Letters

To the Editor: The expert working party that developed the Australian Medical Council (AMC) draft code of professional conduct referred to by Komesaroff and Kerridge1 was chaired by Joanna Flynn, past President of the Victorian Medical Practitioners Board (MPB [Vic]). Herein lies the crunch. The AMC is surely meant to be an independent and objective body — yet if it is aligned with the MPB (Vic), how can this be the case? Komesaroff and Kerridge state that the appendices to the AMC’s draft code “quote extensively (without attribution) the conclusions of guidelines developed by the Royal Australasian College of Physicians” and that “in the AMC’s version, the evidence, context and argumentation are omitted and the recommendations are presented as legally binding”.1 If this is the case, there is cause to question the integrity of the drafters of the code, to fear the code’s implications, and to request “that the whole process that gave rise to it be rigorously reconsidered”.1 Plagiarism cannot be condoned. To attribute honestly and give credit where credit is due is central to ethical practice, scientific discovery, education, accountability and learning. Similarly, context matters. In my opinion, integrity, the basis of ethics and morality, is measured by the extent to which context is valued and conceded. Ethical conduct demands both honesty and integrity. Doctors and the public, and government surely, place their trust in the AMC to objectively evaluate governing practices, laws and regulations, such as the Health Professions Registration Act 2005 (Vic) (“the HPR Act”), under which the MPB (Vic) operates, as well as professional conduct. Yet the authors of the AMC draft code fail to address the issue of the accountability of regulatory bodies and the fact that the HPR Act contains no benchmark for excellence: because context is omitted from the Act, “unprofessional conduct” cannot be defined and becomes relative. This leaves it open for any third party, including members of the regulatory authority itself, to abuse doctors and patients by being dismissive of the patient’s view (and thus, context), while claiming to protect patients and guide doctors. By contrast, the Medical Treatment Act 1988 (Vic), which is not mentioned in the AMC draft code, provides a benchmark for excellence in clinical practice with reference to both doctors and patients. This Act specifies (a) that the wishes of the patient to refuse treatment be respected, and (b) that medical practitioners who act in good faith in accordance with the patient’s expressed wishes be protected from any civil or criminal liability or disciplinary action by the regulatory board.2 As doctors, we are the naturally appointed advocates of our patients’ health preferences and wellbeing. Ensuring that choices are made for the patient’s benefit requires honesty and integrity at all levels of government.1,3,4 When a failure occurs in the system, it is imperative to have avenues of awareness, transparency, protection and evaluation available through public action and professional debate.1,3,5

John B Myers

In reply: The debate about the proposed national code of conduct (“the Code”) has raised a number of important issues, including those highlighted by Myers. The original draft aroused serious concern in the community about the potential role of a centralised bureaucracy with the power to enforce a set of precepts derived from a narrow, largely discredited, philosophical perspective. Although the revised draft now circulated for public comment is admittedly less objectionable than its predecessor, significant concerns remain relating to both its form and its content. The main issues are still the purpose and role of the Code and the confusion between ethical and legal discourses on which it is based. In a multicultural society in which pluralism and diversity are themselves regarded as inherently valuable, the very concept of a unitary set of criteria that define good practice is questionable. In this setting, the proper roles of codes of conduct and of ethics are not to enforce particular kinds of outcomes, but rather to inform and enrich practice. If the Code were devised as an educational process to stimulate clinicians to reflect critically on their existing practices and underlying values, it would be much more likely to change behaviour and increase community wellbeing.

Paul A Komesaroff · Ian H Kerridge

To the Editor: The relationship between population, climate warming and environmental impact has been little discussed in the Australian medical media and often ignored in the wider Australian media. All doctors should have a good working knowledge of the science of climate change and its correlation with increased human activity. Six billion humans (circa 2000 ad) have a greater environmental impact than one billion humans (circa 1800 ad), and this increase correlates with deterioration in nature’s “free goods”, such as clean air and water. Globally, demand for food is outstripping supply, resulting in malnutrition and starvation for the world’s poorest. Nationally, changes in the Australian climate have the potential for increased prevalence of tropical diseases, and extreme weather events can cause damage to infrastructure (including health facilities), social dislocation, injury and death. Guillebaud and Hayes argue that doctors must lead the discussion on population growth and climate change.1 They point out that the global population increase of 1.5 million each week equates to a huge new city ... which destroys wildlife habitats and augments world fossil fuel consumption. Every person born adds to greenhouse gas emissions ...1 Those who insist on the right to a large family must also consider the wider social implications of population growth,2 although there is little to be gained by recriminations against those who have already formed large families. We should take the perspective of retired physician Bryan Furnass: address the problems — population, pollution and poverty — with the solutions — ecology, education and ethics.3 Those doctors who understand the methods used by the tobacco industry to subvert the community’s appreciation of the risks of smoking will also understand that similar tactics can and are being employed by those with vested interests in high carbon-emitting industries. Their arguments are based on a belief that technology can solve all problems, while hiding the relationship between increased total consumption, profit and population growth. We need to understand and lead the community’s discussions on global overpopulation and health reduction. Australian doctors are lagging behind in this. British doctors are already publishing on this topic,4 and the Australian Parliament has commenced discussion on the need for a population policy.5 It is time for Australian doctors to read, discuss, research, write and, following the lead of Walters,6 publish constructively on population growth and its impact.

Robin I W Collin

To the Editor: On my way to Canberra for the Charles Darwin exhibition at the National Museum of Australia, I diverted to Pambula, on the far south coast of New South Wales, for two reasons. Pambula is part of the Australian connection with Darwin through Syms Covington, who, at the age of 15, sailed as a cabin boy on the Beagle in 1831. Darwin soon came to rely on Covington to collect specimens, excavate fossils and act as his personal assistant. During the Beagle’s brief visit to Sydney, Covington was impressed by the colony. In 1840, after a period of employment with Darwin in England, he returned to Australia and eventually became a wealthy man. At first he lived in Sydney, but by 1854 had moved to Pambula, where he became postmaster. His entrepreneurial activities included buying large tracts of land around the Pambula River and the little township of Pambula. On a large block, he built a house of solid sandstone bricks with cedar woodwork throughout — “Covington’s Retreat”. Covington continued to correspond with Darwin and, at the latter’s request, collected specimens for him. He died in 1861. The house, at 28 Quondola Street, still stands and has been listed by the National Trust of Australia (NSW) in Heritage Council File HC32549. After being used for various purposes, including as an inn and as a police station, it became the residence of the local doctor, probably around the start of the 20th century — hence my second reason for visiting Pambula. The subsequent careers of some of the Pambula general practitioners, all of whom lived in the house, are of considerable interest. All came to Pambula from outside the area. Grace Cuthbert (later Cuthbert Browne), MBE, left Pambula in 1929. She was Director of the Division of Maternal and Baby Welfare of the NSW Department of Public Health (1937–1965) and, among many other positions, President of the Australian Federation of Medical Women. Naomi Wing, CBE, and her husband Lindon practised in Pambula from 1929 to 1936. She was an early advocate of rehabilitation medicine as a medical discipline and became President of the Australian Association of Physical and Rehabilitation Medicine. The Naomi Wing Rehabilitation Centre in Zetland, Sydney, was named in her honour. Her husband, Lindon Worlledge Wing, KStJ, was an early practitioner of occupational medicine in Sydney. Their son, Emeritus Professor Lindon Michael Harper Wing, was Dean of the Medical School at Flinders University, Adelaide, from 1998 to 2007. From 1936 to 1945, the house was owned by Keith Jones, who went to World War II from Pambula and whose name is on the town’s war memorial. After the war, he became a surgeon and, over the years, undertook a wide range of community activities. He was President of the Australian Medical Association (1973–1976), Chairman of the Australasian Medical Publishing Company Limited (1976–1982) and, for a time, Acting Editor of the Medical Journal of Australia. He was knighted in 1980. Covington’s Retreat is now a Thai restaurant called “Covingtons Thai”.

