Volume 195 Issue 1

No-fault compensation, based on the ethical principle of redistributive justice, should form a cornerstone of Australia’s immunisation strategy Australia has an enviable reputation for its publicly funded vaccine program — a program that has benefited Australian children and adults over many years. In 2010, the National Immunisation Program funded 12 vaccines, twice as many as a decade previously. To monitor outcomes from this program, the Australian Childhood Immunisation Register, which commenced data collection in 1996, provides a detailed record of vaccine uptake by children.1 Funding for the register and for incentives to general practitioners to improve vaccine uptake are part of the total budget for Australia’s vaccine program, estimated to exceed $400 million annually.2,3 One area for improvement in the vaccine program is monitoring of adverse events following immunisation (AEFI). Another would be the introduction of a no-fault compensation scheme for serious adverse events which can be confidently attributed to vaccination. An investigation into the unexpectedly high number of febrile convulsions in children aged less than 5 years after they had received the influenza vaccine in 2010 — in some cases, with devastating consequences4 — provided a forceful reminder that timely vaccine safety monitoring is needed in Australia.5 More active adverse event surveillance is certain to uncover more AEFI but many of these will only be coincidental, while others will be of a transient or relatively trivial nature. On rare occasions, a serious AEFI with long-term sequelae will be recognised. A decision will then need to be made on whether the vaccine was responsible for that serious event. The World Health Organization defines four categories of serious AEFI: hospital admission or prolongation of an existing hospital admission; permanent disability; any event that is life threatening; or death.6 Using these criteria, 8% (193/2396) of the AEFI reported by passive surveillance in Australia in 2009 were judged to be serious.7 However, unlike many countries where compensation schemes exist for adverse events attributed to a vaccine, Australia has no routine approach to making the assessment of attribution. Parents of children or adults who believe they deserve compensation for a serious adverse event that they attribute to a vaccine are therefore required to make their case through the adversarial legal system. This requires the demonstration that an individual or an organisation was at fault. However, fault is often difficult to demonstrate and an adverse event may be caused by vaccination through no fault of the vaccine manufacturer, the regulator or the person who administered the vaccine. We have previously argued that a Queensland child who developed transverse myelitis after receiving oral polio vaccine was an example of an adverse event following vaccination where no fault was attributable to any party.8,9 Despite detailed epidemiological evidence that was consistent in this case with the causal criteria for an AEFI promulgated by the Institute of Medicine of the National Academies in the United States,8 and despite laboratory evidence showing that the polio virus recovered from this child was similarly pathogenic to a polio virus that has been accepted as causing vaccine-associated paralytic polio,9 the polio expert committee concluded that the evidence was insufficient to support a causal relationship between the oral polio vaccine and transverse myelitis. As causality has not been accepted, this child has received no compensation. The general principles associated with this case raise a number of pertinent questions for Australia. First, should a child who may have been injured by a vaccine, which was endorsed and paid for by the community, be compensated by the community when the serious adverse event may be attributed to the vaccine? Second, what are the criteria for accepting an attributable relationship between receipt of the vaccine and a subsequent adverse event? Third, what is the best method for financing a compensation scheme? Each question may highlight a potential barrier to the implementation of a no-fault AEFI compensation scheme in Australia. By 2010, 19 countries around the world had implemented no-fault AEFI compensation, implicitly answering “yes” to the question of whether the community owes a duty of care to an individual injured by a vaccine.10 There is also a strong ethical argument for this position, based on the concept of redistributive justice. Any person who is injured while helping to protect the community — for instance, by contributing to herd immunity, such that there are sufficiently many people immunised to prevent widespread disease transmission within the community — should not bear the consequences of injury alone. In essence, the community owes a debt of gratitude to that person. Temporal association of an adverse event with receipt of a vaccine does not establish causality and the underlying notion of causation used in most compensation schemes is similar to that used in epidemiology.10 The World Health Organization has published guidelines on causality for an AEFI.11 An adverse event considered to be very likely or certainly due to a vaccine would comprise a “Clinical event with a plausible time relationship to vaccine administration, and which cannot be explained by concurrent disease or other drugs or chemicals”.11 To simplify and expedite determinations of causality in the US, a vaccine injury table is used to predetermine causality if a vaccine injury is included in the table.10 However, determining causation is a complex issue. Recognising this, most countries have a designated committee, comprising medical and legal members, which deliberates on the attributable relationship between receipt of the vaccine and subsequent adverse event.10 Concerns about funding a no-fault compensation scheme is another of the probable barriers to its implementation in Australia. Schemes are currently funded by one of four methods: a vaccine levy; compensation for AEFI as part of a much broader injury compensation scheme; specific AEFI compensation funded through general tax revenue; and funding in association with industry.10 Funding through a vaccine levy has been self-sustaining in the US. Despite compensation payments having been made to 2580 claimants since 1989, the compensation fund there has a surplus of about US$3 billion.12,13 No-fault vaccine-injury compensation programs are based on the premise that any adverse event attributable to vaccination is not due to the fault of a specific individual or organisation, but due to an unavoidable risk that is acknowledged as being associated with vaccines. Germany has been operating a no-fault AEFI compensation scheme for 50 years.10 France restricts its compensation to serious AEFI, since these are likely to have long-term implications for the injured party.10 Restricting compensation to events with long-term consequences, above a nominated clinical threshold, may be an acceptable model for Australia. We have previously argued that Australia should follow the lead of other advanced countries and implement a no-fault compensation scheme.14 We continue to argue that such a scheme, based on the ethical principle of redistributive justice, should form a cornerstone of Australia’s immunisation strategy. Disclaimer The views expressed are those of the authors and have not been endorsed by any institution or organisation with which the authors are affiliated or by any committees of which the authors are members.

Heath A Kelly BSc, MB BS, MPH · Clare Looker MB BS, MPH · David Isaacs MD, FRACP, FRCPCH

Avoidance of allergenic foods in the first year of life is no longer recommended Since the 1980s, the world has experienced an epidemic of allergic disease. The prevalence of asthma rose rapidly during the 1990s, followed by increases in the prevalence of eczema and allergic rhinitis, both of which continue to rise. Of great concern is new evidence that yet another allergic condition — food allergy — is also on the rise, particularly in infants and young children. An estimated 10%–15% of the population report symptoms of food allergy,1 although the prevalence of IgE-mediated food allergies (ie, symptoms such as urticaria, angioedema, vomiting or anaphylaxis within minutes of food ingestion, in the context of a positive skin prick test result or food-specific serum IgE level) has not, until recently, been adequately studied at the population level. Results of population studies examining food allergy prevalence have been hampered by small sample sizes, selection bias related to sampling methodology and response rates, and use of parental or self-report of allergy or a skin prick test result as a proxy for food allergy diagnosis. Even studies that have used the diagnostic gold standard of oral food challenge, where the allergen of interest is fed to the child, have been limited by a lack of predetermined objective criteria to define the outcome. However, there have now been reports that hospitalisations for food allergy-related anaphylaxis — the most serious and life-threatening manifestation — have increased markedly since 1990 in the United Kingdom, the United States and Australia,2 most dramatically, with a fivefold increase, in 0–4-year-olds. The HealthNuts study was recently mounted to describe the prevalence of food allergy in 1-year-old infants in Melbourne, using a sampling frame designed to recruit a representative population sample and predetermined criteria to assess food allergy outcomes at oral food challenge.3 Recruitment occurred at childhood vaccination sessions. Participants’ parents completed a questionnaire, and the infants received skin prick testing for commonly allergenic foods. Among 2848 participants (73% participation rate), those with any sensitisation to one of three foods (egg, peanut and sesame) were invited to attend an allergy research clinic for formal oral food challenge. Using this method, the study found population-based prevalences of 2.9% (95% CI, 2.3%–3.6%) for peanut allergy, 8.9% (95% CI, 7.8%–10.0%) for egg allergy, and 0.8% (95% CI, 0.5%–1.1%) for sesame allergy in 1-year-old infants.4 Certainly, these rates are the highest yet reported in the Western world, with up to 10% of 1-year-old infants in this study population exhibiting signs of IgE-mediated food allergy in a challenge setting. Although it is anticipated that many of those with egg or cows milk allergy will develop tolerance to these foods in the first 3–4 years of life, the high prevalence of peanut allergy remains concerning, as only 20% of children are expected to achieve resolution of this allergy by 5 years of age.5 Furthermore, there is now evolving evidence that food allergy, including cows milk and egg allergy, may represent the first step on the allergic pathway referred to as the “atopic march”.6 As such, the question remains as to whether this reported high prevalence of food allergy may reflect a second and evolving epidemic of allergic disease, with an early onset in the form of food allergy that will translate into increased rates of asthma and other chronic allergic disease later in life. The reasons behind this apparent increase in serious food allergy are unknown and there is little evidence to guide effective prevention. One of the most topical theories for the rise in allergic disease in general — the hygiene hypothesis — states that very early exposure to microbial antigens promotes healthy immune development and reduces the risk of developing allergies. However, this hypothesis has not been examined specifically with regard to risk of food allergy. Another theory relates to vitamin D insufficiency, with recent reports in both the northern and southern hemispheres showing increasing rates of food allergy with increasing distance of children’s residence from the equator.7 A further factor that has been thought to be important in the development of food allergy is food allergen exposure. Until very recently, expert guidelines for infants with a family history of allergy typically recommended delaying introduction of allergenic foods (including avoiding eggs until 2 years and nuts until 3 years of age in the US), as well as delaying solid foods until after 6 months of age, and breastfeeding for at least 12 months, to reduce the risk of food allergy. Until the publication of the HealthNuts study,4 no population study had directly examined the relationship between infant feeding in the first year of life and risk of challenge-confirmed infant food allergy. Data from the HealthNuts study were used to assess the impact of timing of introduction of allergenic foods. Compared with introduction at 4–6 months, introducing egg into the diet later was associated with higher rates of egg allergy (adjusted odds ratio for introduction after 12 months, 3.4 [95% CI, 1.8–6.5]).8 Most interestingly, introducing cooked egg (such as scrambled, boiled or fried) was more protective than simply introducing egg in baked goods (such as cakes and biscuits). Those introduced to cooked egg at 4–6 months of age were five times less likely to develop egg allergy than those waiting until the normally recommended age of 10–12 months, even after adjusting for confounding factors. There was no protective effect among infants who first had egg in baked goods introduced into their diet between 4 and 6 months of age, presumably because exposure to a lower dose does not provide protection. A further possibility is that early introduction of egg might increase the dose of vitamin D in the diet, and therefore the effect might indeed be mediated through a unifying concept of vitamin D sufficiency. These results are the first evidence-based findings to inform recently revised feeding guidelines, in Australia9 as well as in Europe and the US, that avoidance of any allergenic food in the first year of an infant’s life is no longer recommended. The findings also represent the first report of a modifiable lifestyle factor found to be associated with food allergy and, if these results are replicated in randomised controlled trials, it will have important public health implications for infant feeding worldwide. The emergence of this new epidemic of allergic disease poses significant questions relevant to ensuring a healthy start to life for future generations of children, including whether some aspects of the modern lifestyle, which includes unquestionable improvements in public health, have had an unexpectedly adverse effect at the population level. We also need to understand whether this new wave of food allergy in early childhood is likely to persist into later childhood, and further assess whether early-onset food allergy plays a role in the development of other chronic allergic diseases such as asthma.

