Volume 191 Issue 10

General practitioners hold the key to expanding access to treatment Hepatitis C virus (HCV) is an important cause of morbidity and mortality in Australia. More than 200 000 people are estimated to be living with chronic HCV infection, with over 80% of these infections resulting from unsafe injecting drug use. About 10 000 new infections occur annually, although incidence is thought to be declining.1 Following primary HCV infection, persistent viraemia and chronic hepatitis occurs in 50%–80% of patients; after 20 years approximately 7% develop cirrhosis, and a small proportion of these patients develop hepatocellular carcinoma.1 Treatment of HCV infection has advanced over the past 10 years, leading to improved outcomes; the most effective current treatment is pegylated interferon combined with ribavirin. The aim of treatment is viral eradication, and treatment is deemed successful if a patient has a sustained virological response (SVR).2 The subsequent reduction in liver disease progression in patients who obtain an SVR3 suggests that the burden of advanced liver disease could be reduced if more patients received treatment. Treatment uptake has increased over the past 10 years, but has remained low. The removal of restrictions to prescribing for treatment — including the requirement for patients to have abnormal alanine aminotransferase levels or liver biopsy results (restrictions that were removed in 2005 and 2006, respectively) — has increased access,4 but the total number of individuals being treated for HCV infection in Australia remains low, at around 3500 individuals per year.5 Estimates vary, but recent modelling suggests that at least 6000, and closer to 10 000, people with chronic HCV infection need to be treated annually to reduce the burden of advanced liver disease in the future.1 While we acknowledge that not all people want or can have treatment for HCV infection, the number could be increased. HCV treatment can only be prescribed by certain medical practitioners or specialists, or at liver clinics, and cannot be prescribed by most general practitioners. Opportunities for treatment in tertiary hospitals and opioid pharmacotherapy clinic settings need to be expanded,6 but equally important is increasing GPs’ capacity to manage and treat patients living with HCV. GPs are usually the initial point of contact for patients with or at risk of HCV. It is imperative that GPs provide clear, accurate and up-to-date advice on HCV risk, prognosis and management. Several surveys in the past 10 years have reported that most GPs want further education about treatment, interpretation of test results, pre- and post-test counselling, and referral information.7,8 Many GPs’ knowledge of HCV is limited. A study undertaken in the period 2005–2006 found that, although GPs were aware of which patients are at risk of HCV (injecting drug users in particular), many underestimated the large number of Australians infected with HCV.9 A 2002 study reported that 39% of surveyed GPs mistakenly believed that positive results from HCV serological testing, as opposed to positive results from HCV RNA testing, differentiated current and resolved infection.7 An anti-HCV antibody test only provides information on whether a patient has ever been exposed to HCV — a positive result does not necessarily indicate an ongoing infection. An HCV RNA test is required to determine whether a patient has an ongoing infection or has spontaneously cleared their infection. GPs’ awareness of HCV treatment was also limited. The 2005–2006 study showed that only 42% of surveyed GPs were aware of the effectiveness of current HCV treatment, and only 28% were aware of the eligibility criteria for access to subsidised treatment.9 The 2002 study showed that 52% of GPs were not aware that pegylated interferon–ribavirin combination therapy was the most effective HCV treatment.7 Other studies have shown that fewer than 52% of people living with HCV in Australia had ever been referred to a specialist liver clinic10,11 despite the general acceptance that this should occur for the vast majority of patients with HCV. In addition, many GPs have reported being uncertain about when to refer patients to hepatitis specialists.9 Ongoing education is vital if GPs are to remain up to date on the management of HCV infection. A range of options are required to meet the needs of different GPs and their patients. One option is training GPs to fully manage their own patients, including training to become accredited prescribers of pegylated interferon and ribavirin under the federal government’s Section 100 (s100) Highly Specialised Drugs Program. Currently, the availability of such training is limited and varies between states and territories. A shared care model is a second option. Some GPs could be actively involved in the management and follow-up of patients without being an s100 prescriber. This model could suit GPs who manage only a few patients with HCV infection, as well as nurse practitioners and GPs in rural and regional areas. A specific training program could be developed to provide GPs and nurse practitioners with the necessary knowledge and skills, particularly for managing the side effects of HCV treatment. A third option should be provided to potentially the largest group of GPs — those who have patients at risk of or infected with HCV, but who do not want to be directly involved in HCV management. Through ongoing and regularly updated training programs, these GPs need to stay up to date on who is at risk of HCV infection, what tests should be ordered to diagnose and monitor HCV infection, and when patients should be referred to a specialist. In addition, all GPs need to have a broad understanding of what HCV treatments are available, that current and recent injecting drug users are eligible for HCV treatment, and that a liver biopsy is no longer required for a patient to have access to treatment (Box). Encouraging GPs to undertake HCV training in a setting of competing education priorities is a major challenge. Perhaps the first step should be to highlight that HCV occurs in about 1% of the population and that treatment options and outcomes for their patients have improved considerably during the past 5 years and are likely to continue to do so. Hepatitis C virus (HCV): what general practitioners should know HCV is common — more than 200 000 Australians have ongoing infection. Approximately 25% of people infected with HCV spontaneously clear their infection.12 An anti-HCV antibody test only detects whether a patient has ever been exposed to HCV — it does not detect ongoing infection. An HCV RNA test is required to determine whether a patient has an ongoing infection or has spontaneously cleared their infection. HCV can be successfully treated with pegylated interferon combined with ribavirin. The most common HCV genotypes in Australia are genotype 1 and genotype 3.1 Genotype 1 HCV infection usually requires 48 weeks of treatment, and genotype 3 usually requires 24 weeks of treatment; the chance of successfully clearing the virus with such treatment is approximately 45% and 75%, respectively.13 Treatment is deemed successful if a patient has a sustained virological response — defined as having a negative HCV RNA test result 24 weeks after completion of treatment. After successful treatment, patients will be HCV RNA negative but will remain anti-HCV antibody-positive in the vast majority of cases. Subsidised treatment is available to people older than 18 years who are anti-HCV antibody-positive, have detectable serum HCV RNA levels, have compensated liver disease, and have not had prior treatment with pegylated interferon or interferon alfa.

Margaret E Hellard FRACP, PhD, FAFPHM · Yung-Hsuan J Wang MB BS, FRACGP, MAppEpid

To empower patients, we need to apply the knowledge gained from research The final report of the National Health and Hospitals Reform Commission, A healthier future for all Australians, has rightly stimulated debate in Australia about what it takes to create an equitable and sustainable health care system.1 The report draws attention to the importance of strengthened consumer engagement, boldly described as “giving people real control and choice about whether, how, where and when they use health services, supported by access to evidence-based information that facilitates informed choices”, as a platform for creating an “agile and self-improving health system”.1 Building health literacy is identified as a key strategy that will underpin strengthened consumer engagement. This ambitious commitment is long overdue. Research indicates that those who actively participate in health care decisions generally achieve better health outcomes compared with those who do not, and that most patients are not currently involved in health care decisions to the degree they would like to be.2 Those most likely to participate in health care decision making tend to be younger, female and educated. Regardless of personal preferences, not everyone is equally equipped to participate in health care decisions. The Commission’s report recognises this in its advocacy of action to build health literacy. Health literacy can be simply defined as the capacity to acquire, understand and use information for health. A 2006 Australian Bureau of Statistics survey examined health literacy in Australia using data derived from the Adult Literacy and Life Skills Survey, which assessed respondents’ prose and document literacy, numeracy, and problem-solving skills.3 From these data, information relating to respondents’ health literacy was derived, using specific questions related to health issues. The study found that 60% of Australians lack basic health literacy, described as the “minimum required for individuals to meet the complex demands of everyday life and work in the emerging knowledge-based economy”.3 In a country that prides itself on achieving high rates of functional literacy, this is surprising, and indicates that individuals with higher levels of general literacy may not be able to consistently apply it in situations requiring specific content knowledge, or in an unfamiliar environment. For many individuals, as patients, carers and members of the public, health care settings are unfamiliar environments in which alien vocabulary and concepts are used. The relationship between literacy and the quality and outcome of health care has gained increasing attention, especially in the United States.4 Research shows that people with poor health literacy are less responsive to health education and use of disease prevention services, are less able to successfully manage chronic disorders such as diabetes and asthma, and incur higher health care costs.5 This has led to progressive testing of interventions designed to mitigate the effects of poor health literacy through modified communication and improved health service organisation.6 The limited research on health literacy conducted in Australia, such as the article by Adams and colleagues in the current issue of the Journal, confirms both the findings of the Australian Bureau of Statistics survey on the extent of the problem, and the established link between poor health literacy and poor health outcomes.7 Research from New South Wales provided insight to the needs and preferences of people with low literacy in the development of clinical decision aids.8 Given the policy recommendations and potential importance of their impact, this remains an underdeveloped area of research.8 Although the Commission’s attention to health literacy is encouraging, the practical actions proposed in its report are underdeveloped and will require early attention to seize this opportunity for action. Health literacy is best developed through education that is customised to individuals and their specific priorities. The recommendation that health literacy be incorporated into the National Curriculum for school children is commendable; however, the educational needs of a person with diabetes who is receiving patient education, or a pregnant woman attending antenatal classes, or a carer of a person with long-term mental illness will be greatly different. School health education will not prepare us for the different individual health challenges we may face. If we are to see “real control and choice about whether, how, where and when [people] use health services”,1 three strategies are required. First, health care providers and those responsible for patient management and administration need to demonstrate greater sensitivity to the needs of patients with poor health literacy by creating a less alienating health care environment that is more responsive to patient needs. Second, greater care needs to be taken to improve the quality of patient communication and the materials that support it. Both of these strategies require further research, and both can be achieved in part through modification of basic and continuing education. Third, outside the health care system, as well as investing in school education, Australia would do well to follow the lead of the United Kingdom in adopting innovative adult education programs such as the Skilled for Health program, which brings health content into an adult basic skills program.9 It is over 15 years since national goals and targets for health literacy were first proposed in Australia.10 Since then, our understanding of health literacy has grown considerably. If this knowledge is not applied, the policy goal of achieving meaningful control and choice by patients is unlikely to be met. Worse, increasing patient participation without specific interventions to address low health literacy could exacerbate existing health inequalities by further alienating those with poorer literacy skills and less confidence in using the health care system.

Don Nutbeam PhD, FFPH (UK)