George D Repin

To the Editor: We both are ear, nose and throat (ENT) specialists at a tertiary university hospital and cover 1–2 nights of emergency calls each month. Over 8 months in 2008, we witnessed four emergency patients (aged 25–39 years; three men, one woman) who had sore throat, mild fever and pain on swallowing, without any respiratory distress symptoms. One patient presented with “hot potato voice”. All had had a palatine tonsillectomy in childhood. On examination, the oral pharynx appeared normal to mildly hyperaemic, without any suppuration. To exclude potentially fatal epiglottitis, all patients underwent transnasal flexible laryngoscopy, which revealed swollen lingual tonsils covered with fibrinous exudate typical of streptococcal infection. Distal structures, including the epiglottis and endolarynx, were normal. Acute lingual tonsillitis was diagnosed, and the patients quickly responded to penicillin therapy. Some degree of infection of the lingual tonsils probably occurs when the pharynx is otherwise infected, but is usually left undiagnosed because it is not easily visible without laryngoscopy.1 Although none of our patients had any life-threatening symptoms, this condition could potentially cause upper airway compromise, and the course would certainly be more arduous without antibiotics. The flexibility of our health care system in Croatia allows for some emergency patients’ to refer themselves to the relevant specialty services. If these patients had presented to general practice rather than to our department, where we performed transnasal laryngoscopy, this diagnosis would have probably gone unnoticed, and antibiotic therapy would not have been prescribed. Thus, is acute lingual tonsillitis a neglected cause of severe sore throat? A search of the current literature and ENT textbooks did not reveal many reports of this disease.2,3 Even if our observations referred to rare cases, considering our hospital catchment population for ENT emergencies of more than 300 000, they still outnumbered all cases of epiglottitis treated at our emergency service during the same period. Therefore, it is our opinion that acute lingual tonsillitis should be at least kept in mind as a condition that can cause severe sore throat that is oropharyngoscopically silent or mimics simple viral infection, but is effectively and readily treated with antibiotics.4 Because the base of the tongue cannot be visualised by routine intraoral examination, confirmation of the diagnosis must be made by an ENT specialist who will perform laryngoscopy.

Sasa Janjanin · Drago Prgomet

To the Editor: We read with interest the work presented by Markovic and Natoli, highlighting the importance of recognising the nutrient density of foods in managing overweight and obese patients.1 We present data to support their observation that it should not be assumed that a patient who is overweight or obese has a nutritionally adequate diet. Our data were obtained as part of the Geelong Osteoporosis Study from an age-stratified sample of men randomly selected from electoral rolls for the Barwon Statistical Division in Victoria. Dietary intake was estimated using a food frequency questionnaire developed by the Cancer Council Victoria.2 Basal metabolic rate (BMR) was estimated from the Schofield equations, based on age and weight. Data were excluded if the ratio of energy intake (EI) (from food and alcohol combined) to BMR was < 0.9. The sample comprised 1175 men aged 20–93 years (median age, 56 years [interquartile range, 39–73 years]; mean weight, 81 kg [SD, 14 kg]; mean height, 1.75 m [SD, 0.07 m]). Participants were grouped by body mass index (BMI) into three categories: normal weight (BMI < 25 kg/m2), overweight (BMI 25.0–29.9 kg/m2) and obese (BMI ≥ 30 kg/m2). Estimates of physical activity were derived from self-report. Written, informed consent was obtained from participants, and the study was approved by the Barwon Health Human Research Ethics Committee. We investigated the breakdown of macronutrients, vitamins and minerals listed in the “virtual” case report presented by Markovic and Natoli1 and expressed intakes as a percentage of recommended dietary intake (RDI).3,4 Despite adequate EI, the diets of men in all BMI categories were low in zinc, calcium, folate and fibre (Box). We acknowledge that there are limitations posed by self-reported dietary intakes and physical activity levels. The EI–BMR ratio decreased with increasing BMI (median [interquartile range], 1.4 (1.2–1.7), 1.3 (1.1–1.6) and 1.2 (1.0–1.5) for normal weight, overweight and obese subjects, respectively), suggesting that under-reporting may have been more common with increasing BMI. We also acknowledge that RDIs are not thresholds for dietary deficiencies. Within these constraints, however, these data suggest that where there are nutritional shortcomings in diets, they are not limited to men of normal weight-for-height, but are also apparent among those who are overweight and obese. These shortcomings suggest that nutrient-dense foods, such as whole grains and vegetables (particularly leafy green vegetables) are underconsumed, while processed foods with high saturated fat and salt content are consumed excessively. These observations underscore the importance of recognising the nutrient density of foods so that nutrition is not compromised when EI is restricted. Nutritional intake expressed as a percentage of recommended dietary intake (RDI) in a cohort of 1175 men,* by weight category† Nutrient RDI3 Normal weight (n = 471)‡ Overweight (n = 530)‡ Obese (n = 174)‡ Energy (kJ) § 92% (78%–111%) 97% (83%–119%) 105% (88%–124%) Protein (g) 64 (20–70 y); 81 (> 70 y) 139% (109%–181%) 143% (115%–185%) 157% (124%–195%) Total fat (g) 70* 124% (97%–158%) 123% (97%–153%) 127% (102%–173%) Saturated fat (g) 24* 146% (112%–190%) 145% (109%–188%) 154% (115%–206%) Carbohydrate (g) 310* 77% (64%–94%) 78% (65%–92%) 77% (65%–90%) Sugar (g) 90* 117% (90%–142%) 115% (88%–148%) 106% (84%–131%) Fibre (g) 30¶ 78% (60%–100%) 80% (61%–99%) 80% (64%–98%) Iron (mg) 8 173% (136%–225%) 180% (148%–223%) 185% (151%–229%) Zinc (mg) 14 88% (69%–110%) 92% (74%–113%) 93% (79%–120%) Calcium (mg) 1000 (20–70 y); 1300 (> 70 y) 87% (66%–117%) 89% (70%–116%) 90% (68%–109%) Folate (μg) 400 78% (62%–99%) 81% (64%–99%) 82% (67%–102%) Vitamin C (mg) 45 279% (194%–402%) 283% (204%–409%) 294% (213%–434%) Vitamin A (μg) 900 100% (80%–131%) 104% (82%–126%) 104% (82%–127%) Sodium (mg) 460–920¶ 306% (247%–399%) to 611% (494%–799%) 314% (259%–382%) to 628% (518%–764%) 345% (258%–412%) to 690% (515%–824%) BMI = body mass index. y = years. * As no National Health and Medical Research Council (NHMRC) RDIs exist for total fat, saturated fat, carbohydrate and sugar, we used Food Standards Australia New Zealand RDI values for these nutrients.4 † Normal weight, BMI < 25 kg/m2; overweight, BMI 25.0–29.9 kg/m2; obese, BMI ≥ 30 kg/m2. ‡ Data are presented as median (interquartile range). § RDI for energy was based on age and height and a physical activity factor derived from self-report. ¶ Adequate intake.

