Volume 195 Issue 7

Registries have an important role in monitoring outcomes of complex diseases In the 1950s, a diagnosis of cystic fibrosis (CF) brought with it a high likelihood of dying from lung disease and a low expectation of surviving beyond 10 years of age.1 By 2011, expectations of survival for people living with CF have been transformed; mean age at death now approaches 27 years,2 and over 90% of patients survive beyond 17 years of age.3 Two studies reported in this issue of the Journal provide a broad overview of recent outcomes achieved in the management of Australian patients with CF.2,3 Both of these Australian studies recognised improved survival among people with CF, but reasons for this improvement remain unclear. Many factors probably contribute, including improvements in medical care, such as anti-pseudomonas antibiotics and better chest therapy in general, and the proven benefit of a high-fat diet for maintaining normal growth and nutritional status.4 Improved socioeconomic status may be a factor: a recent analysis of mortality rates among people with CF in the United Kingdom emphasised that lower socioeconomic status (based on two UK government classifications) contributes to higher mortality rates.5 In addition, a fall in the number of early deaths from CF with the advent of newborn screening has been clearly demonstrated.6 Newborn screening was commenced in New South Wales in 1981 and is of particular significance in the Australian setting. Recent data demonstrate a significant survival advantage for a cohort of babies who were diagnosed with CF during the first 3 years of screening compared with a non-screened cohort. Mortality among the non-screened population after 25 years was nearly twice that among the screened population (66% v 32%).7 Unfortunately, the data for the studies reported in this issue2,3 did not allow calculation of the median survival age, which has been the accepted measure for assessing survival of patients with CF.8 However, to give a perspective on the Australian outcome, in a comparable German study that reported a median age of death of 23.7 years, the median age of survival in 2005 was 37.4 years.8 Considering the higher median age of death in the Australian study, the median age of survival could well approach 40 years. This would also compare favourably with data from France and the United States showing median ages of survival of 36.4 years in 2003 and 37.4 years in 2007, respectively.8 Nevertheless, it is likely that we are behind the Canadian achievement of a median age of survival in 2009 of 46.7 years.9 The Australian studies suggest that further research needs to answer two specific questions: Why does the greatest decline in lung function occur during adolescence? Why is there a “gender gap” of significant survival disadvantage among female patients (with the rate of mortality events among girls more than twice the rate among boys2)? Certainly, it would be important to assess adolescent behavioural issues, including compliance; and the described increase in energy expenditure of over 10% in females during adolescence similarly warrants further investigation.10 A 2009 Canadian Cystic Fibrosis Patient Data Registry report9 confirms that a higher proportion of female adolescents with CF are underweight, and the cause remains enigmatic. The databases used by the Australian investigators — the Australian Cystic Fibrosis Data Registry (ACFDR)3 and the General Record of Incidence of Mortality (GRIM)2 — have provided invaluable outcome data for comparison of Australian clinics and thus have a benchmark function. CF centres can measure their performance and, at least in part, justify the estimated annual government expenditure on care for patients with CF of A$67 million.3 The investigators emphasise the importance of known factors that influence the effectiveness of databases, including clinic compliance and the painstaking entry of confirmed and accurate data that conforms with standards for international databases. They also have concerns about the longevity of the ACFDR, given that it depends on ad-hoc private funding. Shortfalls in funding will necessitate shortcuts in data entry that will inevitably compromise the completeness and value of the project. It is essential that governments and the community ensure the sustainability of clinical registries that can identify and report on the cost-effectiveness of treatment plans in complex diseases such as CF.

Kevin J Gaskin MD, FRACP · Bridget Wilcken MB ChB, MD, FRACP

High public interest does not guarantee affordability Alcohol dependence is a common, disabling and costly medical condition that affects 4% of Australian adults.1,2 Several pharmacological therapies are now available in Australia to treat alcohol dependence, including disulfiram, acamprosate and naltrexone. While all three medicines are registered in Australia by the Therapeutic Goods Administration (TGA), only acamprosate and naltrexone are listed on the Pharmaceutical Benefits Scheme (PBS). Recent reviews show that supervised administration of disulfiram is both effective and safe. Accordingly, disulfiram should be made more available and accessible through PBS listing. Disulfiram helps to achieve abstinence by inhibiting aldehyde dehydrogenase. This leads to the temporary accumulation of acetaldehyde, which causes a potentially severe aversive reaction with nausea, flushing, agitation and dizziness, thereby usually deterring future drinking. Although the treatment has a logical basis, early studies found only mixed evidence for its efficacy.3 Consequently, disulfiram fell into disfavour. Recently, however, the original studies of the efficacy of disulfiram were reviewed. When studies of supervised and unsupervised dispensing of disulfiram were compared, well supervised treatment was far more effective, often achieving excellent results.4 Indeed, the few available direct comparisons of supervised disulfiram and other medications for alcohol dependence found disulfiram to be more effective.5-7 At first glance, this would seem like unqualified good news: a well known, registered, and relatively inexpensive medicine (costing about $70 per month, including pharmacy dispensing fees) has been found to be effective for a condition that is often ineffectively treated and is estimated to cost Australia as much as $36 billion per annum.2 But the definition of “inexpensive” is a relative one — many of the patients who need disulfiram cannot easily afford even $70 per month, especially on a continuing basis. At present, these patients can access subsidised disulfiram only through ad hoc mechanisms, such as appealing to hospital drug committees. Listing disulfiram on the PBS is the obvious solution — not only because the drug is effective and inexpensive, but because there is reasonable evidence that it is more effective and less expensive than other treatments listed for alcohol dependence. But therein lies the problem: because disulfiram is an inexpensive and old drug, there is little incentive for a pharmaceutical industry sponsor to underwrite the expensive process of applying to the PBS for listing. While professional associations (such as the Australasian Chapter of Addiction Medicine of the Royal Australasian College of Physicians) could submit an application, they too are likely to be deterred by the costs involved. The PBS is also unlikely to take this on, because it has an interest in controlling expenditure and because the cost of applications to the PBS is usually recovered by charges collected from the sponsor of the drug.8 We are left with a situation in which a treatment is not listed on the PBS despite being effective, relatively inexpensive, likely to save health care resources and, somewhat ironically, recommended for use in government-funded treatment guidelines.9 There is, however, a mechanism by which disulfiram could potentially be listed on the PBS that is analogous to the TGA’s “orphan drug” provisions:10 the PBS is willing to list certain drugs in the public interest and waive the associated application costs. For disulfiram to be listed in this way, an economic justification (however crude) would need to be made, support from the relevant clinical organisations would be required, and the sponsor would need to be willing to supply the drug under arrangements proposed by the Pharmaceutical Benefits Advisory Committee that might or might not be commercially appealing. PBS listing of disulfiram would have to be contingent on its proper clinical use. Disulfiram is not a first-line therapy; it should not be used in the elderly or in patients with cerebrovascular or cardiovascular disease; and patients must be able to understand the consequences of drinking alcohol when taking disulfiram. Most importantly, disulfiram is effective only when administered daily under strict supervision (by a health professional, family member, employer, police officer or probation and parole officer) for at least 12 months.4 While we would not wish to discourage the prescribing of disulfiram in general practice and in rural areas, prescribers would need to be familiar with its side effects and able to provide the necessary counselling. We believe that current evidence is more than sufficient to justify listing disulfiram on the PBS, but continued PBS listing of disulfiram would need to be contingent on further evidence demonstrating relative efficacy and cost-effectiveness. Improving treatment outcomes for patients with alcohol dependence is a very worthwhile goal — especially for critical populations such as Indigenous Australians, recidivist drink-drivers, and people with a long history of repeated alcohol-related violence. Increasing the affordability and use of disulfiram, by listing it on the PBS, would be an important step towards this goal.

Wendy L Lipworth MB BS, MSc, PhD · Alex D Wodak FRACP, FAChAM, FAFPHM · Paul S Haber MD, FRACP, FAChAM · Richard O Day MD, FRACP

As yet in Australia, there is no systematic provision of reliable guidance for practitioners Physicians are quite as intolerant as theologians. They never had the power of burning at the stake for medical opinions, but they certainly have shown the will. Harriet Beecher Stowe, Little foxes (1865)1 In a world populated by rapid-diffusion media, varied cultures, widespread literacy, extraordinary means of communication and media veneration of the might of the scientific method, one might expect that the “marketplace of ideas” would be extraordinarily open, lively and free from censorship or restrictions. In such a world, dogma would fail to develop roots and could not survive. Evidence would triumph and, in its absence, both experts and the broader citizenry would hold on to healthy doubt. In such a world, one might expect that medicine would shine like a beacon of open-mindedness and acceptance of new ideas and that it would foster the development of challenges to operative paradigms. Finally, one might even expect that we, the doctors, aware of the course of science, would know that all the dogmas of today are destined to be footnotes in the annals of the history of medicine. Alas, it is not so. We are not very good at letting go of dogma. There are several potential explanations for medicine’s persistent love affair with dogma. First, perhaps, is the fact that it is difficult to advocate major medical or surgical interventions by explaining to patients that serious uncertainty surrounds such decisions. Thus, doctors need “internal dogma” to function. Imagine a cardiac surgeon saying to a patient: “I intend to perform a bypass operation on your coronary arteries and intend to do it without using the heart–lung machine because I believe (internal dogma) it is a better operation”. Then imagine him saying: “Actually, in a large trial in the USA, more people having surgery without the heart–lung machine had worse outcomes than those who had surgery using the heart–lung machine.2 But, look here, that’s the way I was taught and I am a better surgeon than those US guys. Trust me. I will do a better job”. Not many patients would front up for the surgery next week. Or imagine an intensive care doctor saying to a mother: “Your child has an infection and low blood pressure. I am going to give him a whole lot of intravenous fluids because we know (internal dogma) that’s going to make him better”; or, “Look here, there has never been any comparative study of giving or not giving lots of intravenous fluids to children with low blood pressure and infection, and a recent study in more than 3000 children in Africa showed that it increased their chance of dying by 50%,3,4 but, hey, trust me, let me do it, that’s the way I was taught and Aussie kids are made of sterner stuff”. One wonders how many mothers would ask for a second opinion. The cognitive “illusion of knowledge” also plays a role. We have to believe we know the answer and that there is only one answer, the one we have. To accept that we do not know the answer, or that other people might know the answer while we do not, is emotionally challenging and calls into question our very professional essence. Best to believe that what we think we know is actually true. As Thomas Kuhn5 would have it, at any time in history we operate within “paradigms”, the “soft” (but often strongly enforced) dogmas — that blood-letting saves lives; that lobotomy cures mental illness; that radical mastectomy is necessary to cure breast cancer;6 that immediate fluid resuscitation will save lives in patients with penetrating torso injuries;7 that early oral feeding after colorectal surgery is dangerous;8 that tight glucose control will save lives in intensive care patients;9 and that fluid resuscitation will save children with severe sepsis.3,4 We use such paradigms as totems and make challenging them a professional taboo.10 Dogma is further protected by the emotional impact of physiological gain. Large randomised controlled trials that test effects on major clinical outcomes take years to complete and are difficult and expensive. Every day, however, doctors can see that something “works” because it changes physiology in front of their eyes. Thus, they can see the immediate physiological gain but are blind to the long-term consequences.11,12 Alas, the link between physiological gain and final outcome is tenuous, to say the least.3,4,6,11,12 Dogma probably protects patients from rogue behaviour. We need to make sure that not all treatments are allowed. Rules (dogmas) do exist for a reason. In 2011, it is not acceptable to treat meningitis without rapid and appropriate antibiotic therapy, manage myocardial infarction with ST-segment elevation without intervention, ignore persistently elevated arterial blood pressure, and so on. The difficulty, however, occurs in situations where the evidence that a particular action is needed is not so clear, or, just as frequently, when the practitioner is not aware that such evidence even exists. In a world where the evidence generated every week is substantial, we simply do not know what we do not know. In such a state of permanent flux, it is a lot easier to “stick to what you know” (received dogma) and never change until retirement. This is a problem, because while such a stance might have been justified in 1911, it seems spectacularly out of touch in 2011. Indeed, together with the obstinate adherence to such “medical school” dogma, knowledge management (knowing what one does not know and knowing what one should know) may now be one of the major challenges of modern medicine. Finally, in a world full of “experts”, controversy and opinion, holding on to dogma is reassuring and may well have life-saving functions. Yet, dogma has a dark side and its dangers may be as great as its benefits. Doctors would do well to maintain a degree of cautious skepticism for both bold new fashions and received wisdom, whether generated by the world or by the self. They would do even better to question what they do and see such questioning as an asset. It is everyone’s responsibility to find out how to ask questions systematically, find answers from searching the literature, critically appraise the literature and apply the results to practice. At a national level, Australia needs to think of better ways of providing doctors with reliable guidance. Resources need to be allocated to national bodies, such as the National Health and Medical Research Council, colleges and medical schools to make this process of questioning dogma and obtaining up-to-date high-quality evidence a national priority. Unless this is done, dogma will continue to rule medical hearts and minds.

