Volume 179 Issue 10

Most of the solutions lie beyond the emergency department Hospitals represent essential infrastructure. Engineers who run an essential community resource such as the water supply system at 100% of capacity might expect to lose their jobs the first time consumers had to queue to use a tap. In contrast, some hospital funding models include activity targets that reward administrators who run at 100% of capacity — a level that guarantees queuing in the emergency department for coronary care beds and other critical inpatient services. The community accepts the use of price and denial (eg, restrictions of hours or allowed uses) as a rationing mechanism for the water supply, but not for hospital beds — queuing is the only rationing method currently accepted in the hospital system. Rationing is an essential feature in modern medicine,1 and queuing has long been used to ration elective services. But queuing is fundamentally an inefficient means of rationing care for time-critical illness. Access block — the inability of patients in the emergency department (ED) to access hospital beds — is the major issue currently facing emergency medicine in Australasia2 and, indeed, the whole Western world. Given a fixed physical resource and a relatively fixed labour force, increased average total ED time,3 also called ED length of stay (EDLOS), will decrease the resources available for providing care to acutely ill patients. Access block decreases access to emergency care (eg, measured as waiting time),4 and the resultant overcrowding is associated with adverse outcomes for ED patients.5,6 It is certainly in the interests of ED staff and patients to decrease EDLOS. . . . restricting the access and quality of initial care because of inability to provide timely later care is ethically dubious . . . The article by Liew et al in this issue of the Journal 7 adds to the growing evidence for an association between EDLOS and outcomes beyond the ED.8 The authors used a multivariate approach to study the relationship between EDLOS, other confounding factors, and subsequent inpatient length of stay in three Melbourne metropolitan hospitals. They found a positive association between EDLOS and inpatient length of stay after adjusting for casemix, time of presentation, and patient age. Whether this relationship is causal is a subject for further study. The Australasian College for Emergency Medicine has committed resources to such research through the Emergency Medicine Research Foundation. From an administrative perspective, the underlying mechanism is less important than the result. Increased inpatient length of stay after correction for casemix is financially undesirable: it is in the interest of hospital management to reduce both EDLOS and inpatient length of stay. Emergency departments are specialist multidisciplinary units with expertise in managing acutely unwell patients for the first few hours in hospital. Neither the facilities (generally poor privacy, small trolleys, 24-hour lighting) nor the staff are appropriate for providing longer term inpatient care. Very few patients who require an inpatient bed benefit from staying in the ED longer than 4 hours, and no ED benefits by caring for patients beyond this time. If the 30% or so of patients who are admitted spend twice as long in the ED, this represents a 30% increase in workload for ED staff with no change in conventional measures of activity (presentations, admission rate). Steadily worsening delays in accessing inpatient beds have been documented in many EDs over the past decade,9 suggesting there might be an underlying incentive