Julie A Pasco · Margaret J Henry · Mark A Kotowicz · Geoffrey C Nicholson

To the Editor: Markovic and Natoli draw attention to the frequent presence of nutritional deficiencies in obesity.1 While the authors detail various nutrient deficiencies that may arise from a nutrient-poor diet, they do not discuss the possibility of vitamin D deficiency. Normally the main source of vitamin D is that synthesised in skin exposed to ultraviolet B radiation. A nutrient-rich or nutrient-poor diet alone is unlikely to provide adequate vitamin D unless foods are supplemented with vitamin D. Vitamin D deficiency in obese people is prevalent, and Holick has described an inverse relationship between body mass index and 25-hydroxyvitamin D levels, with sequestration of vitamin D in body fat reducing its availability.2 Vitamin D deficiency is associated with various conditions for which obesity is a risk factor, including cancer, depression, altered glucose metabolism and cardiovascular disease.2 A prospective study would be required to determine whether vitamin D supplementation is able to modify some of these associations. Increasing vitamin D levels are associated with improved muscle strength,2 and thus vitamin D supplements may be of benefit in obese patients with reduced vitamin D levels. Furthermore, combined vitamin D and calcium supplementation may have a small beneficial role in preventing type 2 diabetes.3 Pending more evidence, it would be prudent to consider measuring 25-hydroxyvitamin D levels in obese people and correcting any deficiency. In view of the large amount of adipose tissue in obese people, it is likely that they would require higher than normal doses to achieve repletion of their vitamin D stores.

Barbara Depczynski

To the Editor: We concur wholeheartedly with Gill and colleagues1 in support of recognising obesity as a public health issue, and we dispute claims that the current problem of obesity is being exaggerated. Gill and colleagues point out that obesity trends have climbed over decades, and state that 6%–8% of Australian school children are affected.1 While this is a substantial burden of over a quarter of a million children, we also consider that restricting definitions of obese to arbitrary cutoff points may underestimate the problem, given that the entire distribution of childhood weight is increasing, not just the extreme group classified as obese. Adiposity is related to cardiovascular outcomes such as myocardial infarction and stroke in a (curvi)linear fashion. Defining obesity by arbitrary cutoff points is vulnerable to differences between sexes, ethnicity and age, and limits our understanding of obesity-related diseases. It is well known that cardiovascular risk factors cluster, particularly the adiposity-driven components of the so-called metabolic syndrome. In the Western Australian Pregnancy Cohort (Raine) Study, we have used cluster analysis to identify a group of children at risk of future cardiovascular disease with features of the metabolic syndrome.2 The differences in characteristics are shown in the Box. The “high risk” and “low risk” cluster groups differ widely in terms of not only body mass index, the most widely used measure of obesity, but also waist circumference (a measure of central adiposity), insulin resistance, blood pressure, and levels of triglycerides, high-density lipoprotein cholesterol, total cholesterol (data not shown) and low-density lipoprotein cholesterol (data not shown). Not only the conventionally used 95% confidence intervals, but also the 99% confidence intervals do not overlap for any of these intermediate cardiovascular risk factors. We found that 29% of children were in the high-risk cluster at the age of 14 years2 and a similar analysis suggested that even at age 8 years, 25% of children were at increased risk of future obesity, cardiovascular disease and diabetes.3 C-reactive protein (CRP) level is known to be associated with future cardiovascular diseases in adults,4 and with an adverse metabolic profile in children.5 The “high risk” children had significantly higher CRP levels at the age of 14 years than their low-risk counterparts. Certainly, the magnitude of this problem, affecting up to a third of our youth, needs to be addressed by government and health-planning bodies. We suggest our approach of cluster analysis will help identify earlier those children at substantially increased risk of cardiovascular and other adiposity-related disorders in Australia. Features of the cluster groups with respect to components of the metabolic syndrome, showing 99% CIs* BMI = body mass index. HOMA = homeostatic model assessment (for quantifying insulin resistance). SBP = systolic blood pressure. HDL = high-density lipoprotein cholesterol. * From Huang et al.2 Reprinted with permission from the American Diabetes Association.

Rae-Chi Huang · Fiona J Stanley · Lawrence J Beilin

To the Editor: There is a substantial volume of evidence from a range of national and state-based surveys illustrating increases in the rates of obesity and overweight among Australian children over the past two decades,1 concurring with trends observed in most developed countries.2 The recent article by Gill and colleagues highlighted questions that have been raised publicly regarding the extent and impact of levels of obesity and overweight among Australian children, including whether trends have been exaggerated.1 To examine these issues using the latest data available, we present data from the three most recent national surveys in which weight and height of Australian children were measured: the Australian Health and Fitness Survey (1985),3 the National Nutrition Survey (1995),4 and the Australian National Children’s Nutrition and Physical Activity Survey (2007).5 We examined overweight and obesity levels among young Australians from comparable age groups at three time points over more than 20 years, using the same internationally accepted definitions of childhood overweight and obesity. For 1985 and 1995 data, we used the figures reported by Magarey et al in 2001,6 which compared results from the 1985 and 1995 surveys using new standard international definitions to classify overweight and obesity among Australian children and adolescents.7 We calculated body mass index for the 2007 Australian National Children’s Nutrition and Physical Activity Survey using the raw data file obtained through the Australian Social Science Data Archive,8 categorising children as overweight or obese based on the same international definitions used by Magarey et al.6 We based our calculations on the age group common to each of the three surveys: 7–15-year-olds. As shown in the Box, the prevalence of overweight and obesity in boys aged 7–15 years has risen from 11.0% (95% CI, 10.99%–11.01%) in 1985 to 20.0% (95% CI, 19.97%–20.03%) in 1995 and 23.7% (95% CI, 23.68%–23.72%) in 2007. In 7–15-year-old girls, the prevalence of overweight and obesity has increased from 12.2% (95% CI, 12.19%–12.21%) in 1985 to 21.5% (95% CI, 21.47%–21.53%) in 1995 and 25.8% (95% CI, 25.78%–25.82%) in 2007. While data from additional time points are required to map national trends more comprehensively, our analysis clearly indicates an upward trend in overweight and obesity levels in both boys and girls aged 7–15 years between 1985, 1995 and 2007. This trend is cause for alarm, given the widely recognised body of evidence on the significant short-term and long-term consequences of childhood obesity.9 Prevalence of overweight and obesity in Australian children aged 7–15 years, 1985–2007 * Data weighted for age, sex and region with the weighting variable in the raw data file obtained from the Australian Social Science Data Archive.8