Katrina J Allen MB BS, FRACP, PhD

HbA1c may be a practical alternative to blood glucose for the diagnosis of diabetes For more than 15 years, glycated haemoglobin (HbA1c) has been recommended as the key tool for assessing glycaemic control in people with diabetes. Only in 2009 did the first advice to use HbA1c levels for diabetes diagnosis appear, using a cut-point of ≥ 6.5%.1 To date, no clear argument has been articulated to explain why HbA1c levels have been deemed superior to laboratory-determined blood glucose levels for determining the need for insulin therapy, but not for diagnosing diabetes; however, it is likely that implications of the former are greater than those of the latter, for both individuals and society. Blood glucose values are considered the gold standard for diabetes diagnosis, but they have significant limitations. Day-to-day variability in glucose levels is considerable, and the glucose concentration in a plasma sample falls within a short period, even if the blood has been collected in a fluoride tube. In addition, when stable samples are tested in two different laboratories, the results will differ by at least 14% in more than a third of cases.2 Furthermore, even when using a single laboratory, only 70% of people with a blood glucose value that indicates a diagnosis of diabetes have the diagnosis confirmed by repeat testing 2 weeks later, compared with 83% for HbA1c.2 So, is HbA1c the answer to the challenges of diabetes diagnosis? Until recently, the problem with HbA1c has been the concern that results vary considerably between laboratories. In the 1990s, laboratory differences of more than two percentage points were not uncommon, but the United States National Glycohemoglobin Standardization Program (NGSP) has progressively driven improvements in assay standards. The latest results from the largest global survey of quality of HbA1c measurement show that, for reference samples with HbA1c levels of 4.0%–6.0%, 91% of more than 3000 laboratories could obtain an HbA1cvalue that was within 6.0% of the target.3 In a recent Australian study, whole blood samples were sent to more than 200 laboratories and more than 90% obtained HbA1c values that were within 6% of the median.4 Thus, for a sample with a median value of 5.3%, over 90% of laboratories obtained values within the range 5.0%–5.6%, and for a median value of 7.4%, over 90% obtained values within the range 7.0%–7.8%. In addition, combined data from eight studies conducted between 1988 and 2004 (using assays in eight different laboratories, none of which may have performed as well as those available now) showed that HbA1c levels were at least as strongly correlated with diabetic retinopathy as were blood glucose levels.5 HbA1c is not without limitations. First, an HbA1c test is more expensive than a fasting glucose test, but costs about the same as an oral glucose tolerance test. The extra cost of using HbA1c instead of fasting glucose as the initial blood test needs to be weighed up against the potential for the HbA1c test (which does not require the patient to fast) to be used more widely, to identify more undiagnosed cases of diabetes, and to save money by preventing complications of diabetes. To our knowledge, no cost–benefit analyses comparing the HbA1c test with the fasting glucose test have been published — this should be a high priority. Second, HbA1c can be unreliable in the presence of haemoglobin variants or alterations in red blood cell turnover. Most HbA1c assays are now able to adjust for the most common haemoglobin variants, but where there is uncertainty relating to the reliability of HbA1c, blood glucose will remain the preferred test. If the potential exists to use HbA1c for the diagnosis of diabetes, how can a practitioner know whether a particular laboratory can be relied on? A joint working party of the Australian Diabetes Society, the Royal College of Pathologists of Australasia, and the Australasian Association of Clinical Biochemists is developing a formal laboratory and clinical framework within which the diagnosis of diabetes by HbA1c testing can be undertaken. In the meantime, it would be reasonable to think that a laboratory can be relied on, in the context of using HbA1c as a diagnostic tool, if the routine coefficient of variation is ≤ 3.0% (the 2010 accreditation target used by the NGSP) and the external quality assurance results are consistently within the Royal College of Pathologists of Australasia Quality Assurance Programs method-specific performance targets (allowable limits of performance). This information should be available from laboratories on request. Practical aspects of using HbA1c for the diagnosis of diabetes remain to be finalised. One option may be to request a fasting glucose test and HbA1c test at the same time, with the HbA1c to be performed only if the fasting glucose level is ≥ 5.5 mmol/L. This strategy would limit the additional costs of HbA1c testing while decreasing the number of patients who are lost to follow-up for an oral glucose tolerance test. The cost of an HbA1c test that is used for diagnosis is not currently reimbursed by Medicare. However, when used appropriately, the HbA1c test appears to be at least as useful for diagnosing diabetes as a blood glucose test. Australia may soon be ready to join countries such as the United States and Japan in using HbA1c, a measure of chronic glycaemia, for the diagnosis of diabetes, a disease of chronic glycaemia.

On behalf of the Joint HbA1c Working Party of the Australian Diabetes Society, the Royal College of Pathologists of Australasia, and the Australasian Association of Clinical Biochemists

Promising outcomes from the Australian register include a fall in fetal malformation rates associated with changes in antiepileptic drug prescribing The burden of epilepsy for those with the disorder is significant. For women of childbearing age, the uncertainty surrounding their ability to bear children who are free of the disorder, without birth defects, and cognitively and psychologically normal adds to this burden. Although factors other than medication exposure influence these questions, there is no doubt that antiepileptic drugs (AEDs) used to prevent seizures, such as valproate, have a significant, and possibly preventable, role in teratogenicity.1 Pregnancy registers are now showing promising results in elucidating this role and influencing changes in practice for the benefit of women with epilepsy and their children. Some detailed information on the relative risks associated with AEDs has emerged over the past three decades,2 but it has largely been based on small-scale retrospective studies, with various and incomplete methods of recording data, no set protocols, and other shortcomings. It was clear that better information regarding teratogenicity, preferably from prospective studies, was needed. It was also clear that the expectant mother, as well as the infant, should be a primary consideration. The process of studying pregnancies in women with epilepsy should start well before conception and requires extensive consultation with the expectant mother about the planned management of her pregnancy and medication administration.3 In the late 1990s, these issues provided the rationale for setting up registers of pregnant women with epilepsy who were taking AEDs. There are now several international collaborative, independent and pharmaceutical company-initiated registers. The latter are concerned with single drugs and are not prospective. The collaborative and independent registers generally aim to collect prospective observational data from participating women according to an extensive protocol, with the data computerised for subsequent analysis. None of the registers dictate treatment and all have ethics approval, as well as informed consent from the participating women.4 The major registers are the International Registry of Antiepileptic Drugs and Pregnancy (EURAP),4 which includes data from 46 countries in Europe and elsewhere, and registers in North America, Denmark and the United Kingdom that publish reports independently. The Australian Pregnancy Register of Antiepileptic Drugs for Women in Pregnancy with Epilepsy and Allied Conditions (the Australian Pregnancy Register), established in 1999, is affiliated with EURAP, but also publishes its findings independently. It collects data from women who have volunteered to participate through a series of five interviews held at various times during pregnancy and after the infant’s birth.5 Over the past decade, all these registers have contributed considerable knowledge, improved prescribing practices and, although they were initially intended to focus on teratogenicity, have been extended to examine maternal wellbeing and seizure control, and cognition of the offspring. In terms of teratogenicity, the data collected in the registers can be used to assess the contributing roles of heredity, social factors, substance misuse, alcohol consumption, social status, intake of other medications, and accurately defined type and activity of epilepsy. The registers represent prospective studies on treatment efficacy and compliance, seizure freedom before pregnancy, interactions between AEDs and hormones, the role of folate supplementation, and many other factors involved in producing normal pregnancies and outcomes. The international registers have not used untreated control groups until recently — the North American register has used historical controls but is now enrolling a control group of pregnant untreated women, while EURAP compares the effects of different drugs. The Australian Pregnancy Register has from the outset collected data from a control group of untreated women with epilepsy, comprising about 10 per cent of the total, as well as (less successfully) women receiving AEDs for non-epileptic indications such as pain or bipolar disorder. Although there is no ideal control group, collecting data from untreated women with epilepsy provides an important comparison baseline.6 Recent analyses of data from the Australian Pregnancy Register have examined the role of AEDs in teratogenicity. For several decades, the use of AED polytherapy has been enshrined in the international literature as being harmful to the fetus, but our recent analysis of register data casts doubt on this, suggesting that it is the specific composition of polytherapy that is critical, not intake of multiple drugs per se.7 Most recently, analysis of register data has focused on dose issues that are associated with most of the AEDs, and examined the question of whether lower doses of drugs such as valproate may be effective in achieving seizure control without posing a higher risk of teratogenicity than other, less effective drugs.8 The role of AEDs in teratogenicity has become even more complicated as a series of new second-generation drugs have become available, because it takes a long time with many participants to define their role compared with the traditional drugs.9 Findings from the Australian Pregnancy Register have shown that seizure freedom before conception is demonstrably important in predicting the course of future pregnancies; the longer a woman is seizure-free, the better the outlook. The question of repeated pregnancies in women who have had a malformed baby while taking an AED, and advice to women contemplating extending their family, has also been studied. Findings such as these are of immediate importance to women and their babies, contribute to medical knowledge and have demonstrably altered prescribing practices in Australia and internationally. Recent data indicate that, while prescribing of valproate has risen in the general Australian population, possibly as a result of increasing use for patients with psychiatric illness, especially bipolar disorder, there has been a fall in the number of prescriptions and doses of valproate for women of childbearing age.10 This change in prescribing, which was influenced by register data, has been associated with a fall in fetal malformation rates.11 Increasing the number of women enrolled in the Australian Pregnancy Register is highly desirable to continue study of these important and complex topics. Pregnancy is an important health issue, and we must all collaborate to make it safer for women and their children.