We need a national register of home oxygen therapy Oxygen has been used for therapeutic purposes for centuries, but until relatively recently no scientifically rigorous trials had confirmed its true benefits. In the early 1980s, two landmark randomised trials — the Medical Research Council (MRC) trial and the Nocturnal Oxygen Therapy Trial (NOTT) — showed that continuous or semi-continuous oxygen therapy for between 15 and 24 hours a day provided a mortality benefit in patients with chronic obstructive pulmonary disease (COPD) and severe hypoxaemia.1,2 Survival rates for those prescribed “continuous” oxygen (in reality about 19 hours per day) in the NOTT were around 80% at 2 years, compared with around 60% for the “nocturnal” group using oxygen for only 12 hours per day. In the MRC study, in which patients were randomly allocated to receive oxygen for 15 hours per day versus no oxygen, survival rates at 5 years were 67% versus 45%, respectively. This evidence-based treatment is now enshrined in guidelines for managing chronic lung disease locally and worldwide. The Thoracic Society of Australia and New Zealand’s position statement on home oxygen also suggests it may be beneficial for those whose resting daytime oxygen levels are satisfactory, but who experience oxygen desaturation only at night or only during exertion. However, the statement acknowledges the lack of a strong evidence base for use of home oxygen for either of these indications.3 Research to bolster the knowledge base for use of oxygen nocturnally or during exertion, and to examine the effects on mortality of continuous oxygen therapy for patients with COPD and only mild hypoxaemia, was identified as a high priority at a recent workshop on oxygen therapy in COPD initiated by the United States National Heart, Lung, and Blood Institute.4 The MRC trial and the NOTT included only patients with COPD. The patients studied were predominantly men, aged under 70 years, and with few comorbidities. Today, patients commencing long-term oxygen therapy are often older and sicker, they frequently suffer from several other serious illnesses, and more women are affected than previously. Although COPD is still the most common reason for commencing home oxygen therapy, many patients have lung diseases other than COPD. In 2004, the users of home oxygen in South Australia were reported to have a mean life expectancy of 2.9 years; this compared unfavourably with the life expectancy of a demographically similar French population of oxygen users (5.2 years),5 and with the survival data from the original MRC trial and the NOTT. Although ethical issues would preclude conducting further randomised trials to confirm a survival advantage in current oxygen users, we should monitor the use of this intervention to maximise benefits as well as to inform future research. Recent data suggest that nearly one in five Australians over the age of 40 years has COPD6 and, with these numbers expected to rise as our population ages, the number of Australians requiring oxygen therapy will also increase. To maximise the mortality benefit, patients need to use their oxygen as prescribed — for at least 15 hours or more a day. The few studies of adherence to a home oxygen regimen have found adherence rates of only 40%–50%.7 Understanding the difference between the use of oxygen to relieve dyspnoea (which may or may not occur), and its use for prolonged periods of the day to lower mortality by relieving hypoxaemia, requires intensive patient education. Accordingly, the distribution of oxygen should not (as, for example, has been the case in Victoria) occur simply as a component of an “aids and equipment program”, with eligibility for oxygen therapy being determined in the same way as for wheelchairs and walking aids. Oxygen therapy should be regarded as drug therapy, with regular follow-up and clinical review required after prescription and distribution. An explanation for the higher mortality rates in South Australian oxygen consumers, compared with those in France, could be the home care and review program that French patients receive, which may enhance their survival.8 The article by Serginson and colleagues in this issue of the Journal is very opportune,9 coming at a time when the National Health and Hospitals Reform Commission has highlighted the fragmentation of our health system, with its complex divisions of funding responsibilities and performance accountabilities between different levels of government.10 Serginson and colleagues show that there is considerable variability in prescription rates of oxygen, costs of oxygen therapy, and types of oxygen services provided across different Australian states and jurisdictions. The total direct cost of oxygen therapy in Australia in 2005, to treat a little over 20 000 Australians, was estimated by these authors to be $31 million. At the time of their audit, state government funding was not provided for portable oxygen therapy in Queensland and, in New South Wales, it was only available in some areas and for some patients. In New South Wales and Queensland, a means test was applied to determine eligibility for all types of oxygen therapy. Prescription rates were found to vary greatly, from 44 per 100 000 population in the Northern Territory to 133 per 100 000 in Tasmania. Explanations for the differences were not apparent from this important but retrospective observational study. Much work still needs to be done to determine who benefits from oxygen therapy and whether those Australians currently using oxygen — and the community, as a whole — are getting the best value they can from this treatment. Serginson and colleagues call for a national register of domiciliary oxygen therapy.9 Similar recommendations were made by the Australian Lung Foundation in their funding submission to Treasury in 2006.11 We endorse these recommendations wholeheartedly. A scheme to monitor variability in applying guidelines; the use of and adherence to oxygen therapy; and the costs and clinical outcomes of oxygen treatment — both mortality and morbidity — is overdue. Are the disappointingly poor survival data reported from South Australia reflective of survival data in other states? Scrutiny of costs and benefits in health care is currently on the agenda, and taxpayers have the right to expect that outcomes will be reviewed in a systematic way to ensure best practice. It will be important to involve consumers in such a process; we have very little qualitative data about how Australians using home oxygen feel about their treatment. The available qualitative research suggests patients may consider oxygen therapy a burden and adhere poorly to recommendations regarding its use.7 While we await the results of further studies examining the questions still to be answered about oxygen therapy, we should ensure that data about patients requiring oxygen in Australia are kept in a national home oxygen therapy registry, and that information regarding usage, adverse effects and outcomes is collected. This will enable prioritisation of resources and encourage high-quality research to inform future oxygen use.

Christine F McDonald MB BS(Hons), FRACP, PhD · Alan J Crockett PSM, MPH

The conference highlighted the need for new policy development using quantitative methods The Fourth Emerging Health Policy Research Conference was held at the Menzies Centre for Health Policy, University of Sydney, on 19 August 2009. This national gathering of “new and emerging” policy researchers came as the Rudd government’s commissions and taskforces delivered their recommendations on improving Australian health. The conference showcased a critical mass of diverse and innovative research projects that push the boundaries of traditional policy enquiry. Forty-two up-and-coming health policy researchers from Australia and New Zealand presented papers on an exciting range of topics within nine concurrent sessions. Researchers with expertise in the fields of medicine, anthropology, sociology, psychology, economics, nursing, history, law and political science exposed multiple disciplinary perspectives on critiquing and addressing current and future health policy problems.1 Hopes for substantial health reform around the world have been challenged by the global financial crisis. Professor John Wyn Owen (Chair of the Board of Governors, University of Wales Institute, Cardiff, and former Secretary of the Nuffield Trust, London), opened the conference with his keynote speech on the challenge to global health posed by macroeconomic emergencies. Health policy development requires an appreciation of the changing nature of capitalism and an assessment of the global health consequences of economic vulnerability. Although public awareness of the need for concerted action has never been higher, public health emergencies, from severe acute respiratory syndrome to swine flu, have weakened economies, lowering the resources that can be mobilised. Owen stressed the importance of the central discipline of health policy analysis — namely, understanding the context in which problems emerge, research is applied and political forces are mobilised. Christine Bennett (Chair, National Health and Hospitals Reform Commission, Canberra) also gave a spirited account of the principal recommendations of the National Health and Hospitals Reform Commission report.2 Major policy themesThree major policy themes emerged in the remainder of the conference: improving chronic illness prevention and management, the intersections between health and other sectoral policy, and new policy instruments. Improving chronic illness prevention and managementThe desperate need for health systems and preventive health initiatives to combat the growing epidemic of chronic disease was raised in several presentations. For example, Renee Slade (Research Officer, Diabetes Unit, University of Sydney) described a capacity development process that is critical to improving the care and management of type 2 diabetes in the Pacific Islands and could provide a useful model for similar settings. Elizabeth Dunford (PhD candidate, George Institute for International Health, Sydney) demonstrated that, although action to reduce salt in Australian foods is being taken up by industry, full buy-in by the Australian government is necessary for widespread adoption of this initiative. Intersections between health and other sectoral policyThe importance of developing cross-sectoral collaboration in developing and implementing policy to tackle challenging issues such as health equity and the social determinants of health also featured strongly in many presentations. The analysis by Emma Webster (DrPH candidate, Discipline of Public Health, Flinders University, Adelaide) of women’s decision making around disbursement of the Baby Bonus payment suggests that an unintended consequence of this social policy has been to entrench social distinction, undermining its effectiveness as a public health intervention. Mandy Nielson (PhD candidate, School of Social Work and Human Services, University of Queensland, Brisbane) pointed to a silent epidemic of chronic pain — much of which has little or no identifiable pathology — and argued that multidisciplinary “biopsychosocial” models need to take the “social” element more seriously. The integration of commonly siloed sectors was pushed further in an analysis by Remo Ostini (Senior Research Officer, Faculty of Health Sciences, University of Queensland, Brisbane) of the implications of low health literacy for illness management, arguing for a national health literacy strategy. Such a strategy would require collaboration between the health, education, housing, employment and welfare sectors to gain any traction. New policy instrumentsDeveloping effective strategies to allow researchers to better engage with and influence the policy process emerged as the final theme of the conference. For example, Mat Walton (PhD candidate and Research Fellow, Department of Public Health, University of Otago, Wellington, New Zealand) discussed his use of complexity theory to untangle the complex social systems that influence children’s nutrition and, in particular, how such findings could be applied to improve child nutrition policy in New Zealand. Gabriel Moore (Senior Project Officer, Sax Institute, Sydney) presented her proposal for a knowledge translation framework that integrates a pathway of interventions, including analysis of research need, development of policy–research partnerships, knowledge brokering, knowledge exchange and advocacy. Carol Holden (Chief Executive Officer, Andrology Australia, Monash University, Melbourne) looked at past failures to develop effective interventions in men’s health, identifying strength of stakeholder networks as the crucial variable and proposing a more strategic approach to health promotion. Methodology underpinning health policy researchMuch of the research presented was qualitative, reflecting interest in experiences of policy outcomes, broader factors influencing policy outcomes, and participatory policy development. Qualitative methods — mainly interviews with stakeholders such as industry representatives, youth and members of the wider community — were used to assess experiences of policy implementation and effectiveness, as well as to directly inform new policy development. Another method employed was linguistic analysis. For example, Denise Fry (Project Officer, Health Promotion Service, Sydney South West Area Health Service), outlined an analysis of the keywords used in health promotion, showing how language can shape and frame policy issues. This helps to explain the persistence of behaviourist models in health promotion, which focus on individual motivation and exclude broader concepts of social determination. Qualitative methods are influential as a policy tool as long as the findings are interpreted in a way that is sensitive to current and emerging policy opportunities. This point was reinforced by Tanisha Jowsey (Research Officer, Serious and Continuing Illness Policy and Practice Study, Australian National University, Canberra) in her presentation on how to translate qualitative findings into practical, relevant and feasible policy options to improve chronic illness management. The policy process was analysed to gain a better understanding of factors influencing policy uptake and implementation. For example, Kathy Flitcroft (Research Fellow, School of Public Health, University of Sydney) presented an analysis of the relative roles of research evidence and other factors in decision-making and implementation processes regarding bowel cancer screening. Similarly, qualitative methods such as ethnographic and historical research tools were used to analyse the broader context of health policy making and to investigate factors affecting policy implementation and equity issues, such as access to care. Many of the evaluations of policy outcomes used mixed methods research, combining data on measurable outcomes with interview data reflecting stakeholder experiences. The conference also highlighted the need for new policy development using quantitative methods, such as epidemiological studies, economic analyses of cost-effectiveness, randomised controlled trials and carefully evaluated policy experiments. Natalie Plant (Research Officer, Menzies Centre for Health Policy, University of Sydney) presented on the development of a randomised controlled trial to compare patient management strategies in coordinating the hospital and community care of patients with serious and chronic illnesses. The concluding speech was presented by Mary Ann O’Loughlin (Executive Councillor and Head of the Secretariat of the Council of Australian Governments [COAG] Reform Council), who described the COAG Health Reform Project, which has been largely forgotten amidst other more headline-grabbing commissions and reports. Recent COAG reforms will require annual report cards on the progress of state and territory governments and (in a break from the past) the federal government, measuring their progress in meeting targets on prevention, hospital and primary care reform, and Indigenous health. Australian policy researchers will have comprehensive data to compare the performance of governments and identify models to improve practice. The Emerging Health Policy Research Conference was convened in response to concerns about the limited research culture in Australian health policy.3 The 2009 conference saw a doubling of papers and attendance compared with the previous year, so the future is looking a bit brighter.

James Gillespie PhD · Beverley Essue BSc(Hons), MPH · Stephen R Leeder MD, PhD, FRACP · Anne Marie T Thow BScNutr(Hons), MPubPol

Objective: To measure the level of functional health literacy (FHL) in an Australian population, and to explore the level of risk associated with level of FHL.Design, setting and participants: Cross-sectional, random population survey administered to 2824 South Australians aged ≥ 15 years, September – October 2008.Main outcome measures: Newest Vital Sign as a measure of FHL, self-reported general health status, and use of health services.Results: 24% of respondents were at risk of limited FHL, and 21% had a high likelihood of inadequate FHL; this increased with age (≥ 65 years, 50% v 25–44 years, 11%). In multiple logistic regression models, a high likelihood of inadequate FHL was significantly more common among those with lower education (left school ≤ 15 years of age, odds ratio [OR], 8.1; 95% CI, 4.8–13.6); with lower annual income (< $20 000, OR, 4.1; 95% CI, 2.3–7.4); who were born in countries other than Australia, New Zealand, the United Kingdom and Ireland; and with poorer health status (OR, 1.6; 95% CI, 1.2–2.2). Inadequate FHL was significantly less common among females (OR, 0.6; 95% CI, 0.5–0.8). People with inadequate or at-risk FHL were significantly more likely to report having diabetes, cardiac disease or stroke, and significantly less likely to have recently attended a doctor. Respondents aged ≥ 65 years with inadequate FHL were more likely to have been admitted to hospital (OR, 2.2; 95% CI, 1.1–4.5).Conclusion: Many Australians are likely to have limited health literacy, and this is a risk to effective health care delivery and health improvement across the community.

Robert J Adams MD, FRACP · Sarah L Appleton BSc · Catherine L Hill MD, BS, FRACP · Mark Dodd BEc · Christopher Findlay BEc, MEc, PhD · David H Wilson MPH, PhD

Objective: To describe the patterns of screening for hepatitis C virus (HCV) infection in methadone-maintained pregnant women and their infants.Design, setting and patients: Retrospective review of medical records from one rural and two metropolitan hospitals in New South Wales for pregnant women on methadone maintenance treatment and infants born to these women between 1 January 2000 and 31 December 2006, as well as records for pregnant women who were not on methadone treatment.Main outcome measures: Rates of anti-HCV antibody and HCV RNA testing for pregnant women and their infants, and ages at which infants attended follow-up appointments.Results: Of 295 pregnant women on methadone maintenance treatment, 288 were tested for anti-HCV antibodies (98%), compared with 1995 of 9987 women who were not on methadone treatment (20%) (P < 0.001). Seropositive results were obtained for 243 women in the methadone group (84%) and 54 in the non-methadone group (3%) (P < 0.001), of whom 44 (18%) and 17 (31%), respectively, were subsequently tested for HCV RNA (P = 0.03). HCV RNA test results were positive for 31 (70%) and 10 (59%) seropositive women in the methadone and non-methadone groups, respectively (P = 0.39). Of infants of HCV-seropositive methadone-maintained mothers, 27% of those for whom we had follow-up attendance data received HCV screening, and one of these infants tested positive for anti-HCV antibodies and HCV RNA.Conclusions: Screening for HCV infection in the high-risk population of pregnant women on methadone maintenance treatment and their infants is inadequate. This could lead to significant underdetection of active HCV infection in this high-risk population, and their infants. Current screening guidelines may therefore need to be revised.