Rinaldo Bellomo MD, FRACP, FCICM

The full content of this article is available by downloading the PDF.

The full content of this article is available by downloading the PDF.

Health promotion expert Garry Egger argues that obesity is a sentinel of broader environmental causes of chronic disease Any important disease whose causality is murky, and for which treatment is ineffectual, tends to be awash in significance. Susan Sontag, Illness as metaphor1 Evidence in science requires time, but when that evidence arrives, it may suggest that we need to think about things differently. In the case of research into the relationship of obesity to chronic disease, the accumulating weight of evidence has meant a rethink of what obesity means, and what we are trying to achieve in “treating” obesity. After three decades of rapid increases in mean national bodyweight, we now seem to accept that we have a problem. Around one in two Australians are overweight (body mass index [BMI] > 25 kg/m2), and more than one in three are obese (BMI > 30 kg/m2).2 However, now that the message has hit home, the evidence relating obesity to chronic disease has started to shift. Some question whether obesity really is the issue. Should we be focusing instead on those factors (such as lifestyle, environment and social factors) that may (or may not) cause obesity? Why the change of heart? There is little doubt that obesity is linked with the dysmetabolism associated with much chronic disease, and particularly type 2 diabetes. But there are also more distal drivers, which may or may not require obesity in the causal pathway for chronic disease to occur, and these may not be considered if the focus is purely on obesity. This has become clear with the concept of “metaflammation”3 — a form of low-grade, persistent systemic and chronic inflammation, which is associated with much, and perhaps most, chronic disease. While the classical form of inflammation has a healing role in acute disease, metaflammation, because of its persistence, may have a causal role in aggravating and perpetuating chronic disease. Linked not just to obesity, it is also associated with a range of “inducers”, some of which directly cause obesity (overnutrition, inactivity, stress), but also many that are not direct causes.4 These include environmental factors like pollution and passive smoking, a newly identified group of endocrine-disrupting chemicals, and social and occupational factors such as inequality, perceived injustice and even shift work. Together, these make up a group of inducers of chronic disease that could be called “anthropogens” — human-made environments, their by-products, and associated lifestyles. Some of these may be detrimental to human health; all have arisen since the industrial revolution and seem to be foreign to our ancient physiology. These anthropogens may be considered to be the “germs” behind many chronic diseases. A focus just on the proximal causes of obesity and associated individual behaviours could have the adverse impact of blaming individuals for the environment that surrounds them. It deflects criticism from more distal social and environmental causes, where the recognition of an anthropogen-based causality would get to the heart of chronic disease causation. Given this, what would be the point of targeting the “fit fat” — the 35% of obese individuals who have no obvious health risk (apart from mechanical and possibly psychological issues) — and ignoring the approximately 25% of lean people who fit the “lean unhealthy” phenotype and have all the risks expected of the obese?5 The current focus is on visceral fat, which gets close to the issue, but we need to think about what is causing visceral adiposity in the first place. All this points to obesity as an intermediary as much as an offender in chronic disease — it is a sentinel of problems in the broader environment. This is not to suggest that weight loss is not a justifiable goal; of course it is. But to do the job properly, it should be accompanied by broader initiatives aimed at targeting the anthropogens that are using obesity as their cover.

Garry Egger MPH, PhD

Public health expert Ken Harvey believes that they should In theory, allowing people to make their own choices about purchasing products, unfettered by a “nanny state”, sounds fine. However, this assumes that consumers can make informed, rational choices about the cost, risks and benefits of a given product, and that their decisions have no impact on others. In practice, humans are far from rational. We have problems controlling consumption and behaviour, such as how much we eat, drink, or smoke, and how much we spend on poker machines. Advertisers aim to maximise the apparent benefits of products and minimise their risks, and to convince us that expensive, branded products are worth more than no-frills ones. They argue, with the powerful voice of large corporations, that interventions to reduce our consumption of harmful products are an affront to our autonomy. Furthermore, many of our individual decisions do affect others: smoking in enclosed shared spaces and drink-driving cause harm, injury and death to others; and gambling addiction destroys families. Such individual actions have societal costs — premature death, hospitalisation and the need for remedial services — problems often most prevalent in poorer, more disadvantaged populations; some industries specifically target these groups.1 Clearly, the problem of unhealthy consumption and the associated health consequences are societal problems that require a societal approach. Public health policy, appropriately based on relevant evidence and research, is key to a societal approach. Public health is defined as “what we, as a society, do collectively to assure the conditions in which people can be healthy”.2 To know if governments need to restrict people’s choices for the sake of public health, we need evidence about the causes of ill-health, and the effectiveness of proposed interventions. For example, the link between smoking, lung cancer and other diseases is well established, but establishing how much obesity is “caused by” advertising of junk food is harder to quantify. We also need to know if interventions work, and their potential for both benefit and harm in different segments of the population. However, where evidence supports it, policy should be formulated to appropriately limit choices that impact on health. The range of options available to government and policymakers can be thought of as a ladder of interventions, with the rungs representing the degree of freedom individuals should have to make individual choices about their health.3 In considering which “rung” is appropriate for a particular public health goal, the benefits to individuals and to society must be weighed against the erosion of individual freedom. Economic costs and benefits need to be considered alongside health and societal benefits. At the top (most restrictive end) of the intervention ladder, legislation eliminates choice (eg, compulsory seatbelt legislation, banning smoking in public places and random breath testing). One rung down from this, the range of options available are restricted (eg, removing unhealthy ingredients from foods, or unhealthy foods from shops or restaurants). On the next two rungs down, a full range of choices may remain available, but (i) fiscal or other disincentives can be used to influence behaviour (eg, taxes on cigarettes, alcohol and junk food; precommitment limits on gaming machines), and (ii) people can be encouraged to make beneficial choices (eg, by subsidising the cost of nicotine patches through the Pharmaceutical Benefits Scheme). A variant of this is leaving a full range of options available, but changing a default policy so that people need to actively “opt out” (eg, changing from chips to salad as a standard side dish on a restaurant menu, with chips only available as an option). Near the bottom of the intervention ladder, a full range of choices is available, but people are empowered to make beneficial choices. Choice can be enabled (eg, offering participation in “stop-smoking” programs, providing free fruit in schools and building cycle lanes) or the public can simply be provided with information (eg, good food labelling, campaigns to encourage adequate daily fruit and vegetable intake, and encouraging people to walk more). At the bottom of the ladder, the approach is to simply monitor the situation, but this may have its own adverse outcomes. The above policy options are not mutually exclusive. Implementing less restrictive policy options (such as information provision) can increase public acceptance of more restrictive (and often more effective) interventions. Australians have accepted compulsory seatbelts, random breath testing, increasingly tighter regulation of the advertising and sale of alcohol, and smoking bans in enclosed spaces. The Productivity Commission’s proposal for a comprehensive, coordinated and carefully sequenced package of reforms to gambling regulation is a recent example of the public health approach.4 The public has a right to better health. Evidence-based public health strategies, appropriately implemented, are vital to this effort. This may entail impinging on individual freedoms. However, when informed of the benefits, people are prepared to accept sensible curtailment of choice for a better life for themselves and the community as a whole.

