties between Indigenous people’s wellbeing and the “health” of their “country” create significant indirect impacts of climate change.3,4 We argue that it is vital to acknowledge the significance of this situation now, so that anticipatory adaptive policies can be implemented. Such policies should ensure that adequate resources are provided to mitigate some of the worst impacts of climate change on these communities, in a way that encourages community participation in decision making. We now know that, across northern Australia, climate change is expected to bring hotter day- and night-time temperatures.5 Elevated temperatures and increases in hot spells are expected to be a major problem for Indigenous health in remote areas, where cardiovascular and respiratory disease are more prevalent and there are many elderly people with inadequate facilities to cope with the increased heat stress. However, while the literature is not clear on the exact effects of increasing heat on people and communities, it does imply that these effects are likely to be less in regions where people are already acclimatised to hot conditions. Communicable diseases such as bacterial diarrhoea, which are more common in hot, dry conditions, may increase in incidence unless additional preventive action is taken. One study predicted that a 1.0–3.5oC increase in average temperature by the year 2050 would lead to an estimated 5%–18% increase in diarrhoea cases in Alice Springs.6 Dengue fever, spread by mosquitoes, also presents a climate-related risk to Indigenous communities. Although the virus is not currently endemic in Australia, there are sporadic epidemics, with occasional cycles over winter in the local mosquito populations in northern Queensland.7 The conceptual divide between Indigenous and non-Indigenous Australians about perceptions of “health” also needs to be recognised and accommodated.8 The Indigenous concept of health is broad and multifaceted, reflecting a different world view to that of the Western biomedical model. For many Indigenous people, a connection with “country” — a place of ancestry, identity, language, livelihood and community — is a key determinant of health.9 If community-owned country becomes “sick” through environmental degradation, climate impacts, or inability of the traditional owners to fulfil cultural obligations through ongoing management and habitation of their land, the people of that land will feel this “sickness” themselves. That is, the elements contributing to Indigenous health and wellbeing are often abstract and based on social interactions with people and the non-human landscape. Thus, as ecosystems change in response to biophysical impacts and extreme weather events, many traditional owners living in remote areas are likely to face increased physiological, psychological, economic and spiritual stress as it becomes more difficult to “look after their country”. At both international and national levels, there is some recognition of the specific needs of indigenous people in relation to the impact of climate change. The World Health Organization’s Commission on Social Determinants of Health and the United Nations Permanent Forum on Indigenous Issues have recently acknowledged the importance of tackling climate change, particularly with respect to health, for the world’s 350 million indigenous people. In Australia, the Garnaut Climate Change Review has recognised the importance of some non-quantifiable costs, including the specific intangible costs associated with improving Indigenous health.10 A challenge for medical practitioners dealing with this issue in the Australian context will be to look beyond the limitations of traditional epidemiology and scientific reductionism to embrace a more ecologically focused, social-determinants approach to health.11 This approach would enable the “health of country” and its inextricable links with human health to be considered in climate impact assessments. To address these different paradigms of health, the first step is to begin discussions with Indigenous people to prioritise activities. This process will certainly require a significant increase in the capacity of medical professionals and health systems in northern Australia, as well as increased education and training programs for Indigenous trainees and cross-cultural programs for nurses and local Indigenous support staff. Changes also need to be made in teaching practice across Australia. Currently, Indigenous health still occupies a peripheral place in many medical school curricula, with government funding and research disproportionally supporting high-cost, acute-care medicine at the expense of preventive and primary health care. In tandem with well planned, properly resourced programs that support strong livelihood activities in remote communities, there is the potential to begin to reduce the additional risk for many Indigenous communities from climate change. There are multiple co-benefits of this approach that would raise social and economic indicators. Ignoring the warning signs and failing to take action is no longer an option.