Anthony J W Liu,* MB BS, FRACP, MPH · Ethan I An,* BMedSc, MB BS(Hons) · Henry G Murray MB ChB, MRCOG, FRACOG · Emma Tetstall BSc(Hons), MB BS(Hons) · Marcel J Leroi FRACP, FRCPA, MMed(ClinEpi) · Ralph K H Nanan Dr med Habil (Germany), FRACP

Objectives: To compare the use of evidence-based pharmacological and invasive treatments and 12-month mortality rates between patients with and without diabetes who present with acute myocardial infarction (MI), and to explore the relationship between these treatments and late clinical outcomes.Design and setting: Prospective, nationwide multicentre registry: the Acute Coronary Syndrome Prospective Audit (ACACIA).Patients: Patients presenting to 24 metropolitan and 15 non-metropolitan hospitals with acute coronary syndrome (ACS) and a final discharge diagnosis of acute MI between November 2005 and July 2007.Main outcome measure: All-cause mortality at 12 months.Results: Nearly a quarter of 1744 patients with a final diagnosis of acute MI had a history of diabetes on presentation. Patients with diabetes were older, with a greater prevalence of comorbidities than non-diabetic patients, and were less likely to be treated at discharge with evidence-based medications (aspirin, clopidogrel, a statin and/or a β-blocker) or to receive early invasive procedures. After adjusting for baseline characteristics and therapeutic interventions, diabetes at presentation was independently associated with a higher mortality at 12 months after MI (hazard ratio, 1.79; 95% CI, 1.18–2.72; P = 0.007). Early invasive management and discharge prescription of guideline-recommended medications were associated with a significantly reduced hazard of mortality at 12 months.Conclusion: Patients with diabetes have a higher risk than non-diabetic patients of late mortality following an acute MI, yet receive fewer guideline-recommended medications and early invasive procedures. Increased application of proven pharmacotherapies and an early invasive management strategy in patients with diabetes presenting with ACS might improve their outcomes.Study protocol number (sanofi-aventis): PML-0051.

Joseph Hung FRACP, FACC, FCSANZ · David B Brieger PhD, FRACP, FCSANZ · John V Amerena FRACP, FACC, FCSANZ · Steven G Coverdale MB ChB, FRACP · James M Rankin MB BS, FRACP · Carolyn M Astley RN, BN(Hons) · Ashish Soman MB BS, MRCP(UK) · Derek P Chew MB BS, MPH, FRACP

Objective: To develop a tool to allow Australian hospitals to monitor the range of hospital-acquired diagnoses coded in routine data in support of quality improvement efforts.Design and setting: Secondary analysis of abstracted inpatient records for all episodes in acute care hospitals in Victoria for the financial year 2005–06 (n = 2.032 million) to develop a classification system for hospital-acquired diagnoses; each record contains up to 40 diagnosis fields coded with the ICD-10-AM (International Classification of Diseases, 10th revision, Australian modification).Main outcome measure: The Classification of Hospital Acquired Diagnoses (CHADx) was developed by: analysing codes with a “complications” flag to identify high-volume code groups; assessing their salience through an iterative review by health information managers, patient safety researchers and clinicians; and developing principles to reduce double counting arising from coding standards.Results: The dataset included 126 940 inpatient episodes with any hospital-acquired diagnosis (complication rate, 6.25%). Records had a mean of three flagged diagnoses; including unflagged obstetric and neonatal codes, 514 371 diagnoses were available for analysis. Of these, 2.9% (14 898) were removed as comorbidities rather than complications, and another 118 640 were removed as redundant codes, leaving 380 833 diagnoses for grouping into CHADx classes. We used 4345 unique codes to characterise hospital-acquired conditions; in the final CHADx these were grouped into 144 detailed subclasses and 17 “roll-up” groups.Conclusions: Monitoring quality improvement requires timely hospital-onset data, regardless of causation or “preventability” of each complication. The CHADx uses routinely abstracted hospital diagnosis and condition-onset information about in-hospital complications. Use of this classification will allow hospitals to track monthly performance for any of the CHADx indicators, or to evaluate specific quality improvement projects.

Terri J Jackson PhD · Jude L Michel BHlthInfoManagement(Hons) · Rosemary F Roberts MPH, MBA · Christine M Jorm MD, PhD, FANZCA · John G Wakefield FRACMA, FACRRM, FRACGP

Objectives: To determine the rate of prescription of and government expenditure for domiciliary oxygen therapy (DOT) in Australia, and to identify interstate differences in rates, costs and service provision.Design: Retrospective observational study.Participants and setting: Government departments and health services (state and federal) that funded DOT in Australia in the 2004–05 financial year (including the Department of Veterans’ Affairs [DVA] and the Department of Health and Ageing [DoHA]).Main outcome measures: Prescription rates, cost of DOT in 2004–05, and services provided in each jurisdiction.Results: In 2005, 20 127 patients were using DOT, giving a national prevalence of 100 prescriptions per 100 000 population. The total cost was about $31 million. State governments, the DVA and the DoHA funded 13 899 (69%), 4084 (20%) and 2144 (11%) patients, respectively. Prescription rates varied threefold between the states, ranging from 44 (Northern Territory) to 133 (Tasmania) per 100 000 population. Cost per patient per year varied fourfold between the DVA and the DoHA. All jurisdictions funded oxygen according to the clinical criteria of the Thoracic Society of Australia and New Zealand, but considerable variability in service provision was identified.Conclusion: DOT prescription rates and costs vary considerably between jurisdictions. An urgently needed national DOT register would enable the current variability to be understood and allow service planning and benchmarking of clinical outcomes.

John G Serginson RN, BN, MCN · Ian A Yang MB BS(Hons), PhD, FRACP · John G Armstrong MB BS, PhD, FRACP · David M Cooper MB BS, MSc, FRACP · Anthony M Matthiesson MB BS, FRACP · Stephen C Morrison MB BChir, PhD, FRACP · Judy M Gair MHSc · Barbara Cooper MB BS, FRACMA, FRACGP · Paul V Zimmerman MB BS, MD, FRACP

Objectives: To examine patterns of nicotine dependence, the value of the Fagerström Test for Nicotine Dependence (FTND) and its correlation with self-reported tobacco use and urinary cotinine concentrations among pregnant Indigenous women in Townsville.Design, participants and setting: Cross-sectional study of 201 consecutive women who self-reported tobacco use at their first antenatal visit to Townsville Aboriginal and Islander Health Service (TAIHS) between 1 November 2005 and 31 October 2007. All smokers were to be assessed by FTND, and 108 women participating in the Tilly’s Tracks project (a randomised trial of an intervention to reduce smoking in pregnant Aboriginal and Torres Strait Islander women) were to have a comprehensive smoking history taken and urinary cotinine samples collected.Main outcome measures: Self-reported smoking status, FTND scores and urinary cotinine concentrations.Results: Of 302 Indigenous women presenting to TAIHS, 201 (66.6%) identified as current tobacco users at their first antenatal visit; this proportion rose to 79.6% in women aged < 20 years. An FTND was completed for 152 women (75.6%), with a median score of 4, and 40.1% scoring 3 or less, indicating low levels of nicotine dependence. There were significant correlations between the FTND and number of cigarettes smoked (ρ = 0.56; P < 0.001) and urinary cotinine concentrations (ρ = 0.25; P = 0.030). Of those who provided comprehensive smoking histories, the median age of starting smoking was 15 years, with a median of two previous quit attempts; 71.4% reported partners who smoked and 27.3% reported smoking occurred inside the house.Conclusion: The use of the FTND in Indigenous pregnant women may assess physical nicotine dependence, thus providing information that will help in preparing quit-smoking plans, including tailoring of pharmacological support to individual need. Quit-smoking programs that better address the behavioural and psychological aspects of smoking within the Indigenous community in Australia are needed.

Kathryn S Panaretto MB BS, FAFPHM · Melvina R Mitchell EN · Lynette Anderson EN · Conor Gilligan BPsych, PhD · Petra Buettner PhD · Sarah L Larkins MB BS, MPH · Sandra Eades MB BS, PhD

The delay in transfer of imaging studies when a patient moves between hospitals and between public and private systems has been a barrier to expedient and safe patient management. There is also suboptimal reporting when patients have serial imaging undertaken partly in the private sector and partly in the public sector, because of inability to access previous imaging for comparison. Availability of a DICOM (Digital Imaging and Communications in Medicine) server enables sharing of health information, including imaging data, across various sites and jurisdictions. In Perth, Western Australia, we have successfully introduced electronic image transfer between five public teaching hospitals and three large private practices with different picture archiving and communication systems.

Turab Chakera MB ChB, FRCP, FRANZCR · Yusuf Nagree FACEM · Swithin Song FRANZCR · Philip Jones DipAppSc

The major problem of access block to acute hospital admissions in Australia needs a more radical response than a focus on increasing inpatient beds, as suggested recently. Australia needs to take on board recent changes in United Kingdom hospital systems, which have revolutionised patient flow during acute admissions and dramatically improved efficiency, clinical quality and outcomes. Accident and emergency departments in the UK became recognised as part of acute hospital dysfunction. Now, increasingly, patients needing admission are directed as soon as possible to an acute medical assessment and admission unit (AMAAU), thus freeing accident and emergency staff for re-defined core priorities. AMAAUs require supervision by a new style of acute general physician, who drives timely management of acute medical patients, defines patient needs, estimates the likely date of discharge, and selects the most appropriate inpatient clinical stream. These reforms are staff-intensive and expensive, but cost-effective and patient-focused. They highlight the need for an adequate scale for acute clinical services and defined streams of care within individual hospitals, as well as explicit networking at a regional level to guarantee specialist acute services when needed.