Lyn M Roberts · Tessa R Letcher · Alexandra A Gason · Tim Lobstein

To the Editor: Davis and colleagues stated that the Framingham and United Kingdom Prospective Diabetes Study (UKPDS) cardiovascular risk equations are not suitable for predicting risk in an Australian population with type 2 diabetes.1 If confirmed, this would be extremely disappointing. However, before accepting this conclusion the following important considerations should be noted. Davis noted that the Fremantle Diabetes Study (FDS) patient group differed significantly from the UKPDS baseline group (eg, 38% of the FDS patients were aged outside the validated age range of the risk engine [25–65 years] and were assessed by non-validated extrapolation). Similarly, it cannot be assumed that the FDS group is representative of patients in general practice and hospital diabetes clinics around Australia. Moreover, it would be interesting to know how well the engine performs in FDS patients in the age group in which it was validated (ie, patients diagnosed with diabetes at age 25–65 years). It is likely that the low rate of cardiovascular events in the FDS (4.8% with at least one myocardial infarction, and 2.9% with at least one stroke)1 affects the accuracy of the results obtained with the UKPDS risk engine. The Framingham risk score has already been found to vary considerably in accuracy between populations, with predicted-to-observed ratios ranging from underprediction of 0.43 to overprediction of 2.87.2 Further, the UKPDS risk engine recently overestimated the risk of cardiovascular disease events in a UK general practice population.3 In purely pragmatic terms, most patients with type 2 diabetes aged over 50 years are at “high risk” for cardiovascular events (cardiovascular risk of more than 20% over 10 years),4 and the UKPDS risk engine is unlikely to influence prescribing practice significantly. However, we have found the engine to be a useful educational tool for explaining risk to patients. Even if the UKPDS risk engine is not optimally calibrated, the FDS analysis revealed that the coronary heart disease risk equation had modest discrimination (area under the receiver operating characteristic curve [AUC], 0.68), and the stroke risk equation had good discrimination (AUC ≥ 0.86),1 identifying those at highest risk. We believe that, rather than being irrelevant in Australians, the UKPDS risk engine continues to identify those at highest risk for cardiovascular events, operates well within its validated age group, and provides a motivational tool for encouraging changes in patient behaviour. Until a large dataset is pooled from various Australian studies, we believe the UKPDS risk engine should not be discarded.

Roland W McCallum · John R Burgess · Timothy M Greenaway

In reply: We thank McCallum and colleagues for their comments. In relation to their specific points: The Fremantle Diabetes Study (FDS) cohort is representative and drawn from a typical Australian urban centre.1 The 488 cardiovascular disease-free FDS participants with type 2 diabetes who were aged 25–65 years at both diagnosis and study entry had 22 coronary heart disease (CHD) events compared with 72 predicted, with a similar area under the receiver operating characteristic curve (AUC) to that for all 791 patients who were included in the analysis2 (0.66 v 0.68). Calibration indicated significant discrepancies between predicted and actual outcomes (P ≤ 0.02), and positive predictive values were low (≤ 3.5%). Therefore, restricting our patient sample to a “UKPDS” cohort did not alter our conclusions. We agree that the low observed CHD event rate in the FDS compared with that predicted by the UKPDS risk engine undermines its validity in Australians with type 2 diabetes. There was a similarly low CHD event rate in the FIELD study, which included many Australasians.3 Contemporary diabetes care clearly differs from that during the Framingham Study and UKPDS. Although the study cited by McCallum and colleagues, in a UK general practice population, is not strictly comparable to our study, it also found that the UKPDS cardiovascular disease risk engine performed only moderately (AUC, 0.72).4 Accurate risk prediction should be a basis for cost-effective care. We have developed an FDS risk calculator which should improve clinical management for Australians with diabetes.5

Wendy A Davis · Stephen Colagiuri · Timothy M E Davis

To the Editor: The federal government is to be applauded for its decision to re-introduce the “alcopops” tax Bill to Parliament and to try to retain the $300 million raised so far for expenditure on services, programs and research to reduce alcohol-related harm in Australia. The alcopops tax was paid by consumers in the form of higher retail prices, which will fall dramatically if the government again fails to pass legislation to retain the tax. If it transpires that the government cannot retain the revenue already raised, it should be given to an independent public health body (such as the National Health and Medical Research Council [NHMRC]) and not to DrinkWise via distillers and distributors, as has been suggested.1 DrinkWise is a “putatively independent body that was originally funded by the alcohol industry”;2 six of the 11 current members of its board are senior alcohol industry figures. The alcohol industry profits from drinking that contributes significant harm to individuals and communities,2 and it can be relied upon to oppose policies that are known to reduce alcohol consumption across the population.3,4 DrinkWise and similar industry-backed organisations around the world promote industry-friendly programs that do not have an evidence base or are ineffective (such as education campaigns or tepid television advertising),5 while lobbying against the adoption of effective evidence-based interventions, such as higher taxes on alcohol, as these would affect profits.2-4 The Chief Executive of DrinkWise, Chris Watters, recently revealed the organisation’s position on the alcopops tax, reportedly asserting that it did not recommend “fiddling with alcohol tax” because it was “old thinking” and that “the facts just don’t stand up”, and noting that DrinkWise funds many educational programs across the country.6 There is a clear consensus among public health experts worldwide that increasing the price of alcoholic beverages is one of the most powerful and cost-effective strategies that governments have at their disposal to reduce unhealthy alcohol use.7-10 Other effective strategies include drink-driving legislation, random breath testing, increasing the minimum legal age for drinking or purchasing alcohol, restrictions on trading hours and numbers of licensed premises, and better enforcement of existing liquor laws. In contrast, comprehensive reviews of the evidence show that, by themselves, alcohol education programs are ineffective.11,12 Alcohol industry-sponsored agencies have adopted similar public relations strategies to those used by the tobacco industry.3 These strategies distract attention from their concurrent lobbying against the adoption of policies that would actually make a difference. The laudable policy action taken thus far by the government in its attempt to implement the alcopops tax would be enhanced by supporting an independent body, such as the NHMRC, that has transparent funding strategies and criteria, based on an independent peer-review system, to distribute funding for alcohol-related research. We, along with the more than 50 other scientists and health experts listed at <http://www.webcitation.org/5gbwQWf9J> who endorse and are signatories to this letter,13 will not seek or accept funding from DrinkWise. We call on other researchers and community agencies to consider their positions.