Frank J E Vajda MD, FRCP, FRACP · Terence J O’Brien MB BS, MD, FRACP · Cecilie M Lander MB BS, FRCP, FRACP · Mervyn J Eadie MD, PhD, FRACP

Objective: To assess the influence of area-level socioeconomic status (SES) on incidence and case-fatality rates for stroke.Design, setting and participants: Analysis of pooled data for 3077 patients with incident stroke from three population-based studies in Perth, Melbourne, and Auckland between 1995 and 2003.Main outcome measures: Incidence and 12-month case-fatality rates for stroke.Results: Annual age-standardised stroke incidence rates ranged from 77 per 100 000 person-years (95% CI, 72–83) in the least deprived areas to 131 per 100 000 person-years (95% CI, 120–141) in the most deprived areas (rate ratio, 1.70; 95% CI, 1.47–1.95; P < 0.001). The population attributable risk of stroke was 19% (95% CI, 12%–27%) for those living in the most deprived areas compared with the least deprived areas. Compared with people in the least deprived areas, those in the most deprived areas tended to be younger (mean age, 68 v 77 years; P < 0.001), had more comorbidities such as hypertension (58% v 51%; P < 0.001) and diabetes (22% v 12%; P < 0.001), and were more likely to smoke (23% v 8%; P < 0.001). After adjustment for age, area-level SES was not associated with 12-month case-fatality rate.Conclusions: Our analysis provides evidence that people living in areas that are relatively more deprived in socioeconomic terms experience higher rates of stroke. This may be explained by a higher prevalence of risk factors among these populations, such as hypertension, diabetes and cigarette smoking. Effective preventive measures in the more deprived areas of the community could substantially reduce rates of stroke.

Emma L Heeley MSc, PhD · Jade W Wei BPharm · Kristie Carter PhD · Md Shaheenul Islam MB BS, MPH, MSc · Amanda G Thrift PhD · Graeme J Hankey MD · Alan Cass PhD · Craig S Anderson MD, PhD

Objective: This study examined the knowledge of stroke warning signs and risk factors among the general public, including what they would do if they were to develop such symptoms.Design, setting and participants: Population study of randomly selected members of the general public in Adelaide, South Australia. A simple survey assessed knowledge of stroke warning signs and gave four options for management. The survey was conducted on three separate occasions: before, immediately after and 3 months after the National Stroke Foundation’s National Stroke Week in 2009.Main outcome measures: The outcome measures were the public perception of risk factors and warning signs of stroke and what the members of the public would do if presented with a range of warning signs. They were also asked about their knowledge of the Face, Arms, Speech, Time (FAST) test.Results: The three surveys were completed by 251 members of the public. Hypertension and smoking were recognised as risk factors for stroke by 71% and 53% of respondents respectively. Before National Stroke Week, slurred speech was identified by 51% and both slurred speech and upper limb sensory loss was identified by 62% as warning signs to provoke presentation to an emergency department (ED). Amaurosis, upper limb sensory loss, upper limb numbness and upper limb weakness were correctly identified individually as warning signs to attend an ED by fewer than one-third of respondents. There was no significant difference in the survey results following National Stroke Week. Conclusions: Public awareness of the symptoms of stroke, and what to do about them, is limited. There was little improvement after the national week-long awareness campaign. The lack of public awareness about stroke warning signs must be addressed to reduce mortality and morbidity from stroke.

J Ian Spark MD, FRCS, FRACS · Nadia Blest MB BS · Sheralee Sandison RN, MN · Phillip J Puckridge MB BS, FRACS · Hafees A Saleem MB BS, MRCSEd · David A Russell MB ChB, MD, FRCS

Objective: To assess the impact of the quick-service restaurant industry (QSRI) self-regulatory initiative on fast-food advertising to children on Australian commercial television.Design and setting: Analysis of advertisements for foods on the three main free-to-air commercial television channels (channels 7, 9 and 10) in Sydney, Australia, over 4 days in both May 2009 and April 2010 in terms of: number of advertisements; types of food (coded core [healthy] foods, non-core [unhealthy] foods, miscellaneous foods; or fast foods); whether advertised meals were intended for children; whether advertisements were broadcast during children’s peak viewing times; and whether the company in question was a signatory to the QSRI initiative.Main outcome measures: Change in the mean frequency and rate of food advertisements per hour from 2009 to 2010; change in the types of fast-food meals (healthier alternatives [at least one nutrient-dense, low-energy food considered part of a healthy diet for children], non-core [high in undesirable nutrients and not considered part of a healthy diet for children], and other) being advertised; and proportion of children’s energy requirements provided by fast-food meals.Results: From 2009 to 2010, the mean frequency of fast-food advertisements increased from 1.1 to 1.5 per hour. While non-core fast foods comprised a lesser share of fast-food advertising in 2010 than 2009, the mean frequency at which they were advertised during times when the largest numbers of children were watching television remained the same (1.3 per hour in both 2009 and 2010). Family meals advertised for children’s consumption in 2010 provided energy far in excess of children’s requirements.Conclusions: Children’s exposure to unhealthy fast-food advertising has not changed following the introduction of self-regulation, and some fast foods advertised for children’s consumption contain excessive energy. The limited impact of self-regulation suggests that governments should define the policy framework for regulating fast-food advertising to children.

Lana A Hebden BND · Lesley King MPsych(Hons) · Anne Grunseit PhD · Bridget Kelly MPH, BSc(Nutr)(Hons) · Kathy Chapman MNutrDiet, BSc

Objective: To identify characteristics of doctors who are repeated subjects of complaints by patients.Design and setting: Case–control study of doctors about whom patients had complained to the Victorian Health Services Commissioner between 1 January 2000 and 31 December 2009.Participants: 384 doctors in private practice; cases comprised 96 doctors who were the subject of four or more separate complaints; and the control group comprised 288 doctors who were the subject of a single complaint over the study period.Results: Among doctors in private practice in Victoria, 20.5% (95% CI, 19.7%–21.3%) experienced at least one complaint over the decade. Among doctors who were the subject of a complaint, 4.5% (95% CI, 3.6%–5.4%) had four or more complaints, and this group accounted for 17.6% (95% CI, 16.3%–19.0%) of all complaints to the Victorian Health Services Commissioner. Multivariate analyses showed that surgeons (odds ratio [OR], 8.90; 95% CI, 3.69–21.50) and psychiatrists (OR, 4.59; 95% CI, 1.46–14.43) had higher odds of being in the complaint-prone group than general practitioners. Doctors trained overseas had lower odds of being complaint-prone than those trained in Australia (OR, 0.31; 95% CI, 0.13–0.72).Conclusions: A small group of doctors in private practice in Victoria account for nearly 18% of complaints. Interventions to improve patient satisfaction and public confidence in health services should target complaint-prone subgroups of practitioners.

Marie M Bismark MB ChB, LLB, MBHL · Matthew J Spittal BSc(Hon), PhD · David M Studdert LLB, ScD, MPH

A recently published critique of a set of Australian clinical practice guidelines (CPG) highlighted problematic issues in guideline development concerning conflicts of interest of guideline panellists, validity and strength of recommendations, and involvement of end users and external stakeholders. Management of financial or intellectual conflicts of interest requires: full disclosure; limitations on industry or agency financial support during guideline development; a representative panel that includes conflict-free members; and only conflict-free panellists to be involved in drafting guideline recommendations. Guideline panels should consider adopting the GRADE (Grading of Recommendations Assessment, Development and Evaluation) system to assist in determining the validity and strength of recommendations. Guideline panels should seek formal feedback from external stakeholders and end users. Enacting such policies aims to lend greater transparency and credibility to CPG, limit protracted and unhelpful interpretive debates, and promote wider use of CPG.

Ian A Scott FRACP, MHA, MEd · Gordon H Guyatt MD, MSc, FRCP(C)

Lower urinary tract symptoms (LUTS) are common among Australian men over the age of 45 years; most men with LUTS will have benign prostatic hyperplasia (BPH), overactive bladder (OAB), or both. The cause of LUTS should be diagnosed by assessing symptom severity and excluding of medical or pharmaceutical causes. All men with LUTS should undergo digital rectal examination; other diagnostic tools include urine and blood testing, voiding charts and imaging. Depending on disease severity, impact on quality of life, patient preference, presence of complications and fitness for surgery, BPH is managed with watchful waiting, pharmacotherapy (α-blockers or 5-α-reductase inhibitors), minimally invasive surgical therapies or surgery. OAB is initially treated with behavioural therapy; if this is ineffective, pharmacotherapy (usually antimuscarinics) can be used. Patients with LUTS with a provisional diagnosis other than BPH or OAB, or with complications or poor response to pharmacotherapy, should be referred to a urologist.

Henry H Woo MB BS, FRACS · Michael P Gillman MB BS, FRACGP · Robert Gardiner MB BS, MD, FRACS · Villis Marshall MD, FRACS · William J Lynch MB BS, MSc, FRACS

Medical academics Christine Jorm and Michael Frommer believe it is simply the right thing to do For vast amounts of performance data are collected in the Australian health system, many of which are released by agencies such as the Australian Institute of Health and Welfare, state and territory health departments and the Australian Bureau of Statistics. However, merely releasing performance data is different from publicly reporting such data. Public reporting incorporates interpretation and comparisons that make the data meaningful for the community. Public reporting of health care performance has three major uses: (i) to ensure accountability — the Australian public, which pays for health care, is entitled to assess the effectiveness and efficiency of health care and to press for change as needed; (ii) to stimulate action by health care providers that leads to improvements; and (iii) to give consumers information on which they can base their expectations of health services and individual health care choices. All of these uses are important, and the scrutiny afforded by public reporting of performance should therefore be welcomed. It is difficult to determine what types of reporting represent the best investment, because the consequences of public reporting are difficult to measure. The quantum of research on the effects of any complex health policy intervention is scant. Unsurprisingly then, evidence on the value of public reporting is currently limited.1,2 What have we learnt from the international experience? Research in the United Kingdom and the United States shows a thirst among consumers for publicly reported performance data, while pointing out the difficulty of producing data that people can readily use for making health care choices.2 In neither the UK nor the US has patient choice in itself been shown to have had a reliable influence on health care quality. However, when the public is made aware of poor health care service performance, calls for political action are common. This is a desirable outcome. Public reporting — particularly reporting of institutional performance — consistently stimulates health care providers to improve quality.1 For example, after the first publication of comparative cardiac surgery outcomes in New York State, some surgeons who recognised that they were outliers on performance scales voluntarily changed their scope of practice, or retired. More commonly, it is institutions that undergo performance evaluations, and they usually respond vigorously to improve care processes and patient outcomes. This is especially so when public reporting is framed by expectations that people understand and value, such as accompanying goals and targets.2 Does performance measurement corrupt the delivery of health care? It is secrecy that corrupts. The absence of public reporting generates suspicion and cynicism among both clinicians and the public. Notably, the Australian Medical Association submission on the National Health Reform Amendment (National Health Performance Authority) Bill 2011 advocated stronger investigative and disciplinary powers for the National Health Performance Authority and, importantly, a mandatory requirement to release reports. Opponents of public reporting highlight the potential for merely improving the data rather than the quality of care (for instance by finding more risk factors to include or reclassifying chairs as beds) and for neglect of high-risk patients, but evidence from the UK suggests that both are rare. The introduction of targets and public reporting of emergency department waiting-time data drove real reform.3 In a study of more than 27 000 patients who had cardiac surgery, risk-adjusted mortality fell after the introduction of public reporting, and there was no evidence that fewer high-risk patients were offered surgery.4 Some Australian clinical leaders choose to focus their opposition to public reporting on the impossibility of providing adequate risk adjustment — that is, of fully accounting for the differences between individuals and their circumstances. This is an argument that, when taken to extremes, would invalidate most of the evidence base for medical practice. However, reporting of process indicators can reduce the need for, and the debate over, sufficient risk adjustment. Rather than corrupting delivery, the Queensland experience — where there is timely return of data to health care providers, and performance measures are accompanied by reporting on the institutional responses to the data — has shown that public performance reporting can create a culture of improvement.5 Could the personal cost to the clinicians and managers be too great to justify implementation of public reporting? Public reporting affords protections and benefits, and should be welcomed as the price of public service and funding. The risk of unfair reproach will be mitigated by the use of reliable performance measures, timeliness, high-quality data, rigorous analysis, and integrity and sensitivity in reporting results. Review, comparison and criticism are essential components of professional practice. The National Open Disclosure Standard requires clinicians to share uncomfortable truths about adverse events with individual patients. Honesty is a central value of professionalism, and the wellbeing of patients must take precedence over professional self-interest. Public performance reporting promotes strong adherence to these values and therefore should be at the core of good health system governance.

