Letters

In reply: Our study found that both subtypes of influenza caused substantial morbidity and mortality, but that there was no difference in outcomes between patients infected with seasonal and pandemic (H1N1) 2009 influenza.1 The large numbers of cases of pandemic (H1N1) 2009 infection, and especially those requiring intensive care unit (ICU) management, is not disputed — 37 537 cases, 655 ICU admissions and 191 deaths in Australia had been reported as of 18 December 2009.2 However, this is not a function of enhanced virulence of the pandemic strain, but rather a function of vast numbers of infected individuals in a naïve population. The article by the Australian and New Zealand Intensive Care study investigators supports our conclusions, as they found no difference in outcome between pandemic (H1N1) 2009 and seasonal influenza.3 As specimens were tested in “real time”, RNA degradation is unlikely to have resulted in incorrect categorisation. The real impact of influenza has probably been under-reported before this pandemic, as virological testing of respiratory specimens has not been routine. Influenza per se is a significant disease, and thus appropriate planning, including resource allocation for ICU management and routine virological testing of respiratory specimens should be undertaken.

Iain B Gosbell · Sebastiaan J van Hal · Peter M Spencer · Ya-Shu Chang · Peter W Collett

To the Editor: Chang and colleagues suggest that the clinical course and outcomes of patients infected with pandemic (H1N1) 2009 influenza virus are comparable to those with seasonal influenza infection, and that increased hospital and intensive care unit (ICU) admissions with influenza reflected a higher incidence of disease in the community rather than enhanced virulence of the pandemic influenza virus.1 However, this conclusion was based on an analysis of data from a single hospital, which did not examine whether the community incidence of influenza was increased or whether infection with pandemic (H1N1) 2009 influenza increased the risk of admission to a hospital or ICU compared to infection with seasonal influenza. Seasonal influenza co-circulated with the pandemic influenza strain during the recent influenza epidemic in New South Wales.2 We used the results of influenza tests (excluding rapid antigen tests) performed at eight major NSW public laboratory services to estimate the risk of admission to an ICU with pandemic (H1N1) 2009 influenza compared with seasonal influenza A infection. These public laboratories confirmed 95% of people admitted to hospital with pandemic (H1N1) 2009 influenza, and 84% of all laboratory-confirmed pandemic influenza cases in NSW. For the weeks ending 5 June to 2 October 2009, 38 060 specimens were tested for respiratory viruses, of which 7602 were positive on polymerase chain reaction for influenza A. Of these, 4172 (55%) were identified as pandemic (H1N1) 2009 influenza. During the same period, we collected data on all patients admitted to an ICU with influenza A infection.3 In total, 274 patients with influenza A were admitted to NSW ICUs — 229 with pandemic (H1N1) 2009 influenza, 38 with seasonal influenza A and seven with unsubtyped influenza A infection. Excluding the seven unsubtyped influenza A cases, we calculated a relative risk of 4.9 (95% CI, 3.5–7.0) for admission to ICU with pandemic (H1N1) 2009 influenza compared with seasonal influenza A infection. A sensitivity analysis assigning the unsubtyped influenza A cases admitted to ICUs to either pandemic (H1N1) 2009 influenza or seasonal influenza A produced no significant change in our findings, with a relative risk of admission to ICU with pandemic influenza compared with seasonal influenza A infection of 5.1 (95% CI, 3.6–7.1) and 4.2 (95% CI, 3.1–5.7), respectively. Although we attempted to collect data on all patients admitted to an ICU with influenza A infection, repeated testing for pandemic (H1N1) 2009 influenza in ICU patients may have resulted in identification of pandemic (H1N1) 2009 influenza in a greater proportion of ICU patients than community patients. However, our results suggest there was a significantly increased risk of admission to an ICU with pandemic (H1N1) 2009 influenza infection compared with other seasonal influenza A strains circulating in NSW. Given the potential for a subsequent pandemic wave, this provides support for maximising rates of community vaccination with a pandemic-specific vaccine.

Craig B Dalton · Michelle A Cretikos · David N Durrheim · Ian M Seppelt · William D Rawlinson · Dominic E Dwyer

To the Editor: Kelly showed that the pandemic (H1N1) 2009 influenza epidemic experience in Victoria was similar, overall, to a moderately severe influenza season.1 As with seasonal influenza, 0–4 year olds had the highest hospital admission rates,2,3 with those in the first year of life most likely to be admitted to intensive care units (ICUs). “Swine flu” did have differences to seasonal flu, with “younger” people having disproportionally more serious illness.2,3 However, these younger groups were not necessarily what most would regard as young. Eighty per cent or more of deaths associated with pandemic (H1N1) 2009 influenza were among those aged over 35 years, and most had identifiable risk factors.2,3 The peak 5-year age group for ICU admissions was 50–54 years.2 Those aged over 65 years seemed relatively protected — presumably because most had pre-existing immunity resulting from infection with H1N1-type viruses circulating since 1918. Pre-existing immunity was also not uncommon in others. In 18–65-year-olds, 30% had protective antibody levels to pandemic (H1N1) 2009 influenza before vaccination.4 Using data from New South Wales, we can ascertain the severity of pandemic (H1N1) 2009 influenza in different age groups.2 In NSW last winter, 1214 people were hospitalised, 225 were admitted to ICUs and 48 died with pandemic (H1N1) 2009 influenza (17.2, 3.2 and 0.7 per 100 000 population, respectively). Pregnant women had a 10 times higher risk of death (1.4 per 100 000) than other women of their age. For the overall population aged under 40, the death rate was 0.4 per 100 000, with most having identifiable risk factors. Thus, the death rate for those aged under 40 years, but with no known risk factors, was about one per million people. Most of the mortality predictions for this epidemic have been consistently wrong and exaggerated. Some were suggesting 10 000 deaths in NSW alone.5 These, and other predictions of second and third killer waves, have generated needless fear and inappropriate responses.6 Many experts and even health departments were postulating that more than 20% of the population would become infected, with an associated case fatality rate of 1% or more. That translates to a population mortality rate of 200 per 100 000 people, which is 300 times higher than what actually occurred. We need to learn from our recent experience so we can better plan and act in the future. Analysis such as that performed by Kelly is essential if we do not want to repeat the mistakes we made during this pandemic, caused by a virus of relatively low virulence.