E Haydn Walters DM, FRCP, FRACP · David J Dawson MD, FRCP

We present the first clinical descriptions of immune-mediated paradoxical reactions to effective antibiotic treatment for Mycobacterium ulcerans infection, which result in clinical deterioration after initial improvement. Recognition of this phenomenon could prevent unnecessary changes to antibiotic regimens, and might obviate the need for, or reduce the extent of, further surgery. (MJA 2009; 191: 564-566) Clinical recordsPatient 1A 46-year-old man presented with a 3-month history of a slowly enlarging asymptomatic lesion on the lateral aspect of his right leg, that ulcerated and reached a size of 1.5 cm in diameter. A diagnosis of Mycobacterium ulcerans infection was confirmed by histopathological examination, which showed the classic appearance of a necrotic lesion involving the dermis and subcutaneous tissue, with a sparse acute inflammatory reaction, fat cell ghosts and large numbers of extracellular acid-fast bacilli (AFB)1 (Box, A and Box, B). In addition, culture and polymerase chain reaction (PCR) tests of excised tissue were positive for M. ulcerans. The ulcer was excised with primary skin closure and clear histological margins, and adjunctive antibiotic therapy (with 300 mg rifampicin and 500 mg ciprofloxacin, twice daily) was commenced with a planned duration of 3 months. This lesion had not recurred in the ensuing 7 months. However, in the 2 days before the first lesion was treated, the patient spontaneously developed, proximally, an area of erythema and swelling over the right knee. Although secondary M. ulcerans infection at the site was considered, bacterial cellulitis or bursitis was possible, so it was decided to observe the response to intravenous therapy with cephazolin. Initially, the amount of induration and erythema decreased significantly, but did not resolve completely. About 5 weeks later, the area became increasingly inflamed and, over the following month, became fluctuant but not ulcerative. An aspirate of the lesion confirmed the presence of M. ulcerans with AFB seen on microscopy, and a positive M. ulcerans PCR. The patient, therefore, underwent further wide excision of the lesion with a split-thickness skin graft. The antibiotic regimen was changed by replacing ciprofloxacin with clarithromycin (500 mg twice daily) while continuing with rifampicin. Histopathological examination of the excised tissue showed extensive undermining necrosis in the fat and subcutaneous tissue, accompanied by a florid mixed inflammatory reaction with multinucleated giant cells (Box, C). However, only a few sparse AFB were seen (Box, D). Mycobacterial cultures of the aspirate and the excised tissue were negative at two separate laboratories. The patient completed a further 7 weeks of postoperative antibiotic therapy and, after 6 months, there was no evidence of further M. ulcerans lesions. Patient 2A 66-year-old man presented with a 6-week history of a painless ulcer on the left elbow, with significant surrounding induration. A diagnosis of M. ulcerans infection was made, and antibiotic therapy (300 mg rifampicin and 500 mg ciprofloxacin, twice daily) was commenced. One week later, a wide excision and split-thickness skin graft was performed, although not all the indurated area was excised. Culture and PCR of excised tissue was positive for M. ulcerans. Histopathological examination of the excised lesion showed classic features of M. ulcerans infection, with necrosis of the dermis and subcutaneous tissue, a limited and focal inflammatory response, and large numbers of extracellular AFB. These changes extended to the deep excision margin. The clinical appearance of the indurated area that was not excised improved significantly after surgery. However, 6 weeks later and while still taking the antibiotics, over 48 hours, the patient developed erythema and induration of the left elbow region that extended inferiorly from the lower edge of the excisional wound onto the forearm; the condition had the clinical appearance of cellulitis. This was thought to be a secondary bacterial infection, but it worsened despite intravenous therapy with cephazolin. The patient, therefore, underwent further operative exploration, during which extensive liquefied fat extending distally into the forearm was found and debrided. Histopathological examination of excised tissue showed inflamed granulation tissue with lymphocytes, histiocytes and occasional multinucleated giant cells, and scattered necrotic foci. There were no AFB detected on microscopy and, although PCR of the tissue was positive, cultures were negative for M. ulcerans. The antibiotic regimen was changed by replacing rifampicin with clarithromycin (500 mg twice daily), and the patient took clarithromycin for a further 3 months and ciprofloxacin for a further month. The wound healed completely by secondary intention, and there has been no evidence of recurrence of M. ulcerans infection 10 months after the second operation. DiscussionA “paradoxical” reaction describes a deteriorating response to treatment of an infection after initial improvement.2 Such reactions have frequently been described in infections with a number of mycobacterial species, including those causing tuberculosis, avium-intracellulare complex and leprosy, and although they occur most commonly in severely immunosuppressed patients with HIV/AIDS who are undergoing antiretroviral therapy, they can occur in immunocompetent hosts.2,3 The pathogenesis relates to an enhanced immune response to mycobacterial antigens on treatment that produces deleterious clinical effects.1 Its immune basis means that this phenomenon is also referred to as “immune reconstitution syndrome”. M. ulcerans causes necrotising lesions of skin and subcutaneous tissue. Despite large numbers of extracellular mycobacteria, lesions are characterised by a poor inflammatory response.4 This is probably induced by immuno-inhibitory characteristics of mycolactone, the exotoxin produced by M. ulcerans,5,6 which plays a crucial role in the pathogenesis of infection with this organism. Treatment primarily involves surgical excision; however, recent evidence has shown that antibiotics can have an effective role,7,8 and their use is now recommended.9,10 Clinical paradoxical reactions during the treatment of M. ulcerans have not been previously described. Clinical deterioration during antibiotic treatment can be interpreted as treatment failure, leading to further expensive and potentially disfiguring surgery, and a change in antibiotic regimens or a prolongation of their use. In the two cases we describe, involving treatment of M. ulcerans infections in patients from an endemic area in the Bellarine Peninsula of south-eastern Australia,7 initial improvement during antibiotic therapy was followed by a paradoxical worsening in the clinical appearance. This was first interpreted as treatment failure, but we believe it was subsequently shown to result from an immune-mediated reaction to effective antibiotic treatment. We feel that in Patient 1, the lesion on the right knee represented a secondary M. ulcerans infection that was present at the time the lower right leg lesion was treated. It showed initial improvement with antibiotic therapy, but there was subsequent clinical deterioration consistent with a paradoxical reaction to mycobacterial antigens at the site. Likewise, in Patient 2, the clinical postoperative deterioration at the wound margins after initial improvement in an area of incomplete excision of the mycobacterial infection represented a paradoxical reaction to remaining mycobacterial antigens. To our knowledge, these are the first clinical case reports describing paradoxical reactions during the treatment of M. ulcerans. There is published histological evidence to support M. ulcerans-associated paradoxical reactions in patients being treated with antibiotics. Antibiotic therapy for M. ulcerans has been shown to lead to an apparent reversal of the immune-tolerant state of active M. ulcerans infection, with phagocytosis of mycobacteria and a rapid onset of local cellular immune responses.1 These responses are characterised by the formation of epithelioid granuloma with multinucleated giant cells and large clusters of lymphocytes. It is likely that antibiotics facilitate this immune reaction by reducing the production of the immuno-inhibitory exotoxin mycolactone,1 and also by liberating mycobacterial antigens from dead organisms. The evidence for a paradoxical reaction in our cases included: (i) persisting M. ulcerans organisms in affected tissue after the initial surgery; (ii) an initial clinical improvement in the M. ulcerans lesions during antibiotic therapy, followed by significant clinical deterioration 1–2 months after antibiotic therapy was commenced; (iii) negative cultures from aspirates and excised tissue, suggesting that remaining mycobacteria were not alive as would be expected in a lesion that was worsening as a result of uncontrolled infection; (iv) the lack of mycobacteria seen on microscopy of the excised tissue, compared with active lesions that usually show large numbers of extracellular mycobacteria;4 and (v) significant inflammatory reactions evident on histopathological examination of excised tissue, in contrast to what was observed in the initial active lesions, and consistent with recent descriptions of immune responses in successfully treated M. ulcerans infections.1 Thus, we propose that rather than progression of the lesions because of failure of antibiotic treatment, these cases represent an adverse consequence of effective antibiotic treatment. By applying lessons learnt from the management of immune-mediated reactions to infections with Mycobacterium tuberculosis,2 the recognition of paradoxical reactions during treatment of M. ulcerans infections might significantly influence the management of these infections. First, rather than ceasing the antibiotic therapy or changing the regimen, we advocate that therapy be continued, and that it not be changed unless there is evidence of antibiotic failure on histopathological examination or culture. Further, prolongation of the intended duration of antibiotic therapy is probably not required. Second, it may be possible that repeated needle aspiration for fluctuant lesions, as we described in Patient 1, may be effective in settling the lesion. This has been shown for lesions caused by M. tuberculosis,11 and would avoid further surgery, which, in Patient 1, included costly and disfiguring skin grafts. Finally, adjunctive corticosteroid therapy may help to settle the lesion and obviate the need for, or reduce the extent of, surgical intervention.12 We feel that the descriptions of these cases are important, as they can alert clinicians to the possibility of paradoxical reactions occurring during antibiotic treatment for M. ulcerans. We recommend that when initial improvement on antibiotic treatment is followed by clinical deterioration of lesion, clinicians perform histopathological examination and mycobacterial culture of involved tissue to assess the possibility of a paradoxical reaction. Lesions in Patient 1 First lesion, before antibiotic treatment showing: (A) a sparse acute inflammatory reaction around necrotic fat and subcutaneous tissue (haematoxylin and eosin stain; original magnification, ×100 ; and (B) high numbers of extracellular acid-fast bacilli (pink) on Wade–Fite stain (original magnification, × 400). Second lesion after 11 weeks of antibiotic treatment showing: (C) a dense inflammatory reaction including multinucleated giant cells (haematoxylin and eosin stain; original magnification, ×100; and (D) only one small cluster of extracellular acid-fast bacilli on Wade–Fite stain (original magnification, × 400).

Daniel P O’Brien MB BS, FRACP · Michael E Robson MB BS, FRCPA · Peter P Callan MB BS, FRACS · Anthony H McDonald MB BS, FRACS

Clinical record In 2008, a 42-year-old man with spina bifida, and an ileal conduit since childhood, presented to our emergency department (ED) with right-sided flank pain. He had experienced episodes of stone formation throughout his adult life, most recently in 2003 when an obstructing right renal pelvic stone was treated at another hospital with a percutaneous nephrostomy and antegrade stent. He failed to attend follow-up appointments, and the stent remained in situ. In the 3 years before he presented to our hospital, he was treated at different EDs for acute pyelonephritis, and on all occasions neither the presence nor significance of the retained stent was recognised. X-rays of the kidneys, ureters and bladder obtained on the patient’s admission to our ED confirmed the presence of the retained stent, as well as showing large encrustations associated with proximal and distal coils (Figure, A). Computed tomography (CT) demonstrated marked hydronephrosis with significant cortical thinning, consistent with longstanding obstruction (Figure, B). Subsequent mercaptoacetyltriglycine renography confirmed minimal residual function of the right kidney. A right nephroureterectomy was planned, but 2 weeks before surgery the patient re-presented with recurrent fevers, anorexia and weight loss. Pyonephrosis was suspected, and a nephrostomy was placed percutaneously, which drained frank pus. Repeated cross-sectional imaging showed marked retroperitoneal lymphadenopathy, which was presumed reactive because of its rapid onset. The sepsis resolved with drainage and broad-spectrum antibiotics, and we performed a difficult right nephrectomy at 6 weeks. Macroscopic examination of the specimen revealed an end-stage hydronephrotic kidney with an extensive soft-tissue mass involving the renal pelvis and entire length of the ureter (Figure, C). Microscopic examination showed a moderately differentiated squamous cell carcinoma with widespread invasion through the renal substance and ureteric muscle into fat, extensive vascular invasion and widely positive margins. The patient had a prolonged postoperative stay in hospital because of local infection, but was discharged home in the third week. However, he re-presented within 2 weeks of discharge with recurrent fevers, cachexia and right upper-quadrant pain. Repeat CT imaging showed a rapid increase in the volume of retroperitoneal lymphadenopathy, as well as the appearance of multiple, low-density lesions within the liver. Image-guided biopsy of the largest of these lesions confirmed metastatic squamous cell carcinoma. Following extensive discussion with the medical oncology team, the patient was treated palliatively and died shortly thereafter. Stent placement is one of the most common procedures performed in urological practice, as a stand-alone procedure to relieve renal obstruction, or as an adjunct to an increasing array of complex endourological procedures.1 Although urological stents are well tolerated by most patients, stent-related complications are frequent and a common cause of patients re-presenting. The most common side effects are irritative voiding symptoms, suprapubic discomfort and haematuria, usually related to irritation from the bladder coil, or flank pain related to urinary reflux on micturition. Long-term stents, particularly those placed for the management of ureteric strictures or compression not amenable to reconstruction, are prone to encrustation, blocking and subsequent infection.2 The prospect of a “missed” stent is a constant source of anxiety to the practising urologist. Stents that have been inadvertently left in situ for many months act as niduses for stone formation, particularly at the proximal and distal coils, which may prevent easy stent removal. Encrustation increases stent fragility and may lead to its fragmentation, even during careful attempts at removal. Multiple procedures may be required to remove the stent completely. Encrustation may also impair urine drainage, resulting in unrecognised renal obstruction and silent kidney damage, necessitating nephrectomy. As in our patient, long-term obstruction may cause persistent infection and recurrent episodes of clinical pyelonephritis and subsequent pyonephrosis. From a biological viewpoint, it is not surprising that the combination of stent irritation and infection would lead eventually to malignant transformation,3 although to our knowledge this is the first reported case of ureteric carcinoma associated with a retained ureteric stent. Many strategies have been proposed to prevent the occurrence of “missed” stents. In current Australian practice, clinicians rely on a paper-based system that requires manual entry and interrogation to identify overdue stents, and in general this system operates efficiently. However, in a large tertiary hospital where health care is often delivered by a number of different visiting medical officers or junior medical staff, difficulties with a paper-based system may arise. In our experience, the main difficulty is capturing data in unusual circumstances; for example, a stent placed either out-of-hours or at the request of other services in non-urological theatres may not be entered into the system. Recently, a computerised system has been described that addresses this problem.4 However, it is yet to be seen if this can be successfully introduced into other institutions. Although computerisation of medical records may circumvent the potential morbidity of many missed stents, it is unlikely to have helped our patient. He was aware he had a stent in situ and was contacted many times to arrange to have it removed, but did not do so. However, all his ED presentations with acute pyelonephritis in the years before the stent’s removal were missed opportunities to reconnect him with the appropriate urological services. Expedient stent removal may have relieved him from recurrent infection and prevented the fatal squamous cell carcinoma. Lessons from practice Missed ureteric stents are a frequent source of morbidity, repeated procedures and occasional mortality. No stent should be placed without an appropriate removal plan. Retained stents can cause recurrent urinary tract infections, which are typically difficult to clear; occasionally, they cause flank pain, fevers and night sweats secondary to suppurative infection. Patients with urinary tract infection and a history of urological intervention, particularly for stone disease, need a plain x-ray of the abdomen. Identification on x-ray of a stent that has remained in situ for longer than 6 months (unless this was planned) should prompt urgent referral to an appropriate urology service for removal.