Christine M Jorm MD, PhD, FANZCA · Michael S Frommer MB BS, MPH, FAFPHM

Health services experts Jeffrey Braithwaite and Russell Mannion doubt the value Against the idea that publicly reported performance measurement, like apple pie, parenthood and the national flag, deserves a warm, uncritical glow of universal support should be roundly rejected. Introducing any costly new initiative must always be analysed with a cool head for its risks and potential downside. Where is the Australian business case, or the international cost–benefit analysis or cost-effectiveness analysis, applied to Australia, that compels us to not only accept, but insist on its introduction? These have not been provided by proponents to date. It is a considerable logistical exercise to collect, process, analyse and distribute national data, and it is therefore very costly. Do the benefits outweigh the costs? Almost everyone will have their doubts. There is probably no clinician or manager who has not reported information to some system or other, and never heard about it again. Health care is renowned for “hoovering up” data, which get stuck in the system. Will a national performance measurement initiative fare any better? We prefer to maintain a healthy scepticism. Most experts in favour of performance measurement argue that the twin aims are to improve accountability and enhance the system’s performance.1 But health care’s enormous complexity must be acknowledged. There are many stakeholders, a complicated multiplicity of services and products delivered through many public and private providers contributing millions of encounters across acute, aged, primary and tertiary sectors, with increasing emphasis on prevention, promotion and community care. There is heavy political involvement in health care, and much media attention, both of which distort priorities. Against this heady mix of systems changeability, key challenges are to determine what should be measured, and how, and from whose perspective, while ensuring fairness and objectivity. These questions have not been answered satisfactorily. Even if they were, there are several other problems. One is how to solve technical issues about data quality and the effectiveness of measurement. For example, are the input data collected in the same way, are they gathered systematically by all providers or according to different coding and institutional rules, and what is the extent of gaming (ie, portraying or modifying data to one’s strategic advantage) by participants? How accurately do the data reflect actual performance, are apples being compared with apples and how good are the information systems or the data collection measures that produce the data? It is well known that it is extremely hard to measure performance because of difficulties in risk adjusting. Different risk adjustment models give rise to different outcomes.2 Another issue is whether this initiative will have the desired outcomes. There are many examples of performance measurement systems which, even when they have solved some of the main technical problems, have failed to have meaningful effects. The reporting data are ignored, argued over or politicised, improvement efforts founder, or targets and indicators have perverse effects.1 Indeed, public performance measures are not neutral assessments of performance, but can alter behaviour in unintended and dysfunctional ways. All this gives rise to the potential for Type 1 errors (higher performing organisations or services are assessed as underperforming) or Type 2 errors (lower performing organisations or services are assessed as adequately performing). Traditionally, the attention has been on avoiding Type 1 errors, but since high-profile inquiries at Bristol Royal Infirmary in the United Kingdom, King Edward Memorial Hospital in Western Australia, Campbelltown and Camden hospitals in New South Wales, and others,3 attention has shifted to avoiding Type 2 situations.4 It is very tricky to get the balance right. No performance measurement systems internationally claim to have done so. There are also timing and attribution issues that need to be resolved. Performance measurement systems are necessarily backward looking, as it takes time to assemble and disseminate data. By the time a problem is spotted, it may be too late to do anything about it. There is also the attribution problem: when good or bad performance is observed, is it causally related and assigned correctly? In systems where many things are changing simultaneously — and health is the par-excellence exemplar of this — this is an ongoing issue. So what can contribute to success? Apart from a good data collection system and agreed definitions, targets and indicators (none of which we have at this point), we need excellent partnerships between sectors, agencies and health departments; leadership, not politics; incentives to participate; really good communication of outcomes; fair media reporting of results; and well designed mechanisms to improve performance. It remains doubtful whether these can be readily achieved in Australia. All in all, performance measurement systems often have little impact on changing behaviour or improving performance.5 As that is the point of them, and until the fundamental problems we describe are sorted out, we respond with a resounding no to the proposition.