Ken J Harvey MB BS, FRCPA

Anaesthetist Michael Keane says no In Melbourne, a prominent billboard summarises: “Alcohol does not cause violence. Blame and punish the individual”. Ironically, this simple message articulates a far more comprehensive understanding of the complete body of relevant knowledge than many public health academics who advocate reactionary, prohibition-like controls on the voluntary consumption of ever more products. Public health traditionally focused on the health consequences of unwanted phenomena. Nobody wanted to drink faeces-flavoured water, but they did want convenient disposal of sewage.1 In contrast, today’s public health focuses increasingly on restricting the active and deliberate consumption of desired products and services, thus imposing government lifestyle mandates (GLMs) on the population. Alcohol, fast food, cigarettes, shopping, soft drinks, gambling and other “vices” unquestionably bring utility as well as harm. What price for the enjoyment of, say, a night of alcohol intoxication? Only the individual knows the answer. The long-established principle of autonomy acknowledges that only the individual can apportion the appropriate weighting to each of the myriad factors in any harm–benefit calculation. GLMs are health interventions, and, like any intervention, need to be consistent with contemporary medical ethics. Sensationalist studies of harm are inadequate to justify enforcing health interventions against peoples’ will. Political scientist Eli Feiring summarises: “Given that respect for the autonomous choices of patients runs deep in modern healthcare, there are strong reasons to value the claim that competent and well-informed individuals are the best interpreters of their own interest and that they should be free to make choices others would regard as non-beneficial to them”.2 Furthermore, it is meaningless to present the sum of harm resulting from a product without reference to fault. A fully established societal and legal principle is that harm caused to oneself is treated differently from harm caused to others. There is certainly no academic basis to nihilistically accept that people who are “glassed” in the face or killed by drunk drivers are merely victims of alcohol-related harm. The solution is not to apply prohibitionist measures to collectively punish everyone. Unfortunately, it is this same failure to rationally distinguish between responsible and reckless use that frustratingly perpetuates the stalemate in the war on illegal drugs. Internationally, challenges to the limits of restrictions (of even smoking) are being countenanced, when the harm is only to the user.3 Similarly, the “freedom to endanger others behind a car wheel with a lead foot or a skinful”4 cannot be equated with the volitional use of products that harm only the user. A common straw-man argument implies that antipathy towards GLMs is a concern only about the overreach of government to run our lives. Admittedly, many public-health-inspired intrusions are minimal, such as the perennial example of seatbelts. But this example is then misused to justify extreme mission creep, up to and including prohibition-like measures. All behaviour can ultimately be coded as health-related in our system and, by reductio ad absurdum, a truly Orwellian state can be justified. Where does it end? Who decides? Yes, Prime Minister’s Sir Humphrey Appleby, or some other fictitious public servant? A more potent concern with the nanny state is the propagation of the “disease” model, which promotes society-damaging, malignant lack of personal responsibility — “it’s not my fault, it’s my disease”. Conceptualising the degree of responsibility for one’s behaviour is at the intersection of neuroscience, ethics and, ultimately, philosophy within the burgeoning field of neuroethics.5 If decision making is a function of the brain, should individuals really be held responsible for their decisions? With this neuroscientific and philosophical uncertainty, “addictions” should not be equated with other diseases in medicine. While the concept of addiction is complex and evolving,6 the current tendency to regard even the most reckless, selfish and antisocial behaviour as the biologically bound phenomena of a particular product is essentially just an expression of opinion and ideology. Regarding autonomy, does an individual who is smoking, drinking, gambling, eating junk food and being indiscriminate about sexual partners (“sex addiction”) really employ a sophisticated risk management equation and decide that the benefits outweigh the costs? Ultimately, public health advocates believe that such people are incapable of making the right decisions; we, the “elite” who know best, therefore have the right to decide what’s good for them. A further justification to usurp established ethical principles is based on the divisive and emotive argument that we have the right to control people because they cost us money in the form of health care expenditure. However, contradictory economic analyses on the real costs of alcohol, cigarettes and fatty foods abound. History and the human condition teach us that it would be dangerously naive to enforce interventions against peoples’ will on the basis of conflicting, often ideologically inspired economic analyses. Crucially, again, government overreach would then make it legitimate to forcibly treat individuals against their will, if it meant a reduction in government expenditure. Let me opt out.

Michael J Keane FANZCA

Aspiration pneumonia occurs most commonly in patients with a predisposition to aspiration (eg, those with neurological bulbar dysfunction). There is limited evidence regarding the involvement of anaerobes in most cases of aspiration pneumonia. Most patients respond to treatment for aspiration pneumonia without specific anti-anaerobic therapy such as metronidazole. Metronidazole has adverse side effects, and widespread use where not indicated can promote carriage of multiresistant intestinal flora such as vancomycin-resistant enterococci. Use of metronidazole may be appropriate in patients with aspiration pneumonia and evidence of a lung abscess, necrotising pneumonia, putrid sputum or severe periodontal disease.

Jason C Kwong MB BS, BMedSci · Benjamin P Howden MB BS, PhD, FRACP · Patrick G P Charles MB BS, PhD, FRACP

A view from the front line In Australia, medical colleges set the standards for specialty education within an accreditation framework managed by the Australian Medical Council (AMC). They also play a critical role in ensuring that vocational trainees are appropriately supervised and supported during their training. Despite the critical value of evaluation in specialty education, it can be difficult to obtain anonymous program feedback from trainees who fear being identified.1-3 In this context, the Australian Medical Association (AMA) Council of Doctors in Training undertook its Specialist Trainees Survey to ascertain trainee opinion on key aspects of vocational education. The April 2010 survey was an online, self-report questionnaire based on the AMC’s standards for specialty education programs. The survey methods are outlined in the footnote to the Box, and the full report is available online (http://ama.com.au/specialist-trainees-survey). Selected results (Box) show that colleges are performing well in many areas, including selection, alignment of clinical experience with learning objectives, and access to supervision. While there was a high level of satisfaction with work and training, several areas attracted negative results. These included appeals processes, capacity to raise concerns without fear of recrimination, recognition of prior learning, provision of remediation, responsiveness to cases of bullying and harassment, and cost. Concerns about appeals processes and fears of recrimination are consistent with the findings of a 2010 literature review and discussion at a recent AMC workshop on trainee feedback and course evaluation.3 It is critical that colleges adopt appeals procedures that conform to best-practice models, which characteristically ensure natural justice, have clear criteria, follow due process and minimise the risk of litigation. A concerning finding of the Specialist Trainees Survey is the perception of inadequate responsiveness to claims of bullying and harassment. Bullying occurs in Australian health workplaces,4 and trainees are at risk because distinctions between workplace and training supervisors can be blurred. It is critical that colleges have well defined and transparent processes for dealing with these matters, which are the responsibility of educators as well as employers. In the absence of such processes, trainees, supervisors and colleges remain vulnerable. The survey’s findings in relation to recognition of prior learning are not surprising, and reflect suboptimal integration of stages and pathways of training. Efforts to align and recognise components of clinical education will create efficiencies that will benefit trainees, colleges and health services. The survey’s most negative response was in relation to value for money of training fees. Further, 40% of respondents reported that the cost of their training program had caused them financial hardship. Ensuring reasonable costs for training and assessment is integral to minimising the adverse consequences of study debt.5 It is equally important that colleges are transparent about how they apportion fees. Notwithstanding the limitations of its methods, the results of this survey should help colleges reflect on their performance against the AMC standards for specialty education. Reassuringly, most areas attracted positive responses. The AMA plans to repeat the Specialist Trainees Survey every 4 years to continue to identify trends and emerging issues. Selected Specialist Trainees Survey* data Statement Agree or strongly agree Weighted average score I am satisfied with my training program 68% 0.29 The selection processes for entry into the training program are fair and transparent 69% 0.34 My training posts provide the necessary clinical experience to meet the objectives of my training program 75% 0.36 I am satisfied with the level of supervision I receive 84% 0.46 I am confident that I will not be disadvantaged if I raise issues of concern with my college 31% − 0.04 The college grants appropriate credit for relevant prior training and experience 25% − 0.09 The college provides unsuccessful candidates with appropriate remediation 16% − 0.14 The college has an effective appeals process 16% − 0.03 The college responds in a timely and appropriate manner to cases of bullying and harassment 11% − 0.04 The costs of the college training program represent value for money 23% − 0.30 * The survey had 55 items, each scored on a five-point Likert scale. All 10 649 hospital-based vocational trainees were eligible to participate, although only trainees on the Australian Medical Association database were directly sent a link via email. There were 538 respondents from 18 disciplines. Results for responses of “agree” and “strongly agree” were expressed as a percentage, and a weighted average score was calculated by dividing the sum of vote values (strongly agree, 1.0; agree, 0.5; neither agree nor disagree, 0; disagree, − 0.5; and strongly disagree,− 1.0) by total sample size.

Rob D Mitchell BMedSc(Hons), MB BS(Hons) · Alexandra L Markwell BSc, MB BS(Hons), FACEM · Rick J Fielke MB BS · Michael A Bonning BAppSc(Hons), MB BS · Andrew W Perry MB BS · Dror Maor MB BS

To the Editor: Outpatient non-attendance remains a major problem that significantly drains the ability of hospitals to provide efficient and effective outpatient services.1,2 Our earlier pilot study demonstrated the effectiveness of short message service (SMS) text message reminders in improving attendance at the outpatient department in Melbourne’s Royal Children’s Hospital (a 250-bed tertiary referral hospital).3,4 We present the results of a follow-up retrospective cohort study that examined the effect of the following eight factors on failure to attend (FTA): sex, native language, distance lived from hospital, day of appointment, time of appointment, wait time (days from scheduling to appointment), socioeconomic status (SES), and SMS reminders. Data included all outpatient appointments (65 535) in the period July 2005 to January 2006. Incomplete data meant that 44 appointments were excluded, leaving 65 491 episodes for the analyses. The patients were classified into three SES groups: low (G1), middle (G2) and high (G3). This classification was based on the Jarman score (a proxy for SES) derived from the patient’s residential postcode.5 Similarly, patients were classified into three groups based on distance between the patient’s residence and the hospital: < 25 km, 25–50 km and > 50 km. Univariate and multiple logistic regression analyses confirmed that all factors other than sex were significantly associated with FTA. We also found that the two populations with and without SMS reminders were significantly different. We conducted a stratified analysis for the two groups and the summary results are presented in the Box. Our analysis shows that FTA rates improve by 5.34% (from 14.85% to 9.51%), and confirms the effectiveness of SMS reminders in lowering FTA. It shows that native language, distance lived from hospital, SES and wait time are significantly associated with FTA across both groups. Although SMS reminders resulted in higher improvement in attendance for non-English speaking patients compared with English speakers (8.33% versus 4.1%), those patients still had higher odds of missing an appointment. Lower SES was associated with an increased likelihood of defaulting. Longer waits until the appointment resulted in lower odds of attending, and odds of attending improved with increased distance from the clinic. Together these results suggest that in addition to SMS reminders, interventions targeted at specific groups may improve attendance rates and cost effectiveness. Stratified analysis of factors contributing to outpatient failure-to-attend rates, by SMS reminder No SMS reminder (n = 20 871) SMS reminder sent (n = 44 620) Factor FTA OR FTA OR Aggregate 14.85% 9.51% Native language English 13.04% 1* 8.94% 1* Non-English 21.35% 1.62† 13.02% 1.30† Distance lived from hospital < 25 km 15.89% 1.36† 10.28% 1.51† 25–50 km 13.77% 1.20†† 8.71% 1.28† > 50 km 11.36% 1* 7.16% 1* Socioeconomic status Low (G1) 17.51% 1.37† 12.28% 1.57† Middle (G2) 14.84% 1.34† 9.26% 1.22† High (G3) 12.11% 1* 8.26% 1* Wait time (from scheduling to actual appointment) < 15 days 8.40% 0.42† 5.94% 0.45† 15–30 days 16.40% 0.90‡ 9.48% 0.74† > 30 days 18.13% 1* 12.40% 1* SMS = short message service. FTA = failure to attend. OR = odds ratio. * Baseline comparison group: OR = 1. † OR significant at P < 0.001. ‡ OR significant at P < 0.05.