Peter J Collignon

To the Editor: The debate raised by Sitas and colleagues about whether smoking status should be recorded on death certificates1 represents data acquisition at the last point. What needs to be considered is not the merits of the proposal, but the systematic failure to record this crucial data in patients’ clinical records. The argument I present here concerns cancer, but may be extrapolated to other smoking-related diseases. The absence of smoking history from the clinical records of patients with cancer up until now is understandable. Unlike the situation with infectious diseases, causative agents have had no relevance to the prognosis or the treatment of malignancy. Even if this pregenomic outlook persisted, the evidence we now have, showing that smoking affects response to therapy (eg, in prostate cancer),2 would warrant documentation of smoking history for every cancer patient. Among developed countries, the risk attributable to smoking in lung cancer is 70%–90%. In single-gene terms, polycyclic aromatic hydrocarbons and tobacco-specific nitrosamines such as 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone mediate malignant transformation by point mutations in onocogenes and tumour suppressor genes, typified by G-to-T transversions in codons 157, 158, 245, 248 and 273 of TP53; mutations in the KRAS gene and in the gene for epidermal growth-factor receptor (EGFR) are likewise relevant.3 Enough distinction can thus be made between smoking-related and non-smoking-related lung cancer to identify two entities.3 Patients with non-small-cell lung cancer, with exon 19 and 21 mutations in the EGFR gene are typically non-smokers, and their tumours have an 80% response rate to erlotinib.4 Indeed, these tumours respond better to chemotherapy than in patients lacking such mutations.4 As the single-gene era closes, smoking history will be required for all relevant biospecimens to avoid making genomic-wide data on pathways consequent on tobacco-related etiology — representing hundreds of tumours — inaccessible.5 Tobacco smoking causes cancer of the oral cavity, oropharynx, nasopharynx, and hypopharynx, oesophagus (adenocarcinoma and squamous-cell carcinoma), stomach, colorectum, liver, pancreas, nasal cavity and paranasal sinuses, larynx, lung, uterine cervix, ovary (mucinous), urinary bladder, kidney (body and pelvis), ureter and bone marrow (myeloid leukaemia), and possibly causes female breast cancer.6 The prospect of genomic-wide data for these tumours not being accompanied by data on smoking is daunting. The case for smoking data in relation to clinical trials has been made previously.7 Beyond this, the immediate goals for Australia are that smoking history be recorded for tobacco-related malignancies in hospital-based tumour-specific clinical cancer registries and for biospecimens. The need is for the adoption of uniform national vocabulary and coding methods. This will require leadership by an authority such as the National Health and Medical Research Council (NHMRC), the Cancer Council Australia, the Clinical Oncological Society of Australia, or Cancer Australia.

Bernard W Stewart

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

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

To the Editor: Having been closely involved with the initiation of the practitioner impairment and performance processes of the New South Wales Medical Board, I appreciate Breen’s generous remarks about the efficiency and fairness of the existing medical boards’ processes.1 In addition to wholeheartedly endorsing his concerns about the proposed medical regulation legislation, I consider that the profession should not lose sight of the origin of these “reforms” — the Productivity Commission’s report on the health workforce.2 This government “workforce” initiative is far removed from the concerns of any registration body — namely, “standards”. Our medical boards have hitherto rightly divorced themselves from workforce considerations. The profession should be concerned that an inquiry into the health workforce has resulted in a national standards body. This mismatch suggests a hidden agenda behind the new legislation to be adopted by all states and territories. Can our governments, Labor or Coalition, be trusted not to combine their powers over the new registration authority and over Medicare to exercise ham-fisted controls over doctors? Australians have already suffered the disastrous Wooldridge reduction in Medicare provider numbers in 19963 — resulting in today’s scramble to train more doctors. Breen says that most doctors have not opposed the proposed scheme.1 As one of the minority who do, I claim that the Emperor has no clothes. The devil is not in the detail, but in the principles. Breen correctly identifies the only valid, but weak, argument for national registration — that “the existing regulatory system [is] somewhat inefficient in terms of interstate mobility”.1 Australia’s health care problems relate primarily to lack of coordination between governments,2 not to standards. There is little regarding standards that could not have been ironed out by the state and territory medical boards and the Australian Medical Council. We are about to witness a horrendous waste of public money by governments whose primary goal, I suspect, is control over our profession — over our numbers, over our education, over our registration, over our postgraduate training, over our standards, and over the nature and location of our eventual practice of medicine. Today’s and tomorrow’s doctors have my sympathies.

Peter C Arnold

To the Editor: The evaluation by Hicks and colleagues of the centralised ethics review system in New South Wales1 codifies important additional time delays facing researchers conducting multicentre trials that include NSW. These delays have direct financial consequences that continue to limit the viability (especially when staff are on time-limited grants) and productivity of multisite research in Australia, without adding value to the ethical conduct of the research.2 There is also inconsistency between the approaches of the lead ethics committee (LEC) and site-specific ethics committees in the way they deal with protocol amendments and adverse event governance, further compounding the delays in initial review. Five multicentre clinical trials are currently being conducted by the Palliative Care Clinical Studies Collaborative (PaCCSC),3 a national initiative to improve the evidence for symptom therapeutics at the end of life. Submissions for ethics review occurred between May 2008 and July 2009 across nine sites in five states. As in the study by Hicks et al,1 ethics review submissions included the NSW LEC, but because these submissions were more recent than those reported by Hicks et al, they were submitted on the National Ethics Application Form (NEAF). Hicks and colleagues state there is benefit in standard documentation, but using the NEAF does not reduce the need for collating complete sets of documentation for each site-specific approval and any subsequent amendments or adverse events.4 For the PaCCSC, LEC and site-specific review in NSW achieved approval in a median of 119 days (range, 76–209), compared with 107 days (range, 6–172) for individual committees in other states. Hicks and colleagues1 did not quantify the costs generated by these delays. Given that staff are often employed to prepare ethics submissions and then retained for the definitive study, additional delays in approval are costly, especially with finite, competitive grants funding. Costs of multisite ethics review applications have previously been quantified in Australia,2 but the additional delays in NSW from the requirement for site-specific approval are estimated to have cost the PaCCSC about $4000 per study per site in salaries and on-costs. Across three NSW sites and five studies, $55 000 has been spent without measurable ethical or research governance benefits. Theoretically, LEC review should streamline protocol amendments and adverse events reporting, as they are the responsibility of the LEC. But although protocol amendments are supposed to be reviewed only by the LEC, some site-specific committees continue to insist on approving all amendments.4 Efforts to consolidate adverse event reporting have made some progress.5 All adverse events are reported to the LEC for review, and any required response should be shared with site-specific committees. Again, some non-lead sites continue to insist on separately reviewing adverse events rather than using the LEC as intended.