Jeffrey Braithwaite PhD, FACHSM, FAIM · Russell Mannion PhD, FRSA

A husband and wife became unwell after eating a fish from the Calder River in northern Western Australia. Gnathostomiasis was diagnosed, and treated with ivermectin and albendazole. Serological testing was positive for gnathostomiasis, and there has been no recurrence. These appear to be the first proven endemically acquired cases of gnathostomiasis in Australia, and demonstrate the difficulties in diagnosis and treatment. (MJA 2011; 195: 42-44) Clinical recordsPatient 1A 52-year-old man developed epigastric discomfort, nausea, diarrhoea and lethargy 10 days after eating a fish (identified by the patient as “black bream”, possibly Acanthopagrus berda or Hephaestus jenkinsi) caught from the Calder River in northern Western Australia (Box 1). The fish had been pan-fried whole over a camp fire, but the duration and thoroughness of cooking is unclear. The patient’s epigastric discomfort persisted, followed a week later by fevers and myalgia and then pruritic subcutaneous swellings and skin thickening over his chest and abdomen. He had no response to a prescribed course of antibiotics. His abdominal symptoms and myalgia continued and, over the next 2 months, multiple episodic swellings developed over his abdomen. The swellings progressed to involve both thighs and were associated with feelings of movement under his skin. Examination revealed right thigh oedema and skin induration with a “peau d’orange” appearance. Blood investigation showed marked eosinophilia (7.27 x 109/L; reference range, < 0.5 x 109/L). Doppler ultrasound examination showed no evidence of deep venous thrombosis, and results of computed tomography of the abdomen and pelvis were normal. Serological evaluation for vasculitis and autoimmune disease was unremarkable. A presumptive diagnosis of parasitic infection was made, and ivermectin 12 mg was prescribed. Rapid improvement occurred, with a reduction in the patient’s eosinophilia to 1.6 x 109/L. Serological evaluation for schistosomiasis, cysticercosis, filariasis, angiostrongyliasis and strongyloides was negative. Eight weeks later, recurrent swelling of the patient’s right leg was treated with ivermectin. Three months later, further cutaneous symptoms were treated with three doses of ivermectin, with a subsequent eosinophil count of 0.44 x 109/L. A serological test for gnathostomiasis was positive (24 kDa immunoblot test conducted by the Department of Helminthology, Mahidol University, Bangkok, Thailand) 8 months after initial onset of symptoms. A simultaneous enzyme-linked immunoabsorbent assay (ELISA) for Gnathostoma antibody was positive (titre, 0.901 at 1:20 dilution), and a repeat ELISA 14 months later showed a similar titre (0.823 at 1:20 dilution). No earlier blood sample was available to demonstrate seroconversion. There has not been any recurrence of symptoms or eosinophilia over the subsequent 6 years. Patient 2A 50-year-old woman (Patient 1’s wife) developed fevers and lethargy 12 days after eating the same fish as her husband. Vomiting and abdominal cramps followed, and settled down over 10 days. When she returned to Melbourne 4 months later, the patient’s blood samples revealed an eosinophilia of 1.6 x 109/L. A further 4 months later, a trial of ivermectin (12 mg weekly for two doses) was prescribed for gnathostomiasis, and 4 months later her eosinophil count was 0.23 x 109/L. Serological testing for amoebiasis, strongyloides, filariasis and schistosomiasis was negative. A test for gnathostomiasis (24 kDa immunoblot) was positive 8 months after initial symptoms. An ELISA for Gnathostoma was also positive 8 and 20 months after initial symptoms, with little change in titre (0.903 and 0.886, respectively). Sixteen months after the initial symptoms (9 months after ivermectin), a pruritic swelling over the upper right arm developed with associated eosinophilia. Eosinophilia and chronic symptoms resolved following a single dose of ivermectin 12 mg, and albendazole 400 mg twice daily for 21 days. Two months later, a transient pruritic swelling over the right buttock was treated with repeat ivermectin (12 mg weekly for two doses). Subsequently, the patient had recurrent swelling of the right deltoid muscle and was given three further ivermectin doses. Symptoms have not recurred during 5 years of observation. DiscussionGnathostomiasis is a foodborne zoonosis, a clinical syndrome caused most commonly by infection with the larvae of Gnathostoma spinigerum, but also by several other Gnathostoma species.1,2 Humans may become accidental hosts after ingesting third-stage larvae (Box 2). The larvae are unable to mature further in humans, and they migrate through visceral and cutaneous tissues. Larvae may be found in a range of intermediate and paratenic hosts including freshwater fish, snakes, frogs, snails and fowl.1,3 Consequently, the disease is endemic where these foods are consumed raw or undercooked, including South-East Asia and Japan, but more recently recognised in Latin America, China, India, Africa and in travellers returning from these areas.1,2 Locally acquired infection in Australia has not previously been confirmed.4 The Gnathostoma life cycle is illustrated in Box 2. Following ingestion of viable larvae, patients often develop fever, anorexia, abdominal discomfort, nausea and vomiting as larvae penetrate the gastrointestinal wall. This is usually associated with a marked eosinophilia. Subsequently, symptomatic disease may have either cutaneous or visceral manifestations depending on the larval migration pattern. Cutaneous disease is more common, typically presenting with intermittent migratory erythematous swellings, which may be pruritic or painful. Cutaneous symptoms usually occur within 4 weeks of larval ingestion, and last 1–2 weeks. In untreated patients, larvae may survive up to 15 years and cause recurrent symptoms, by which time eosinophilia may have resolved. Less common cutaneous manifestations include nodular lesions, skin abscesses, panniculitis or creeping eruptions. The main differential diagnoses include cutaneous larva migrans, larva currens, trichinosis and Calabar swellings secondary to loiasis. Visceral disease may involve almost any part of the body. Pulmonary disease may manifest as a cough, pleuritic chest pain, haemoptysis, lobar consolidation or pleural effusions. Gastrointestinal disease may be asymptomatic, but is more frequently associated with sharp abdominal pains or inflammatory masses, or may mimic an “acute surgical abdomen”. Ocular disease has a variety of manifestations and often allows direct visualisation of the larvae. Untreated, gnathostomiasis of the central nervous system (CNS) is associated with the highest mortality (8%–25%), and 30% of survivors have long-term sequelae.1 Typically, symptoms begin with acute radicular pain or headache, lasting up to 5 days, as the larva penetrates the CNS via spinal cord nerve roots. Focal paralysis and cranial nerve palsies usually follow, and may progress to eosinophilic meningoencephalitis or encephalomyelitis. Subarachnoid haemorrhage and other vascular complications are less common presentations of CNS gnathostomiasis. Imaging reveals the haemorrhagic migratory tracts of the larvae. The main differential diagnosis for CNS disease is Angiostrongylus cantonensis. Definitive diagnosis of gnathostomiasis requires parasite extraction and identification, however small parasite size (2–3 mm) makes this impractical, and thus is no longer recommended. Therefore, gnathostomiasis is a clinical diagnosis, supported by epidemiological history, blood eosinophilia (although alone not sensitive or specific) and serological testing. Serological tests have surpassed non-specific antigen injection techniques, and include immunoblot testing (which detects antibodies to specific L3 antigen with a molecular mass of 24 kDa) and ELISA (which detects IgG1 or IgG2 to the crude L3 antigen).6-8 The immunoblot test appears to be the most specific, but is difficult to perform.6-8 In a series of four patients with parasitologically confirmed gnathostomiasis, and 15 patients with a presumptive diagnosis of gnathostomiasis, the 24 kDa L3 antigen immunoblot test had a sensitivity of 100% for parasitologically confirmed gnathostomiasis and 33% for presumed gnathostomiasis.8 The authors commented that the lower sensitivity in presumptively diagnosed cases was probably due to initial incorrect diagnoses. In the same series, 64 patients with other parasitic infections and 19 healthy control subjects were also tested, with only one positive result, giving a specificity of 99%.8 An ELISA to detect subclass immunoglobulin levels for crude L3 antigen, avoiding the difficult purification step, has been proposed as an alternative diagnostic test. Detection of IgG1 has the greatest sensitivity (98%) making it an attractive initial test, and IgG2 does not appear to cross-react with other parasitic species, thus providing the best specificity (88%) for diagnostic confirmation of gnathostomiasis.7 Neither test is available commercially, but both the immunoblot and ELISA are performed at the Department of Helminthology, Mahidol University, Bangkok, Thailand. Nevertheless, serological investigations for gnathostomiasis have limited validation, making precise estimates of sensitivity and specificity difficult. Cross-reactions may occur, so caution with interpretation is paramount. In the patients described, an evaluation for other parasitic infections was made in order to reduce the possibility of a false positive result. Data comparing the outcomes of treatment regimens are limited to observational studies only. In a series of 49 patients treated with albendazole 400 mg twice daily for 21 days, over 93% achieved a cure at 6 months.9 In the same series, the efficacy was similar in 21 patients treated with ivermectin 0.2 mg/kg as a single dose.9 There are few data comparing combinations of ivermectin and albendazole. Longer observational studies indicate that treatment failures are common, as demonstrated in the two patients above, and thus repeat treatment is recommended if symptoms recur.10 Proven endemic human gnathostomiasis has not previously been reported in Australia, although cases suspected to have been locally acquired were described in the 1970s (non-specific antigen injection was used for confirmation).4 Gnathostoma infection of mammals has been described in Australia.11,12 Therefore, we believe these cases are the first confirmed cases of locally acquired human gnathostomiasis in Australia. The two patients had clinical syndromes compatible with gnathostomiasis, associated blood eosinophilia, positive serological results and supportive epidemiological history, and they responded to treatment. Importantly, neither of the patients had previously travelled outside Australia. Weaknesses of this report include that we were unable to definitively identify the fish species or determine how thoroughly the fish was cooked. Although it is a rare disease, gnathostomiasis needs to be considered in patients coming from endemic areas, and also in patients who have not left Australia, who present with migratory cutaneous lesions and associated peripheral blood eosinophilia. Visceral disease may be more difficult to diagnose due to the broad differential diagnoses, but gnathostomiasis must be considered in those with eosinophilic neurological syndromes due to the high mortality in untreated disease. 1 Calder River, West Kimberley region, northern Western Australia, where the “black bream” was caught 2 Gnathostoma life cycle5

Cameron J Jeremiah MB BS · Chanad S Harangozo MB BS, FRACP · Andrew J Fuller MB BS, FRACP, FRCPA

Medical students and junior doctors are increasingly interested in opportunities to practise their craft abroad. Some will undertake a medical elective, others will assume training positions in foreign hospitals and research institutes. Many will commit to an extended period of time working in a humanitarian or development setting. Organising a placement is not a straightforward task, however. Navigating the quagmire of available resources can be laborious and confusing. And while good sources of information do exist — travel books, websites and databases among them — identifying current and targeted content can be a challenge. This Guide aims to provide practical information that will help medical students and junior doctors undertake work abroad that is meaningful and rewarding for their own personal and professional development and, more importantly, for their host community. While it has been developed with all international settings in mind, the focus is on medical practice in under-resourced environments. The Guide was launched as an MJA eSupplement by MJA editor Dr Annette Katelaris and guest speakers Professors Rob Moodie and Mike Toole at AMA House, Victoria, on 21 June 2011. This was a joint project by the Australian Medical Students’ Association, the AMA and the MJA, and is freely available on the MJA website. http://www.mja.com.au/public/issues/194_12_200611/working_abroad.html. Left to right: Dr Annette Katelaris, Editor MJA; Mr David Humphreys, co-author of the Guide; Dr Rob Mitchell, co-author and Council of Doctors-in-Training Deputy Chair; Dr Jenny Jamieson, Prof Rob Moodie, Nossal Institute for Global Health; Prof Mike Toole, Burnet Institute; Dr Hamish Graham, co-author; and Dr Sarah Mansfield, co-author. Co-authors not pictured: Dr Jake Parker, Dr Fred Hersch, Dr Kate Brennan

Jake Parker · Rob Mitchell · Sarah Mansfield · Jenny Jamieson · David Humphreys · Fred Hersch · Hamish Graham · Kate Brennan