Peter G Miller · Kypros Kypri · Tanya N Chikritzhs · Steven J Skov · George Rubin

In reply: I write in response to the letter from Miller and colleagues, recently published online.1 Their letter is an attempt to influence non-government senators as the Australian Government reintroduces the Bill to increase the tax on some alcoholic beverages. There must have been a better way to do this than by besmirching the good work of DrinkWise and its directors. DrinkWise Australia is not an industry-dominated body. It has a balanced board of six members from the alcohol industry and six distinguished community members. Miller and colleagues should know that, in criticising DrinkWise, they also attack the reputations of board members Professor Ross Kalucy, Chair of Psychiatry at Flinders University; Noel Turnbull, Adjunct Professor in Communications at the Royal Melbourne Institute of Technology; Neil Comrie, former Chief Commissioner of Victoria Police; and Terry Slater, who led the Australian Government’s public health programs before heading up the National Food Authority and the Therapeutic Goods Administration. The sixth community representative position on the board is currently vacant and has been offered to the federal health department. DrinkWise does not advocate for or lobby government in respect of alcohol taxation policy for a very sensible reason — alcohol industry leaders advocating for or agreeing on matters affecting price could constitute a breach of the Trade Practices Act 1974 (Cwlth). DrinkWise programs are strictly evidence-based, drawing on specifically funded high-level independent research executed by leading academics at universities including Griffith, Macquarie, Monash, Deakin, Flinders, and the Hunter New England Institute. Moreover, the DrinkWise “Kids Absorb Your Drinking” advertising campaign was developed through qualitative, quantitative and ethnographic research, as well as the findings of an extensive literature review by child heath experts and academics.2-9 Campaign tracking results show that 28% of adults surveyed in March 2009 reported having reduced the amount of alcohol they drink in front of their children in the previous 12 months. When parents who had seen the DrinkWise advertising were asked about its impact on their drinking behaviour, 39% said they were more self-conscious of how they drink in front of their children, 18% had changed their drinking patterns, and 14% had actually cut down how much alcohol they consume when their children are around.10 DrinkWise Australia: receives funding from the federal government and the alcohol industry for the development of both its evidence base and its programs; has no associations with any international alcohol or tobacco lobby groups; undertakes research through Australian universities to develop the evidence base for its interventions; does not interfere with specification of the research hypotheses, research design and techniques, or publication of results; ensures that the research it funds is undertaken in accordance with the universities’ protocols for conducting independent research; and grants the researchers it funds a “non-exclusive, royalty-free, perpetual license to use, reproduce, adapt and publish Project IP [intellectual property] for research, education, academic and consulting purposes”.11 I was particularly surprised that the letter’s authors would trivialise the importance of education in successful drug intervention programs and instead advocate for increased reliance on supply-side strategies. DrinkWise delivers interventions in a variety of settings, not only through the Kids Absorb Your Drinking campaign, but also through practical tools such as a website (http://www.drinkwise.com.au), information materials and discussion forums, as well as working at the grassroots level with groups such as local government, school organisations, community newspapers, Sports Challenge Australia and the Good Sports program. Educational programs informed by scientific literature, that are implemented and evaluated effectively and not used as a standalone intervention strategy, can work.12 We at DrinkWise hope that anyone with a strong commitment to public health will be able to work with us and not against us. This will ensure that we will be able to continue to run evidence-based initiatives to reduce alcohol-related harm in Australia.

Trish M Worth

To the Editor: Skov puts the case for an alcohol taxation policy in Australia.1 Few people, if any, in public health would disagree that alcohol is a serious public health issue in Australia, and few would doubt that higher prices will reduce consumption. But why tax the consumers directly? Why not tax the providers? I propose a tax on the advertising budget of alcoholic beverage producers. Further, this tax should be weighted according to the alcoholic content of the products they sell. Yes, this would mean higher prices for drinkers, but set in this way the incentive mechanism is to get sales and consumption down, firstly by reducing advertising, and secondly by lowering the amount of alcohol in what is sold. It has been estimated that more than a quarter of a billion dollars are spent each year on advertising alcoholic beverages in Australia.2 An average 200% tax, graded by alcoholic content of products, would mean a lot of money for the government! It might well make up for the estimated loss from the defeated “alcopops” tax of $1.6 billion over 4 years.3 Indeed, we should hope that it would not bring in half a billion dollars a year, as both advertising budgets and average alcohol content fall. An advertising tax would almost certainly make much greater inroads into reducing alcohol consumption than would the alcopops tax. It would raise the price for consumers, but to a lesser extent for lower alcohol-content beverages. It would severely discourage advertising, especially of high alcohol-content drinks, and would encourage manufacturers to produce beverages that are lower in alcohol. Any increase in cost to the consumer through taxation risks being regressive and might make the poor even poorer if they continue to drink, with a consequent impact on their health. This needs to be watched. But using the revenues raised to devise a targeted counselling program for those who do want to reduce their consumption (and for those who perhaps cannot do so without help) cannot be beyond the wit of Treasury and the health department.

Gavin H Mooney

To the Editor: I write in response to the article by Skov on alcohol taxation policy,1 and in the context of the recent defeat of the “alcopops” tax legislation, which is soon to be reintroduced to the Australian Senate. Our democratic political system has held us in relatively good stead, with a reliable system of checks and balances. However, the rejection of the alcopops legislation arguably represents a failure of democracy and a retrograde step for public health, defeating the first Australian public health-centred alcohol tax policy. For this, Senator Fielding and the Opposition should be held accountable. Yes, the tax is not all encompassing, and expansion to broader initiatives, as proposed by Senator Fielding, is not without merit. However, health experts supported the alcopops tax initiative as an important first step, as outlined in Skov’s evidence-based article.1 Skov highlighted the key issues, including that alcohol-related harm is at unacceptable levels, that action is overdue, and that good evidence from Australia and internationally supports taxation and pricing as being among the most effective measures to reduce alcohol consumption and harm.1,2 Overall, the positives of this initiative clearly outweigh the negatives, and defeating it was arguably naïve and ill informed. Historically, both policy and funding are crucial to public health successes. Following awareness of the problem, change must start somewhere, before broadening over time to deliver health benefits (eg, smoking, seatbelts, speeding — all crucial and effective public health campaigns). The most important aspect of the alcopops tax initiative is likely to be that it is a start and a successful avenue to raise revenue. Extension to a full alcohol content-based tax, education, incentives and regulations will come — but much more belatedly now. The defeat of the alcopops tax legislation has threatened this opportunity to significantly contribute to the fight against alcohol misuse. While opposition is by definition the trademark of Opposition parties, bipartisanship should prevail when community benefits are clear. Perhaps more concerning is that a single politician holding the balance of power can disregard history, expert opinion and popular support, and defeat important public health-centred legislation. The manipulation of our political system with the rejection of the alcopops tax legislation was profoundly disappointing. This initiative should not be defeated again. Our politicians should take heed of history, evidence, expert opinion and public sentiment and vote in the nation’s interest to support the alcopops tax legislation on its return to the Senate.