Tania Shelby-James · Meera R Agar · David C Currow

To the Editor: Hicks and colleagues presented a study contrasting the ethics review system in two multicentre trials.1 They concluded that the introduction of a centralised ethics review process in New South Wales did not reduce the overall time taken to receive approval, but did help to reduce the time and resources involved in preparing applications. We are establishing a multicentre trial to prospectively evaluate and refine a model to predict patient outcomes after endovascular aortic aneurysm repair.2 This will involve collaboration between vascular surgeons at over 40 sites throughout Australia, one site in the United Kingdom and six sites in New Zealand. We, along with Hicks and colleagues, have experienced difficulty in establishing our multicentre trial. Multiple individual ethics applications have been submitted to human research ethics committees (HRECs) throughout Australia. The National Ethics Application Form (NEAF) was created to minimise inconsistencies and reduce the time and resources required when submitting ethics applications to multiple HRECs. Although the NEAF was designed to increase efficiency and quality,3 in reality it has done little to facilitate the submission process. It has been useful in NSW and Queensland, which have processes to allow the review of multicentre trials, but few HRECs in other Australian states accept the entire form, and often they have their own specific requirements. This has resulted in increased costs and time, as well as different interpretations of the trial protocol — effects that Hicks and colleagues found were reduced with a centralised ethics system. We are at least 9 months behind schedule in establishing our trial after having submitted over 25 individual applications. This has resulted in substantial losses in patient recruitment and research time. Other researchers have also reported on the excessive time and resources required to submit ethics applications.4 Like Hicks and colleagues (and no doubt other researchers), we are advocates of the Harmonisation of Multi-centre Ethical Review (HoMER) initiative.5 This national system would allow single ethics review that would be recognised by all institutions participating in a collaborative research project, without re-review by their institutional HREC. It is uncertain how many HRECs will adopt the HoMER initiative, but we remain optimistic that HoMER can solve problems that the NEAF has not. Central coordination of the ethics review process may help standardise documentation, as demonstrated by Hicks and colleagues, but clearly other factors, such as the time required for approval, need to be addressed.

Kate L Fitzpatrick · Margaret Boult · Robert A Fitridge

To the Editor: Hicks and colleagues are to be commended for reporting the benefits of the single ethics review system for multicentre trials in reducing the time taken for review, reducing unnecessary duplication of effort, and standardising documentation.1 They based their analysis on the overall time to approval, which included both an ethics and a governance component. The single ethics review model introduced by NSW Health in July 2007 separates scientific and ethics review from business or governance review (which requires site-specific approval). The Australian Research Ethics Database, developed by Infonetica for NSW Health, is used by the Cancer Institute NSW Clinical Research Ethics Committee (CREC) to track and manage multicentre research projects. It uses a 60-calendar-day clock to measure the time from submission to approval.2 The 60-day period sets a benchmark and represents a reasonable target review time. This clock stops, for example, when the CREC has sent a letter to the investigator and is awaiting a response. This method of measurement makes the total number of days for ethics review even shorter — for example, for the CO.20 trial described by Hicks and colleagues,1 the total number of days would be 66 rather than the 77 days they reported. It should be noted that if the CREC, which I chaired, sought changes to the participant information sheet after the first review of a research submission, the response was approved by the executive of the committee between full committee meetings. We used executive review more extensively than other committees to save time. This and other efficiencies, such as reducing the time between submission and the first ethics committee review and using a paperless review system, make it more likely that we will achieve a review time of less than 60 days as the committee becomes more experienced. This makes the adoption of a single ethics review system even more attractive.

Ian N Olver

To the Editor: Mitchell raises issues that strongly reflect on the professional standing of the medical profession.1 His particular focus is on the pharmaceutical industry, and on much needed changes as highlighted by Medicines Australia.2 Similar concerns exist in the medical technology industry where the transparency of relationships is becoming increasingly important. Mitchell highlights the fact that self-regulation by the medical profession has been largely ineffective.1 In this day of international corporate activity in the delivery of health care, the declaration of the Hippocratic Oath is no longer sufficient. The Royal Australasian College of Surgeons (RACS) published a code of conduct in 2006.3 This has been supplemented recently by the code of conduct of the Australian Medical Council.4 Separately, the Medical Technology Association of Australia has published its guidelines for industry groups.5 However, the dominant criticism of these documents is that compliance is voluntary. The RACS believes it is critical that the profession takes leadership in this complex issue to ensure that trust is maintained in the patient–doctor relationship. Consequently, we have recently expanded our code of conduct with a comprehensive policy dealing with interactions with the medical technology and pharmaceutical industries.6 We are introducing a sanctions policy to strengthen compliance. If there is a breach of the guidelines, the fellow or trainee concerned will need to confirm ongoing adherence to the RACS code of conduct. If there is a repeat offence, then cause will need to be given as to why the fellow should not have his or her fellowship removed or the trainee should not be dismissed from the training program. As professionals, these issues of integrity, transparency and trust are fundamental. The doctor–patient relationship must be our primary focus, and should not be violated by any perceived or real conflict of interest.