Haemoglobin A1c (HbA1c — a term that is sometimes used interchangeably with “glycated haemoglobin”) measurements are an indicator of time-averaged blood glucose levels (previous 2–3 months), and are used as the best marker of long-term diabetes control. A recent consensus statement on the worldwide standardisation of HbA1c measurement1 has updated previous international recommendations on the standardisation of HbA1c measurement and reporting.2 Here, we provide the rationale and guidance for implementation of HbA1c reporting in the new Système International (SI) units in Australia. This article represents the views of the Australasian Association of Clinical Biochemists, the Australian Diabetes Educators Association, the Australian Diabetes Society and the Royal College of Pathologists of Australasia, and was prepared by a working party of representatives of these organisations. The International HbA1c Consensus Committee recommends that all HbA1c levels be reported in SI units (mmol/mol, no decimal places) — with results directly traceable to the International Federation of Clinical Chemistry and Laboratory Medicine (IFCC) reference method — and in the currently used, National Glycohemoglobin Standardization Program (NGSP) units (percentage, one decimal place). We recommend that dual reporting in Australia begins in July 2011, and that reporting of percentages ceases 2 years later. In New Zealand, dual reporting commenced in August 2009. The key reasons for implementing this recommendation in Australia are that: the SI units relate to a scientifically valid measure of HbA1c; the SI units remove potential confusion between HbA1c values as a percentage and blood glucose values in mmol/L; the change is in keeping with the international consensus statement;1 and the change has already been initiated in New Zealand and a number of countries in the European Union. Until now, all HbA1c measurements performed in Australia have been reported as percentages (HbA1c as a percentage of total haemoglobin) that are aligned with those produced in the Diabetes Control and Complications Trial.3 These units and this standardisation have been promoted by the NGSP in the United States, and the activities of this organisation have produced marked improvement in the accuracy of HbA1c results worldwide. More recently, the IFCC has developed a reference method that is more specific for HbA1c and more analytically robust.4 The IFCC method is now used as the reference system by the NGSP and for all routine methods for measurement of HbA1c, although a numerical conversion is required during the calibration process. The changes recommended here will provide results that are directly aligned with the IFCC method. As the IFCC method is more specific for HbA1c, not measuring several other haemoglobin–sugar complexes, the results are 10% to 40% lower than those from the NGSP system, depending on HbA1c concentration. Because reporting these results as percentages may lead to confusion (eg, producing a result of 5.3% rather than 7.0%), the units are changed to mmol/mol (millimoles HbA1c per mole of total haemoglobin [53 mmol/mol in the previous example]), which is consistent with the SI units recommended for use in Australia. There is a linear relationship between results from the two methods, and the “master equation” is used to convert results between the two methods: HbA1c SI unit (mmol/mol) = 10.93 × HbA1c NGSP unit (%) − 23.50.5 To make the conversion easier for clinicians, it is important to translate current treatment advice to the new units. A general conversion table for clinical use is provided in Box 1. The general HbA1c target of ≤ 7.0% for patients with type 1 and type 2 diabetes mellitus equates to ≤ 53 mmol/mol, although these values need to be individualised for patients. The recently updated diabetes treatment guidelines are shown with SI units in Box 2 and Box 3,6 and recommendations for reporting HbA1c levels in Australia are summarised in Box 4. In addition, supporting material for doctors and patients will be presented in SI units in the future. The routine reporting of an estimated average glucose (eAG) value may be useful for consultations with individual patients. However, the working party strongly agrees with the revised consensus statement that routine reporting of eAG with all requests for HbA1c analysis is not appropriate.1 The reasons for this include variability in the methods used to measure eAG, the risk of confusing a measure of long-term glycaemia (eAG) with a measure of short-term blood glucose control (actual blood glucose level), and its lack of applicability in the majority of patients with type 2 diabetes (in whom blood glucose levels are not measured at frequent intervals).7 Nonetheless, eAG values will be used as an educational tool at the discretion of individual clinicians, who can assist patients to understand the significance and limitations of the result. 1 Conversion table for haemoglobin A1c (HbA1c) values HbA1c as percentage (old units) HbA1c in mmol/mol (new units) 5.0 31 6.0 42 6.5 48 7.0 53 8.0 64 9.0 75 10.0 86 11.0 97 12.0 108 2 Recommended haemoglobin A1c (HbA1c) target ranges for patients with type 1 diabetes6 HbA1c target General target ≤ 53 mmol/mol, ≤ 7.0%* Specific clinical situations Pregnancy or planning pregnancy ≤ 53 mmol/mol, ≤ 7.0%*† Children and adolescents ≤ 58 mmol/mol, ≤ 7.5%* Recurrent severe hypoglycaemia or hypoglycaemia unawareness ≤ 64 mmol/mol, ≤ 8.0% Patients with major comorbidities likely to limit life expectancy Symptomatic therapy of hyperglycaemia‡ and avoidance of ketosis * Achievement of HbA1c targets must be balanced against risk of severe hypoglycaemia. † An HbA1c level of ≤ 42 mmol/mol (≤ 6.0%) is desirable if it can be achieved safely. ‡ Where practical, suggest blood glucose target level < 15 mmol/L to help minimise risk of infection. 3 Recommended haemoglobin A1c (HbA1c) target ranges for patients with type 2 diabetes6 HbA1c target General target ≤ 53 mmol/mol, ≤ 7.0%* Specific clinical situations Diabetes of short duration† and no clinical cardiovascular disease Requiring lifestyle modification ± metformin ≤ 42 mmol/mol, ≤ 6.0%* Requiring any antidiabetic agents other than metformin or insulin ≤ 48 mmol/mol, ≤ 6.5%* Requiring insulin ≤ 53 mmol/mol, ≤ 7.0%* Pregnancy or planning pregnancy ≤ 42 mmol/mol, ≤ 6.0%* Children and adolescents ≤ 53 mmol/mol, ≤ 7.0%* Diabetes of longer duration† or clinical cardiovascular disease (any therapy) ≤ 53 mmol/mol, ≤ 7.0%* Recurrent severe hypoglycaemia or hypoglycaemia unawareness (any therapy) ≤ 64 mmol/mol, ≤ 8.0% Patients with major comorbidities likely to limit life expectancy‡ (any therapy) Symptomatic therapy of hyperglycaemia§ * Achievement of HbA1c targets must be balanced against risk of severe hypoglycaemia, especially among older people. † In an older adult, long duration might be considered to be > 10–20 years, but for a person who develops type 2 diabetes at a young age, it might be considerably longer. ‡ Examples of major comorbidities include chronic medical conditions, such as chronic kidney disease stages 4 or 5; heart failure stages III or IV (New York Heart Association grading); incurable malignancy; and moderate to severe dementia. § Where practical, suggest blood glucose target level < 15 mmol/L to help minimise risk of infection. 4 Recommendations for reporting haemoglobin A1c (HbA1c) levels in Australia From July 2011, HbA1c levels should be reported in both National Glycohemoglobin Standardization Program units (percentage) and the Système International (SI) units (mmol/mol) by all pathology laboratories and, where possible, from point-of-care devices. The period of dual reporting will be 2 years, after which only the SI units will be used. These recommendations are consistent with international recommendations and are already in place in New Zealand.

Graham R D Jones MB BS, DPhil, FRCPA, Chemical Pathologist · George Barker BHSc, CDE-RN, NP · Ian Goodall BSc, FAACB, FFRCPA · Hans-Gerhard Schneider MD, FRACP, FRCPA · Mark D S Shephard MAACB, FFRCPA, PhD · Stephen M Twigg MB BS, PhD, FRACP

In recent years, lymphogranuloma venereum, which is caused by C. trachomatis serotypes L1–L3, has emerged as a problem among men who have sex with men (MSM). Cases of LGV have been reported among MSM in the United States, United Kingdom, Europe and Australia, and have been overrepresented among HIV-positive MSM.1,2 In contrast to infections seen in developing areas where LGV remains endemic, the more recent reports among MSM in Western countries have been characterised by a predominance of proctitis cases, with fewer genital or inguinal presentations.1-3 Furthermore, nearly all recent cases have involved a clonal strain of the C. trachomatis L2b serovar.4 Genital LGV infections are commonly heralded by transient genital ulceration, followed by lymphatic spread and the development of local lymphadenopathy. A transient genital ulcer reported by Patient 2 had resolved before the development of the bubo. LGV infections causing ulceration and proctitis are readily detected using commercially available C. trachomatis nucleic acid amplification assays such as PCR or SDA. However, for LGV to be confirmed microbiologically, further genotyping is required to identify C. trachomatis serovars L1–L3, as distinct from the more common non-LGV-associated serovars D–K. This requires awareness on the part of the clinician, as LGV genotyping is only available from reference laboratories in most countries. In a symptomatic patient with a positive C. trachomatis nucleic acid amplification assay result, the clinician must specifically request referral of the original specimen or DNA extract for further testing, potentially delaying the final diagnosis. Newer amplification assays that can directly detect C. trachomatis serovars from clinical specimens are under development, but none are commercially available and they may not be cost-effective for routine diagnostic use in most settings.5 C. trachomatis serological testing can sometimes be useful for diagnosing LGV when there is no obvious lesion for sampling by PCR. However, a positive serological result does not discriminate between LGV and non-LGV chlamydial infections.6 In a recent study among MSM in Melbourne, 7% (21/292) of chlamydial rectal infections were associated with the L2 or L2b serovar.7 The distinction between LGV and non-LGV chlamydial infection of the rectum is potentially important, as a single 1 g dose of azithromycin is commonly used for non-LGV chlamydial infection, while more prolonged treatment — usually a 3-week course of doxycycline — is recommended for LGV.8-10 The extent to which inadequate treatment might be contributing to further transmission of LGV between men is not known. The diagnosis of LGV should be considered in MSM with proctitis, anogenital ulcers or inguinal buboes, particularly in HIV-positive men. If LGV genotyping is not readily available, an alternative approach would be to treat such men with a 3-week course of doxycycline or to perform a test-of-cure to ensure that the treatment has cured the patient of LGV. Clinical records An HIV-positive man (Patient 1) presented with a 4-day history of a painful anal ulcer (Figure, A), which was associated with a small, tender left-sided inguinal lymph node. He was not taking antiretroviral therapy and had a CD4 cell count of 648 cells/μL and an HIV viral load of 25 500 copies/mL. The man’s male sexual partner (Patient 2), also HIV-positive, presented on the same day with a lump in the left inguinal region (Figure, B). He was taking antiretroviral treatment and had a CD4 cell count of 494 cells/μL, with an undetectable HIV viral load (< 50 copies/mL). The lump had been present for 4 weeks and had enlarged despite treatment with amoxycillin followed by flucloxacillin given at a hospital emergency department. Two weeks before the lump appeared, the patient reported that there had been a sore on the penis but this had resolved before the lump developed. The inguinal lump had overlying erythema and was slightly fluctuant. Given these men were sexual partners, the diagnosis most likely to explain the presence of an inguinal bubo in one partner and anal ulceration in the other was lymphogranuloma venereum (LGV). Both men were treated with oral doxycycline 100 mg twice daily for 3 weeks. Patient 1 was reviewed 1 week later, by which time the anal ulcer had begun to resolve and a swab taken from the ulcer at the previous visit had tested positive for Chlamydia trachomatis by strand displacement amplification (SDA) assay and negative for herpes simplex virus and Treponema pallidum by polymerase chain reaction (PCR) assay. In both men, serological tests for syphilis returned negative results, and white cell counts were normal. Despite the doxycycline therapy, Patient 2’s bubo had enlarged further when examined 3 weeks later, with increased swelling, erythema and fluctuance. A hollow-bore needle was used to aspirate 5 mL of milky pus from the bubo. Light microscopy of the Gram-stained aspirate showed few polymorphs, and no bacteria, parasites or fungi. No acid-fast bacilli were seen on Ziehl–Neelsen staining, and bacterial culture showed no growth. The aspirate tested positive for C. trachomatis and negative for T. pallidum and Neisseria gonorrhoeae by PCR assay. Cytological examination of the aspirate showed acute inflammation, with no organisms identified. Despite the initial aspiration and continued therapy with doxycycline, the bubo reformed and then spontaneously discharged 2 days later, leaving a sinus (Figure, C). Genotyping of the chlamydia isolates from the anal ulcer and the bubo aspirate confirmed the presence of C. trachomatis serovar L2b in each patient. Both men also tested positive for C. trachomatis IgG and IgA by enzyme immunoassay.

Marcus Y Chen FRCP, PhD, MRACP · Timothy R H Read MB ChB, FACHSM · David E Leslie MB BS, FRACP · Melanie Bissessor MB ChB

General medicine is being challenged by increasing numbers of patients who are presenting with multiple comorbidities and a decline in numbers of suitably trained personnel to manage these patients. A resurgence in generalist care, with collaboration between generalists and specialists, is the key to successfully managing patients who present with acute medical conditions. Better funded collaborative training programs for general physicians, which promote a diversity of skills and address clinical demand in a proscriptive manner, are needed. Research aimed at designing acute services to match local clinical demand is also required.