Sean R Downer · Kannan Sethuraman · Devanath Tirupati

To the Editor: Kinner and colleagues described the high proportion of deaths among recently released prisoners in Australia.1 I had a patient with a history of intravenous drug use who, after a prolonged stay in hospital for osteomyelitis complicating a diabetic foot ulcer, including extensive inpatient rehabilitation, died due to drug overdose on the first weekend after discharge. This tragic death suggests a mortality risk for people with a history of drug misuse who are released from any long-stay institution, including hospitals. It may be appropriate for medical practitioners to discuss this risk frankly with such patients at discharge.

Emma L Duncan

To the Editor: We wish to report Queensland data regarding vitamin D levels during pregnancy, to contribute to the debate on screening during pregnancy raised in Lau and colleagues’ article1 and Ebeling’s accompanying editorial.2 In 2009, we measured serum 25-hydroxyvitamin D (25[OH]D) levels, using a DiaSorin radioimmunoassay (DiaSorin, Stillwater, Minn, USA), in 75 women who attended general antenatal clinics at the Royal Brisbane and Women’s Hospital (RBWH) and Mater Mothers’ Hospital. Both institutions’ Human Research Ethics Committees approved the study. Participants gave written consent. The RBWH Private Practice Fund covered pathology expenses. Fifty-seven of the 75 women were white; the remainder were Asian (five), Indian Subcontinental (seven), Polynesian (four), Middle Eastern (one) and black African (one). Mean age was 28.6 years (SD, 5.4 years), mean gestational age was 28.7 weeks (SD, 2.7 weeks) and mean body mass index was 26.4 kg/m2 (SD, 5.5 kg/m2). Median serum 25(OH)D level was 92 nmol/L (interquartile range, 74–118 nmol/L). Using cut-offs of < 25 nmol/L for deficiency and < 50 nmol/L for insufficiency, two women were vitamin D deficient (one was Middle Eastern and one was South-East Asian) and five women were vitamin D insufficient (three were white, with lowest serum 25[OH]D level of 40 nmol/L, and two were Indian Subcontinental). The result of a Fisher exact test suggested an association with ethnicity (P = 0.01). A χ2 value of 21.36 (P < 0.001) confirmed that the proportions of deficiency and insufficiency in our study population were significantly different to those of Lau et al’s study population. The majority of serum samples (40) were obtained in winter, followed by spring (21), summer (10) and autumn (three). Six of the seven results of deficiency and insufficiency were from samples obtained in winter; the other was from a sample obtained in September. Excluding autumn, categorical and continuous analyses showed borderline significant variation of 25(OH)D level by season (Mann–Whitney U test [P = 0.08] and Kruskal–Wallis test [P = 0.08], respectively). Several factors may account for the difference in vitamin D deficiency and insufficiency prevalence between our study and that of Lau et al. The most obvious is the “Sunshine State” factor, because several studies in southern states have reported higher prevalence of vitamin D insufficiency than in our study.3-5 In Lau et al’s study, a large proportion of women were at high risk of vitamin D deficiency (only 19% were white) and the women were recruited from a gestational diabetes mellitus clinic. Care should be taken in extrapolating such findings to the wider population. Although our study was not population based, it included a majority white and healthy general obstetric population, rather than sampling at a clinic where women are at high risk of vitamin D insufficiency. We are not asserting that gestational vitamin D levels are unimportant. The increasing incidence of rickets in Australia,2 along with other potential hazards, dictate that increased awareness is mandatory. However, as opposed to routine screening in all pregnancies, our data suggest that local assessment of vitamin D status and demographic risk factors (in gestational diabetes mellitus and general obstetric populations) should be the priority.

Donald S A McLeod · Katherine A Scott · Karin M C Lust · H David McIntyre

To the Editor: We published a case in the Journal in 2009 titled “Spontaneous chylothorax in a 2-year-old child”.1 Subsequently, it has come to our attention that trauma is likely to have been the cause of the chylothorax. At the time of caring for the child, and submission of our article to the Journal, we had no evidence of this. We had specifically asked for a history of trauma and looked for external signs of injury. The chest x-ray and computed tomography (CT) scan had been reviewed with our radiology staff at the time and we did not detect abnormalities of the vertebrae or paravertebral tissue, and no such abnormalities were detected during surgery. However, the child presented with serious injuries 9 months later and died on arrival at hospital. At autopsy, a CT scan showed a paravertebral haematoma and vertebral injury in the lower thoracic vertebrae where the thoracic duct traverses the diaphragm and ascends on the right side (it was a right-sided chylothorax). On further review of the original chest x-ray and CT scan, it was possible to see that some of these findings were evident at the initial presentation with chylothorax. At the time of submission of our article, we speculated that vomiting could have caused injury to the thoracic duct. We now wish to highlight that apparently spontaneous chylothorax may be due to trauma. In children, non-accidental injury must be considered as a possible cause.2

Manuel E Soto-Martinez · Vanessa Clifford · Tom Clarnette · Sarath Ranganathan · R John Massie

To the Editor: A 38-year-old man with genotype 1b chronic hepatitis C infection had been treated with 48 weeks of pegylated interferon (IFN)-α and ribavirin. Autoimmune serology performed just before treatment showed positive perinuclear antineutrophil cytoplasmic antibodies (ANCA) accompanied by an elevated antimyeloperoxidase antibody level (22 U/mL; reference range [RR], < 5 U/mL). Notably, the patient was ANCA-negative 12 months previously. The treatment course was uneventful. One month after the completion of therapy, the patient presented with a subacute onset of fever, haemoptysis, breathlessness and generalised arthralgia. Laboratory investigations demonstrated raised levels of C-reactive protein (128 mg/L; RR, < 5 mg/L) and creatinine (159 μmol/L; RR, 64–104 μmol/L), low albumin concentration (28 g/L; RR, 35–46 g/L), a low haemoglobin level (64 g/L; RR, 135–180 g/L), and microcytic hypochromic anaemia. Autoimmune serology showed persistence of a positive ANCA and an elevated antimyeloperoxidase antibody level (29 U/mL). A high-resolution computed tomography scan of the chest showed features of interstitial lung disease (Figure, A) and a renal biopsy demonstrated pauci-immune necrotising glomerulonephritis (Figure, B). These findings were consistent with a diagnosis of microscopic polyangiitis. Despite treatment with intravenous cyclophosphamide and pulse methylprednisolone, the patient deteriorated and was admitted to the intensive care unit for ventilatory support, haemodialysis and plasmapheresis. This admission lasted 4 weeks and was complicated by line-related sepsis and persistent anaemia requiring multiple blood transfusions. The patient remains clinically well 14 months after discharge, with negative ANCA and negative hepatitis C virus RNA polymerase chain reaction consistent with a sustained viral response. Autoimmune disease is a well recognised complication of IFN-α therapy in chronic hepatitis C infection. The clinical manifestations of IFN-α-related autoimmune disease can be either organ-specific (thyroiditis, psoriasis) or, less commonly, systemic (rheumatoid arthritis, lupus-like disease, sarcoidosis).1 IFN-α-based treatment in chronic hepatitis C infection unmasks silent autoimmune processes, or induces de novo autoimmune diseases or autoantibodies.2 A predisposition to autoimmunity, together with the presence of baseline auto-antibodies, has been demonstrated in most instances of IFN-α-mediated autoimmune diseases,1 as observed in our case. Although rare, the diagnosis of microscopic polyangiitis needs to be considered in patients treated with IFN-α-based therapy for chronic hepatitis C infection presenting with skin rash, fevers, arthritis, an active urine sediment, renal failure or pulmonary haemorrhage. One could consider reducing the duration of therapy in patients who achieve negative RNA polymerase chain reaction at Week 4 of treatment. There is emerging evidence that 24 weeks of response-guided therapy in genotype 1b chronic hepatitis C infection is as effective as the standard-of-care treatment for 48 weeks in rapid responders.3 We also suggest that, in the presence of a positive ANCA at baseline screening, a chest x-ray and urinalysis be performed before initiating IFN-α-based treatment, and that patients be monitored clinically and with urinalysis during treatment. A chest x-ray should also be performed at the completion of treatment. The presence of auto-antibodies alone is not a contraindication to IFN-α therapy, but it does mandate careful monitoring and a high index of suspicion of an immune diathesis. A: High-resolution computed tomography scan of the patient’s chest showing patchy foci of ground glass opacification and nodules bilaterally. B: Renal biopsy showing focal crescentic necrotising glomerulonephritis (haematoxylin-eosin stain; original magnification x 400).

Stephen Y Oh · Brett E Jones · Suran L Fernando

To the Editor: In a recent article that appeared in newspapers such as Melbourne’s The Age and Sydney Morning Herald on 19 Jan 2011,1 one of us (P Z) argued that it is both ineffective and inaccurate to blame those who are overweight and obese for their health problems. It was highlighted that our social, economic, cultural and physical environments are all “obesogenic”,2 acting as barriers to achieving a healthy lifestyle. The article by Proietto in the August 2011 issue of the Journal similarly argued that the obesogenic environment, and its interaction with a person’s genetic make-up, is to blame for the increasing prevalence of overweight and obesity.3 Neglecting to address the role of environmental factors in lifestyle disease may lead to a number of unintended negative consequences. First, healthy eating and being physically active are not easy choices. If attempts are not as successful as first hoped, and if the response from health professionals is simply “try harder”, feelings of guilt and despair can result, which then make it even harder to engage in healthy behaviours. Second, a sole emphasis on individuals’ responsibility for their own health has led governments at all levels in Australia to be passive on this issue. Governments seek to protect us in other ways (eg, legislation to restrict the use and advertising of tobacco), so they now need to be encouraged to take steps towards reducing the obesogenic nature of our environment (eg, introducing policy that ensures affordable and sustainable fruit and vegetable production).4 Finally, focusing on individual health behaviours alone may create or reinforce a social stigma around obesity and related chronic conditions, such as type 2 diabetes.5 When individual behaviour change is the sole focus of prevention and management efforts, the subtext is that the individual is to blame if he or she develops the condition. The astonishing and immediate public response to the aforementioned newspaper article — almost 300 comments were posted online on The Age and Sydney Morning Herald websites alone within hours — reflected an entrenched attitude of blame towards people who are overweight or obese. Given that type 2 diabetes can only be prevented in about 60% of cases,6 these comments reveal and perpetuate a limited understanding of the multiple causes of lifestyle diseases. It remains critical to encourage people to pursue healthy lifestyle choices. However, addressing the obesogenic elements of our environment is just as important. Encouraging patients to become involved in organisations such as The Parents’ Jury, an online network dedicated to improving children’s food and physical activity environments (www.parentsjury.org.au), or to become familiar with community-based initiatives such as Victoria Walks (www.victoriawalks.org.au) may be beneficial. More broadly, it is important for health professionals and their professional bodies to make known to governments their support of policy and other initiatives that make our environ-ment conducive to healthy choices.