such as increased efficiency in a different part of the health system. This research demonstrates an association with increased opportunity costs rather than any benefits. There is a clear need to reduce EDLOS for patients, but most of the solutions lie beyond the ED.10 Changes within the ED can mitigate the effects of increased workload, but, because of access block, they cannot shorten EDLOS. Much can be done to improve our hospital systems, including use of protocols for common conditions, transparent bed-management processes, and a focus on efficient use of the available beds, particularly through admission and discharge planning. Clinicians must be willing to trial different methods of management, such as treatment in the home and accelerated discharge, and to evaluate the outcomes rigorously.10 The study by Liew et al identifies the elderly as a group with the greatest potential for effective intervention. There have been significant achievements and more can be expected, but process change will not completely address the underlying mismatch between demand for inpatient beds and resources available. The primary problem is the lack of acutely available beds.11,12 The scarcer those empty beds become, the more difficult they are to access. Queuing for care at the entrance to ED is managed by triage, which stratifies patients by urgency — the most time-critical cases have the shortest queues. Queuing for a bed at the exit of ED is managed by bed allocation, which tends to stratify patients by their nursing load — the least intensive cases generally have the shortest queues. Elementary queuing theory predicts the accumulation of patients, but the daily variation in emergency medical activity has for too long allowed both emergency staff and others to assume the ED has “rubber walls” and that the marginal cost of the ED absorbing additional care to inpatients is low. The study by Liew et al7 and other studies on the effects of overcrowding5,6,13 now provide clear evidence that this is not the case. Emergency departments are expert at triage to achieve “the greatest good for the greatest number”, but, when prioritising, even emergency physicians are reluctant to consider denying care to patients with whom they have begun a therapeutic relationship. EDs are faced with the ridiculous situation of providing many hours of care to patients whose conditions were urgent on arrival but stable after treatment, while potentially unstable patients of similar initial urgency languish in the waiting room or in an ambulance for want of an ED trolley and nurse. It is time that hospitals addressed this inequity: restricting the access and quality of initial care because of inability to provide timely later care is ethically dubious14 and is likely to lead to adverse outcomes and medicolegal exposure. These weighty issues cannot be addressed by EDs alone. Demand for emergency services has increased9 while bed numbers have decreased,15 and demographic projections indicate that these trends are unlikely to reverse. Unless practices change, our EDs will cease to function in their designated role, and will instead inappropriately spend most of their resources providing care to patients who should be in inpatient beds. Hospitals, communities, and government must debate and decide the allocation of resources to EDs and wards and agree on a sensible approach to providing appropriate care in both environments. The debate is no longer about the level of resources our EDs deserve, but rather about how to ensure that ED resources are directed to those who need them — the patients in the waiting room.