Ian R Gough · Ian Dickinson · Guy Maddern · Michael Grigg · David J Hillis

To the Editor: There is no doubt that the relationship between doctors and the pharmaceutical industry, described by Mitchell,1 is a complex one. Mitchell states that: “There are few, if any, analogies for the relationship between the medical profession and the pharmaceutical industry”.1 We contend that, as medical professionals are to the pharmaceutical industry, nutritional health professionals are to the food industry. Nutritional health professionals, like medical professionals, span the health care spectrum — from research and public health to tertiary care — and include doctors, dietitians, nutritionists and nurses. The food industry is more expansive than the pharmaceutical industry, encompassing primary producers, manufacturers, retailers and parts of the pharmaceutical industry. Some definitions include alcohol as part of the food industry. As well as this difference in magnitude, there are other substantial differences between the pharmaceutical and food industries. Contact between the food industry and health professionals is ubiquitous and unavoidable, but lacks the oversight provided by the, albeit voluntary, Medicines Australia code of conduct.2 It is unrealistic to suggest that health professionals should be completely divorced from the food industry. The alcohol industry is, however, the exception.3 Appropriate engagement between health professionals and the food industry has the potential to improve population health.4 Product reformulation (to improve the nutrient profile, such as reducing salt or fat content) and repackaging (to make smaller portions) are examples of successful partnerships between health professionals and the food industry. The food industry must work with health professionals to respond to consumer demand for healthier foods. Yet many of these foods are still of questionable nutritional quality, or of benefit only in very specific cases. Medications, on the other hand, must be proven before they enter the market. Finally, the food industry is able to advertise directly to the public and use health professionals to promote their products. This creates opportunities for endorsement — perceived or otherwise — of specific foods or brands by key opinion leaders, like doctors or sporting icons, who have varying degrees of nutritional expertise but are nevertheless viewed by the public as credible. Increasing rates of obesity legitimately prompt greater scrutiny of food industry activity. Analogous to the relationship between the pharmaceutical industry and doctors, it is equally necessary to “. . . expeditiously formalise a relationship of integrity and transparency . . .” between health professionals and the food industry.1 A code of conduct, equivalent to that of Medicines Australia, may be a necessary next step.

Iain S Pratt · Clare L Hughes · Terry J Slevin

To the Editor: In his article on the relationship between doctors and the pharmaceutical industry, Mitchell highlights moves to bring about greater transparency.1 While such moves are important, they do not go nearly far enough. Mitchell states that “it is not the relationship between medical practitioners and the pharmaceutical industry per se that is the problem, but how that relationship is enacted”.1 I disagree. The marketing activities of pharmaceutical companies are often justified by reference to the role that they play in the development of new medications, summarised in the statement “we need them”. In fact, the vast majority of the world’s most valuable medications were discovered and, in most cases, developed without pharmaceutical company involvement. Even recent advances, such as 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors, originated with the brilliant work of researchers in the basic biological sciences.2 The progression from discovery to the development, testing and approval of a new drug does require large investments by pharmaceutical companies, but they do this for commercial reasons, in the hope of delivering profits to their shareholders. Naturally, they endeavour to promote their products and maximise their profits. As Mitchell outlines, their means include gifts, honoraria, sponsorship of events, “key opinion leaders” and “ghost writing”.1 As Mitchell also outlines, it is well established that all these manoeuvres are effective in altering doctors’ prescribing practices.1 Mitchell recommends that “we go down the route of disclosure of earnings from industry”.1 But is transparency enough? Is it enough to read that the keynote speaker at a symposium received an honorarium from a pharmaceutical company? Is it enough to know that delegates’ meals, entertainment or travel were paid for by a pharmaceutical company? Is it enough to know that your pen was provided by the manufacturer of X? (Isn’t that why the company’s name is written on it?) The fact that we need pharmaceutical companies to develop new drugs does not justify any of these activities, all intended to influence our decisions about whether and when to use their products. The fact that pharmaceutical companies cannot advertise or sell directly to their customers (ie, patients) in no way justifies marketing through intermediaries (ie, doctors and pharmacists). The recent report of the Association of American Medical Colleges is clear and forthright in proscribing many of these activities.3 Mitchell summarises their recommendations nicely, so I am surprised and disappointed that he does not go on to recommend proscription himself, rather than just transparency.

Richard Kelly Barnes

To the Editor: We read with some dismay the article by Winch and Henderson1 critically reviewing the introduction into health care of process improvement methods pioneered in manufacturing and service industries. We take issue with the article at several points. While the article is titled a “critical review”, it has more of the character of a personal view. For instance, the authors single out “lean thinking” for particular criticism, but the examples cited are in fact a mixture of business process re-engineering, hospital or health system restructuring, and total quality management. These differ substantially from lean thinking, but this is not acknowledged in the text. Then the authors claim that lean thinking has been accepted “somewhat uncritically”, but this is not so. The current peer-reviewed literature contains a number of articles critical of lean health care that have not been referenced by Winch and Henderson (for example, an article by Young and McClean2). The authors’ principal argument is that fragmentation of health care delivery reduces the quality of care provided. We agree. They then argue that process redesign increases the fragmentation and impairs quality of care, but we reject this view. The process redesign programs we have been involved with have been aimed at increasing the time that staff can spend with patients. They explicitly involve staff in designing systems that will deliver this. Rather than trying to “[reduce] the richness of professional health care practice to impoverished snippets of work”,1 we are trying to put broken care processes back together. The authors close by implying that process redesign may “add to the problems of hospital misadventure . . . rather than solve them”, but they provide no evidence for this assertion. In fact, the existing evidence points the opposite way. For example, a recent report from the ThedaCare group in the United States showed a reduction in mortality after coronary artery bypass grafting from 4% to effectively zero as a result of process improvement.3 Here in Australia, the Flinders Medical Centre in Adelaide has seen a striking reduction in serious adverse events after implementing a process redesign program based on lean thinking.4 Interest in process redesign is increasing in health care. All improvement methods benefit from critical discussion, but critiques that are also well supported by evidence are likely to be the most influential.