Jessica L Browne · Paul Zimmet · Jane Speight

To the Editor: A daunting idea for health care providers is the statistic that, for many medications, only about half of the patients given standard doses will receive the desired therapeutic benefit.1 In the past decade or so, it has been argued that some of this variation in response may be attributed to genetic differences between individuals in mechanisms responsible for the pharmacokinetics and pharmaco-dynamics of many drugs.2 The disparity in health standards among Aboriginal and Torres Strait Islander people compared with non-Indigenous groups is a cause for concern, and requires a concerted political effort to instigate adequate solutions.3,4 Some of the problems include a higher rate of diseases such as hypertension, diabetes, obesity, cardiac disease and depression.3,4 The range of medicines prescribed for these conditions is broad, and some people may not receive the full therapeutic benefit, or may have more severe side effects compared with others. Genetically determined variables contribute to the pharmacokinetics and pharmaco-dynamics of these drugs. Many medications used to treat such diseases are metabolised by the cytochrome P450 (CYP) hepatic enzyme systems, and/or their pharmacokinetics are altered by drug influx and efflux systems. Many of these mechanisms are under genetic control and their efficiency may vary between individuals. Despite this, there are few data on the pharmacogenetics of Indigenous populations generally, and the data on Aboriginal and Torres Strait Islander populations are particularly scant.5 Of the few genetic studies of Indigenous Australians, one found that CYP2C19 and CYP2D6 allele frequencies in a group from remote north-western Australia differed significantly from those for Australians of European ancestry, but were similar to those for East Asian populations.5 An altered CYP2C19 allele could mean alterations in levels of drugs such as phenytoin and clopidogrel, and an altered CYP2D6 allele could mean alterations in levels of drugs such as tricyclic antidepressants, selective serotonin reuptake inhibitors, codeine and tamoxifen. We urgently need to identify clinically relevant issues relating to the capacity of people from these groups to metabolise certain medicines. Screening for genetic variations in drug metabolism and transport mechanisms may highlight significant variations in capacity. This may influence whether people benefit from or are harmed by commonly prescribed medications for hypertension, type 2 diabetes, cardiac disease and depression. The high and increasing prevalence of these diseases among Aboriginal and Torres Strait Islander populations supports a detailed, methodical assessment of the genetics of their drug-metabolising capacity.

Joseph D Tucci

To the Editor: NSW Health’s latest initiative, www.emergencywait. com.au, is a website that presents real-time information about estimated waiting times at 58 emergency departments (EDs) in New South Wales. Similar websites have been used in other Australian states, including South Australia, Western Australia and Victoria, as well as overseas, in Ontario, Canada, and in Memphis, Tennessee. I am concerned that this initiative will be counterproductive and will add further congestion to our already overcrowded EDs. Extended waiting times are a longstanding problem at EDs. They have traditionally been attributed to staff shortages, delays in pathology and imaging tests,1 and inadequate funding. However, there is another major contributor to waiting times that rarely attracts attention in the lay media — the overwhelming number of patients who inappropriately seek medical attention in EDs and would be better served by a general practitioner. Much of the work in EDs involves treating patients with non-acute and non-urgent problems. Recent examples from my personal experience include a man requesting a prescription for antiepileptic medication, a perimenopausal woman with many months of irregular menstrual bleeding, and a young man with a common cold. All of these patients bypassed their GPs, despite their attendances being within normal business hours. A logical outcome of www. emergencywait.com.au is an increase in the number of non-acute, non-urgent presentations to EDs that are seen to be “quiet”. For alongside each hospital’s estimated waiting time, the website presents a list of nearby hospitals with the number of patients waiting at each, thereby enabling patients to compare EDs and attend the least busy one. Formal studies are scant, but crude American data indicate a 6%–10% increase in ED patient volume since waiting times were publicised.2 Although the transparency of www.emergencywait. com.au may help our EDs to share more equitably the burden of inappropriate patient attendances, I expect that it will increase the overall number of such attendances and ultimately increase waiting times. Australian EDs provide excellent, prompt care for patients who have been in accidents or emergencies, but they are neither equipped nor designed to look after individuals who meet neither of these criteria. The solution to overcrowded EDs lies not in websites that publicise waiting times, but in convincing the public that emergency rooms are for emergencies.

Alexander M Owen

Carpal tunnel syndrome, resulting from median nerve compression at the wrist, is a common and often disabling mononeuropathy. Risk factors include female sex, family history, repetitive hand use, obesity, pregnancy and a variety of medical comorbidities including diabetes mellitus, rheumatoid arthritis, and other connective tissue diseases. In many cases, an accurate diagnosis can be reached on the basis of clinical history and supportive examination findings alone. Neurophysiological investigations are essential for confirming the diagnosis, assessing severity and excluding more generalised neuropathies, as well as providing a baseline preoperative index of median nerve function. Wrist splinting and local corticosteroid injection are effective treatments in the short term, but long-term data are lacking. Surgical (endoscopic or open) carpal tunnel release is effective and nearly always required to enable a return to work for patients with occupationally induced carpal tunnel syndrome.

Marion A Simpson MB ChB(Hons), MRCP(UK) · Bruce Day MB BS, FRACP

Objective: To assess mortality trends among people with cystic fibrosis (CF) in Australia.Design and setting: We augmented Australian summary data for deaths from CF registered during 1979–2005 with information from Australian transplant centres on lung transplantation among CF patients for 1989–2005 to allow us to follow trends in all “mortality events” (death or lung transplantation).Main outcome measure: Age at death or lung transplantation.Results: Between 1979 and 2005, the mean age at death increased from 12.2 years to 27.9 years for males and from 14.8 years to 25.3 years for females. Overall, female deaths in childhood (0–14 years) occurred at an age-standardised rate of 0.40 per 100 000 (95% CI, 0.34–0.45) during 1979–2005, which exceeded the corresponding rate for males of 0.24 (95% CI, 0.20–0.28) per 100 000. Among 0–14-year-old boys, event rates declined markedly after 1989, but they declined later and more gradually for girls, with the result that the age-standardised rate for girls was 2.38 times that of boys during 1989–2005 (95% CI, 1.69–3.36).Conclusions: The pattern of CF mortality in Australia has changed substantially. Mortality rates continue to be higher for girls than for boys, but death in childhood has become uncommon. Survival has increased since 1979, but females continue to have reduced length of life.

David W Reid BSc, MB ChB · C Leigh Blizzard PhD · Dace M Shugg RN · Ceri Flowers BSc · Catherine Cash BSc · Hugh M Greville MD

Objectives: To describe the demographics, clinical features and outcomes among people with cystic fibrosis (CF) in Australia and to estimate incidence of the disease.Design and setting: Cross-sectional analysis using data from the Australian Cystic Fibrosis Data Registry for 2009.Main outcome measures: Numbers of diagnoses, pulmonary and anthropometric measurements, microbiological culture results, rates of hospitalisation and transplantation, and numbers of medical complications and deaths.Results: In 2009, data were submitted on 2986 people (48% female). Median age was 17.6 years and 49% of people were aged 18 years or over. Seventy-eight people were newly diagnosed. Fourteen people died and 14 people underwent lung transplantation in the year. Lung function and nutrition were relatively normal among children but deteriorated (more rapidly) among adolescents. With increasing age, progressive respiratory disease was apparent, and the frequency of CF-related complications and use of health care resources increased. In all age groups, there was a wide range in severity of lung disease and nutritional status.Conclusions: CF remains a progressive respiratory disease and is associated with multisystem complications. The acceleration in disease severity in adolescence and early adulthood suggests that better treatment at these stages is required to further improve survival.

Scott C Bell MB BS, MD, FRACP · Peter T P Bye MB BS, PhD, FRACP · Peter J Cooper MB ChB, FRACP · A James Martin MB ChB, MRCP, FRACP · Karen O McKay LLB(Hons), PhD · Phillip J Robinson MD, PhD, FRACP · Gerard F Ryan MB BS, FRACP · Geoff C Sims BComm, GradDip(Pop health), GradCertBiostats

Objective: To investigate how Australian print news media portray psychiatric genetics.Design and setting: Content and framing analysis of a structured sample of print news items about psychiatric genetics published in Australian newspapers between 1996 and 2009.Main outcome measures: Identify dominant discourses about aetiology of mental illness, and perceived clinical outcomes and implications of psychiatric genetics research.Results: We analysed 406 eligible items about the genetics of psychiatric disorders. News coverage of psychiatric genetics has steadily increased since 1996. Items attributing the aetiology of psychiatric disorders to gene–environment interactions (51%) outnumbered items attributing only genetic (30%) or only environmental factors (20%). Of items that referred to heritability of mental illness, frames of genetic determinism (78%) occurred more frequently than probabilistic frames (22%). Of frames related to genetic prophesy, genetic optimism frames (78%) were used more frequently than frames of genetic pessimism (22%). Psychosocial and ethical implications of psychiatric genetics received comparatively relatively little coverage (23%). The analysis identified 22 predictions about psychiatric genetic discoveries and the availability of molecular-based interventions in psychiatry, most of which (20/22, 91%) failed to manifest by the predicted year.Conclusions: Excessive optimism about the power of genetic technology in psychiatric health care, perceived clinical benefits, and largely unfulfilled predictions about availability of these benefits could encourage unrealistic expectations about future molecular-based treatment options for mental health.

Alex Wilde BSc(Hons),PhD · Catriona Bonfiglioli BA(Hons), PhD · Bettina Meiser PhD · Philip B Mitchell AM, MD · Peter R Schofield PhD, DSc

Objective: To evaluate the effectiveness of the Practitioner Asthma Communication and Education (PACE) Australia program, an innovative communication and paediatric asthma management program for general practitioners.Design: Randomised controlled trial.Setting: General practices from two regions in metropolitan Sydney.Participants: 150 GPs, who were recruited between 2006 and 2008, and 221 children with asthma in their care.Intervention: GPs in the intervention group participated in two 3-hour workshops, focusing on communication and education strategies to facilitate quality asthma care.Main outcome measures: Patient outcomes included receipt of a written asthma action plan (WAAP), appropriate medication use, parent days away from work, and child days away from school or child care. GP outcomes included frequency of providing a WAAP and patient education, communication and teaching behaviour, and adherence to national asthma guidelines regarding medication use.Results: More patients of GPs in the intervention group reported receipt of a WAAP (difference, 15%; 95% CI, 2% to 28%; adjusted P = 0.046). In the intervention group, children with infrequent intermittent asthma symptoms had lower use of inhaled corticosteroids (difference, 24%; 95% CI, − 43% to − 5%; P = 0.03) and long-acting bronchodilators (difference, 19%; 95% CI, − 34% to − 5%; P = 0.02). GPs in the intervention group were more confident when communicating with patients (difference 22%; 95% CI, 3% to 40%; P = 0.03). A higher proportion of GPs in the intervention group reported providing a WAAP more than 70% of the time (difference, 23%; 95% CI, 11% to 36%; adjusted P = 0.002) and prescribing spacer devices more than 90% of the time (difference, 29%; 95% CI, 16% to 42%; adjusted P = 0.02).Conclusions: The PACE Australia program improved GPs’ asthma management practices and led to improvements in some important patient outcomes.Trial registration: Australian New Zealand Clinical Trials Registry ACTRN12607000067471.