Drew B Richardson MB BS(Hons), FACEM

Even for a simple genetic condition, screening the general population is not straightforward Hereditary haemochromatosis has been touted as the “poster child” for public health genetics. Most cases of haemochromatosis are due to homozygosity for a single mutation leading to iron overload. It is considered to be an ideal candidate for population genetic screening because genetic susceptibility is common, testing is inexpensive, and iron studies can detect early stages of disease. Most importantly, venesection is a simple and effective way to both prevent and manage the potential sequelae of iron overload, which include severe fatigue, arthritis, impotence, cirrhosis, diabetes, and cardiomyopathy. However, even though most cases of haemochromatosis are due to a single mutation, it is still unclear how many people homozygous for this mutation will develop serious disease. Consequently, there is uncertainty as to the benefit of screening. Following characterisation of the HFE gene in 1996,1 genetic testing for hereditary haemochromatosis has become available. In Australia, Medicare claims for testing for genetic susceptibility to hereditary haemochromatosis have risen from 14 414 in 1999 to almost 30 000 in 2002.2 It is predicted that about one in 200 Australians are homozygous for the C282Y mutation, which accounts for about 90% of cases of hereditary haemochromatosis identified to date in high-risk families.3 A person carrying two copies of the C282Y mutation is at risk of developing iron overload and subsequent disease. However, like all diseases, haemochromatosis is defined by pathology, and a person does not have hereditary haemochromatosis unless body iron stores, as reflected by abnormal iron indices (serum ferritin and fasting transferrin saturation), are elevated. There is a wide spectrum of potential consequences of iron overload, and while about 60% of C282Y homozygotes will eventually develop iron overload,3,4 it is not known what proportion will progress to serious clinical disease. The answer is complicated by the long latency for development of disease (probably many years) and the possible modifying effects of sex, diet, environment and other genes. Recent population-based studies have shed light on disease expression in people genetically susceptible to hereditary haemochromatosis. In the Busselton study, 16 homozygotes were identified from a sample of 3011 adults (1 in 188) with a median age of 52.7 years (range, 20–79 years).3 Twelve were not previously aware of their genetic risk, and of these, seven had elevated serum ferritin levels and the four with normal iron studies were premenopausal women. Half of the original 16 had clinical features consistent with hereditary haemochromatosis, although the prevalence of symptoms in non-homozygotes of the same age was not presented for comparison.3 A recent study in California identified 152 homozygotes from a sample of 41 038 individuals (1 in 270) with mean age 57 years (SD, 14).4 Among these homozygotes, 76% of men and 54% of women had raised serum ferritin levels. Homozygotes were twice as likely as controls to report liver problems (8.1% versus 4.1%), but there was no evidence for a higher prevalence in homozygotes for any other symptom associated with hereditary haemochromatosis. The authors estimated only a small percentage of homozygotes would develop frank clinical haemochromatosis.4 However, exclusion of people with pre-existing disease may have biased this estimate downwards.5 Although it is possible that disease expression is greater in Australia, owing to our relatively higher meat and alcohol intake,6 the results of the Californian study indicate that further population-based studies are necessary. The key factors in considering population screening of asymptomatic people are whether it will do more benefit than harm and whether it is cost-effective.7 International expert opinion has been cautious about population genetic screening for hereditary haemochromatosis,8,9 given the limited population data and possible adverse effects of screening, such as the potential for insurance discrimination in the United States. In Australia, health insurance is population-rated and discrimination is illegal. For life insurance, an agreement has been reached with the insurance industry that considerably reduces the risk of discrimination.10 Because cost–benefit analyses depend upon the number of people for whom disease can be prevented, enthusiasm for population screening for hereditary haemochromatosis has been dampened by the Californian findings. Even if these results are confirmed in whole or in part, it could be argued that, in Australia, there is minimal “cost” to genetically susceptible individuals in becoming blood donors, which virtually eliminates their risk of disease.11 However, until it can be demonstrated that benefits or savings outweigh any potential harm or costs, population genetic screening programs — paid for by the public purse — are on the backburner. The current standard of care remains cascade screening (ie, testing the HFE mutation status of first-degree relatives of individuals who have developed iron-related disease), because it is reasonable to assume that familial homozygous individuals are more likely to express disease.12 Genetic testing for HFE mutations is also appropriate as a follow-up in people with abnormal iron studies (ie, elevated serum transferrin saturation and serum ferritin). Iron studies should be considered for patients with unexplained symptoms or conditions consistent with hereditary haemochromatosis, such as severe fatigue, liver disease and diabetes, although the predictive value of such testing is likely to be low. C282Y homozygotes found to have high serum ferritin levels, with or without increased transferrin saturation, should have regular therapeutic venesection. Those with normal iron studies should be monitored expectantly, but do not require venesection unless they develop persistent abnormalities in serum ferritin levels. The Human Genome Project has made a great step forward in mapping tens of thousands of genes, but it may be decades before we can predict which individuals are most likely to develop serious disease. Even for a condition as apparently straightforward as hereditary haemochromatosis, the path to general population genetic screening has proven more complicated than initially expected.

Dorota M Gertig MB BS, DSc, FAFPHM · John L Hopper MSc, PhD · Katrina J Allen MB BS, FRACP, PhD