David I Ben-Tovim · Duncan Stuart · Maarten Kamp · Paul Cullen

To the Editor: As one who works in paediatrics and sees parents bringing their children to hospital for day surgery, and then taking them home again a few hours later, I concur with Winch and Henderson in their critique of “lean thinking” ways of delivering health care.1 Nowhere is this more obvious, and nowhere is it applied with less critical assessment, than in day admissions. This process, which we are told is best for families, may not be. It is best for the hospital, of course, as it means that care can be delivered for a fraction of the cost of keeping people in for several days. But is it best for families? What are we doing to parents when we send them home with a child fresh from surgery? While we might give them some education about what to do if the child has an adverse event, there is not enough time to make sure the parents have understood, are able to read effectively, and have taken any information on board (with their ability to do so potentially hampered by their state of anxiety). How do we know what the infection rates are after surgery? If the child develops an infection, the parents are likely to take the child to a general practitioner rather than return to the hospital, and busy GPs may not report back to the hospital on the child’s visit and the need for treatment. We do not ask parents what financial burden we are placing on them. Have they taken days off work or used their holiday time to look after the child? Does that mean financial hardship for the family? Do we ask them what emotional burden it is placing on them? As a highly educated health professional who knows the ropes, I can only imagine how anxious young parents must be with a child who has just had an operation and for whom there is no health care support at home. Of course, my comments about children are just as salient for adult day surgery admissions. I believe that lean thinking and its penultimate expression in health delivery, the day admission, should be critically re-examined, and there needs to be much more research on the immediate and long-term effects on patients and their families.

Linda E Shields

To the Editor: It is pleasing to see the acknowledgement by contributors of the fundamental premise that the fragmentation of health care may reduce the quality provided, which was a key argument of our article.1 Our aim was to provide space for critical appraisal of “lean thinking” and its application to health care, by questioning the assumed theoretical basis from which this approach is derived and enquiring about the evidence for long-term benefits relating to patient outcomes. We wished to engender discussion and debate rather than provide a systematic review of existing literature. To this end, we think our aim has been achieved. Returning to the central thesis of our article, we argue that the notion of quality is rapidly being subsumed by quantity (understood as patient throughput and the number of measurable errors). This is reflected in the focus of Ben-Tovim and colleagues on process rather than practice.2 We believe that medicine is grounded in the human condition,3 and thus ideas of quality must relate to patient experience, including harms that are not readily measurable. We acknowledge that health care is becoming more and more complex, and increasingly requires the exercise of practical wisdom that informs clinical reasoning.4 Individual differences between patients mean that each situation has to be considered in its own context. Recognition of this difference provides the opportunity for some of the richness and satisfaction inherent in medicine. Finally, medicine and health care are far from immune to adopting and repeating the mistakes of other professions and industries. It has been suggested that the continued rationalisation of health care, such as occurs with “lean” approaches, may contribute to the deprofessionalisation of medicine over time.5 In turn, this may promote the “McDonaldization”6 of health care, whereby efficient turnaround becomes the primary goal. We suspect that, while meeting a need at one level, this would provide little long-term satisfaction for health care providers or patients.

Sarah Winch · Amanda J Henderson

To the Editor: The recent rapid increase in popularity of low-carbohydrate (“low-carb”) beers in Australia, such as Foster’s Pure Blonde and Lion Nathan’s Hahn Super Dry, may represent an insidious health risk. The perception that low-carb beers represent a healthy alternative may result in some consumers: confusing low-carb beers with low-alcohol beers; believing that there will be a significant health benefit associated with consumption of low-carb beers (such as weight loss); drinking more beer in the belief that there are fewer health consequences associated with low-carb beers; or drinking low-carb beer in situations where the consumption of regular beer may be contraindicated because of health conditions such as diabetes or cardiac vulnerability. Particularly vulnerable risk groups include younger people and especially young women, who are often highly body image-conscious, as well as others with weight or health problems. Nutritional information for some of the major beers on the market in Australia is shown in the Box.1-3 The new generation of low-carb beers contain about 0.9 g of carbohydrate per 100 mL. However, there is little, if any, difference in either the amount of alcohol or the total energy content of traditional and low-carb beers, suggesting “low-carb” may not be a nutritionally significant improvement. Given that alcohol is a known cause of short- and long-term problems such as cancer, cirrhosis of the liver, strokes and violent behaviour, we contend that the alcohol content of beer is a far more important health issue than its energy content. Additionally, the alcohol content itself contributes directly to energy intake (1 g of alcohol contributes 29.8 kJ of energy, compared with sugar’s 15.4 kJ).4 Consuming alcohol may also indirectly lead to weight gain because of its association with unhealthy eating behaviour, such as increased snacking, junk food consumption and overeating.5 The Box clearly demonstrates that drinkers are better off consuming low-strength beers in terms of both alcohol content and energy intake. Recognising this fact, the European Parliament adopted the resolution that “Beverages containing more than 1.2% by volume of alcohol shall not bear health claims”.6 We believe that the Australian Government, particularly through its current Review of Food Labelling Law and Policy, should move quickly to enact similar legislation to protect the Australian public from the marketing claims of brewing companies. The message should be made explicit: low-carb beers are not a “healthy choice”. Nutritional information for major beers on the market in Australia1-3 Beer Alcohol by volume Carb (g/100 mL) Energy (kJ/100 mL) Full strength Redback 4.7% 3.6 172 Hahn Premium 5.0% 3.2 172 Cascade Pale Ale 5.0% 3.0 170 Crown Lager 4.9% 3.1 169 Cascade Premium Lager 5.0% 3.0 169 Foster’s Lager 4.9% 3.1 168 Victoria Bitter 4.6% 3.0 165 Carlton Black 4.4% 3.3 161 Tooheys New 4.6% 3.1 161 Tooheys Extra Dry 5.0% 2.5 161 Melbourne Bitter 4.6% 2.9 158 Tooheys Old 4.4% 3.0 156 Carlton Draught 4.6% 2.7 155 Swan Draught 4.5% 2.7 153 XXXX Draught 4.5% 2.1 147 Mid–low strength XXXX Gold 3.5% 1.9 121 Hahn Premium Light 2.6% 3.1 119 Carlton Sterling 2.5% 3.1 114 Cascade Light 2.6% 3.0 114 Hahn Super Dry 3.5 3.5% < 1.0 104 Low-carb Carlton Dry 4.5% 1.9 139 Bondi Blonde 4.5% < 2.0 130 Tooheys Maxim 4.6% 1.6 126 Hahn Super Dry 4.6% 0.9 126 Pure Blonde 4.6% 0.9 125 Carb = carbohydrate.