Smita Shah MB ChB, MCH · Susan M Sawyer MB BS, MD, FRACP · Brett G Toelle DipAppSc(Nursing), BA(Psychology), PhD · Craig M Mellis MPH, MD, FRACP · Jennifer K Peat PhD · Marivic Lagleva BSc(Hons) · Timothy P Usherwood MD, FRACGP, FRCP · Christine R Jenkins MB BS, MD

Objective: To evaluate the effectiveness of formal assessments of prevocational medical trainees (ie, interns, first-year residents and international medical graduates undergoing supervised training).Design and setting: Retrospective review of structured assessment forms that are completed by all prevocational trainees and their supervisors in New South Wales public hospitals. We reviewed the first 3390 assessment forms, representing assessments of 1072 trainees at 43 training sites (83% of all prevocational trainees in NSW) since January 2009.Main outcome measures: (i) Trainee ratings on 19 assessment items by self-assessment and by supervisor assessment; and (ii) quantity and quality of written comments provided in assessments.Results: At the end of term, 43% of trainees assessed themselves as performing “at expected level” on all 19 rating items. Nearly 99% of trainees were assessed by their supervisors as performing at or above the expected level on all assessment items. Written comments by supervisors were generally short and encouraging, but lacked specific feedback that trainees might use to guide improvements in performance.Conclusions: As currently used by trainees and supervisors, the assessment forms may underreport trainee underperformance, do not discriminate strongly between different levels of performance of trainees or the training system, and do not provide trainees with enough specific feedback to guide their professional development.

Craig M Bingham MA, DipEd · Roslyn Crampton MB BS, FACEM

Clinical record A 17-year-old girl presented to her general practitioner with a 1-week history of fever, arthralgia, general malaise and dry cough. She had a history of systemic onset juvenile idiopathic arthritis (SOJIA), diagnosed at age 2 years and treated with aspirin, and had been in remission for 13 years. She was initially treated by her GP with oral roxithromycin, and admitted to hospital 3 days later with worsening of her symptoms. Her admission chest x-ray (Box 1) revealed bilateral perihilar infiltrates. A diagnosis of severe community-acquired pneumonia was made and broad spectrum antibiotics were commenced, including vancomycin, moxifloxacin, and oseltamivir. Despite this treatment, her condition deteriorated. On Day 3 of admission she required endotracheal intubation and circulatory support with noradrenaline 18–50 μg/kg/min, and was admitted to the intensive care unit (ICU). She remained hypotensive, with a mean arterial pressure of 50 mmHg, and with sinus tachycardia of 132 beats/min, and subsequently required renal replacement therapy. She remained febrile for the first 3 days after admission (temperature range 37.5°C–39°C), and her temperature settled to normal after appropriate therapy was initiated. Investigations included a computed tomography scan of her abdomen, which showed hepatosplenomegaly, and liver function tests, which showed elevated conjugated bilirubin (36 mmol/L; reference range [RR], < 4 mmol/L), γ-glutamyl transferase (84 U/L; RR, < 24 U/L), lactate dehydrogenase (3540 U/L; RR, 150–280 U/L), alanine aminotransferase (108 U/L; RR, 10–30 U/L) and aspartate transaminase (388 U/L; RR, < 30 U/L). Other abnormal parameters were her haemoglobin level (93 g/L; RR, 120–160 g/L), platelet count (65 x 109/L; RR, 150–400 109/L), white cell count (2.9 x 109/L; RR, 4.5–13 x 109/L), international normalised ratio (2.1; RR, 0.9–1.2) and fibrinogen level (0.9 g/L; RR, > 2.5 g/L). Elevated inflammatory markers included C-reactive protein (301 mg/L; RR, < 5 mg/L) and serum ferritin (50 500 μg/L; RR, 7–140 μg/L). A transthoracic echocardiogram showed a left ventricular ejection fraction of 60%, a mild reduction in right ventricular contractility, and a right ventricular systolic pressure of 48 mmHg. A full screen for sepsis was performed, including a nasopharyngeal aspirate, bronchoalveolar lavage, blood cultures and serological testing; all were unremarkable. Other immunological tests performed were for Mycoplasma pneumoniae antibodies, Streptococcus pneumoniae urinary antigen, Legionella pneumophila urinary antigen, herpes simplex virus, cytomegalovirus, Epstein–Barr virus (EBV) IgM and IgG, influenza A and B, H1N1 influenza RNA, respiratory syncytial virus, parainfluenza and adenovirus DNA, Q fever (Coxiella burnetti) IgM and IgG, and serological tests for hepatitis, dengue fever IgM and Leptospira IgM, all of which were non-reactive. Urinalysis revealed a white blood cell count of 140 x 106/L (RR, < 10 x 106) and an erythrocyte count of > 500 x 106/L (RR, < 10 x 106/L) with no microbial growth on culture. A bone marrow aspirate with trephine was performed on Day 4 (Day 2 in the ICU), and EBV DNA was detected in the resulting sample using a qualitative DNA test. The patient’s failure to improve, in combination with her past history of SOJIA, hepatosplenomegaly and a very high ferritin level led to a preliminary diagnosis of macrophage activation syndrome (MAS). Immunosuppressive treatment in the form of high-dose methylprednisolone (10 mg/kg daily) and intravenous immunoglobulin (1 g/kg daily) were commenced. Inotrope and ventilatory requirements improved within 24 hours of this treatment. On Day 9 of admission she was extubated, and was discharged home on high-dose steroids 8 days later with no complications. Her bone marrow aspirate histological examination showed haemophagocytosis which confirmed the diagnosis of MAS (Box 2). Macrophage activation syndrome (MAS) is a severe, potentially fatal condition associated with paediatric rheumatic diseases. It is a form of secondary haemophagocytic lymphohistiocytosis (HLH) with uncontrolled activation and proliferation of well differentiated macrophages and T-lymphocytes.1,2 The central pathophysiological abnormality in HLH is cytokine dysfunction, resulting in uncontrolled accumulation of activated T-lymphocytes and activated histiocytes (macrophages) in many organs. High levels of cytokines are found in these patients due to ineffective natural killer cells and T-lymphocytes (a positive feedback loop started by ineffective T-cells, triggering an unopposed release of cytokines that attracts further T-cells).3 Hyperactivated macrophages cause damage in different tissues, and this is thought to be the origin of the high serum ferritin levels characteristic of these conditions. The cause of the macrophage activation is multifactorial. Ineffective cytotoxic immunity is due to underactive natural killer cells and reduced perforin production. Secondary HLH can be precipitated by infection, drugs, malignancy and rheumatic diseases. SOJIA has been linked to polymorphisms in genes controlling production of cytokines, such as tumour necrosis factor. This could in turn be a cause for MAS, leading some authors to postulate that MAS and SOJIA could be part of the same disease.4 Clinical manifestations include fever (91%–100%), hepatomegaly (90%–92.3%), splenomegaly (77%–84%), lymphadenopathy (41%–62%), neurological symptoms (47%) and rash (43%).5,6 The central nervous system is commonly affected,7 and patients may present with agitation, seizures, coma, respiratory failure from adult respiratory distress syndrome, and multiorgan failure.7 MAS has a mortality of up to 22%.8 To our knowledge, this is the only reported case of MAS in a patient nearing adult age and with a long inactive rheumatic disease period. MAS is well described in the paediatric population with SOJIA, and has a median age of 5 years at the time of presentation.9 The mean time between initial diagnosis of SOJIA and presentation with MAS is 4 years.8 Our patient was aged 17 years at the time of presentation with MAS, and had not had symptoms of, nor required treatment for, SOJIA for 13 years. Diagnosis was described by Ravelli and colleagues,7 and is based on clinical findings such as organomegaly and laboratory findings such as hypofibrinogenaemia, thrombocytopenia and elevated serum liver enzymes. A bone marrow aspirate can aid diagnosis in uncertain cases, the pathognomonic feature being the presence of well differentiated macrophages actively phagocytosing haemopoietic cells.8 Infections, medications and malignancies have all been identified as triggers for MAS. EBV DNA was found in the patient’s bone marrow aspirate, and EBV has been identified as one of the more common triggers for MAS.5,7 It is likely that EBV was the trigger for this patient’s MAS. Treatment is based on immunosuppression using steroid therapy. Cyclosporin has been used as the first-line treatment, or used in combination with corticosteroids. Other treatment options include plasma exchanges or intravenous immunoglobulins.10 This patient presented with fever, prominent respiratory failure and cardiovascular collapse. Her initial systemic symptoms and radiological findings suggested severe sepsis, most likely respiratory in origin, her SOJIA had been in remission for over 10 years, and there was no neurological involvement. These factors made clinical suspicion of MAS difficult, but her hepatosplenomegaly and highly raised ferritin levels suggested the diagnosis, which was supported by her laboratory test results (leucopenia, thrombocytopenia, hypofibrinogenaemia and abnormal liver function test results) and bone marrow aspirate histological findings (Box 2). Despite MAS predominantly presenting in a paediatric population with active disease, this case report emphasises the need to exercise diagnostic vigilance in treating young adult patients with multiorgan failure and a distant history of rheumatic disease. Lessons from practice Multiorgan dysfunction and vasodilatory shock may not be of infectious origin. If a patient fails to improve when treated with broad spectrum antimicrobials, alternative diagnoses should be sought. Although macrophage activation syndrome (MAS) primarily affects children with active rheumatic disease close to the time of diagnosis, it may occur in adults after a prolonged disease-free period. Diagnosis of MAS is based on history, clinical examination and laboratory findings. Demonstrating haemophagocytosis in a bone marrow aspirate can aid uncertain diagnosis. 1 Chest x-ray of the 17-year-old patient, taken on admission, showing bilateral perihilar infiltrates 2 Macrophage (long arrow), containing a red blood cell (arrow head), seen in the bone marrow aspirate taken from the 17-year-old patient (May–Grünwald–Giemsa stain x 100)

David Gutierrez MD · Louis Guy MB BS · Veera S Katikireddi MB ChB(Hons), MRCP(UK) · Jason P Butler MMedSci, FRACP, FRCPA · John Gowardman FRACP, FCICM