Helena J Teede

There is nothing a government hates more than to be well informed; for it makes the process of arriving at decisions much more complicated and difficult. — John Maynard Keynes, 1938. To the Editor: I would like to contribute to the debate raised by Skov’s timely article1 on the recently defeated “alcopops” tax legislation — the Excise Tariff Amendment (2009 Measures No. 1) Bill 2009.2 Senator Fielding’s requirement for a ban on alcohol industry advertising during sporting events as a condition for his support of the alcopops tax legislation is rational, visionary and affordable from the additional tax raised. Many of the high-profile individual and public health incidents related to alcohol misuse have been among athletes sponsored by the alcohol industry, and around sporting arenas. As the positive outcome of banning tobacco industry sponsorship of sporting events has demonstrated, such bans have at least as strong an impact as would the increased tax on alcopops on reducing exposure of young people to alcohol.3 It is estimated that the alcohol industry contributes up to 23% ($288 million) of the $1.25 billion in annual sports sponsorship in Australia.4 If the government had agreed to Senator Fielding’s prerequisite amendment, and had also fully taken over sports sponsorship responsibilities, it would have achieved two important public health objectives — a reduction in binge drinking and banning of sports sponsorship by the alcohol industry — and would still have had at least $100 million left to address alcohol-related issues; assuming of course that the real objective of the alcopops tax policy was to prevent alcohol-related harm among youths. Had the government agreed to simultaneously ban alcohol industry advertising in sport and maintain the new alcopops tax structure, it would then be on a moral high ground to implement other important alcohol-related public health measures that require no more than strong political will, such as mandated warnings on alcoholic products at the point of sale. In this respect, the French National Cancer Institute’s recent report that alcohol-related colorectal, breast, oesophageal and liver cancer risks increase from one glass per day, and that the consumption of alcoholic beverages of any type is not advised for anyone,5 is instructive.

Niyi Awofeso

To the Editor: A 70-year-old woman presented to the emergency department with intense pain, erythema, oedema and haemorrhagic bullae of the right lower leg. Twenty-four hours earlier, she had fallen into warm seawater on the south coast of New South Wales, sustaining a penetrating wound by an unknown object. She reported developing excruciating pain and the noted leg changes within hours of the injury. She had a history of systemic lupus erythematosus (SLE), managed long-term with 7.5 mg oral prednisone daily. Soon after presentation, she rapidly developed septic shock, becoming hypotensive, tachycardic, hypoxic and confused. She was experiencing rigors and required inotropic support. On examination, there was marked cellulitis of the right lower leg with purpura and bullae. No crepitus was detectable in the tissues. There was no clinical or laboratory evidence of disseminated intravascular coagulation. Broad-spectrum empirical antibiotic treatment with intravenous gentamicin, cephazolin and metronidazole was commenced, and urgent, extensive surgical debridement of the lower limb was performed (Box). Wound culture swabs and tissue samples were sent for microbiological and histopathological examination. On Day 2, blood cultures taken at initial presentation were positive for Vibrio vulnificus, as were tissue swabs. Based on susceptibility testing, antibiotic therapy was reduced to a single agent, intravenous ciprofloxacin 400 mg twice daily. The patient’s postoperative clinical recovery was slow, but her SLE did not flare up, and on Day 23 she was transferred to a tertiary referral centre for lower-limb skin grafting. Cellulitis is a common presentation to emergency departments, and common organisms are usually implicated. However, in some cases, the presence of more unusual pathogens, such as V. vulnificus, should be considered. V. vulnificus is a virulent halophilic (salt-loving) gram-negative bacterium associated with seawater temperatures (usual range, 18°–24°C). It has two distinct clinical presentations.1,2 The first, well recognised, is septicaemia after ingestion of raw or undercooked seafood, such as oysters, causing acute gastrointestinal disease. The second, not always considered, is necrotising wound infections, as in this case. Open wounds can be directly inoculated with V. vulnificus from seawater containing the organism. “Vulnificus” is a Latin term meaning “inflicting wounds”. Hippocrates described perhaps the first recorded case of a fisherman with pain in the foot, fever, delirium and blistering skin.3 Patients with primary wound infections caused by V. vulnificus develop painful, rapidly progressing cellulitis. More unusually, our patient developed fulminant sepsis from an open wound infection. Patients who are immunocompromised, especially those with alcoholic liver disease, hepatitis B or hepatitis C, have a higher risk of infection with V. vulnificus, as well as patients, like ours, who take long-term steroid therapy.2 Management requires timely recognition, antibiotic therapy and prompt surgical review. Cellulitis of right lower leg caused by infection with Vibrio vulnificus

Tamara C Preda · Veronica A Preda · Allan P Mekisic

To the Editor: A 27-year-old man who had recently emigrated from Sudan was admitted to our department with a 7-hour history of constant peri-umbilical pain. Physical examination revealed inconstant voluntary guarding of the lower abdomen. Full blood and electrolyte examinations were unremarkable. Urinalysis showed protein and traces of blood. A condition requiring surgery was considered unlikely and further investigations were undertaken. Significant bladder calcification was noted from an abdominal x-ray. A computed tomography scan confirmed this finding (Box), and also revealed circumferential distal ureteric calcification, appendiceal thickening with appendicolith, and adjacent fat stranding. Repeat abdominal examination demonstrated right iliac fossa tenderness with a positive Rovsing sign. Acute appendicitis was diagnosed and an inflamed, thickened, retrocaecal appendix was removed laparoscopically. The patient was discharged 2 days later, but did not attend his post-operative review. Histological examination of the appendix demonstrated transmural neutrophil infiltration, without eosinophils. Within the lumen there were numerous oval-shaped helminth ova, some with terminal spines, consistent with acute appendicitis caused by schistosomiasis. The patient did not have a general practitioner, therefore a referral to an infectious diseases clinic was made. He was thereafter lost to follow-up. Infection by schistosomes leads to chronic granulomatous inflammation in many body systems, including the gastrointestinal tract. Adult worms are not usually harmful to the host — eggs provoke a Th2-mediated immune response.1 Three major species of Schistosoma cause schistosomiasis in humans, of which two are endemic in sub-Saharan Africa — Schistosoma mansoni and Schistosoma haematobium. S. haematobium migrates against portal venous flow to the vesical venous plexus, causing urinary tract calcification through chronic inflammation and fibrosis. This species has also been described as a cause of appendicitis.2 Examinations of appendices removed from patients with acute appendicitis in endemic areas have demonstrated schistosomiasis in 2.3%–4.2% of samples, with 2.7% having histological evidence of acute schistosomal appendicitis in one study.3,4 Schistosomiasis can be diagnosed by histological analysis, or urine and stool microscopy. Serological testing cannot be used to differentiate past and present infection, however positive serological results are the basis for treatment of patients in endemic areas. After diagnosis, praziquantel should be prescribed. It is assumed that our patient did not receive praziquantel. He thus risks significant morbidity and mortality from possible gastrointestinal, hepatic, urinary, pulmonary and neurological complications related to chronic schistosomal infection. Surgeons and pathologists should be aware of the atypical pathology of acute schistosomal appendicitis. The number of immigrants arriving in Australia from endemic areas has increased markedly in recent years and further presentations may occur. Non-contrast computed tomography scan of a 27-year-old man with schistosomal appendicitis Calcification of the bladder (black arrow) and distal ureters (white arrows) is evident.