Peter G Miller · Stephen P McKenzie · Florentine P de Groot · Sondra L Davoren · Evie R Leslie

To the Editor: Influenza causes around 8% of community-acquired pneumonia (CAP) episodes,1 and during the (H1N1) 2009 influenza pandemic, concurrent bacterial infections were detected in up to 29% of fatal infections.2 Determining microbial aetiology of CAP can guide antibiotic and antiviral therapy. To investigate the usefulness of microbiological diagnostic testing for CAP, we undertook a retrospective review of our pathology department’s electronic database of patients admitted with CAP to a tertiary referral centre (365 beds) and two suburban teaching hospitals (314 and 280 beds) between 1 May 2007 and 30 April 2008. Inclusion criteria were: International Classification of Diseases, 10th revision codes J09–J22 (respiratory tract infections); age ≥ 18 years; and consolidation on a chest radiograph performed within 48 hours of admission. Exclusion criteria were: hospitalisation within the previous 14 days; admission to a unit managing predominantly immunosuppressed patients; HIV infection; active tuberculosis; chest injuries; and previous inclusion in the study. Basic demographic data and microbiological investigation results were collected. We adopted the Australian CAP Study’s criteria for aetiology and classification of good-quality sputum.1 Change in management was indicated for patients with bacteria not covered by empiric regimens recommended in Therapeutic guidelines: antibiotic, version 13, or organisms with public health and infection control implications.3 Continuous variables were analysed using either Student’s t test or the Wilcoxon rank-sum test, and categorical variables with the Fisher exact test. Statistical significance was set at P < 0.05. From 2436 admissions, 341 patients met inclusion criteria. Mean age was 71.1 (SD, 17.1) years, and 72 patients (21.1%) were in residential care. Most patients (251; 73.6%) had investigations to determine aetiology (Box). Ninety-three organisms were identified from 83 patients (33.1%), most commonly Streptococcus pneumoniae (33; 13.1%), Haemophilus influenzae (14; 5.6%), influenza (11; 4.4%) and Legionella spp (9; 3.6%). Good-quality sputum taken within 8 hours of presentation had the highest diagnostic yield (47.1%). Changes to management were indicated for 37 patients (14.7%). Aetiology was identified more often in the suburban hospitals, where S. pneumoniae and Legionella spp were more common than in the tertiary centre (27.7% v 8.1% and 9.2% v 1.6%, respectively; P = 0.001). Patients in the suburban hospitals were younger and less likely to be in residential care than those in the tertiary centre (mean, 67.6 v 72.6 years and 13.7% v 24.3%, respectively; P ≤ 0.03). The Australian antibiotic guidelines recommend appropriate investigations to determine aetiology of CAP.3 Our analysis suggests that usefulness of microbiological investigations varies between different patient populations, and their value may be maximised by using algorithms similar to the recommendations for CAP investigations in United States guidelines.4 Contrary to widespread belief that microbiological diagnostic tests for CAP are low-yield and not helpful, we found that aetiology could be established in up to 55% of patients and a change in management made in 15% by using a combination of diagnostic tests. Our findings should be generalisable to other parts of Australia, as the aetiologies we observed mirror those seen in the Australian CAP Study.1 Diagnostic yield of investigations used to determine microbial aetiology for patients hospitalised with community-acquired pneumonia No. positive/no. tested (% positive) Investigation Suburban hospitals Tertiary centre Total Sputum microscopy, culture and sensitivities 14/40 (35.0%) 23/103 (22.3%) 37/143 (25.9%) Blood culture 5/42 (11.9%) 7/131 (5.3%) 12/173 (6.9%) Urinary antigen test Streptococcus pneumoniae* 14/40 (35.0%) 11/105 (10.5%) 25/145 (17.2%) Legionella pneumophila serogroup 1* 4/39 (10.3%) 1/104 (1.0%) 5/143 (3.5%) Respiratory multiplex PCR† 1/6 (16.7%) 6/17 (35.3%) 7/23 (30.4%) Bronchoscopy‡ 0/2 3/12 (25.0%) 3/14 (21.4%) Serology§ 4/27 (14.8%) 7/66 (10.6%) 11/93 (11.8%) Total patients investigated 36/65 (55.4%) 47/186 (25.3%) 83/251 (33.1%) PCR = polymerase chain reaction. * P = 0.02 for comparison of % positive between hospitals. † Nasopharyngeal swabs tested for influenza A and B, picornavirus, parainfluenza, adenovirus and respiratory syncytial virus. ‡ All bronchoscopy specimens cultured for Legionella spp, bacterial and fungal pathogens, and other investigations as requested by clinicians. § Serological tests for influenza A and B, Legionella spp, Mycoplasma pneumoniae, Chlamydophila spp and Coxiella burnetii.