Failure to provide public funding for clinical trials may come at a high cost to the community in the long term Large-scale morbidity–mortality trials have become fundamental to the evaluation of most new drugs intended for long-term administration. Such trials have the unique ability to determine the net balance of positive and negative outcomes from the long-term use of drugs and allow consumers to feel confident that long-term therapy is safe in otherwise healthy individuals. A randomised controlled trial is the only study design that can provide reliable and unbiased estimates of the moderate treatment effects of interventions for most chronic diseases. Smaller studies measure surrogate outcomes or are underpowered to answer important clinical questions. If underpowered, they may be unethical and also squander the community altruism that underpins trial participation. Large-scale trials are major logistical exercises. They involve several thousand people allocated randomly to different treatment groups and monitored for 4–6 years. Depending on the recruitment strategy and the mode of follow-up, the cost is typically $20–$50 million.1 Past attempts to interest Australian research organisations in funding such studies have floundered because of this cost. In spite of this, there are a number of groups in Australia with an excellent track record in initiating and running high-quality large-scale clinical trials (many of the “public good” variety), indicating local capacity to conduct this type of research. However, these trials have largely been the province of the pharmaceutical industry. Although industry-funded studies have yielded firm scientific foundations in many areas of clinical practice, they are almost all directed towards testing superiority or equivalence of specific products, or other aspects such as greater convenience of new agents or technologies over the existing ones. Indeed, it is naïve to believe that the interests of industry will align with broader societal interests in securing effective and affordable care.2 The failure of non-industry concerns, including governments, to fund large-scale clinical trials leaves some conspicuous gaps in evidence where the consequences may be forgone savings for the public purse. In other cases, the result may be prolonged community exposure to older agents whose long-term risks have not been adequately assessed. Some recent examples highlight the importance of this problem. Antihypertensive drugs make up a large component of the Australian pharmaceutical budget — $516 million for the Pharmaceutical Benefits Scheme (PBS) for the newer agents in the financial year 2002–03 alone.3 For many years, there has been a trend towards these newer, more expensive agents replacing older, cheaper drugs for first-line management of mild hypertension.4 The justification was provided by small trials involving surrogate endpoints, such as effects on blood pressure control, vascular changes, and other risk factors. However, clinical trials with surrogate endpoints do not provide an appropriate basis to underpin long-term drug therapy: they can not provide reassurance of the drug’s long-term safety or determine the balance of desirable and undesirable effects of new agents. When the necessary studies of antihypertensive drugs were finally undertaken, they demonstrated that the advantage of newer agents over diuretics was marginal, at best.5,6 In this instance, a lack of appropriate trial data on management of hypertension probably led to years of unnecessary expense to the PBS that greatly outweighed the cost of a large-scale trial. It is clearly in the public interest to ensure that PBS funds are not being spent on expensive therapies when much cheaper agents are just as effective. We recently estimated that the failure to provide funding for trials probably cost Australian taxpayers between $45 million and $108 million in 1998 alone.4 Another example of the false economy of failing to fund clinical trials is the recently reported Women’s Health Initiative study.7 Before the results of this trial were published, a generation of women was prescribed hormone replacement therapy (HRT), despite the lack of rigorous long-term safety data that could only have been obtained from a large-scale trial. There was little commercial imperative to fund such a long-term trial when large markets of regular users existed. Eventually the US National Institutes of Health (NIH) recognised the importance of funding such a study, as indeed they have funded a number of other “public good” studies. Release of the study results has led to a sharp drop in the use of combined HRT, except for short-term use to relieve significant perimenopausal symptoms. The “dividend” for the Australian government was $16 million less expenditure on HRT in the financial year 2002–03.3 A failure to learn from these experiences may cost the community in the future. For example, low-dose aspirin is an effective antiplatelet agent whose use has recently been advocated in the United States for people with a 10-year risk of coronary events and stroke of 10% or more.8 This recommendation may lead to widespread use of aspirin for primary cardiovascular prevention in the elderly, despite a lack of data to indicate that its benefits in this age group outweigh the risk of haemorrhage.9,10 There is little likelihood that commercial interests will supply the funding to overcome this lack of data. It is more likely that industry would fund a study using a newer, more expensive antithrombotic agent in the hope of establishing it as standard therapy. The means must be found to identify and target strategically important research questions that require public funding. A budget (in the order of $100 million) for national research funding of these large “public good” trials should be established and administered by the National Health and Medical Research Council (NHMRC). This sum, representing 12% of the NHMRC budget and 0.2% of the recurrent health expenditure of $60 billion, is commensurate with the importance of such trials to clinical medicine and public health. Using the NIH as a model, trials would involve a mix of requested and investigator-initiated research. Research groups, either alone or (more likely) collaboratively, would apply for competitive funding. Although this would be administered by the NHMRC, a number of other stakeholders would benefit, including federal and state governments and their agencies, departments of health, the Health Insurance Commission, and the PBS. New funds should be made available from these sources. States should contribute to this initiative as large-scale trials are usually multicentred, allowing research capacity building and employment in both metropolitan and rural areas throughout Australia. Failure to develop a policy that supports such strategic research may well lead to waste of public funds and a delayed recognition of unfavourable risk–benefit ratios.