Peng-Kung Yang MB BCh, AO · Dinesh Agarwal FRACS(Urol) · Niall Corcoran PhD, AFRCSI

To the Editor: Hospitalisation rates for seasonal influenza are highest among young children and people aged over 65 years.1-3 Calculation of laboratory-confirmed infection rates is difficult because influenza testing is not consistently performed. Using diagnostic codes to identify hospitalisations for acute respiratory illness provides one measure of the relative burden of pandemic (H1N1) 2009 (pH1N1) virus infection compared with influenza virus infections in previous influenza seasons. On 26 May 2009, the first pH1N1 virus human infection in New South Wales was identified, and between June and August 2009, pH1N1 was the predominant circulating influenza virus strain (found in 15%–82% of influenza A-positive specimens).4 In July 2009, the Hunter New England Area Health Service (HNEAHS) (population, 866 000) in NSW established population-based surveillance for hospitalisations for acute respiratory illness at all 35 HNE public hospitals admitting patients with respiratory illness. Data on hospitalisations coded with eight International Classification of Diseases (10th revision) codes (Box 1) were analysed by age group and year. Data for 2007 and 2008 (relatively severe and relatively mild influenza seasons, respectively)5 were used for comparison. Monthly hospitalisation rates for acute respiratory illness were calculated for 1 January 2007 to 31 August 2009. Over the period June to August in 2007 and 2008, 1736 and 1267 hospitalisations for acute respiratory illness occurred, respectively, and monthly hospitalisation rates peaked during August in both years (859 [9.7/10 000 persons] in 2007 and 517 [5.8/10 000 persons] in 2008). The highest hospitalisation rates occurred in children aged 0–4 years (113 [20.6/10 000 persons] in 2007 and 37 [8.9/10 000 persons] in 2008) and in people aged ≥ 62 years (276 [16.3/10 000 persons] in 2007 and 212 [12.1/10 000 persons] in 2008). In 2009, over the same 3-month period (June to August), there were 2378 hospitalisations for acute respiratory illness, with monthly hospitalisation rates peaking in July (1029 [11.4/10 000 persons]). Between May 2009 (before pH1N1 circulation) and July 2009, the monthly hospitalisation rate for acute respiratory illness in the HNEAHS increased by 260% (from 385 [4.3/10 000 persons] to 1029 [11.4/10 000 persons]). During the same period, age-specific hospitalisation rates increased more than threefold among children aged 0–4 years (from 31 [5.5/10 000 persons] to 101 [17.9/10 000 persons]) and 5–16 years (from 36 [2.5/10 000 persons] to 140 [9.8/10 000 persons]), and more than sixfold among people aged 17–31 years (from 43 [2.6/10 000 persons] to 281 [16.9/10 000 persons]) (Box 2). In July 2009, age-specific hospitalisation rates among people aged 5–61 years exceeded respective peak age-specific hospitalisation rates for 2007, while hospitalisation rates among children aged 0–4 years and people aged ≥ 62 years remained below 2007 peak rates for their respective age groups. Although our analysis calculated hospitalisation rates for various types of respiratory illness (including infections with non-influenza viruses) and may be affected by changes in health care-seeking behaviour and coding practices, comparison over multiple seasons suggests several unique features of the 2009 influenza season in the HNE region. Compared with 2007 and 2008, the HNEAHS experienced a rapid, early increase in hospitalisations for acute respiratory illness, coinciding with the emergence of pH1N1. Furthermore, a disproportionate burden of hospitalisations occurred among people aged 5–61 years (particularly those aged 17–31 years), with a relatively lower burden among those aged ≥ 62 years. Ongoing surveillance will determine whether these age-specific trends continue in the 2010 influenza season. 1 Emergency department ICD-10 separation codes used for acute respiratory illness hospitalisation surveillance Code Disease J11 Influenza, virus not identified J11.1 Influenza with other respiratory manifestations, virus not identified J11.8 Influenza with other manifestations, virus not identified J12.9 Viral pneumonia, unspecified J15.9 Bacterial pneumonia, unspecified J18.9 Pneumonia, unspecified J22 Unspecified acute lower respiratory infection J96.9 Respiratory failure, unspecified ICD-10 = International Classification of Diseases (10th revision). 2 Monthly hospitalisation rates for acute respiratory illness in the Hunter New England Area Health Service region, May–August 2009, compared with peak monthly rates in 2007 and 2008* * Hospitalisation rates are per 10 000 residents of the Hunter New England Area Health Service region.

Fatimah S Dawood · Craig B Dalton · David N Durrheim · Kirsty G Hope

To the Editor: Bronchiolitis, most often associated with respiratory syncytial virus (RSV), is a major cause of hospitalisation in young children. Those with chronic lung and congenital heart disease (the latter affecting about 192 births annually in Western Australia) are at particularly high risk.2 Immunoprophylaxis with the RSV monoclonal antibody palivizumab is effective in reducing severe RSV-related hospitalisations, and monthly immunoprophylaxis is recommended in high-risk children.2,3 Monthly immunoprophylaxis is costly; therefore, the most cost-effective schedule follows the times of peak RSV activity4 — usually the winter months, May to October. Using the Western Australian Data Linkage System,5 we investigated the seasonality of bronchiolitis hospitalisations (International Classification of Diseases-10 code J21) from 1996 to 2005 as a proxy for RSV-related illness. Data specifically for RSV-related illness were considered unreliable because some children may not have been tested for RSV, test results may not have been documented on hospital discharge notes, or RSV immunofluorescence tests may have given false negative results. Furthermore, RSV codes (B97.4, J12.1, J20.5, J21.0) were not used by hospitals in WA until July 1999. We identified 11 988 hospitalisations for bronchiolitis throughout WA among 245 249 births. Most bronchiolitis admissions (81%) were in children younger than 12 months. In the Perth metropolitan region, there was a clear winter seasonal pattern, with hospitalisations peaking in July. However, in the Kimberley region in northern WA, there was a sustained bimodal seasonality, with a peak in April and second peak in August (Box). Moreover, only 51.5% (469) of bronchiolitis admissions in the Kimberley and 61.5% (444) in the Pilbara–Gascoyne (located in mid-north WA) occurred between May and October, as opposed to 84.3% (6354) in the metropolitan region. These data support an earlier implementation and longer dosing schedule with palivizumab for high-risk children in the Kimberley and Pilbara–Gascoyne than for those in Perth. Our study has some limitations. Not all bronchiolitis hospitalisations may be caused by RSV. However, when we investigated only those hospitalisations with a specific RSV code, the monthly distribution showed a similar pattern. Additionally, timing of RSV activity, and therefore bronchiolitis, may vary from year to year. Although the numbers were too small to allow separate analysis by calendar year, bronchiolitis hospitalisations in the Kimberley showed extended seasons in 8 of the 10 years. Our findings support the need for each jurisdiction to know its seasonal pattern of bronchiolitis and RSV hospitalisations, and to implement recommended palivizumab schedules accordingly. Such use of extended prophylactic regimens may well require its cost-effectiveness to be reconsidered. Our analysis highlights the relevance of population-based data linkage studies to clinical care policy. Monthly distribution of bronchiolitis hospitalisations by region of child’s birth, 1996–2005

Hannah C Moore · Anthony D Keil · Peter C Richmond · Deborah Lehmann

To the Editor: In 2008, considerable publicity was given to the diagnosis and treatment of prostate cancer in two Australian celebrities: retired Australian Football League player Sam Newman and radio announcer Alan Jones. Newman’s cancer was reported on 5–9 March 2008, culminating in a 12-minute item on the high-rating Australian television program 60 Minutes, when Newman said, “Be tested and enjoy life”. Jones’s announcement of his forthcoming surgery was reported on 3–4 July 2008, and his recovery on 16–27 July. We investigated whether this publicity was associated with changes in the rate of prostate specific antigen (PSA) testing. We used Medicare Australia data on claims for Medicare Benefits Schedule item 66655 (which allows “one annual PSA test for an individual without prior prostate disease”) to determine the mean number of PSA tests and age-standardised testing rate between January 2002 and March 2009. We fitted a linear regression model to the log of the age-standardised rates, modelling secular trends using natural splines with two degrees of freedom (splines were piecewise cubic within the data range and otherwise linear), with indicators set for the average effect of the second, third and fourth quarters and an indicator for the second quarter of 2008. We calculated predicted values and prediction intervals (which take into account both uncertainty in the predicted mean and individual variation), excluding observed data for the second quarter of 2008 (Box). The mean monthly number of PSA tests was 72 064 in the 12 months before April 2008, increasing to 107 633 in April 2008, and 90 813 in July 2008. The seasonally adjusted age-standardised rate of PSA tests rose 17% above the secular trend in the second quarter of 2008 (95% CI, 8%–27%), with the observed data point falling outside the prediction interval (Box). This represented an additional 39 000 PSA tests during the second quarter of 2008. These data show that prostate cancer screening increased significantly in the quarter after media coverage of Newman’s prostate cancer diagnosis. Screening seemed to have returned to the expected seasonal rate by the time of Jones’s diagnosis, in the third quarter of 2008. The impact of celebrity cancer diagnoses on population screening has been demonstrated previously, most recently by an increase in breast cancer screening following news of pop singer Kylie Minogue’s breast cancer diagnosis in 2005.2 In a survey of US men, almost a third stated they would be more likely to have a PSA test after hearing celebrities endorse prostate cancer screening.3 In addition, coverage of melanoma by 60 Minutes in 1987 was followed by a 167% increase in melanoma detection in the subsequent 3 months. Whether the additional 39 000 PSA tests performed in the second quarter of 2008 result in a surge in diagnoses of prostate cancer remains to be seen. Despite continuing uncertainty about the benefits of PSA testing, but unequivocal evidence of harms,,6 Australian men’s willingness to be screened for prostate cancer appears to have been boosted by this celebrity endorsement. Age-standardised* prostate-specific antigen testing rates in Australia (assessed quarterly) Prostate-specific antigen (PSA) testing rates showed a consistent seasonal pattern, with the highest rates in the third quarter (July–September) for all years except 2008, when they were highest in the second quarter. * Standardised to Australian 2001 population.

David P Smith · Mark S Clements · Melanie A Wakefield · Simon Chapman

To the Editor: The recent article by Lowthian and colleagues raises some important concerns regarding current management of warfarin therapy in Australia, especially the provision of quality warfarin education.1 While the study focused on the uncertainty surrounding who is responsible for this task, additional barriers to providing warfarin education include limited access to suitable resources and a tendency to rely on a single verbal counselling session and/or the supply of written material, often just before discharge from hospital.2 As Lowthian et al note, it is plausible that warfarin education was provided to the patients interviewed; it may simply have been inadequate to meet their needs or delivered at the wrong time or place. It is not always feasible for health care providers to reliably provide the necessary education in busy health care settings (eg, general practitioners when prescribing warfarin, pharmacists when supplying it). The authors note a potential role for practice nurses in providing this education; we would also like to highlight the role of accredited pharmacists, who can visit patients in their homes and provide targeted medication-related education. An annual Home Medicines Review can be provided for patients taking high-risk medications such as warfarin.3 Under the Fourth Community Pharmacy Agreement Research and Development Program, the Pharmacy Guild of Australia has funded two projects that are attempting to meet the education needs of patients taking warfarin. One project is trialling a comprehensive postdischarge service involving a series of follow-up home visits by trained accredited pharmacists, to provide not only warfarin education but also point-of-care international normalised ratio monitoring, in liaison with the patients’ GPs. The other project is piloting a process whereby community pharmacists can identify potential candidates for patient self-monitoring of warfarin and, with GP collaboration, organise suitable training, with ongoing support from the pharmacist and GP. Patient self-monitoring, although not widely practised in Australia, has been shown to provide the best clinical outcomes for suitable candidates.4 An important component of these two projects is a website, launched in late 2008, containing a range of free, downloadable educational resources for both consumers taking warfarin and health care professionals responsible for its management (http://www.anticoagulation.com.au). Education is crucial in achieving optimal health outcomes for patients taking warfarin, and health care professionals should cooperate to ensure their patients are well educated. This should involve regular reinforcement of consistent messages, and can also involve better use of existing services and educational tools.