Donna Green PhD · Ursula King FACRRM, MPH · Joe Morrison MA

The Medical Journal of Australia (MJA) is published by the Australasian Medical Publishing Company (AMPCo), a wholly owned subsidiary of the Australian Medical Association (AMA). The Journal is available on subscription and is included as part of the membership package of the AMA. Since 2001, AMPCo has published an Internet version of the MJA (eMJA) to which readers have enjoyed free open access since its inception. The eMJA now contains 6350 pages of valuable information, which, while formidable, unfortunately comes with increasing production and maintenance costs. Because of these essential costs, the Board of AMPCo has decided that, commencing with the first MJA issue in 2009, access to certain content in the eMJA will require a subscription. In this move, the MJA will follow the steps taken by other prestigious medical journals, including the Journal of the American Medical Association (JAMA), the Annals of Internal Medicine (the journal of the American College of Physicians), the BMJ and The Lancet. Much information, including all previously published articles, current editions of In This Issue, plus guidelines, position statements and supplements, will remain on open access. Research articles will be freely accessible online for 2 weeks following publication, after which a subscription will be required. Twelve months after publication, all articles will revert to open access. This policy will be continually reviewed. Naturally, open access will be provided for any articles we consider to be of urgent public health importance. Importantly, all current AMA members will continue to enjoy free access to all content of the eMJA. Information about how to access the eMJA is available at http://www.mja.com.au/access_policy.html. The Medical Journal of Australia Martin B Van Der Weyden, Editor.