John J McNeil PhD, FRACP · Mark R Nelson PhD, FRACGP, FAFPHM · Andrew M Tonkin MB BS, MD, FRACP

On 9 March 2003, during the New South Wales state election campaign, Premier Bob Carr announced that a re-elected Labor government would convene a state summit on alcohol. The 1999 NSW Drug Summit and the 2002 Obesity Summit were obvious models. The 1999 Drug Summit, also conceived during a state election campaign, was generally considered to have been successful. It developed a realistic policy framework and substantially increased funding to improve prevention, community and treatment services to reduce problems resulting from illicit drug use in NSW. However, the problems arising from alcohol greatly exceed those of illicit drugs, and, as our favourite drug provides both considerable benefits as well as sizeable costs, these problems are more complex for communities to grapple with. The Alcohol Summit was held in the NSW Parliament from 26 to 29 August 2003, and involved key government departments (including Health, Police, Gaming and Racing, and the Cabinet Office), as well as health professionals, such as Emeritus Professor Ian Webster, the doyen of the alcohol and drug field in Australia, and industry and community representatives. The Summit comprised plenary sessions with national and international invited speakers who are international authorities on the prevention of alcohol-related problems (eg, Professor Tim Stockwell, Director of the National Drug Research Institute, Perth; and Professor Sally Casswell, Chair of the World Health Organization Committee on the Prevention of Alcohol-Related Problems); 10 working groups addressing specific issues; and site visits to drug and alcohol services to enable parliamentarians to inspect treatment facilities at first hand. All members of the NSW Legislative Assembly and Council were invited to attend the Summit along with 131 delegates from diverse backgrounds. Two one-day satellite meetings preceding the Summit addressed alcohol problems in young people and Aboriginal people, respectively. BackgroundThe Summit began with expert reviews on several topics, including the history of alcohol in Australia, the epidemiology of alcohol problems and the evidence base for effective prevention of alcohol problems. About half the alcohol-related morbidity and mortality in Australia results from acute intoxication, and includes injury, road trauma and suicide. The remaining half results from chronic excessive consumption, and includes cirrhosis, stroke and other medical complications. A large proportion (39%) of the alcohol consumed in Australia is drunk at levels that confer moderate-to-high risk of chronic harm, while 51% of the alcohol consumed poses short-term risks to the drinker.1 Mr Ken Moroney, NSW Commissioner of Police, stated that people intoxicated with alcohol and perpetrating domestic and other violence account for up to 75% of the workload of the NSW police. Furthermore, alcohol-related problems are very unevenly distributed. For example, the NSW town of Walgett, with a total population of 2000, has 10 liquor licences and one in three of the adult male population has had at least one conviction for alcohol-related violence. The debateMany initiatives were reviewed, especially primary prevention methods to limit intoxication, such as increasing the price (by raising taxes) of cask wine and other beverages particularly associated with severe intoxication. Secondary prevention initiatives proposed included improving enforcement of existing laws concerning responsible service of alcohol. Enforcement of these laws was acknowledged by senior NSW police to be less than adequate, and penalties were generally considered to be insufficient. Installation of breathalysers in bars could enable patrons to test their breath alcohol level before driving home. Tertiary prevention measures were also considered, such as expanding measures focused on problem drinkers. These included ignition interlocks to reduce recidivist drink-driving by requiring participants to pass a breathalyser test before starting their car engine. Numerous delegates expressed concern about the ready availability of alcohol to under-age youth. The alcohol beverage industry rejected the evidence that under-age drinking is an increasing problem. Anecdotal reports suggested that provision of alcohol by adults to under-aged young people is widespread and quite widely accepted. To address this problem, education of adults and young people was proposed, along with a range of measures to increase enforcement of the law and to increase penalties for offenders (Summit communiqué resolutions 