Luke R E Bereznicki · Leanne Stafford · Ella C Jeffrey · Gregory M Peterson · Shane L Jackson

In reply: Bereznicki and colleagues have reinforced the importance of patient education in optimising warfarin safety, while highlighting the need for role clarification in its provision. We applaud the Pharmacy Guild of Australia’s sponsorship of research projects trialling different models of service delivery, such as the coordination of postdischarge warfarin home care by pharmacists and support of patient self-monitoring programs, where appropriate. The success of such care models will be enhanced by a collaborative partnership between the patient and all members of the warfarin care team.1 In addition, appraisal of patient suitability for programs such as patient self-monitoring requires systematic and regular evaluation of cognitive function, compliance and health literacy, to reduce the likelihood of adverse events.2-4 Likewise, ongoing education with resources tailored to individual patients’ capabilities will optimise patient safety.5

Judy A Lowthian · Basia O Diug · Sue M Evans · Ellen L Maxwell · Alison M Street · Leon Piterman · John J McNeil

To the Editor: Lowthian and colleagues ask who is responsible for the care of patients treated with warfarin therapy.1 In Melbourne, it seems that this devolves mainly upon the pathology laboratory, whereas in other states, general practitioners manage care for their own patients, in my own experience. Where management of warfarin dosing, based on the international normalised ratio (INR) result, is performed by the laboratory, this is done as a courtesy to GPs. This practice possibly evolved from competition between private laboratories and, as such, may have been intended to induce other pathology requests to the service provider. Larger metropolitan private pathology services may have sufficient pathologists with haematology training to provide warfarin dosing to patients, but this may not always apply in smaller laboratories. In some laboratories, warfarin dosing may be provided to patients by scientific staff. Although warfarin therapy can sometimes be challenging, its difficulties are not usually insurmountable. Problems for pathologists arise because they are expected to give a warfarin dose by telephone to a patient they do not know and have never seen. The patient’s phone number may be not supplied or incomplete, and the call may not be answered. If answered, a brief history of previous INR results, dosages and test intervals may or may not be elicited from a person who may have poor English, who may be the patient, a relative, friend or neighbour; or a message may have to be left. If the message is received, it may not be acted on, depending on memory, understanding or level of compliance. If the message is not received, the patient and the patient’s GP may be unreasonably irate, even though multiple attempts to contact the patient may have been made. It is not hard to understand why some GPs prefer to pass this often frustrating and time-consuming aspect of treatment to pathologists — who may also be pressed for time. Problems are further compounded if warfarin dosing devolves to pathology laboratory scientists, which may be required by their employer. Scientists would be, in effect, performing drug dosing without medical training or medical registration and may be exposing themselves to litigation risk, without carrying medical indemnity. In other Australian states, it seems that GPs do provide treatment and dosing of warfarin for their own patients. In my view, this is the safest and most satisfactory outcome for patients, pathologists and scientists. With the projected advent of point-of-care testing with reliable INR results2 and new anticoagulant alternatives1 that would enable easier management of anticoagulant therapy by GPs, this whole issue could potentially be resolved.

John C Roberts

To the Editor: I appreciated Brukner’s perspective on treatment of venous thromboembolism (VTE),1 but I do feel some additional considerations and clarifications are in order. Quotes from Kearon2 and Kearon and colleagues3 about the duration of therapy are missing an important caveat. The suggestion for longer duration and possibly “indefinite” anticoagulant therapy after a first deep vein thrombosis or pulmonary embolism is in reference to unprovoked VTE. Brukner1 mentions a plane flight from China to Australia 3 days before he experienced a symptomatic pulmonary embolism. According to guidelines issued by the American College of Chest Physicians, such a flight (although I cannot comment with certainty on its duration) is likely to represent a reversible minor risk factor for VTE — “prolonged travel (eg, > 8 h)”.3 Indeed, Kearon2 and the authors of a related research article to which he refers4 make the important distinction between provoked and unprovoked VTE. Kearon comments: For patients with a minor reversible risk factor, the risk of recurrence is about 5% in the first year after stopping anticoagulant therapy. This is considered low enough to justify stopping anticoagulant therapy at the end of 3 months.2 Additional factors and preferences are also important when considering prolonged anticoagulant therapy for individual patients. For instance, I can empathise with the 25-year-old who wants to discontinue warfarin therapy after 6 months following a first unprovoked VTE — another 50 years of warfarin therapy might seem a disheartening burden. And certainly we must take into account other variables that may increase a patient’s risk of bleeding complications while receiving warfarin therapy, such as older age, the presence of other acute or chronic illnesses and the use of other medications, particularly antiplatelet therapy.3 For someone such as Brukner,1 who claims that his anxiety about a recurrence of VTE is reduced by staying on warfarin therapy, I would probably say, “That’s OK by me, as long as you are aware of the risks and implications of provoked and unprovoked VTE”. For other patients with unprovoked VTE who may not want to continue indefinite anticoagulant therapy, there are other management options worth discussing. First, there is the possibility of further risk stratification for VTE recurrence by testing D-dimer levels. This strategy is receiving considerable study and validation as a useful tool for predicting VTE recurrence.5,6 Second, for patients who refuse to continue warfarin therapy but would consider other therapies for reducing their risk of having a recurrence of VTE, I would suggest taking a daily low dose of vitamin E, which has shown some benefit in reducing VTE.7 Finally, the ASPIRE (Aspirin to Prevent Recurrent Venous Thromboembolism) Trial, which is currently underway, should provide a definitive answer as to whether aspirin is a safe and effective option for secondary VTE prevention. If the trial supports the use of aspirin for this purpose, it would offer another VTE risk-reduction option for those who prefer not to take warfarin indefinitely.8

James A Fink

To the Editor: Brukner’s personal perspective in a recent issue of the Journal highlights the inherent difficulty of managing patients taking warfarin.1 Although Brukner advocates life-long warfarin therapy for patients who have experienced a pulmonary embolism, we believe few clinicians would be willing to expose their patients to the increased risk of haemorrhage associated with long-term warfarin therapy, especially if a transient risk factor for venous thromboembolism (VTE) existed (such as frequent air travel, in Brukner’s case). There is an abundance of conjecture regarding the appropriate duration of warfarin therapy for VTE, with guidelines and clinical intuition often differing. But it is possible that, in the future, decisions about the appropriate duration of warfarin therapy may be guided by the use of pharmacogenetics. Pharmacogenetics gives clinicians an insight into how a patient’s genetic profile affects his or her ability to metabolise drugs, thereby allowing doctors to better tailor the dose and duration of the patient’s medications. In the case of warfarin, metabolism of S-warfarin (the more potent enantiomer in the racemic warfarin mixture) occurs via the cytochrome P450 system, specifically enzyme CYP2C9.2 Studies have shown that patients who metabolise warfarin normally are homozygous for the wild-type allele CYP2C9*1, whereas patients with polymorphisms in the CYP2C9 allele have reduced warfarin metabolism and increased risk of bleeding.3 The anticoagulation effect of warfarin actually occurs via inhibition of the C1 subunit of the vitamin K 2,3-epoxide reductase complex (VKORC1).4 Numerous polymorphisms have been identified in VKORC1, and it is speculated that VKORC1 polymorphisms alone may account for a significant proportion of response variability to warfarin.4 Validated algorithms have been developed to combine information on a patient’s CYP2C9 and VKORC1 genotypes with factors such as age and body surface area to identify an appropriate warfarin regimen.5 Although the pharmacogenetic information required to employ this algorithm has not been assessed for cost-effectiveness, it is quite possible that clinicians will be able to use such pharmacogenetic information to their advantage in the future. This would allow doctors to identify with greater precision which patients are likely to benefit from warfarin (and how much is required, for how long), rather than relying on equivocal evidence and clinical intuition alone.

Amit K Verma · Ajai K Verma

To the Editor: In their national analysis, Robson and colleagues found less favourable outcomes among term singleton babies born in public hospitals than in private hospitals.1 Most health services research is non-randomised, and it is unrealistic to expect studies such as this to be as internally valid as a randomised controlled trial.2 As noted by others,3,4 in the absence of randomisation, it is difficult to untangle the myriad differences between mothers, babies, and the care provided in private and public hospitals (ie, the results might be subject to confounding). Robson et al statistically accounted for the potential confounding effect of maternal smoking (although these data were only available for about half the mothers), age, Indigenous status, parity, diabetes, hypertension, rurality and method of birth. We replicated their analysis using the Queensland Perinatal Data Collection (July 2005 – December 2007), which included virtually complete data on maternal smoking. Our analysis of 124 300 term singleton babies gave an adjusted odds ratio (AOR) for perinatal mortality of 2.0 (95% CI, 1.4–2.7), which is similar to that reported by Robson et al. Using more detailed data from the Queensland dataset, we statistically adjusted for other potential confounders — including pre-existing and gestational diabetes, pre-existing and pregnancy-induced hypertension, pre-eclampsia, eclampsia, antepartum haemorrhage, anaemia, depression, urinary tract infection, low birthweight (< 2500 g), socioeconomic status (based on area of usual residence5), alcohol and drug misuse, and artificial reproductive technology — and obtained an AOR of 2.1 (95% CI, 1.5–2.9). We are not implying that adding more and more variables to a statistical model is an appropriate way to account for confounding. Our aim is simply to show that Robson et al’s result is robust to statistical adjustment using the available data; this is not the same as saying the analysis is robust to confounding. We found that the higher perinatal mortality in public hospitals was greater for neonatal deaths (AOR, 3.1; 95% CI, 1.8–5.6) than for stillbirths (AOR, 1.6; 95% CI, 1.0–2.4). Excluding lethal congenital anomalies4 did not materially change the result (AOR, 1.9; 95% CI, 1.3–2.8). We also stratified our analysis by level of hospital — tertiary referral (neonatal intensive care unit), base (special care nursery), and community — and obtained a similar twofold mortality excess in each stratum. Although perinatal mortality is uncommon among term singleton babies (1 in 1000 in private hospitals versus 2 in 1000 in public hospitals), any excess risk should be investigated and the reasons for it understood. The results from Robson et al’s article might be due to confounding, but they should not be dismissed and should be investigated with more detailed clinical data. Even if all the excess risk is due to confounding, explicit confirmation of this would be extremely useful. To this end, the Statewide Maternity and Neonatal Clinical Network in Queensland Health will undertake clinical review and classification of term singleton deaths according to national guidelines6 and collaborate with the Australian Maternity Outcomes Surveillance System (AMOSS)7 to enhance prospective monitoring of late gestation perinatal deaths nationally.

Michael D Coory · Guan T Koh · Vicki Flenady · Maarten Kamp

To the Editor: Robson and colleagues found higher crude odds of perinatal death in public hospitals — an unsurprising finding, given the maternal demographics in the public system.1 However, after taking into account known risk factors for poor perinatal outcome by “adjusting for the potentially confounding variables available in the NPDC [National Perinatal Data Collection]”, the authors found that the odds ratio actually went up — implying that the pregnancies of mothers in the private system are higher risk. This is implausible. There are a number of problems with the analysis. The possibility that potentially important maternal information was not included has been acknowledged.1,2 Of greater concern is the omission of a history of low birthweight from the regression model. Since intrauterine growth retardation is a very strong risk factor for perinatal death,3 and since the rate of low birthweight in the public hospitals was double that in the private hospitals, this omission is puzzling. Furthermore, while the authors’ stated aim was to assess the effect of the private model of obstetrician-led interventional care on perinatal outcomes, they included the method of birth and hospital type as independent explanatory variables. Since the interventional nature of obstetric care is, as acknowledged by the authors, a key component of the model of care provided in a private hospital, adjusting for this variable will lessen the usefulness of the study in assessing the impact of private hospital care on perinatal outcomes. Put another way, in deciding what is best for her baby, a mother who is considering giving birth in the private system cannot cherry-pick only the non-interventional side of the obstetrician-led model of care — she must adopt the entire package. Including method of birth as a separate explanatory variable artificially inflates the apparent “riskiness” of the pregnancies of mothers presenting to private hospitals to give birth. These mothers had a 75% increased incidence of caesarean section; however, most of these procedures would be elective rather than emergency. Since this distinction was not made, the women in private hospitals appear high risk despite having had a caesarean section for a low-risk pregnancy. This will have the effect of making perinatal outcomes in private hospitals appear more favourable than they actually are. As currently analysed, the data are of little value to prospective mums and dads in making the first, and one of the most emotive, of the many decisions they need to make as parents.

Daniel C Chambers

To the Editor: Of the many problems with the study by Robson and colleagues,1 the one that concerns us most is the outcome of perinatal death. The headline that this is twice as high in public hospitals has the potential to scare those who have no choice about where they give birth. Both the public and the medical community have a right to expect that this outcome is rigorously and accurately represented. We do not believe this to be the case. The perinatal death rate is made up of stillbirths and neonatal deaths in the first 28 days of life. Stillbirths will comprise 70% of all perinatal deaths, and more than 90% of stillbirths after 37 weeks’ gestation will occur before the onset of labour.2,3 It cannot be excluded that this relates to model of care but, because less than 10% of these stillbirths will have occurred during delivery, it is most certainly not related to the type of birth hospital or the interventions performed during labour. Most likely, it reflects differences in intrinsic risk that have not been controlled for by Robson et al.1 The neonatal death component of this statistic is probably confounded by ascertainment bias. Most neonatal deaths after 37 weeks’ gestation occur for two reasons: intrapartum hypoxia–ischaemia and severe congenital abnormalities. When the latter are diagnosed antenatally, the mothers will often be transferred to tertiary public hospitals for a second opinion and further management. Babies with undiagnosed lethal abnormalities or severe intrapartum hypoxia will invariably be transferred postnatally to a tertiary public hospital neonatal intensive care unit, where death often occurs after withdrawal of intensive care. The midwives data collection form is filled in at the birth hospital, and the baby is categorised as “discharged”, “transferred” or “died”. The 2006 national perinatal data collection report specifically cautions: Ascertainment of neonatal deaths within 28 days of birth is likely to be incomplete. In particular, deaths occurring among babies transferred to another hospital, readmitted to hospital or dying at home may not be known to midwives who collect these data or staff who compile state and territory data.2 Thus, it is unlikely that the difference in perinatal mortality described by Robson et al1 has anything to do with the birth hospital. To represent it as such in the public arena is irresponsible. Further, for the MJA to misrepresent “perinatal mortality” as “neonatal mortality” in the media release about this article defies belief.