Adrian R Tramontana · Vincent Sinickas

To the Editor: We present this case to highlight the differential diagnosis of afebrile seizures in patients from many asset-poor nations. A 3-year-old Congolese girl presented with sustained loss of consciousness after a prolonged generalised seizure. She had migrated, with her family, 12 months previously after a long period in a Zambian refugee camp. She was intubated briefly and given intravenous benzodiazepines. She made an uneventful recovery; she was discharged from hospital after 2 days. This was her first seizure and there was no history of fever, trauma or poisoning. The parents declined long-term anticonvulsants. Apart from mild malaria, she had been previously well and showed normal development. HIV serology and results of blood films for malarial parasites were negative; other blood tests, including an eosinophil count, were normal. Cerebral magnetic resonance imaging (MRI), performed because the diagnosis was unclear and the patient had had a prolonged seizure, revealed a single 8 mm cyst, with an enhancing wall and surrounding oedema, in the left frontal lobe. The cyst contained a scolex, pathognomonic of neurocysticercosis (Box). There were multiple foci throughout the brain, indicating active and resolving cysts. Serology results for Taenia solium were negative at presentation and 3 months later. The child was treated with 8 days of albendazole and 3 days of dexamethasone. Repeat MRI 2 months after presentation showed significant improvement, with a residual 3 mm calcified focus. The child has remained seizure-free for 18 months. Neurocysticercosis is caused by larvae of the pork tapeworm T. solium, which may encyst in the brain, eye or spinal cord, after ingestion of ova-contaminated food or water.1 In contrast, ingestion of encysted larvae (cysticerci) in undercooked meat results in intestinal infection with the adult tapeworm.1 Neurocysticercosis is common in many asset-poor countries, including those in Asia and sub-Saharan Africa from where many people in humanitarian refugee programs originate.2 In areas where it is endemic, T. solium is a leading cause of epilepsy in children and adults.3 The diagnosis of neurocysticercosis is difficult and the diagnostic differential is broad. Cerebral imaging showing typical lesions containing a scolex is diagnostic. T. solium serology is insensitive, especially in children with few cysts. Anticercal antibodies or cysticercal antigens in the cerebral spinal fluid are helpful, but these investigations are not widely available (they are available from the Centers for Disease Control and Prevention, Atlanta, United States). Treatment with anthelmintics is controversial; parasites may die spontaneously and treatment may cause local inflammation (reduced by steroids), which potentially exacerbates seizures or causes local tissue damage.4 Ocular cysticercosis should be excluded before anthelmintic treatment as the resultant inflammation may compromise sight; surgical excision should be considered if ocular cysticercosis is present.4 Empirical anthelmintics, often given before departure or following resettlement to people at risk, may potentially precipitate seizures.5 We treated this child with albendazole as there were multiple lesions likely to contain live parasites, and because anticonvulsants were declined. This case highlights that neurocysticercosis is a possible treatable cause of afebrile seizures in patients migrating from, or with a history of visiting, endemic areas, including resettled refugees. Clinicians in affluent countries are often unfamiliar with the disease, yet are managing increasing numbers of people at risk. Misdiagnosis is of particular concern because brain imaging is not routinely performed in children presenting with their first afebrile seizure. Magnetic resonance image of brain of 3-year-old girl showing cysticercus Encysted scolex of Taenia solium, surrounded by enhancing wall and significant oedema, in left frontal cerebral lobe.

Juliette M Lucey · James McCarthy · David P Burgner

To the Editor: Two recent publications have described programs of carrier testing for cystic fibrosis (CF) gene mutations.1,2 The authors conclude that CF carrier testing of women in early pregnancy and their partners, as well as couples contemplating pregnancy, can successfully identify those who are at risk of having a child with CF and provide them with reproductive choices. The authors use these proof-of-concept studies, in the absence of Australian economic data, to call for all couples to be offered CF carrier testing that is supported by government funding. Although reproductive choice is clearly an individual’s right, what obligation does the community have regarding government funding of specific services to generate information that might assist such couples? Genetic screening policies have often been determined on the basis of technological capability, rather than through a rigorous evidence-based review process.3 Decision making should also take into account evidence of clinically effective screening programs, ethical principles, and opportunity costs, given the limited resources available in the health sector. A simple economic analysis of these publications highlights some issues that need to be addressed. Massie and colleagues identified nine carrier couples by screening 3200 individuals (3000 females) before conception or during early pregnancy (CF carrier frequency, one in 30). Two of the nine carrier couples had affected pregnancies, which equates to a cost of $300 000 per CF case. In Christie and colleagues’ dataset of 1000 individuals, 73% had no family history of CF; 27 of these individuals carried CF mutations, and two carrier couples but no affected pregnancies were identified. Based on population gene frequency statistics (CF carrier frequency, one in 25; 75% of CF gene mutations being p. F508del),1 Massie et al’s screening model2 would, on average, require 3585 women to be screened to detect one affected pregnancy, costing about $740 000. Christie et al’s expanded one-step model1 would require about 3763 couples to be screened to detect one affected pregnancy, at a cost of more than $430 000. Among the 270 individuals with a family history of CF who were screened in the latter model, 126 were carriers of CF mutations (carrier frequency, one in two). It is clear that cascade screening of those with a family history would be a more effective strategy. There is an ethical argument that projected economic benefits from the termination of affected fetuses should not play a role in decisions to offer testing.4 Nevertheless, technological capability needs to be considered together with evidence of cost-effectiveness and community acceptance before public funding of community CF carrier screening can be justified.

Peter C O’Leary · Susannah J Maxwell · Leanne M Youngs · Kate J Brameld · Ian R Walpole

In reply: Our aims in publishing the outcomes of offering cystic fibrosis (CF) carrier testing to couples were to demonstrate the high acceptability rate and report the reproductive choices made by high-risk couples. Not all decisions resulted in termination. O’Leary and colleagues rightly raise the question of screening costs. Laboratory costs will reduce with economies of scale and centralisation of testing. The recent release of a position paper on population screening for CF by the Human Genetics Society of Australasia1 will influence the demand for testing. It recommends that all couples intending to have children, and women in early pregnancy and their partners, be made aware of the availability of CF carrier testing, and that couples should be offered testing for 10 CF transmembrane conductance regulator gene mutations using an expanded one-step or two-step model. O’Leary and colleagues suggest that cascade testing of those with a family history of CF would be a more effective strategy. However, only 10% of children born with CF have a family history.2 Studies have demonstrated that costs of CF screening are less than the averted medical care costs associated with fewer births of infants with CF.3-5 Although economic considerations are important, these should not form the primary goal of any screening program.

Louise M Christie · Angela J Ingrey · Gillian M Turner · Anne L Proos · Gloria E Watts

To the Editor: Hellard and Wang1 are correct in emphasising the importance of the general practitioner in the management of hepatitis C virus (HCV) infection. As the authors note, HCV infection is a considerable source of morbidity and mortality in the community, and the infection may cause a substantial burden of illness in the future if it is not appropriately managed. The GP plays a pivotal role in managing HCV infection, being the first and most likely point of contact for patients. However, Hellard and Wang fail to note that the GP’s most useful role is to inform patients that “alcohol abstinence is strongly recommended before and during antiviral therapy”.2 The well recognised role of alcohol in disease progression is emphasised in the position papers of both the American Gastroenterological Association and the United States National Institutes of Health.2,3 From a public health perspective, it is difficult to think of a more cost-effective approach to the management of such a public health issue.