1.10, 8.8–8.23 and 10.1).2 Delegates heard that alcohol taxation is one of the prevention measures best supported by evidence of effectiveness.3 However, taxation of alcohol in Australia is riddled with inconsistencies and anomalies. A more public-health-oriented approach involves taxing alcoholic beverages according to alcohol content rather than beverage class or cost. One of the key recommendations of the Summit was to hold a national public inquiry into alcohol taxation (Summit communiqué resolution 2.9). Earmarking some additional tax revenue for prevention and treatment programs is supported by evidence of effectiveness, but was not supported by the Summit. At times, the debate became quite confrontational. Representatives of the alcohol beverage industry denied developing products designed to appeal to under-age drinkers and advertising inappropriately (including appealing to under-age drinkers). The alcohol beverage industry advocated retaining self-regulation of alcohol advertising, despite the evidence presented to the Summit that the current system does not prevent grossly inappropriate advertising. The industry argued vigorously that it already promotes responsible drinking. Curfews for young people were debated but not adopted. The industry expressed a strong interest in developing voluntary partnerships with health and community groups, but argued that funding should be drawn from existing alcohol taxes. Total federal, state and territory government revenue from alcohol exceeds $5 billion annually, not including income from the goods and services tax. Most of this revenue is generated by the federal government, and very little is directed towards preventing or alleviating the adverse effects of alcohol. The outcomeIn the final sessions, resolutions from the 10 working groups were collated into an interim report for debate. Most resolutions were not controversial: all the proposals of several working groups were adopted without significant change. There was strong support for improving the capacity and quality of treatment for people with alcohol-related problems, and for general practitioners to receive support in this endeavour. A fundamental issue for most delegates was the extent to which the alcohol industry should accept responsibility for the manner in which alcohol is consumed. For example, how can a server more reliably recognise intoxication and refuse further service? The final communiqué comprised 44 pages of recommendations, with 315 recommendations to reduce the burden of alcohol-related harms supported by a majority of delegates (Box).2 The outstanding achievement of the Alcohol Summit so far has been returning alcohol control policy to the public health agenda. The resulting policy changes have the capacity to achieve considerable future benefits for the community. However, it is critical that the NSW government maintains its focus on this field and injects new resources to ensure that the Alcohol Summit leads to tangible outcomes. Selected recommendations of the NSW Alcohol Summit* 1. A retailer alerts system should be developed to highlight breaches of the Voluntary Advertising Code. 2. There should be a national public inquiry into alcohol taxation to consider the health, economic, social and community costs and benefits of current and proposed alcohol excise and taxation measures. 3. The liquor industry should be required to set aside a proportion of its advertising budget for harm-minimisation programs. 4. The acceptability of inappropriate alcohol use at sporting events, by both participants and spectators, should be challenged. 5. The distribution of alcohol treatment services in NSW should be reviewed and adjusted to ensure equity of access. 6. The NSW police should investigate the feasibility of random breath testing on waterways. 7. Drink drivers convicted of more serious offences should be required to undertake an alcohol-related brief intervention program before licence reinstatement. 8. The NSW Vice Chancellors’ Committee should be asked to consider the development of additional postgraduate programs for professional and clinical staff in drug and alcohol treatment. 9. Intoxication should be defined in relevant legislation so that responsible service-of-alcohol requirements can be applied by both servers and the police. 10. Existing schemes to divert offenders from the criminal justice system towards treatment should be considered for extension to cover those with alcohol misuse problems, and adequate treatment places should be available to absorb court referrals. *Resolutions have been edited. The full text is available from the Summit website.2