Nick Evans · Girvan Malcolm · Adrienne Gordon

To the Editor: The study by Robson and colleagues1 predictably produced alarming media headlines. However, we feel the study contains potential inaccuracies that seriously undermine the conclusion that the baby toll is lower in private hospitals. Did the authors ascertain the true impact of fetal abnormality or conditions requiring transfer to tertiary care? Women with threatened preterm labour often transfer to the public system and subsequently remain under the care of public high-risk teams. Babies with a known congenital anomaly detected antenatally by private obstetricians may be similarly transferred. This highest level of care is only available in public hospitals, usually those with dedicated subspecialist services in maternal–fetal medicine, neonatology or neonatal surgery. When babies who have been transferred from private hospitals to the public neonatal intensive care system subsequently die within 28 days of birth, this may be recorded as a public hospital death. The authors stated that the “major adverse outcome associated with social disadvantage is low birthweight” but that assessment of the effect of social disadvantage was beyond the scope of their study. Not accounting for the effect of low birthweight is unacceptable. The National Perinatal Data Collection records birthweight accurately and is easily used to remove the bias of low birthweight. An internationally accepted indicator of optimal perineal outcome is the rate of intact perineum. This is known to be lower in private hospitals but was curiously not reported. Further, a prospective data audit in a tertiary hospital revealed that where episiotomy extends to third- or fourth-degree tear, this is only reported as episiotomy.2 Thus, with twice the rate of episiotomy in private hospitals,3 and its association with severe perineal trauma, this outcome could be seriously under-reported in Robson et al’s study. The authors identify the significantly higher rate of caesarean sections in private hospitals as one of the measurable benefits of this model of care and dismiss any concerns as “orthodoxy”. They have overlooked the significant morbidity and mortality among term neonates associated with the rise in caesarean rates, both elective and following labour. Research using detailed Australian and New Zealand Neonatal Network data to ascertain admission rates of babies of ‘‘low-risk’’ women to neonatal intensive care units and special care nurseries not only found higher rates of admission across each gestational age group after elective caesarean section but also reported the death of two infants.4 Such morbidity and mortality is arguably the most important differential of care experienced by women who give birth in private or public hospitals.

Sally K Tracy · Alec W Welsh · Hannah G Dahlen · Mark B Tracy

To the Editor: More than 30 years ago, I was employed by the Commonwealth Government’s Maternal Mortality Committee to identify and evaluate factors contributing to maternal and infant mortality among Aboriginal Queenslanders. At that time, government policy was to transfer all pregnant Aboriginal women from their rural communities or missions to Cairns Base Hospital at 32 weeks’ gestation until 7–10 days after birth. Findings I presented in a report to Queensland Health in 19771 and at the Australian College of Paediatrics Annual Meeting in 19792 included: Babies of women who were compulsorily transferred at 32 weeks’ gestation to Cairns Hospital had lower neonatal death rates. It was assumed that — as Aboriginal women had unreliable gestational age assessments, antenatal care was irregular, and birthweights were lower than for other races3 — the risk of premature deliveries could be avoided by early transfer. There was a lower rate of breastfeeding among mothers transferred to Cairns, largely because if they opted to bottle-feed they could return home after 3–4 days (rather than waiting 7–10 days in Cairns to ensure breastfeeding was established).1 Growth failure was common in the month after weaning.4 Bottle-fed babies experienced slower weight gain and higher rates of illness.5 Suboptimal growth in bottle-fed babies during the early postnatal months predisposed babies to poor growth patterns during infancy6 and increased death rates.7 Women returning to their communities took with them infections acquired during the hospital stay in Cairns. Separation anxiety or maternal deprivation was common among children left in their communities. There was decreased family bonding (eg, between the father and the new child) and sibling resentment at maternal separation. There was unquantifiable resentment at having babies born away from the ancestral lands. Women delayed admitting their pregnancies in an attempt to remain in their communities, resulting in fewer antenatal visits. The antenatal transfer policy has been in effect for 30 years, despite conflict between those who were predominantly concerned with maternal and perinatal mortality (who favoured compulsory delivery in Cairns Base Hospital), and those (myself included) who were concerned about the effects on children’s growth and development. During this time, I have observed weakening family and community bonds, increasing alcohol and substance misuse and sexual abuse, low school attendance, poor employment records and domestic violence. My studies of Aboriginal and non-Aboriginal children born in Cunnamulla in western Queensland followed the same cohort of children from birth8 for 20 years.9 The presence of a father who was employed at the time of the child’s birth acted as a role model for the future and was more effective than all other social interventions with respect to the child’s successful education or employment 20 years later, irrespective of race or subsequent social support or interventions offered to the child during school years.9,10 Arnold and colleagues’ recent article in the Journal records a situation almost unchanged from 30 years ago, with the exception that antenatal ultrasounds have allowed transfer to occur at 36 weeks’ instead of 32 weeks’ gestation.11 Enormous resources of goodwill, effort and money have been spent in these communities over 30 years, yet the family disruption, unemployment and abuse statistics remain at variance with the Queensland norm. Perhaps the time has come to allow low-risk births to occur in selected towns, where the mother can be surrounded by her friends and relations, and be in closer contact with her ancestral land. I endorse the article by Arnold et al and hope they are more successful in implementing change than I have been.

John W Cox

To the Editor: A letter by Scrimgeour1 in the 18 May 2009 issue of the Journal praised an earlier study by Andreasyan and Hoy2 for adding to the evidence that Indigenous people living in small communities (known as “outstations” or “homelands”) in very remote areas are healthier than those living in larger settlements. I believe this was an error. The study found that mortality was lower in both outer regional areas and very remote areas than in remote areas.2 But, unfortunately, this tells us nothing about outstations. The Accessibility/Remoteness Index of Australia (ARIA) classification used by the authors groups larger remote communities and their outstations together — categorising both as “very remote”. Scrimgeour is not alone in overstating the evidence for better health among Indigenous people living in smaller communities. The possible health benefits associated with living in outstations has become a major argument against the Australian Government’s plan to create 26 remote “hubs” that will receive improved services (to the likely detriment of smaller communities)3 and the related plan of the Northern Territory Government to develop 20 larger remote communities.4 For example, Tom Calma, Aboriginal and Torres Strait Islander Commissioner at the Australian Human Rights Commission, was reported as saying that there was “a strong body of research showing that people on homelands lived longer, healthier lives”.5 Calma seriously overstated the evidence we have to date, which consists of two studies from Utopia in central Australia and one study of land management practices in an Arnhem Land community.6-8 Although this research is encouraging, we are a long way from determining the causes of better health among sections of those two communities, and whether residence at outstations/homelands or land management practices are associated with better health in other communities as well. There are many reasons for supporting the growth of outstations, and health may be one of them, but it is crucial that those in the field of Indigenous health get this right. Rather than jumping the gun, we need more research into the effects of outstation life on health and wellbeing.

Emma E Kowal

To the Editor: In an article about Indigenous mortality in the Northern Territory, Andreasyan and Hoy1 concluded that Indigenous residents in very remote areas (VRAs) had a better health status than those in remote areas (RAs) and outer regional areas (ORAs). This result is inconsistent with previous reports and prompted us to examine the authors’ outcome. A central problem with the authors’ analysis lies in the identification of “usual residence” for death registration. The usual residence is defined by the Australian Bureau of Statistics as the dwelling at which a person spends or intends to spend 6 months or more in the year in which the question is asked.2 This definition limits its usefulness for the authors’ purpose, but is further compromised by the common practice by certifying doctors of simply using the last known address as a proxy for usual residence. In either case, the address recorded at death registration may differ from the location where a person lived for the majority of his or her life. The latter is the location more closely associated with health risks, particularly for chronic disease. As a test, we investigated changes of residence for all NT public hospital inpatients who died within a 7-year period by linking multiple hospitalisations between 1 January 2001 and 31 December 2007. We found that 26% of inpatients classified as residents of RAs at the time of death were previously usual residents of VRAs. This “unhealthy migrant” effect can be readily recognised as people relocate due to illness from VRAs, which have limited health services, to RAs or ORAs to access secondary and tertiary health care. The likelihood of inconsistent classification of usual residence in mortality data can also be tested demographically. Assuming the authors’ mortality ratios were correct for a stable population, we estimate that the Indigenous life expectancy at birth in VRAs would be 72.3 years, or 23 years longer than the life expectancy at birth in RAs (49.1 years). Such a large discrepancy is implausible. The age structure of a stable population is determined by fertility and mortality,3 and reported NT Indigenous fertility rates show a lack of substantial variation across regions.4 If the life expectancy at birth in VRAs was significantly longer than the life expectancy in RAs, VRAs would have about five times more elderly people (aged over 75 years) than the current estimates.5 The mobility of residence shown by hospital data and the absence of a substantial elderly population in VRAs suggest that the reported differential mortality rates between VRAs and RAs are the result of misidentification of “usual residence”.

Yuejen Zhao · Steve Guthridge · Shu Q Li · Christine Connors

In reply: We thank Zhao and colleagues for their interest in our study.1 The main issue they raise is misclassification of deaths by remoteness of residence. In our article, we acknowledged the role of migration to larger urban centres to access health services and raised the issue of unhealthy lifestyle and its flow-on effects on mortality. If we were to assume that 26% of deaths in hospital in remote areas were deaths of people who previously lived in very remote areas (as Zhao and colleagues suggest), regional variation in the disparity between Indigenous and total Australian all-cause mortality would narrow but would still remain. A re-analysis of our data based on this assumption1 shows that standardised mortality ratios in remote areas would drop from 875% (95% CI, 799%–956%) to 646% (95% CI, 582%–717%) in 1998–2000 and from 731% (95% CI, 665%–801%) to 540% (95% CI, 484%–601%) in 2001–2003. In very remote areas, the standardised mortality ratios would increase from 214% (95% CI, 193%–236%) to 281% (95% CI, 258%–306%) in 1998–2000 and from 208% (95% CI, 189%–228%) to 264% (95% CI, 242%–286%) in 2001–2003. Furthermore, in our article we stressed the importance of examining Indigenous migration to enable more accurate interpretation of our findings and called for future studies to “clarify the reasons for these differences in mortality by remoteness, with a particular focus on migration”. Our studies of Queensland data and national data (unpublished) have shown a similar pattern of higher Indigenous mortality in remote areas than in very remote areas, but the difference in mortality rates between these areas is highest in the Northern Territory. Thus, the phenomenon of the “methodological” error applies to all of these studies. We propose to undertake a prospective study of Indigenous mortality that will overcome some study design problems inherent in a cross-sectional study.

Karen Andreasyan · Wendy E Hoy

To the Editor: We commend the Indigenous Health issue of the Journal (18 May 2009). Its editorial emphasis — that partnerships with and continued leadership by Aboriginal and Torres Strait Islander peoples will be key to closing the gap between Indigenous and non-Indigenous Australians1 — is supported by preliminary, unpublished findings from our research into improving mainstream general practice care of Indigenous patients. Couzos and Thiele emphasised that closing the gap in health and life expectancy between Indigenous and non-Indigenous Australians depends on Aboriginal community controlled health services (ACCHSs).2 By virtue of their governance structure and focus, these services deliver culturally safe and appropriate primary health care to Indigenous Australians, while addressing issues of Indigenous autonomy and other social determinants of health.2 However, although not all general practices see Indigenous patients, 0.9% of general practice encounters (range, 0.7%–1.6%) are with Indigenous patients, equating to about one million consultations a year. Indigenous Australians present to general practitioners with essentially the same range of clinical conditions as do non-Indigenous Australians, although consultation rates for diabetes and circulatory conditions are higher for Indigenous patients.3 Most Indigenous Australians (76%) live in urban and regional areas, and are widely spread through the general population. They are likely to need mainstream services including general practice and primary care services, at least some of the time and for the foreseeable future. There is clearly a need for initiatives beyond support for ACCHSs, Indigenous workers and communities, to improve mainstream services for Indigenous Australians in a culturally sensitive and appropriate manner.4 Better sociocultural education for health care providers, trainees and students is required to close the gap that exists in mainstream understanding and acceptance of Indigenous cultures and aspirations. The Inala Indigenous Health Service in Brisbane is an example of a mainstream practice successfully developing into an accessible service.5 Our research aims to improve mainstream general practice care for Indigenous Australians with diabetes who live in urban areas of Victoria. As the following statement made by Indigenous participants in focus groups for our research indicated, health services must be patient-centred: We need to hold the health system — and that includes GPs — accountable for delivering help to Aboriginal people. The best one to do that is the consumer. Focus group participants also highlighted the importance of working together: I think we need to take some responsibility ourselves as (Indigenous) workers in organisations and go to these mainstream services. Whether it’s diabetes or drugs and alcohol, we need to say look, you get funded to look after everybody, and we want to come here and tell you how to look after our people when they come to your centres.