Martin B Van Der Weyden

Bring on the debate, but let’s base it on evidence Not long ago, I received an email describing two different health care experiences: Two patients limp into two different medical clinics with the same complaint. Both have trouble walking and appear to require hip replacement. The first patient is examined within the hour, x-rayed the same day, and has a time booked for surgery the following week. The second sees his family doctor after waiting 3 weeks for an appointment, then waits 8 weeks to see a specialist, has an x-ray which isn’t reviewed for another week, and is finally scheduled for surgery a month later. Why the different treatment for the two patients? The first is a golden retriever. The second is a senior citizen. This tale of two treatments may seem to trivialise the gravity of a human experience, but it does serve to highlight the community’s prevailing unhappiness with our health service delivery: the untimeliness of access to doctors. As David Weatherall, Emeritus Regius Professor of Medicine at the University of Oxford, recently noted: . . . the work load of doctors today is such that good doctoring has become almost impossible, especially in an environment in which a medical supermarket mentality has been and continues to be generated by successive governments.1 In the face of medical workforce shortages, governments are looking to displace doctors with alternative health care providers like nurse practitioners (NPs), physician assistants (PAs), and other health professionals such as psychologists and pharmacists to relieve bottlenecks in health care delivery. Displacing doctors in this way, or “role or task substitution” as it is also termed, has been actively pursued in the United Kingdom and United States. In the UK, the number of NPs grew by 27% between 2004 and 2007 to over 47 000; NPs work in such diverse areas as general practice, emergency medicine, anaesthetics, surgery and endoscopy.2 In the US, there were about 69 500 PAs in 2007 and 140 000 NPs in 2004.3 Different strands of the US education sector are delivering courses to train these practitioners. There are university-based PA programs, and nursing schools now provide doctorates of nursing, in which candidates are purportedly trained in skills equivalent to those of primary care doctors, and practise using the title “doctor”.2,4,5 In light of these developments, an obvious question requiring clarification is: “What defines the role of these alternative practitioners?” One recent definition of NPs in an Australian context states: A nurse practitioner is a registered nurse educated to function autonomously and collaboratively in an advanced and extended clinical role. The nurse practitioner role includes assessment and management of clients using nursing knowledge and skills and may include, but is not limited to the direct referral of patients to other health-care professionals, prescribing medications and ordering diagnostic investigations. The nurse practitioner role is grounded in the nursing profession’s values, knowledge, theories and practices and provides innovative and flexible health care delivery that complements other health care providers. The scope of practice of the nurse practitioner is determined by the context in which the nurse practitioner is authorised to practise.6 The Canadian definition of an NP is almost identical.7 These definitions and the ascendency of NPs in the UK prompted the BMJ to run with a front cover (Box) questioning the difference between an NP and a doctor. PAs are starting to appear in Australia. Queensland Health is exploring the use of PAs through pilot programs in the areas of primary and emergency care at Mount Isa Hospital and at Cooktown Multipurpose Health Service, in cardiology at both Prince Charles and Princess Alexandra hospitals in Brisbane and at Specialist Connect, Brisbane for ear, nose and throat. In these pilot programs, two experienced US-trained PAs will be employed at each site to explore whether PA roles are valid in our health system in terms of productivity, quality of care, patient satisfaction, cost-effectiveness, PAs’ ability to work as part of a multidisciplinary team, and whether PAs provide a comfortable social and cultural fit within the Queensland health workforce. (Bronwyn Nardi, Senior Director of Workforce Planning and Coordination, Queensland Health, personal communication). A similar program is underway in South Australia, led by the state’s Health Department. The program is to pilot PAs in major metropolitan hospitals in Adelaide in paediatrics, anaesthetics and surgery.8 More recently, two US-trained PAs were seconded to the Department of Surgery at Queen Elizabeth Hospital in Adelaide to perform designated tasks (Guy Maddern, Jepson Professor of Surgery, University of Adelaide, Queen Elizabeth Hospital, personal communication). In addition to these initiatives, the University of Queensland (UQ) will inaugurate Masters and Diploma graduate programs in PA studies, and James Cook University will be starting an undergraduate program. All are scheduled to commence in 2009. The UQ program will provide broad generalised medical training with an emphasis on primary care, health maintenance and disease prevention, and medical, nursing and PA students will be taught together within the Faculty of Health Sciences to foster an ethos of team work (Peter Brooks, Executive Dean, Faculty of Health Sciences, UQ, personal communication). Nurses also have a defined path to follow to become NPs, including pursuit of a Masters degree, a designated period of clinical work and a final assessment by a multidisciplinary team of examiners (Ged Kearney, Federal Secretary, Australian Nursing Federation, personal communication). How should the medical profession react to these developments? Any discussions on doctor displacement will invariably raise the spectre of turf warfare.9,10 Be that as it may, there are questions that must be widely addressed and vigorously debated. It needs to be acknowledged upfront that the current medical workforce shortage is the outcome of successive past federal governments’ policies to cap the number of medical graduates. Doctor displacement is a solution to the resulting predicament, but no solution should sacrifice quality and safety. Becoming a doctor requires passage through an extremely competitive and rigorous selection process and indepth training in biomedical and clinical sciences to prepare for autonomous practice with its myriad clinical uncertainties. This is followed by a period of mandated, prevocational internship, followed by vocational training as prescribed by the clinical colleges. Doctors undergo 10–15 years of training to reach the stage of autonomous practice. Such rigorous training for doctors surely raises the question as to whether NP or PA programs will inevitably evolve into a truncated alternative route to working as a doctor, especially if their graduates were to be remunerated as independent, standalone clinicians. Importantly, will the advent of independent NPs and PAs effectively result in a two-tiered medical system in which some patients have access to lesser medical care than others? Most proponents of PAs and NPs stress the need for their obligatory involvement in teams focusing on multidisciplinary care, and this is commendable. But just how is this service delivery to be remunerated? Will remuneration be based on service provided by the team, or will individuals be remunerated for individual episodes of care? Who will decide what services can be provided by PAs and NPs and how they should be remunerated? Surely a bureaucratic and indemnity nightmare awaits! This approach will require the untangling of notions of parity — of cognitive and procedural services — and a political commitment to studies of the relative value of services provided by PAs and NPs and other members of multidisciplinary teams. Moreover, thorny problems such as these also touch on an overarching philosophical notion — that one of the primary roles of the doctor is to bring certainty to an undifferentiated illness, and to advise on and supervise an intervention or management plan.11 If this is a unique role for which medical graduates have been specifically trained, how is it to be brought to bear under the proposed new arrangements? Will doctors become mere service supervisors, or will their role continue to stress competence in diagnosis and treatment of individual patients? In any event, it is imperative that doctors are the team leaders. There is also an urgent need for consistent, reliable and agreed competency standards, as well as registered trade titles for PAs and NPs, regulated and supervised by multidisciplinary bodies and transferable between various jurisdictions. Interestingly, the evidence underpinning the effectiveness and cost-effectiveness of doctor displacement schemes and protocols is not particularly rigorous.2,3 Furthermore, there are intrinsic cultural considerations in health care delivery. Any programs of doctor displacement in Australia need to be underpinned by contemporaneous research to provide answers as to their relative efficiency and effectiveness, as well as patient safety and satisfaction. It would be unethical and unconscionable to introduce and sustain programs of doctor displacement without evidence from local research. Finally, the debate on whether we proceed with specific doctor-displacement programs will need to be cognisant of recent medical workforce developments. An impending “tsunami” of medical graduates from the recent expansion of our medical schools will soon flood our health care systems.12 Their education and role in health care delivery should not be compromised by developments in doctor displacement. The Australian Government response of using doctor displacement to alleviate workforce shortages must also take into account current acute and future projected nursing shortages.13,14 Thus, it is absolutely imperative that this entire debate be based on community requirements, rather than on the pursuit of vested interests or ideology-driven political agendas. So, bring on a wide-ranging debate about doctor displacement, but let us ensure that this is an evidence-laden debate — a debate that avoids the trenches of turf warfare. In this debate we need creative leadership from doctors.

Martin B Van Der Weyden MD, FRACP, FRCPA