Paul F Jenkins MA, MB BChir, FRCP · Campbell H Thompson MD, DPhil, FRACP · Alasdair B MacDonald BMedSc, MB BS, FRACP

To the Editor: Young children are at increased risk of severe influenza compared with the general population. Routine vaccination of children using trivalent influenza vaccine (TIV) is recommended in the United States and Canada. The Western Australian government, with support from vaccine manufacturers, has been providing TIV free of charge to all children aged 6–59 months since 2008.1 In 2010, high fevers and an increased incidence of convulsions were observed in children aged < 5 years after administration of TIV. Most reports of adverse events were from WA, owing to higher uptake of vaccination associated with the free vaccination program. The national influenza vaccination program for children aged < 5 years was subsequently suspended,2 and high rates of fever and convulsions were confirmed.2,3 The majority of adverse events occurred after administration of Fluvax or Fluvax Junior (CSL Biotherapies). More than 50% of parents of children who were administered Fluvax or Fluvax Junior reported high fever after vaccination. The incidence of febrile convulsions after vaccination with Fluvax and Fluvax Junior was 4.4 per 1000 doses, significantly higher than expected.3,4 Fluvax and Fluvax Junior are not recommended for children aged < 5 years in the Australian 2011 influenza vaccination program.5 In response to these events, WA Health established an online registry for vaccine-associated adverse events — the Western Australian Vaccine Safety Surveillance (WAVSS). Health professionals are required and members of the public encouraged to report adverse events. In addition, a prospective safety study of the 2011 TIV in children aged < 5 years has commenced at Princess Margaret Hospital for Children and the WA Central Immunisation Clinic. From 15 March to 29 April 2011, 2227 doses of TIV were administered to children aged < 5 years in WA (2130 doses of Vaxigrip [Sanofi Pasteur]; 97 doses of Influvac [Solvay]). Adverse events in four children aged < 5 years have been reported via WAVSS: two with elevated temperature (≥38°C yet < 39.5°C) within 24 hours of vaccination, one with vomiting and diarrhoea after vaccination, and one with fever (not specified) and convulsions 4 days after vaccination (this child had a respiratory tract infection at the time of vaccination). All four children were administered other vaccines with TIV. In the safety study, 144 children were enrolled between 15 March and 29 April 2011. Adverse events after vaccination were reported in 10 children (7%), two of whom received other vaccines in addition to TIV. All 10 children had fever reported, and one child had a temperature > 39.5°C. Two children developed vomiting. No convulsions were reported and none of the children who had adverse events required assistance from a health care professional. These data demonstrate that the significant adverse events that occurred after administration of TIV in 2010 have not been observed in WA during early 2011. Ongoing surveillance is underway and will continue. Poor uptake of influenza vaccination in Australian children is likely to result in increased influenza-related hospitalisation, morbidity and mortality. Data such as those reported here are required to reassure the community of the safety of this vaccination program before the expected start of the 2011 influenza season.

Christopher C Blyth · Tracy Y Markus · Paul V Effler · Peter C Richmond

To the Editor: Australian influenza notification and hospitalisation rates are highest in children aged under 5 years,1 the group most commonly affected by egg allergy (estimated to affect 8.9% of infants aged 12 months in a recent Melbourne study).2 The ability to safely vaccinate egg-allergic individuals is thus an important public health issue, particularly in the context of potentially pandemic influenza. More than 98% of over 4000 egg-allergic individuals have tolerated vaccination under direct medical supervision in published studies.3-6 As a result, Australian and several international guidelines3,5,6 recommend that influenza vaccination of the egg-allergic individual may be undertaken using a two-step protocol (10%–90% vaccine dose, 30 minutes apart with a final 30-minute waiting period), as long as vaccines contain less than 1 μg egg ovalbumin/dose. Prior allergy testing with the vaccine is not recommended. All currently available influenza vaccines for the 2011 season in Australia have less than 1 μg ovalbumin/dose, specifically Influvac (Abbott Pharmaceuticals, < 1 μg/dose), Intanza (Sanofi Pasteur, < 0.05 μg), Vaxigrip and Vaxigrip Junior (Sanofi Pasteur, < 0.05 and < 0.025 μg, respectively), Fluvax (CSL, < 1 μg), Agrippal (Novartis, < 0.20 μg) and Fluarix (GlaxoSmithKline Australia, < 0.05 μg). Based on current evidence, we suggest that the 2011 seasonal influenza trivalent vaccines can be safely administered in a medically supervised primary care setting as a single dose with a 30-minute observation period (rather than the standard 15 minutes) in those with non-anaphylactic reactions to egg. In those with a history of egg anaphylaxis (or positive allergy tests without a history of ingestion), we recommend a split-dose protocol after discussion with an allergy specialist. We acknowledge that these guidelines are at variance with those in the Australian immunisation handbook,7 but they are consistent with more recent evidence and international recommendations. Whether it is also safe to administer vaccines containing more than 1 μg ovalbumin/dose8 awaits confirmation in a larger patient population and is not currently recommended.

Raymond J Mullins · Michael S Gold

To the Editor: Amid debate about growth in the number of Disability Support Pension (DSP) recipients and the increasing percentage of recipients with mental disorders,1,2 the recent federal Budget announced further welfare reforms and significant investment in mental health services.3 There are, however, limitations in the data informing the current discussion. Administrative data are restricted to coding the primary disability of DSP recipients, and do not assess comorbidity. Further, data on the health of recipients receiving other welfare payments are lacking, precluding thorough understanding of the context of the growth in the DSP population. We recently published an analysis of the 2007 Australian Bureau of Statistics National Survey of Mental Health and Wellbeing, in which we estimated the prevalence of common mental disorders in different categories of working-age welfare recipients.4 The main results showed that just over one-third (34%) of income-support recipients had a 12-month affective, anxiety and/or substance use disorder, compared with 20% of non-recipients; that, despite a decade of reform of the welfare and mental health systems and improved economic circumstances, there had been little change in the overall prevalence of mental disorders among welfare recipients since 1997 (Box, A);5 and that most income-support recipients with mental disorders received payments other than DSP. We compared data from the 1997 and 2007 surveys, focusing on welfare recipients with a mental disorder (12-month common mental disorder assessed by the World Mental Health Composite International Diagnostic Interview). Of the 10 641 and 8841 survey respondents in 1997 and 2007, 667 and 362, respectively, were identified as working-age welfare recipients with a mental disorder.5 We estimated that 31% of income-support recipients with mental disorders were DSP recipients in 1997, but in 2007 this had increased to 45% (Box, B). The increased concentration of recipients with mental disorders receiving the DSP was significant in logistic regression models controlling for age and sex (odds ratio, 1.72; 95% CI, 1.05–2.83).5 The increased profile of mental disorders among DSP recipients may reflect shifts between payments within the welfare recipient population. Although this could be due to financial incentives to receive DSP rather than lower-paying allowances (eg, Newstart Allowance), the results may reflect that some income-support recipients with a mental disorder are unable to comply with the new activity or work requirements introduced by recent policy changes.6 Careful consideration is needed of the potential adverse unintended consequences of welfare reforms for the large number of income-support recipients with mental disorders. Changes that promote DSP as the most appropriate option for people with mental disorders risk entrenching their alienation from the workforce. Mental disorders and welfare recipients (with 95% CIs), 1997 and 20075 DSP = Disability Support Pension.

Peter Butterworth · Philip M Burgess · Harvey Whiteford

To the Editor: The Health Practitioner Regulation National Law Act 2009 (Part 8, Sections 140 and 141) enshrines mandatory notification in the new national registration framework. As registered health practitioners, clinician-researchers are bound by the notification requirements. This raises the question of whether mandatory notification has implications for observational research in health services that is conducted by clinician-researchers. In particular, how likely is it that these requirements will lead to reclassification of one’s observations from “research data” to “notification evidence”? Three initial considerations are important here. First, the Act was designed to make health care safer for patients. Its intent is to limit incidents by ensuring clinicians are more open about and address inappropriate care. Second, serious incidents are rarely isolated, instantaneous and therefore easily observable disasters. When something goes seriously wrong, problems tend to be inherent in how teams practise, communicate and support one another over time. Third, observers may encounter instances of substandard care, but these become notifiable only when the threshold of unsafety is surpassed. This threshold is pegged to relatively high levels of severity, frequency and risk.1 In all, observational research can help clinicians to identify existing risks, but it is unlikely to become a source of notification. Human research ethics committees may also feel obliged to acknowledge and consider the possibility of incident notifications arising from observational research. However, it would not be wise to regard the risk of such notification as detracting from a study’s potential for obtaining ethics approval. The situation calls for specification of: how the observers will deal with incidents if and when observed the observers’ understanding of the definition and threshold of notification how the definition of notification is likely to bear on the study how the design of the study affects the likelihood of notification (eg, does the researcher seek to identify care irregularities or track these irregularities over time?) a projection of the relevant service’s vulnerabilities to notification, and plans for addressing and resolving existing vulnerabilities. In addition, mandatory notification does not mean that observational research will be more difficult to “sell” to ethics committees and frontline clinicians. The aim is generally to stimulate learning and raise awareness of problems. Our experience is that if the research is designed with frontline clinicians, and they contribute to its implementation, analysis and publication,2 it attracts considerable interest and support.3 Frontline staff know that the best way to understand the complexities inherent in their everyday work is through observation. Such research takes seriously their specific and unique circumstances, enabling them to actively participate as analysts and improvers of their own practice. Observation encourages reflection, and this means they become aware of and can proactively resolve their own vulnerabilities. Ultimately, the priority for clinician-researchers involved in observational research in health services, as for patients, is to reduce risks and prevent incidents.

Rick A M Iedema · Donella A Piper

To the Editor: We read with interest the case by Nadeem and Khateeb of an elderly man with migratory lung lesions and the concurrent finding of mixed cryoglobulins.1 We are concerned about attributing this man’s symptoms to mixed essential cryoglobulinaemia. The clinical syndrome described in this patient is not typical of cryoglobulinaemia. The establishment of a diagnosis of essential mixed cryoglobulinaemia in this man is problematic, given a lack of cutaneous findings and no definite evidence of peripheral neuropathy and renal disease. Nerve conduction studies to establish the presence of peripheral neuropathy and renal biopsy to confirm membranoproliferative glomerulonephritis were not carried out. Given his age, the confirmation of membranoproliferative glomerulonephritis would potentially necessitate long-term and possibly intensive immunosuppression to prevent subsequent development of renal failure. The cryoglobulins reported in this case fulfil the criteria for type II cryoglobulins. However, they were of relatively low concentration (0.4 g/L of monoclonal IgM/kappa and 0.1 g/L of polyclonal IgG). As well as hepatitis C, type II cryoglobulins can be detected in association with hepatitis B and Sjögren’s syndrome.2 The absence of anti-Sjögren’s syndrome A and anti-Sjögren’s syndrome B antibodies by no means excludes the diagnosis of concurrent, subclinical Sjögren’s syndrome. In addition, hepatitis B and C have not been excluded as the cryocrit was not analysed for hepatitis B virus DNA and hepatitis C virus RNA. Furthermore, the relatively low concentration of cryoglobulin detected and the findings of chest opacities with very high levels of C-reactive protein (that fell to normal levels with antibiotic treatment) could also be due to an infective aetiology.3 We also note that the thermal amplitude of the cryoglobulins should be investigated in such cases, as it has been well described that cryoglobulins of higher thermal amplitudes are more likely to be clinically significant. In conclusion, given the long duration of this man’s admission, repeat cryoglobulin measurements after he was discharged would have helped to more clearly define the role of cryoglobulins in his disease. We therefore recommend caution when interpreting low levels of cryoglobulinaemia in patients who have a clinical syndrome that may or may not be consistent with clinical cryoglobulinaemia.