Forensic medical practitioners urgently require credentials and national guidelines Across Australia, health professionals from differing disciplines provide health care for victims of suspected assault, which may include collection of samples for forensic analysis. Although some have been trained to collect forensic samples, few hold professional qualifications in forensic medicine. The current lack of standards and credentialled training for collection of forensic samples (in a manner that minimises the risk of contamination) poses an unacceptable risk to individual doctors and nurses, the profession and to the criminal justice system. During the past decade, several high profile cases involving DNA contamination of evidence have been reported in the medical, legal and popular media. These cases highlight the costs in economic terms and in terms of human suffering, injustice and loss of confidence in the criminal justice system when errors occur because of DNA contamination. A swab, and materials collected onto a swab, for forensic DNA identification might become contaminated at any time from the collection stage to the final stage of DNA identification. The process of DNA identification is a lengthy one that involves a number of people operating at different locations, at different times. There are many opportunities for a swab, or the genetic material obtained from the swab, to become contaminated with another person’s DNA. It could be argued that there are two levels at which we should consider the need to avoid DNA contamination of swabs. First, there is a need to avoid contamination of a swab with DNA from a member of the public who might be inculpated in a crime. These individuals cannot easily be excluded as suspects. Second, there is a need to avoid contamination of a swab by DNA shed from a professional who has handled the swab or worked in the environment in which the swab was collected. By virtue of their employment, these individuals have a valid reason for their DNA being in the proximity of the swab. They might more easily be excluded as suspects, and most would readily volunteer to donate a reference sample to enable their DNA to be identified for the purpose of excluding them from further consideration in a criminal investigation. The compelling reason to avoid contaminating a swab with DNA from a medical professional or laboratory scientist is that the presence of any extraneous DNA affects the DNA scientists’ ability to interpret electropherograms. When mixed profiles are obtained, confidence in the scientists’ interpretation of the results is reduced. Some laboratories will not provide an interpretation of DNA results when a mixed profile of four or more individuals is obtained. What are the consequences when DNA contamination of a forensic swab occurs?Wrongful convictions of innocent individuals have occurred because of DNA misidentification and other DNA-related errors in Australia and other countries — an outcome regarded as intolerable in a civilised society. Examples of wrongful convictions that appear to have resulted from DNA contamination are shown in Box 1. Wrongful convictions have far-reaching consequences. In regions of the world where the death penalty exists, the outcome can be lethal. How has the legal system responded?As new case law increases everyone’s awareness of the phenomenon of secondary transfer of DNA, and techniques such as low-copy-number DNA amplification increase the risk of amplification of traces of contaminating DNA,6 defence lawyers are demonstrating greater willingness to challenge DNA evidence in court. In the United Kingdom, at Terence and David Reed’s unsuccessful appeal ([2009] EWCA Crim 2698) against their 2006 conviction for the murder of Peter Hoe, the defence counsel argued that shards of plastic said to be from a knife handle and found near the victim were contaminated with the brothers’ DNA. Prosecutors argued that the DNA connected the brothers to the murder weapon. (The appeal was dismissed as there was sufficient evidence for conviction beyond the doubts over the DNA evidence.) In 2008, the UK police conducted a review of the use of low-copy-number DNA amplification techniques in light of the increased risk of erroneous interpretation of DNA identification results.7 In Australia, Canberra man Steven Hillier was acquitted of his ex-wife’s murder at a retrial in April 2010 (R v Hillier [2010] ACTSC 33). He had been convicted of murder in 2004. The conviction was quashed in 2006, and the Australian Capital Territory Director of Public Prosecutions subsequently challenged the appeal and sought a retrial. Hillier’s counsel successfully argued that a possibility existed that his DNA had been secondarily transferred onto his estranged wife’s clothing and doona.2 Prominent Australian lawyers8-10 have provided advice for barristers and judges on matters to consider during cross-examination and guidelines for determining admissibility of DNA evidence in Australian courts. How have forensic scientists responded?Quality assurance activities within laboratories minimise the risk of DNA contamination. National standards exist (National Association of Testing Authorities [NATA]) and DNA laboratory scientists must be credentialled. Most scientists remain alert to the possibility of DNA contamination and openly acknowledge when contamination within a laboratory occurs. On rare occasions, scientists have denied responsibility for contamination or error. For example, the Victoria Police Forensic Services Centre (VPFSC) scientist involved in the contamination of a murdered child’s bib with a rape victim’s DNA suggested that an adventitious DNA match, not laboratory error, was responsible (inquest into the death of Jaidyn Leskie, Coroner Graeme Johnstone, July 2006). At the trial of a man wrongfully convicted of rape, the testimony of a VPFSC scientist suggests that the scientist had limited understanding of the potential for contamination at a site other than the VPFSC laboratory.5 How have clinical forensic medical practitioners responded?Justice Frank Vincent’s conclusions5 about environmental contamination of the swab that led to the wrongful conviction of Farah Jama (Box 1) has been a powerful influence for change in the practice of clinical forensic medicine in relation to suspected sexual assault in Australia. There are a number of areas of improvement driven by the Victorian Institute of Forensic Medicine (VIFM), which has developed, in consultation with others, interim practice arrangements that act as guidelines for the collection of samples for forensic analysis.11 Key areas for improvement include the equipment and procedures used to collect samples and the environment in which samples are collected. Swabs and slides within sexual assault kits should be as free of contaminating DNA as possible. Irradiation of swabs has proven to be an inadequate process for denaturing DNA. An unknown female suspect, linked to several unsolved serious crimes in Germany and Austria between 1993 and 2009, was eventually shown to be a worker involved with the manufacture of the swabs.12 Forensic-supply companies continue to develop and supply swabs, slides and kits that are increasingly easy to use and are designed to minimise the risk that DNA might inadvertently be transferred onto a swab via a swab sheath or equipment used during the procedure. Disposable single-use instruments such as pencils, pens, speculae, forceps and scissors are recommended. Documents for recording samples collected and envelopes used for transporting samples to a laboratory are treated to denature DNA. Currently, there is significant variation between regions in Australia in relation to the design and suitability for purpose of some of the facilities where forensic samples are collected. Some facilities are clearly not “fit for purpose”. The structure of the facility should enable restricted access to a limited number of known individuals, adequate and documented cleaning to DNA elimination standards, furniture and surfaces that are maintained in a DNA-clean state, storage of equipment and supplies that prevents reuse or replacement of supplies that might have been contaminated and appropriate disposal of used supplies. Furniture and equipment within the examining room should be kept to a minimum and all surfaces should be able to tolerate cleaning with bleach. There should be a flow of patients from the entrance area into the examination room then shower facility. Suspects should not be examined in the area where victims are examined. These recommendations were set out in the VIFM submission to the Vincent inquiry. Gloves must be worn and changed regularly, particularly during the interval between collecting samples from different sites and when labelling and packaging samples. In some overseas jurisdictions, medical practitioners shower and change clothing between cases. No agreement has yet been reached about the need for forensic practitioners to wear gowns, masks or hairnets. The requirement to use gowns and masks is likely to meet with opposition from paediatric forensic practitioners who are likely to express concern about the negative emotional impact that this apparel might have on child victims. Cleaning procedures need to be at a standard that will denature DNA. Hypochlorite bleach has been demonstrated in DNA laboratories to denature DNA and is used for routine cleaning of floors and walls, as well as for cleaning work surfaces. Techniques used to collect samples must ensure that material from one site is not inadvertently transferred to another site. Tamper-proof seals are used in some jurisdictions. How have the regulators responded?Following the release of the Vincent report, the Victorian Department of Justice sought to rectify problems within the Victorian centres where sexual assault victims are examined. To date, changes to cleaning practices and modifications to a small number of units have occurred, primarily as a direct request to health services, where most facilities are located. Although it was a clear recommendation in the Vincent report, no reduction in the number of sites where sexual assault victims are examined has occurred. In July 2010, the UK Home Office published the second draft of the Codes of practice and conduct for forensic science providers and practitioners in the criminal justice system.13 The document was informed by a critical review of low-copy-number DNA amplification techniques and the use of this technology within courts. This comprehensive discussion document is regarded to be the first step in a process aimed at achieving better governance and higher standards throughout the sector. In Australia and New Zealand, standards are being developed in line with the strategy for 2009–2012 developed by the Australia New Zealand Policing Advisory Agency National Institute of Forensic Science.14 Forensic science centres are assessed according to explicit criteria that test quality and the reliability of results in order to achieve NATA accreditation. Within government in Australia, particularly Departments of Justice, there is an increasing awareness of the need for standards, monitoring and governance of those standards and the need for caution in relation to the use of DNA evidence in courts. The Public Defenders Office in New South Wales offered succinct advice to the legal profession in relation to the use of DNA evidence in court.15,16 In May 2011, the High Court, the highest court of appeal in Australia, dismissed convicted Canberra rapist Benjamin Forbes’ application for an appeal on the basis that he had been convicted on DNA evidence alone.17 This judgement indicates confidence in DNA technology and its use in the Australian criminal justice system. At present, there is no governing or regulatory body for clinical forensic medical practice. Doctors are accountable to their employer and to the Medical Board of Australia. Nurses are likewise accountable to their employer and the Nursing and Midwifery Board of Australia. Most forensic practitioners belong to professional colleges, such as the Royal Australasian College of Physicians, the Royal Australasian College of General Practitioners, and the Australasian College of Legal Medicine. There is no overarching collegiate body to certify successful completion of forensic medical training. The intercollegiate working group that developed guidelines for genital examinations of girls and young women did not provide explicit advice about the collection of samples for forensic analysis when sexual assault is suspected.18 The Australasian Association of Forensic Physicians has demonstrated an interest in developing standards and guidelines for collection of forensic samples, but this work is in its infancy. Where to now?It is unlikely that the medical profession will ever be able to exclude the possibility that a swab has become contaminated with DNA. The task before us is to minimise the risk, and to be seen to be minimising the risk, of DNA contamination. Forensic medical practitioners urgently require national guidelines and standards to guide and govern forensic medical practice (Box 2). We also need: a national collegiate body to certify that practitioners have met training requirements and have demonstrated required competencies; a national group to negotiate across state boundaries with employers and governments to ensure that we are enabled and supported to provide a high standard of forensic medical care and to maintain an effective workforce; police and forensic scientists to share with us the desire to safeguard the integrity of forensic samples and the results obtained from their analysis; a well informed public that has realistic expectations of forensic services; a legal system that challenges, questions and pushes us to consider our failings; and a health system that supports and encourages us to continue to improve. 1 DNA contamination resulting in wrongful identification of suspect Country Year Case Contamination site Criminal charge Consequences for wrongly accused New Zealand 1998 Profile N1 Laboratory Murder × 2 Financial records seized; intense police investigation; no conviction Canada 2001 Gregory Turner2 Laboratory Murder 27 months’ jail Australia 2004 Steven Hillier3 Before collection Murder Conviction; successful appeal Australia 2008 Russell Gesah4 Laboratory cold-case match Murder × 2 Charges dropped Australia 2008 Farah Jama5 Collection Rape 15 months’ jail 2 A multicomponent plan for national clinical practice standards regarding collection of forensic samples for DNA identification Task Responsible group Strategy Authorising body Determine clinical practice guidelines Forensic physicians, paediatricians and nurses Working group evaluation of evidence; consensus; recommendations Currently none; potentially AAFP Develop national standards for handling of forensic samples ANZPAA National Institute of Forensic Science Multidisciplinary working group evaluation of evidence; consensus ANZPAA National Institute of Forensic Science Determine professional training requirements College or university department of forensic medicine Curriculum development and implementation Currently none; potentially VIFM and/or Monash University Certification of competency College or university department of forensic medicine Successful completion of training program; demonstrated competency Currently none; potentially VIFM and/or Monash University or alternative Governance of professional practice clinical forensic medicine Employing organisations Organisational standards; monitoring practice Multiple, such as state centres providing clinical forensic medicine services Monitor and enforce clinical forensic medicine standards across Australia National body A new national college of forensic medicine Currently none; potentially RACP, Australasian College of Legal Medicine or new national college of forensic medicine AAFP = Australasian Association of Forensic Physicians. ANZPAA = Australia New Zealand Policing Advisory Agency. RACP = Royal Australasian College of Physicians. VIFM = Victorian Institute of Forensic Medicine.