Jordan K Webb · Graeme Thompson

To the Editor: A 4-year-old girl presented with a flyblown scalp to a district aid post outside Madang, Papua New Guinea (PNG). Coincidentally, we were present at the aid post in our capacity as students and lecturers in the tropical paediatrics module of the James Cook University Masters in Public Health and Tropical Medicine course. The child was otherwise healthy, and her scalp had been normal until about 2 days previously, when her mother noticed two developing “sores”. These had deteriorated into circular, foul-smelling ulcers about 1.5 cm in diameter and 2 cm apart on the crown of her head (Box, A), in which live maggots could be seen squirming. The child’s mother had extracted some maggots with a pair of toothpicks (Box, B), and about 10 more were removed at the aid post with tweezers. When no further movement was apparent in the wounds, they were covered with petroleum jelly to suffocate any “stragglers”. No dead larvae were seen the following morning, and the wounds healed rapidly. We believe the most likely culprit was Chrysomya bezziana, or Old World screw-worm fly, although we were unable to preserve a larva for formal identification (by “curing” in very hot water and transporting in 70% ethanol). Old World screw-worm fly is an obligate myiasis-producing fly endemic in PNG. Its larvae are found only in living vertebrate tissues. The child’s mother had not noticed a prior lesion, and we assumed entry was through a graze on the scalp. Although screw-worm fly is endemic throughout tropical and subtropical regions of Asia and Africa, it is not found in Australia. If it became established here, it could devastate the livestock industry, particularly by striking the umbilical region of newborn calves and infesting their abdominal contents.1 The fly is known to be able to travel 100 km,2 further than the distance between the islands of Torres Strait, but has not yet migrated from PNG to Australia. It could also be introduced in livestock vessels returning from Asia or the Middle East; the Australian Quarantine and Inspection Service has strict regulations to prevent this, with all returning vessels thoroughly cleaned before reaching Australian waters. This is justified as it has been documented that sheep shipped from Australia arrived in Bahrain with fly infestation. Presumably, flies were attracted to the ship as it passed the coast of Oman or the United Arab Emirates.3 Infestation is self-promoting, as ovipositing females are particularly attracted to the odour of an existing myiasis, resulting in expansion of the lesion. In our patient, the application of petroleum jelly to the lesions fortuitously covered the odour, reducing the likelihood of reinfestation. Ivermectin is useful in treating affected animals,4 as well as humans5 when the larvae cannot be physically extracted. Scalp of a child with fly infestation A: Circular ulcers on the child’s scalp. B: Removal of larvae with toothpicks.

John S Whitehall · Richard Speare · Heidi E Best · Philippa J Price · Deborah J Mills

To the Editor: A recent review of medical textbooks found that the topic of intravenous fluid therapy is poorly covered.1 Hence, the recent article by Hilton and colleagues provides interesting hypothetical examples of the risk of hypovolaemia and hypervolaemia, as well as imbalances in fluid tonicity, in patients receiving intravenous fluid therapy.2 In particular, the authors recommend the use of intravenous 0.9% saline, as it is reportedly isotonic and hence avoids potential imbalances in serum sodium concentration. However, Hilton and colleagues discuss only tonicity as the determining factor when selecting the type of fluid to give patients. They do not mention that 0.9% saline, also known as “normal” saline, distorts fluid, electrolyte and acid–base balance, despite being isotonic. In healthy subjects, 25% more volume is retained 6 hours after infusion of 2 L of 0.9% saline compared with 2 L of Hartmann’s solution.3 Infusion of 0.9% saline also results in hyperchloraemia, which decreases glomerular filtration rate, and is not seen with infusion of Hartmann’s solution.3 Certainly, the most important side effect of 0.9% saline infusion is metabolic acidosis, caused (according to the Stewart approach) by a reduction in the strong ion difference.4 Using the Stewart approach once again, Hartmann’s solution is “balanced”, ensuring the eradication of infusion-related metabolic acidosis.4 Although tonicity is important in considering the appropriate intravenous fluid therapy, it should not take precedence in the choice of therapy. Such an approach ignores the volume, electrolyte and acid–base disturbances induced by 0.9% saline infusions.

Alexander D Franke

In reply: Franke presents some well known problems associated with intravenous administration of large volumes of 0.9% NaCl, particularly its relatively slow elimination (as compared with Hartmann’s solution), and hyperchloraemic acidosis.1 In isolation, we do not dispute these facts. However, 0.9% NaCl is not unique in having problems — no intravenous fluid therapy is without risk, especially when given in excessive volume, or when the composition is inappropriate for the patient’s needs. It is also important to distinguish maintenance therapy from resuscitation. For postoperative maintenance therapy, we advocate a conservative approach with initial use of minimal volumes of isotonic fluids, to decrease the risk of common complications such as postoperative fluid retention, impaired respiratory function, and prolonged bowel dysmotility. We encourage close monitoring of volume and electrolyte status, and do not exclude the later use of hypotonic fluids.2 Disorders of volume and tonicity (hypo- or hypernatraemia) are the most common serious problems associated with intravenous fluid therapy. The approach we recommend follows the priorities of the kidney: restoration of volume, restoration of tonicity, and restoration of acid–base balance, in that order. If the patient’s requirements for fluid volume and tonicity are met, and tissue perfusion and gas exchange restored, then significant morbidity or death is unlikely to be a direct consequence of isolated 0.9% NaCl-induced hyperchloraemic acidosis.

Carlos D Scheinkestel · Andrew K Hilton · Vincent A Pellegrino

To the Editor: We agree with Smith and Gray that the uptake of telemedicine is slow despite the availability of hardware in many facilities.1 Not every field in medicine is amenable to videoconferencing consultations. Specialties in which the physical examination needs to be performed by the specialist, such as cardiology, are not suitable. However, decisions in medical oncology are based on history, pathology and imaging studies, making the specialty well suited to telemedicine. If physical examination is needed, it can be performed by a proxy examiner. Towns with high patient loads are probably not suited, but towns with fewer patients would be ideal for this method. For the past 2 years, Townsville Hospital’s Department of Medical Oncology has managed cancer patients in Mount Isa (800 km — a 2-hour flight or 10-hour drive — from Townsville, one way) using weekly videolinked clinics. The team comprises a medical oncologist in Townsville, and a senior medical officer (SMO), a chemotherapy nurse, patients and families in Mount Isa. Except for the initial period of familiarisation, running the clinics has been smooth. Forty patients have been managed in Mount Isa in over 200 consultations. Consultations have included new cases, ward consultations and reviews. Four patients were considered for palliation only and were managed in Mount Isa without being transferred to Townsville, which was particularly helpful for those at terminal stages. In 2008, we conducted a survey to assess the level of patient satisfaction and assessed the safety of chemotherapy delivery. We found that all 25 patients who participated in the survey were satisfied with the service, with scores of more than 80% on a five-point Likert scale (ie, “agree” or “strongly agree”).2 Ninety-two per cent of patients would rather “see” the specialist via videoconference than travel to Townsville. All three SMOs and both nurses felt they were able to communicate more effectively with and receive support from the specialists. Thirty-two patients received active chemotherapy between 2006 and 2008. Rate of occurrence of severe side effects among patients in Mount Isa was similar to that of patients treated in Townsville (< 5%). Four patients were admitted for complications, but there were no treatment-related deaths. We believe that this technology is safe and appreciated by patients. The technology can be adopted by medical oncologists to manage patients in rural areas, where travel by specialists and patients is not cost- or time-effective. The major advantages are that the patients have the opportunity to be treated closer to home, and doctors receive specialist support on a weekly basis.