Carl A Kennedy · David Gillis · Richard C W Wong

To the Editor: Katelaris recently asserted: In our society the response to medical error is typically legal, rather than investigative and remedial. This should be deplored by both the profession and the public.1 This polarised orientation seems more political than objective. It acknowledges neither the reticence of medical professionals regarding investigative reviews, nor the costs to patients’ families. Katelaris notes that defensive approaches encourage the concealment of errors. I have long advocated clinical reviews of critical incidents. Having personally set up Queensland Health’s original Suicide Register, I released statewide patient suicide data to health services. Reactions from service providers were decidedly underwhelming, despite the gravity of the outcomes. Katelaris did not explain how clinical reviews can address the problem of income replacement or other major costs associated with catastrophic outcomes for patients’ families. In the 1990s, I reviewed all Australian litigation for failure to prevent suicidal behaviour in care, through a survey of insurers and defendant solicitors.2 Of the 13 non-fatal cases identified, paraplegia occurred in seven patients, with other serious injuries in the remaining six. These were not trivial complaints. I also reviewed what might be learnt from the international literature3 and made known my availability to assist with clinical reviews of patient suicides. Despite having been an expert witness at the Royal Commission into Aboriginal Deaths in Custody and a Royal Australian Navy inquiry into the loss of a sailor who disappeared overboard in 2002, among others, no medical services have sought my assistance over more than 20 years! I understand, from personal experience, how distressing trivial and vexatious complaints against doctors are. I have even received a complaint for providing a report to a plaintiff’s solicitor, in relation to failure to prevent suicidal behaviour, in which I asserted that reasonable care had been provided. I now run a personal-injury psychiatric practice, with alleged medical negligence featuring in about 3% of cases. Mostly I am called by the plaintiff’s side, often following devastating surgical outcomes. Referral bias operates, in that negative surgical outcomes with psychiatric consequences are likely to have been more serious than those without. The outcomes have often been both emotionally and financially devastating to those affected. I long to see a medically mature culture develop with respect to clinical reviews of critical incidents, but my experience suggests we still have a way to go. But even when or if such a medical utopia is achieved, how will the financial disadvantages to patients’ families be overcome?

Christopher H Cantor

To the Editor: I was extremely surprised to note that there was no mention of the Australian Council on Healthcare Standards’ (ACHS) extensive national clinical database (http://www.achs.org.au/ClinicalIndicators) in the recent article by Evans and colleagues on clinical-quality registries.1 Since 1993, commencing with a small set of generic indicators that were of limited value, the ACHS has been collecting clinical data through its clinical indicator (CI) program as part of its accreditation process. Now, with over 300 CIs in use and around 670 health care organisations (HCOs), including some from New Zealand, contributing data, the scope of the ACHS national clinical database is unique in the world. Its longevity makes it one of very few national programs that can display longer term trends in processes and outcomes — both desirable and undesirable — of medical care. The clinical indicators, which form the basis of the database, were all developed in conjunction with providers of medical care, namely, the medical colleges. The validity, reliability and effectiveness of the indicators were established (and published) subsequent to introduction of the more specific indicators into the accreditation process.2 In addition to providing aggregate and peer-comparative data to the contributing HCOs, the ACHS publishes aggregate data with detailed analyses on an annual basis.3 As with similar databases, problems have arisen regarding maintenance of currency and relevance, timelines for reporting, and other issues. However, it seems extraordinary that this valuable aid to determining the quality of health care standards — envied by many countries — could be ignored by Evans et al, as it was similarly ignored by the authors of a recent special MJA supplement that reported on gathering patient-centred health care data aimed at improving care.4

Brian T Collopy, AM

To the Editor: Cancer Voices NSW, a leading organisation for health care consumers, welcomes the coverage in the 18 April issue of the Medical Journal of Australia of gaps in and barriers to research endeavours into cancer. We particularly commend Olver’s editorial which, among other things, calls for more consumer-friendly clinical trial registries to play a role in enhancing patient recruitment by making it easier for them to find suitable trials.1 Cancer Voices NSW (http://www.cancervoices.org.au), the voice of people affected by cancer in our state, has long advocated for such a resource, both centralised and reliable. We are delighted to advise Journal readers that an initiative of ours, the Australian Cancer Trials website (http://www.australiancancertrials.gov.au), is now up and running. It has been publicly available since its launch by Professor Jim Bishop, Australia’s Chief Medical Officer, in November 2010 and is hosted by Cancer Australia. In partnership with consumers, the development of the project was led by a research team that included members from the University of Sydney, the Australian New Zealand Clinical Trials Registry (ANZCTR), Cancer Voices NSW and Cancer Australia. Consumers had considerable input to the website’s development through consultation with members of Cancer Voices NSW and Cancer Australia’s National Consumer Advisory Group. The Australian Cancer Trials website was funded by Cancer Australia with partial funding from the National Health and Medical Research Council project grant (grant reference number 512380). The Australian Cancer Trials website’s consumer-friendly portal offers open access information held on both the ANZCTR and the United States ClinicalTrials.gov registers (http://clinicaltrials.gov/). It currently lists over 1000 cancer trials, and it is updated every day. Consumers can do a “simple search” by cancer type or keyword or an “advanced search” using criteria including cancer status, trial focus, phase of clinical trial, recruitment status and age category. Information about each trial is displayed in a user-friendly format. All cancer trials registered with ANZCTR in Australia for which a few consumer-friendly additional cancer fields are completed at registration will find recruitment easier. Patients with cancer and their specialists will have much easier access to up-to-date clinical trial information. This website is a successful model that can be translated to other diseases and conditions, and indeed, generically.

Sally Crossing

CorrectionsIncorrect statement: In “Fraud in fluid resuscitation research” in the 20 June 2011 issue of the Journal (Med J Aust 2011; 194: 621-622), there was an error in the second-last paragraph (page 622). The second sentence of this paragraph should have read “This code was established by the National Health and Medical Research Council and the Australian Research Council to bolster responsibilities of research organisations.11” The html and pdf versions of this article were corrected when published online on 20 June 2011.

John A Myburgh

CorrectionsIncorrect estimate of number of lives saved by the use of surgical checklists: In “Is money spent on quality improvement better spent on clinical care?” in the 20 June 2011 issue of the Journal (Med J Aust 2011; 194: 641), the order of magnitude of the number of lives potentially saved in Australia by surgical checklists is incorrect. The potential saving is thousands of lives rather than “tens of thousands of lives”. The html and pdf versions of this article were corrected when published online on 20 June 2011.

William B Runciman

Colorectal surgery clot risk The incidence of venous thromboembolism (VTE) is significantly higher among patients undergoing open colorectal resections compared with those undergoing laparoscopic colorectal resections (0.8% v 1.4%; P < 0.001), according to new research of nearly 150 000 patients in the US. The findings persisted after stratification for surgery site and pathological condition. A possible explanation is the fact that the laparoscopic procedures are linked to less pain and postoperative ileus, leading to earlier ambulation and shorter hospital stays. The researchers also looked at what conditions were associated with VTE, and found higher blood clot rates among patients with inflammatory bowel disease, followed by cancer and diverticulitis. Arch Surg 2011; 146: 739-743 Dying young in the USA Although the US has the highest levels of health spending per capita, new research shows that its citizens are not living as long as people in many other countries. In 2007, the US life expectancy at birth was 75.6 years for men and 80.8 years for women, ranking 37th in the world for both sexes. The research found vast disparities between American counties, with life expectancy ranging from 65.9 to 81.1 years for men, and from 73.5 to 86.0 years for women. During the period from 2000 to 2007, the increase in life expectancy in most of the US counties fell behind that in other nations. In some parts of the US, life expectancy in 2007 was equivalent to the life expectancy in 1957 in the world’s best-performing countries. The authors comment that improving risk factors such as smoking, adiposity, high blood pressure and elevated blood glucose could substantially improve life expectancy. Popul Health Metr 2011; 9: 16 (Online 15 June) Statins: still a wonder drug? Statins have sometimes been described as “wonder drugs” for their ability to cut cholesterol, with recent suggestions that everyone over 55 should be taking the pills.1 However a new meta-analysis finds that intensive-dose statin therapy is associated with an increased risk of new-onset diabetes compared with moderate-dose statin therapy.2 The research looked at five randomised clinical trials providing data on 32 752 non-diabetic patients, over an average follow-up of 4.9 years. Among patients assigned to the intensive statin treatment (eg, atorvastatin 80 mg), there were 416 fewer patients with cardiovascular events, but 149 more cases of incident diabetes. The authors comment that the “net cardiovascular benefit in high-risk individuals will still strongly favour statin therapy”; however, they suggest that clinicians should be vigilant for the development of diabetes in patients receiving statin therapy. 1 PLoS ONE 2011 6 (5): e18742 (Online 4 May) 2 JAMA 2011; 305: 2556-2564 The reluctant sickie Taking a “sickie” is arguably something of an Australian tradition, but a comment piece in the BMJ suggests that health care professionals may be reluctant to stay home when they are unwell. The article refers to recent research which found that over a 4-week period, one-third of doctors and nurses worked when they should have taken sick leave (a phenomenon known as “presenteeism”). Presenteeism is said to be more common among those who have a greater responsibility for patient care, a lack of back-up and an accumulating workload during absence. Stimulating workplaces can also promote presenteeism among workers with high job satisfaction. The comment piece points to evidence suggesting that presenteeism increases morbidity including musculoskeletal pain, fatigue, depression and serious coronary events. Going to work when sick is of particular concern in health care settings because of the risk of spreading infections, the author comments. BMJ 2011; 341: d3446 “Coming out” without coming down Doctors who are counselling gay, lesbian or bisexual people about coming out may be interested in new research which found that revealing one’s sexual identity does not always confer psychological benefits. The psychological pay-offs of coming out, such as reduced anger and depression and increased self-esteem, only occur in supportive settings. The qualitative study of 161 gay, lesbian and bisexual people in the US found that among hostile groups, the costs and stigma of identifying as gay cancelled out the benefits. The research found that friends, then families, were perceived as the most supportive and accepting groups, while religious communities and schools were rated as more controlling and judgemental. Soc Psychol Personal Sci 20 Jun 2011 (online)

Sophie McNamara