Siaw-Teng Liaw

In reply: It is unclear how many mainstream general practice consultations involve Aboriginal and Torres Strait Islander patients. Of 485 300 patient encounters attributed to general practices in the BEACH study (2003–2008), 7292 were with Indigenous patients, but 2906 of these encounters took place in Aboriginal community controlled health services (ACCHSs) rather than in general practices.1 If funding to close the gap in Aboriginal disadvantage is being channelled to general practice and the Divisions of General Practice (through recent measures of the Council of Australian Governments), then the Indigenous health outcomes of mainstream services must be carefully attributed.2 The ACCHS sector agrees there is a need to make general practices culturally secure for Indigenous Australians. For example, the Aboriginal Health Council of Western Australia has developed modules for cultural safety training, which are accredited by the Royal Australian College of General Practitioners for GPs’ professional development.3 The National Health and Hospitals Reform Commission report recommends that health services be required, by accreditation processes, to meet specific standards of cultural safety for Indigenous patients to ensure high-quality care.4 Within a quality assurance framework, systematic reforms such as these can potentially improve mainstream services, while supporting Indigenous workers who face unrealistic pressures to improve their local services. As Liaw points out, these initiatives are in addition to the vital role of ACCHSs in closing the health disparity gap.

Sophie Couzos · Dea D Thiele

To the Editor: Finally! An article in the Journal about health reform that carries no spin and decries further futile experimentation in management. Lewis and Leeder are to be congratulated on their insightful review.1 As they point out, social and environmental determinants of health are far more important to a community’s well-being. This was recognised intuitively as long ago as 1986, with the promulgation of the Ottawa charter,2 and its recommendation that health services be reoriented primarily toward promoting heath rather than delivering acute care per se. As Lewis and Leeder articulate, the evidence in favour of this line of thinking is actually quite potent.1 However, as they point out, the thing that surprises students and practitioners in public health is why the “bigger picture” has been so difficult to comprehend and act on. Rather than a need for the “stars to be aligned”, perhaps this is the time for stronger advocacy? And while we’re at it, evaluation tools for health promotion programs need to become more sophisticated if we’re going to convince our colleagues, politicians and the community that we’re spending their money wisely. The transformation that Lewis and Leeder recommend is likely generational in its span, but what better time to make a start?

George Larcos

Incorrect author affiliation: In the article “General Practice Super Clinics — how will they meet their educational objectives?” in the 5 October 2009 issue of the Journal (Med J Aust 2009; 191: 393-395), an incorrect author affiliation was printed. The correct author affiliations are included here.

Alistair W Vickery MB BS, FRACGP · Jennifer Dodd PhD, BASocSci(Hons) · Jon D Emery MB BCh, FRACGP, DPhil

Incorrect graph and wording: In “Avoidable hospitalisation in Aboriginal and non-Aboriginal people in the Northern Territory” in the 18 May 2009 issue of the Journal (Med J Aust 2009; 190: 532-536), there was an error in Box 4 (Li et al). In the panels headed “25–44 years” and “45 years and over”, the lines representing Aboriginal and non-Aboriginal rates were transposed. The correct version of Box 4 appears here. In addition, in the second paragraph of the results section, the wording was potentially misleading. The paragraph should have read: “Although total average avoidable hospitalisation rates were higher in Aboriginal than non-Aboriginal people in the NT, the largest differences were observed in the age groups 25–44 and 45–64 years (Box 1).” 4 Trends in age-adjusted, avoidable hospitalisation rates by Aboriginality and age group, Northern Territory, 1998–99 to 2005–06

Shu Q Li MPH, MB, BNursing · Natalie J Gray MIPH(Hons), MB BS(Hons), BSc/LLB(Hons) · Steve L Guthridge MB BS, MPH, FAFPHM · Sabine L M Pircher MPH, BNutrDiet

Ron Lucas (“Rowdy” to his mates) was one of the most outstanding infectious diseases physicians of his generation. He was a physician’s physician, and the person you would want caring for you if you were ill. Born in Ballarat on 13 August 1932, he was educated at Ballarat Grammar School, where he excelled at football and cricket and was school captain. He studied medicine at the University of Melbourne, graduating in 1956. After a brief period at Horsham Base Hospital, Ron joined the staff at Fairfield Infectious Diseases Hospital, where he remained until his retirement in the early 1990s. Ron’s career spanned a most exciting and eventful era, as the field of infectious diseases was transformed from a largely descriptive branch of medicine, with limited diagnostic tools and therapeutic options, to the science-based discipline of today. Empowered by Medical Superintendent John Forbes’s view that clinical practice would only progress if it was based on strong relevant research, Ron formed a partnership with the laboratory team and helped not only to improve clinical practice but to define many important features of the epidemiology, natural history and control of some of the most common viral diseases. He pioneered techniques for managing patients with fulminant hepatitis, established the first dialysis unit for chronic carriers of hepatitis B virus, established dedicated clinics for the care of patients infected with HIV and, in his role as founding Secretary/Treasurer of the Australasian Society for Infectious Diseases, guided the growth of that organisation. Although shy and quiet to the point of taciturnity, and often hidden beneath a cloud of pipe smoke, Ron had a profound impact on a generation of medical students and was a marvellous mentor of young physicians and laboratory personnel. After his first marriage ended, Ron married Jo Cornish. They built a wonderful mud brick house in Eltham overlooking the Yarra River. With Ron’s craftsmanship and Jo’s cooking and decorative flair, their home became a haven for their host of friends. Some time after his retirement, Ron began to develop signs of the debilitating neurological disease which was to claim his life. He became increasingly immobile and was forced to give up most of the pleasures that sustained him. Eventually, confined to his favourite chair and in the loving presence of Jo and his children Kate, Eric, Michael and David, he continued with calm and dignity to receive a stream of visitors until his death on 13 June 2009.

Ian D Gust · Edwina J Wright · Suzanne M Crowe

Ethics and law for the health professions. 3rd ed. Ian Kerridge, Michael Lowe, Cameron Stewart. Sydney: The Federation Press, 2009 (xxv + 895 pp). ISBN: 978 1 86287 730 6. Comprehensive, accurate and up-to-date references on the law are indispensable in my work, so the third edition of Ethics and law for the health professions will join a couple of others to which I regularly refer. There are chapters on truth-telling, confidentiality, consent, the limits of medical treatment, cardiopulmonary resuscitation, genetics and biotechnology, sexuality and reproduction, abortion, treatment of children, treatment of people with mental illness and with chronic diseases, the elderly, post-coma unresponsiveness, organ donation and transplantation, end-of-life care, public health, infectious diseases, indigenous health care, resource allocation, research, animals and the environment, complementary medicine, and the pharmaceutical industry; each chapter provides succinct accounts of the relevant laws, judgments and legal reasoning. The authors clearly distinguish ethics from the law, both in general and in relation to each of the topics they discuss. They offer an informative introduction to the controversy among jurisprudents about how best to think about the nature of the law. The book also has a useful table of cases, table of statutes and an index. I would have only one minor reservation about recommending the book as a text in bioethics: the ethical content is not as strong as the legal content. As an example, the authors say that, with technological change and the passage of time, our ethics must change. However, this assumes that ethics is a set of very specific, very detailed, very current rules about how we should act. Further, the doctrine of the sanctity of life, properly understood, neither says nor implies that it is morally prohibited intentionally to let a person die or that it is morally prohibited to base decisions relating to the prolongation or shortening of human life on considerations of the kind or quality of a person’s life. That said, Ethics and the law for health professions will be a useful reference work for health care professionals.

Bernadette M Tobin

Preventive cardiology: a practical manual. Catriona Jennings, Alison Mead, Jennifer Jones, et al. Oxford: Oxford Medical Press, 2009 (xvi + 218 pp). ISBN: 978 0 19 923630 5. While cardiovascular disease (CVD) remains the predominant cause of death in our society, books on the topic will continue to find interest in the market, particularly those on preventive cardiology. Relatively few books on prevention, however, are written for health professionals by health professionals. Preventive cardiology: a practical manual, by a group of seven authors, addresses cardiovascular risk management and lifestyle factor assessment and application, for the benefit of and use by health professionals. The authors include representatives of nursing, dietetics, physiotherapy, physical activity and cardiology, so Preventive cardiology provides a uniquely holistic overview. With this multidisciplinary approach, the authors deal with both the assessment of risk factors and the application of findings in the management of patients with cardiovascular risk factors. One of the strengths of this book is its fundamental family-oriented approach. In a clear and concise manner, the authors address the main issues of identifying and treating patients with CVD risk factors, and provide a guide for health professionals in their work of identifying, assessing, treating and managing patients/clients at high risk, and steering them and their families through appropriate programs. The book covers all the usual topics of diet, smoking cessation, risk assessment, physical activity, identification of asymptomatic patients, blood pressure, lipid and glucose management, compliance, and so on. More importantly, it aims to assist the health professional team in getting such vital information lucidly and comprehensively across to patients and their families in a way that is most likely to be of practical benefit. The book comes in a pocket-sized format for easy access, and can be regarded as a ready companion and consistent helper for the cardiovascular professional.

Ian R Hamilton-Craig

Excess of eggs A study linking high consumption of eggs with an increased risk of mortality in men, particularly diabetics, has caused interest and some controversy.1 Based on data from the large, long-term US Physicians’ Health Study, the researchers found an association between the consumption of eggs and mortality, but not with the risk of cardiovascular disease. The association was stronger among diabetic subjects consuming more than seven eggs per week. An accompanying editorial comments that data on low-density lipoprotein cholesterol levels, important dietary factors, and other significant covariates were lacking in the study, leading the author to speculate that the results should be interpreted with caution.2 1. Am J Clin Nutr 2008; 87: 964-969 2. Am J Clin Nutr 2008; 87: 799-800 Gene links to breast cancer The tumour suppressor gene NRG1, which when functioning normally is instrumental in stopping cancer from spreading, has been implemented in a significant number of beast cancers, say researchers from the United Kingdom. The study of breast cancer samples and normal breast tissue showed that NRG1 was expressed much less frequently in the breast cancer cells. The mechanism of silencing the gene appeared to be related to methylation of a site on NRG1. They also showed that reducing NRG1 expression in cell lines in vitro increased cell proliferation. The authors suggest that NRG1 may be a principal tumour suppressor gene involved in the development of breast cancer and possibly other epithelial malignancies. The implications for treatment are positive, with research directed at re-methylation and “switching on” of the gene being an exciting direction for the future. Oncogene 2009; Oct 5 [Epub ahead of print] Jaundice in babies Visual assessment of the cephalocaudal progression of jaundice in hospitalised newborns is not necessarily an accurate estimation of actual bilirubin concentration, according to the results of a US study. The extent of neonatal jaundice was assessed visually by nurses on a five-point scale on the night before discharge, and compared with transcutaneous bilirubin (TcB) measurement. Infants with high TcB had total serum bilirubin performed. The nurses’ assessment of jaundice was only moderately correlated with bilirubin concentration, with similar results in both black and white infants. The correlation was poorer still for babies of less than 38 weeks’ gestational age. Despite these findings, a complete absence of jaundice by visual assessment had a high sensitivity and good predictive value for ruling out significant hyperbilirubinaemia. The authors comment that a visual estimation of extent of jaundice progression should not be used to estimate bilirubin levels, particularly in infants born prior to 38 weeks’ gestation. Arch Dis Child Fetal Neonatal Ed 2009; 94: F317-F322 A pain in the neck If you or your patients suffer from neck and arm pain due to cervical radiculopathy, be advised that rest and a cervical collar, or physiotherapy appear to be more effective than the “wait and see” approach.1 Dutch researchers conducted a randomised trial with over 200 patients with recent onset cervical radiculopathy, treating three groups using a semi-hard collar and 3 to 6 weeks’ rest; 12 twice-weekly sessions of physiotherapy and home exercise for 6 weeks; or continuation of normal routine (control group). The collar and rest group and the physiotherapy group had significantly reduced neck and arm pain compared with the controls, prompting the authors to recommend that treatment with a semi-hard collar and rest is a cost-effective and efficient method of management. An accompanying editorial comments that the best approach might be to allow the patient to decide which approach suits them best, and to be open to a change of treatment depending on the clinical response.2 1. BMJ 2009; 339: b3883 2. BMJ 2009; 339: b3952 Dr Tanya Grassi, MJA

Ann Gregory