Sabe S Sabesan · Pieter Nel · Suresh C Varma

To the Editor: Climate change has an adverse impact on health.1 Procurement, waste production, transport, and energy and water consumption (ie, the ecological “footprint”) all contribute to climate change. If the principle underpinning the work of all health professionals is “do no harm”, addressing the harmful effects of the health care industry on the natural environment must become a priority. We argue that one way to rapidly achieve this would be to mandate more sustainable practices as part of hospital accreditation. The United Kingdom has specifically targeted its health system to reduce its large ecological footprint,2 but in Australia, progress towards environmental sustainability within health care is uncertain and unmonitored. The contribution by health care to Australia’s national carbon emissions is unclear, but we do know that, for example, Victoria’s public hospitals consume 60% of the total energy used by the state’s government departments,3 so we have the opportunity to make a major impact. There are excellent examples of hospital energy- and water-saving projects with financial recovery within 10 years.2,4 The Environment Protection Authorities of several Australian states are now mandating that heavy users of energy and water (including larger hospitals) have Environment and Resource Efficiency Plans to reduce their footprints,5 but action from hospitals has been unclear. Progress has typically been made on an ad-hoc basis by hospitals acting in isolation, although the Institute of Hospital Engineering, Australia is facilitating a more systematic approach.4 The Australian Council on Healthcare Standards (ACHS), through its Evaluation and Quality Improvement Program (EQuIP)6 accredits Australian hospitals against mandatory and preferred criteria. However, EQuIP does not currently include mandatory criteria that address issues such as energy, water and waste auditing, energy efficiency and the presence of a hospital environmental committee. The accreditation process offers an opportunity to encourage hospitals to prioritise these issues. The ACHS has awarded hospitals in the past for “environmental excellence”, but without a solid framework from the ACHS, the goal of all of our hospitals pursuing sustainability seems unlikely. In 2009, it is out of step with Australia’s shift to a low-carbon future that there are no requirements that hospitals achieve more sustainable use of energy, water and transport, and improve procurement and waste reduction. The introduction of broad environmental standards as part of the accreditation process could be a vehicle for achieving rapid improvements in sustainability across the hospital sector and shift our health system to one that “does no harm”.

Forbes McGain · Grant A Blashki · Kevin P Moon · Fiona M Armstrong

To the Editor: A 71-year-old man presented with a firm erythematous painful swelling over the sternoclavicular region. He had undergone coronary artery bypass grafting (CABG) 18 months earlier. A chest x-ray showed the presence of sternal wires and mediastinal clips from the surgery, and pleural thickening in the right costophrenic angle. There were no focal abnormalities seen on the x-ray when compared with pre-CABG radiographs. A computed tomography scan of the chest showed a destructive lesion of the manubrium, with an associated soft tissue mass extending into the pectoralis muscle and anterior mediastinum. A sternal suture was noted within the lesion, and a separate surgical clip was identified in the suprasternal notch region (Box, A). Surgical exploration of the sternotomy wound revealed tumour in the muscle around the proximal sternum, with bone destruction. Histopathological examination of the tumour confirmed the presence of an osteosarcoma (Box, B). (A section of normal trabecular bone [Box, C] is shown for comparison.) There have been few reported cases of primary sternal tumours. To our knowledge, primary osteosarcoma arising contiguous to a surgical suture has never been reported. It is unknown why the osteosarcoma originated in the part of the sternum that contained the sternal suture rather than originating de novo in another part of the bony skeleton. Chronic localised sternal inflammation or mechanical irritation of the proximal sternum by the suture may have been contributory factors in triggering carcinogenesis in this uncharacteristic site.1 However, the effect of trauma and mechanical stimulation on development of primary cancers and their metastases has never been proven. Patients who present with bony tumours frequently have a history of previous trauma to the area where the tumour develops. While there have been numerous reports suggesting some relationship between trauma/chronic inflammation and oncogenesis,1-5 there is no evidence that a single incident of trauma can cause cancer. The combination of trauma, in-situ metal and malignancy after CABG is rare, and there are currently no grounds for suspecting a direct relationship between them. A: Computed tomography scan of the chest showing a destructive lesion in the cortex of the manubrium. A sternal suture, surgical clip and soft tissue mass are visible within the tumour (A = anterior, R = right). B: Histopathological section of osteosarcoma of the sternum. Pleomorphic and hyperchromatic cells are present in a disorganised immature bone matrix (osteoid) (haematoxylin and eosin stain; original magnification, × 20). C: Histopathological section showing normal trabecular bone of the sternum (haematoxylin and eosin stain; original magnification, × 2.5).

Laurence Weinberg · Joseph Mathew

To the Editor: We report a case of reactive arthritis with an unusual cause in a previously well 47-year-old male landscape gardener. The patient presented with acute onset of left ankle arthritis. He had a 10-day history of a productive cough associated with mild fever, back pain and arthralgias. His temperature was 37.7°C and occasional crackles were audible at the lung bases. His left ankle was tender, with decreased range of movement. The provisional diagnosis was atypical pneumonia with reactive arthritis. A chest x-ray was normal. Laboratory tests showed an elevated white cell count of 11.93 × 109/L (reference range [RR], 4–11 × 109/L), with a C-reactive protein level of 326 mg/L (RR, < 3 mg/L). Arthrocentesis showed increased white cells but was negative for crystals and bacteria. Serological tests were positive for Chlamydia psittaci (IgM, IgA and IgG were all elevated and increased during illness), and the patient was also positive for human leukocyte antigen (HLA)-B27. He was initially treated with meloxicam for the arthritis. Oral prednisone was added when his joint symptoms became more disabling. Weaning of prednisone was attempted, but symptoms recurred. Sulfasalazine was subsequently added. Symptoms took about 8 weeks to resolve. Sufferers of psittacosis are infected by inhaling the obligatory intracellular bacterium, Chlamydia psittaci, from the faeces of infected birds in soil or grass. As a landscape gardener, our patient was at risk. Clinical presentations of psittacosis vary considerably, but patients usually present with flu-like and respiratory symptoms.1 Reactive arthritis is unusual, being more commonly associated with pathogens such as Salmonella, Shigella, Campylobacter and Yersinia spp.2 Although reactive arthritis usually involves asymmetrical large joint oligoarthropathies, patients with Chlamydia psittaci infection usually have a polyarticular pattern.3 HLA-B27 has a high association with spondyloarthropathies, including reactive arthritis. Contact with infected birds is often not obvious, making the diagnosis challenging. Microimmunofluorescence (showing a fourfold increase in antibodies or IgG titre greater than 16) has become available for diagnosis. Differential diagnosis of reactive arthritis includes other causes of arthritis such as sepsis and crystal deposition. Management of Chlamydia psittaci reactive arthritis includes early use of the antibiotics doxycycline or erythromycin, or possibly ceftriaxone.4 Anti-inflammatory drugs are the mainstay for symptomatic treatment of all reactive arthropathies. Intra-articular steroid injections may be helpful. There is conflicting evidence regarding the benefit of systemic corticosteroids. Sulfasalazine may be a helpful adjunct.5 For gardeners, preventive measures include the use of masks, gloves and lawnmower catchers.

Peter N Gonski · Bobby Chan