J Anne S Smith MB BS, FRACP

Gambling and diagnostics are related, but strangely reversed, in the way that prior events can affect our clinical judgements The year was 1913; the location, the roulette tables of a Monte Carlo casino. For the previous 10 spins of the wheel, the ball had landed on black. A red was overdue, so the punters began to bet more aggressively against the trend. But the 11th spin produced yet another black number. As did the 12th, and the 13th ... and the longer the run of blacks continued, the more convinced the gamblers became that the subsequent spin would yield a red. Their wagers accelerated. Their losses snowballed. For it was only after 26 consecutive black numbers (by which time few could afford to continue betting) that the streak finally came to an end. It was perhaps the most profitable night in the casino’s history: records were set, fortunes were lost, and the “Monte Carlo fallacy” was born. Also known as the “gambler’s fallacy”,1 it describes the erroneous belief that the outcomes of recent random events have some bearing on future random events. It dictates that if a flipped coin yields 10 consecutive heads, then the likelihood of a subsequent tails is increased, because the coin seems “due” for a tails. Intellectually, we know this law of averages makes no sense: a coin has no memory, so every time it is flipped, there is an equal chance of either side appearing face-up, regardless of what happened on previous flips. Certainly, the odds of flipping heads 10 times in a row are remote — one in 1024, to be exact — yet this number also represents the odds of having any other pattern of heads and tails in a 10-flip series. Although we know this to be the case (undoubtedly, so too did many of the gamblers on that night in Monte Carlo), it is all too tempting to disregard the laws of probability and be seduced by pseudologic. In our clinical practice, it is similarly easy to be fooled by apparent patterns, and unduly influenced by any recent experiences that remain prominent in our minds.2 However, for clinicians, the Monte Carlo fallacy seems to work in reverse: rather than a string of similar events prompting us to think we are “due for a change”, we may instead feel that the “run” is more likely to continue. For example, if, within a short space of time, two patients presenting with hypotension are found to be hypoadrenal, then it may be tempting to look for this unusual diagnosis in all future hypotensive patients, even though other diagnoses may be more common, more likely, and easier to diagnose without expensive investigations. If a patient has a fall while in hospital, and then dies unexpectedly from an unidentified intracranial bleed, we may feel compelled to request a brain scan for any subsequent patient who has such an accident. We may do this even when the patient appears unhurt, and our clinical judgement would otherwise suggest that such a test is not indicated. While the outcome for the first patient was tragic, it in no way affects the likelihood that a second patient’s (unrelated) fall will also have life-threatening complications — just as the first 25 black roulette numbers had no bearing on the outcome of the 26th. Our approach to any clinical situation is guided by the accumulation of our previous experiences, but somehow the most recent ones seem to bear the most weight. Ultimately, we are human, and humans are pattern-seeking creatures. We see faces in amorphous clouds, and stars scattered across the night sky form images before our eyes. And to this pattern-seeking ability we owe much of our understanding of medicine: the linking of infection outbreaks to geographical areas has identified sources of contamination, and the observation of disease trends has revealed unrecognised side effects of drugs. A great deal of our knowledge today has been acquired through observing the unusual, the unexpected and the uncommon, and continuing to do so will certainly teach us more. However, in day-to-day clinical medicine, the old maxim rings true: common things occur commonly.

Alexander M Owen MB BS(Hons), BSc(Med)Hons

Readers who may contemplate referring patients to practitioners of complementary medicine may be interested in the fate of Dr Frederick Axham. He was an English anaesthetist, who was struck off the medical register for medical malpractice in 1911 at the urging of the General Medical Council, having been found guilty of “covering” (ie, professionally assisting a person not on the medical register). Axham had — despite dire warnings — anaesthetised eight patients of Herbert Barker, a renowned bone setter (now a lost art), who had successfully set and stabilised the complex fractures of seven of these eight patients whose fractures had been found to be inoperable by a number of eminent surgeons. Axham, who died in 1926 aged 86 years, still deregistered, was posthumously rehabilitated when the medical faculty of the University of Edinburgh made him a Licentiate of the Royal College of Physicians some weeks after his death.1 The whole affair caused a huge outcry throughout England, leading to a petition to Lambeth Palace, the residence of the Most Reverend Lord Randall Davidson, Archbishop of Canterbury, to make Barker a Doctor of Medicine, in reliance on the Ecclesiastical Licences Act 1533 (25 Henry VIII, c 21). The petition included not only leading members of the aristocracy, but, more importantly, Sir Henry Morris Bt, former President of the Royal College of Surgeons, Sir Alfred Downing Fripp, “Surgeon in Ordinary” to King George V, Sir William Arbuthnot Lane Bt, consulting surgeon to Guy’s Hospital, and physician Sir Bruce Bruce-Porter, all testifying to Barker’s coampetence. It also led George Bernard Shaw to write: Until the General Medical Council, which at present exhibits every constitutional vice that a trade union or professional association can have, is completely reformed by its legal constitution, we shall continue to hasten more and more precipitously to the not far distant day when the vogue of the unregistered practitioners, already very great (Mr. Barker is only a specially famous example of a large and growing body), will become so irresistible that the registered will be shunned by the public and driven to earning a scanty wage by signing death certificates for their unregistered employers.2 Alas, the Archbishop declined to award the degree. A press cuttings file at Lambeth Palace (Davidson’s Papers Vol 404, page 110) shows that he stated on 21 June 1920: The legislation which limits registration to men qualified by the ordinary professional training expressly, and I think rightly, provides that the status acquired by registration is not given by the Degree which the petitioners invite me to confer on Mr Barker.2 In frustration, King George V did the only thing he could do, which was to make Herbert Barker a knight of the realm. Sir Herbert continued bone setting till he died in 1946. Medicine. An Illustrated History

Paul Gerber LLB, DJur

Ken Paver was an outstanding dermatologist with broad vision and a remarkable ability to get things done. To paraphrase one of his maxims, Ken had great ability to which he applied a lot of effort. He was born in Kensington, Sydney, on 24 May 1920 and grew up in Mosman. After gaining his Intermediate Certificate in 1933, he left school to work at an insurance firm to help his family, because his father suffered from debilitating rheumatoid arthritis. During World War II, Ken served as a Private and then Captain in the Coastal Artillery. After the war, Ken studied medicine at the University of Sydney, where he met Elaine Kerr. They married in 1948 and graduated together in 1952. In 1953, after a year of residency at Royal North Shore Hospital, Ken joined a general practice at Merrylands. While working as a general practitioner, he obtained membership of the Royal Australasian College of Physicians (RACP). He received his Diploma of Dermatological Medicine in 1964 and was subsequently awarded the medal of the New South Wales branch of the British Association of Dermatologists. He gained Fellowships of the Australasian College of Dermatologists in 1966 and the RACP in 1971. Ken established a successful private practice in dermatology at Blacktown and was appointed Honorary Dermatologist at St Vincent’s Hospital, Sydney, where he was Chairman of the Department of Dermatology from 1966 to 1975. In 1978, Ken’s drive and momentum led to the establishment of the Skin and Cancer Foundation Australia, of which he was the first Chairman. He was appointed a Member of the Order of Australia in 1988. In 1989, Ken retired to the NSW Central Coast. He became a keen woodworker, an Associate of the Securities Institute of Australia and, in 2005, a Fellow of the Financial Services Institute of Australasia. He also acquired a Bachelor of Arts in sociology and worked on writing the history of the Skin and Cancer Foundation Australia. Ken died on 18 March 2011, and is survived by Elaine and children Graham, Rob, Phil and Cathy.

William Regan

Understanding and responding to pharmaceutical promotion. Mintzes B, Mangin D, Hayes L (editors). Amsterdam: Health Action International Global and World Health Organization, 2010 (online, free). THIS BOOK is a collaborative project by Health Action International Global — an organisation based in Amsterdam and committed to promoting the rational use of medicines — and to increasing access to essential medicines, and the World Health Organization. The editors (Barbara Mintzes, Assistant Professor in the Department of Anesthesiology, Pharmacology and Therapeutics, University of British Columbia, Canada; Dee Mangin, Director of the Primary Care Research Unit at the University of Otago in New Zealand; and freelance scientific editor Lisa Waller-Hayes) all have a background in writing about pharmaceutical promotion. Information on the influence of promotion on medicine use is often lacking. This book is an attempt to remedy this by bringing together studies on various aspects of promotion, including medical journal advertisements, sales representatives, conference sponsorship, physician opinion leaders and direct consumer advertising. There are contributions from many countries including Australia, a world leader in promoting the rational use of medicines. Health professionals are the target of aggressive and sustained promotional pressure by the pharmaceutical industry but are often not sufficiently educated about understanding and responding to such promotion. This book is intended to fill this gap, and it does so admirably. It also teaches readers the importance of using unbiased sources of information. It has been designed as part of a student module on pharmaceutical promotion, but the easy-to-read style incorporating pictures, graphs and well designed boxes and logical organisation ensures that it can be read on its own. I am currently using it to conduct small-group activity-based teaching sessions for second-year students and consider it superior to other initiatives I have used. I especially liked the chapters dealing with pharmaceutical sales representatives and how to avoid the “pharmaceutical industry tango”. The references at the end of each chapter are comprehensive, and numerous web links are provided. However, it lacks an index. The book can be freely downloaded from the Health Action International website (www.haiweb.org) and is sure to be of interest to all health professionals.

P Ravi Shankar

Cause of chylothorax: In “Spontaneous chylothorax in a 2-year-old child” in the 2 March 2009 issue of the Journal (Med J Aust 2009; 190: 262-264), the cause of chylothorax was unknown, but attributed to strenuous vomiting. Additional information has become available and trauma is now thought to have been the cause. In a child, this raises the possibility of non-accidental injury. Further details are published in this issue of the Journal (See Soto-Martinez et al).

Manuel E Soto-Martinez · Vanessa Clifford · Tom Clarnette · Sarath Ranganathan · R John Massie