Anne E Duggan · John M Duggan

In reply: Duggan and Duggan are correct to highlight the well recognised role of alcohol consumption in progression of hepatitis C virus (HCV) infection. Alcohol consumption has been found to increase viral load and accelerate hepatic fibrosis in HCV infection.1,2 While studies have reported that a history of alcohol consumption adversely affects treatment outcomes (with some reporting a dose–response relationship),3,4 treatment success has also been reported among patients who continue to consume moderate amounts of alcohol during treatment.5 Although there are biologically plausible mechanisms through which alcohol consumption might negatively affect treatment, low rates of treatment success among drinkers may also be related to lack of adherence to treatment regimen in this population.1 To date, no study has specifically measured the effect of alcohol consumption during treatment while adequately controlling for the effects of compliance, disease progression and baseline viral load. Until studies are undertaken that measure the direct effect of alcohol consumption on treatment success, while adjusting for compliance, it seems reasonable to advise patients to decrease their level of alcohol consumption before and during HCV treatment. However, given that some patients have successfully completed treatment without abstaining from alcohol consumption, this should not be an automatic exclusion criterion.

Margaret E Hellard · Yung-Hsuan J Wang · Rachel Sacks-Davis

To the Editor: The recent letter by Cox, about transfer of pregnant women from remote communities to Cairns for birthing,1 mirrored my experiences while working in general practice and psychiatric community outreach in rural Australia for many years. The removal of people from their familiar surroundings (especially for extended periods) in itself exacerbates health problems, even more so when they are already hindered by impaired socioeconomic status or ethnic disadvantage. Almost always, the security of their attachment and capacity to maintain resilience are strained. Furthermore, this displacement often occurs in emotionally charged or threatening health situations, where it is likely to be most damaging: childbirth, treatment of life-threatening disease caused by malignant neoplasm or cardiovascular disease, and management of mental disorders or substance misuse. The increasing concentration of “expert” treatment centres in fewer and fewer (usually metropolitan) centres, together with the degradation and de-skilling of rural and remote services that I have observed for the nearly 30 years I have worked in Australia, are sad. However, even worse is the failure of government to do anything to reverse the trend, despite repeated hand-wringing and talking about the rural health “problem”.

Robert D Craig

To the Editor: The Australian Medical Council recognises the importance of clinical experience in general practice for all medical students.1 In their recent article in the Journal, Vickery and colleagues identify three significant barriers to clinical teaching by Australian general practitioners: time, space and opportunity costs.2 They suggest that General Practice Super Clinics will be well placed to address the issue of space and, with additional funding, could also overcome the barriers of opportunity cost and lack of time. The latter claim may be true, but we need to invest in all teaching practices, not just in Super Clinics. The Australian Government is currently committed to establishing 35 Super Clinics. Even if more are set up in the future, it is difficult to see how they will ever make a major contribution to providing general practice placements for the 3000-plus students entering medical training each year. There are many high-quality general practices across Australia that have been committed to teaching for years. For this, they receive a $200 Practice Incentives Program payment per student per day. This amount has not increased since 2004, and is widely seen as insufficient to meet practice teaching costs. There is an urgent need to increase the sessional payment for teaching to an amount that realistically reflects the time and opportunity costs to practices. In addition, a national fund for capital investment in teaching practices would help address the third barrier that Vickery et al identify: many excellent practices are unable to provide student placements due to lack of space.

Timothy P Usherwood

To the Editor: A 69-year-old Indigenous Australian man, with no known Caucasian ancestry, presented in 2008 with a 7-week history of depigmentation of the face and neck, which was initially intensely pruritic and erythematous. He had neither a personal history nor family history of vitiligo, but a 2 mm thick, Clark level III, superficially spreading melanoma had been widely excised from his right lateral calf in 2001; results of a right inguinal sentinel node biopsy had been negative. In 2005, multiple small local recurrences on the right lower leg had been surgically removed. Two years later, further histologically confirmed local cutaneous and subcutaneous recurrences were excised, but new lesions continued to develop. His medical history included type 2 diabetes mellitus, hypertension, atrial fibrillation and coronary artery bypass grafting. He had no family history of melanoma. The onset of facial inflammation and depigmentation over a few days in 2008 was associated with complete regression of some leg lesions and partial regression of others. The facial inflammation settled spontaneously within a week. Computed tomography of the abdomen and pelvis at this time did not show any distant disease. The patient was unconcerned by the depigmentation and declined treatment. Over the following 5 months, the extent of his head and neck depigmentation increased (Box, A) and he developed more melanomas on his right lower leg, including one with a depigmented rim (Box, B). Positron emission tomography identified several areas of focally increased metabolism corresponding to the right lower leg lesions, but no evidence of disease elsewhere. The leg lesions have demonstrated only slow progression, and the patient continues to have 6-monthly follow-up at our department, as well as ongoing local review. Cutaneous melanoma is rare in Indigenous Australians, with only two reported cases of acral lesions.1,2 In melanoma, immunogenic factors may play a key role in disease course. Antibodies that cross-react with antigens on melanocytes and melanoma cells, such as tyrosinase, tyrosinase-related-protein-1 and tyrosinase-related-protein-2, can lead to both vitiligo-like autoimmune depigmentation and tumour regression.3 T-cell-mediated responses to melanoma antigens, such as MART-1 (melanoma antigen recognised by T-cells-1), are also enhanced in melanoma patients with depigmentation,3 which has been reported in approximately 3% of patients with stages III and IV melanoma.4 Vitiligo is a positive prognostic factor and has been reported in association with tumour regression distant from the depigmentation.4 In conclusion, this case of vitiligo-like depigmentation, affecting both the head and neck and a cutaneous metastasis, highlights the immune responsive potential of metastatic melanoma. Vitiligo-like depigmentation associated with melanoma in a 69-year-old Indigenous Australian man A: Extensive depigmentation of the face and neck 5 months after the onset of vitiligo. B: Depigmentation around the largest subcutaneous metastasis on the right lower leg.

Elizabeth M Christou · Diona L Damian · John F Thompson