Paul S Haber MD, FRACP · Katherine M Conigrave FAChAM, FAFPHM, PhD · Alex D Wodak FRACP, FAFPHM, FAChAM

Objective: To examine the association between emergency department length of stay (EDLOS) and inpatient length of stay (IPLOS).Design: Retrospective review of presentations and admissions data.Setting: Three metropolitan hospitals in Melbourne, 1 July 2000 to 30 June 2001.Main outcome measures: Mean IPLOS for four categories of EDLOS (≤ 4 hours, 4–8 hours, 8–12 hours, >12 hours); excess IPLOS, defined as IPLOS exceeding state average length of stay; odds ratios for excess IPLOS adjusted for age, sex and time of presentation.Results: 17 954 admissions were included. Mean IPLOS for the four categories of EDLOS were ≤ 4 hours, 3.73 days; 4–8 hours, 5.65 days; 8–12 hours, 6.60 days; > 12 hours, 7.20 days (P < 0.001). The corresponding excess IPLOS were 0.39, 1.30, 1.96 and 2.35 days (P < 0.001). Compared with EDLOS 4–8 hours, odds ratios (95% CIs) for excess IPLOS associated with the other three categories of EDLOS were ≤ 4 hour, 0.68 (0.63–0.74); 8–12 hours, 1.20 (1.10–1.30); and > 12 hours, 1.49 (1.36–1.63), after adjusting for elderly status, sex and time of ED presentation.Conclusion: EDLOS correlates strongly with IPLOS, and predicts whether IPLOS exceeds the state benchmark for the relevant diagnosis-related group, independently of elderly status, sex and time of presentation to ED. Strategies to reduce EDLOS (including countering access block) may significantly reduce healthcare expenditure and patient morbidity.

Don Liew MB BS, FACEM · Danny Liew MB BS(Hons), FRACP · Marcus P Kennedy MB BS, FACEM

For women with early breast cancer, multidisciplinary care has the potential to reduce mortality, improve quality of life and reduce healthcare costs. In Australia, the diversity of healthcare delivery settings and types of care means that a single model of multidisciplinary care may not be appropriate. The “Principles of multidisciplinary care” were developed to provide a flexible framework for the provision of multidisciplinary care in Australia. The Principles emphasise five key elements: the team, communication, access to the full range of therapies, standards of care and involvement of the woman. This flexible, principle-based approach to multidisciplinary care is unique. The Principles have the potential to be applied to other cancers and other chronic diseases.

Helen Zorbas MB BS · Kathy Rainbird PhD · Karen Luxford PhD · Bruce Barraclough FRACS · Sally Redman PhD

Objectives: To study the relationship of blood pressure to birthweight and current body mass index in a population with high rates of low birthweight (< 2.5 kg).Design: A cross-sectional population screening program conducted between 1992 and 1998, with retrospective retrieval of birthweights.Setting: A remote coastal Australian Aboriginal community with a high prevalence of diabetes, cardiovascular and renal disease.Participants: Eighty-two per cent of the community members (1473/1805) were screened. Birthweights were available for 767 (71%) of the screened participants aged 7–43 years.Main outcome measures: The association between birthweight and current blood pressure, accounting for current body mass index.Results: Mean birthweights were low, and 18% of children and 35% of adults had been low-birthweight babies. In children (7–17 years), blood pressure was not correlated with birthweight, but in adults there was an inverse correlation — a 1 kg increase in birthweight was associated with a 2.9 mmHg (95% CI, 0.3–5.5 mmHg) decrease in systolic blood pressure, after adjusting for age, sex and current weight. Overweight adults with low birthweight had the highest blood pressures.Conclusions: Low birthweight is significantly associated with higher blood pressure in adult life, and the effect is amplified by higher current weight. Given the high rates of low birthweight in Aboriginal people in remote areas, and the detrimental effect of higher blood pressures on chronic diseases (currently present in epidemic proportions), interventions should focus on improving birthweights and on weight control in adolescents and adults. Special attention should be paid to children with low birthweight to avoid their becoming overweight in adult life.

Gurmeet R Singh MB BS, MD, MPH · Wendy E Hoy MB BS, BScMed, FRACP

Objective: To review the results of opinion polls on community attitudes to in-vitro fertilisation (IVF) and other aspects of assisted reproductive technology over a 20-year period.Design, setting and participants: Fourteen Australia-wide interview surveys that included questions relating to IVF were carried out between July 1981 and November 2001 as part of regular Morgan polls of community attitudes on various topics. Each survey involved about 1000 respondents drawn from randomly selected “cluster points” in urban and rural locations.Main outcome measures: The proportion of people who approved or disapproved of various aspects of IVF treatment.Results: Support for IVF to help infertile married couples increased from 77% in 1981 to 86% in 2001. Approval for IVF procedures being supported by Medicare funding rose from 70% in 1981 to 79% in 2000.Conclusions: Community approval of the use of IVF to treat infertility has risen significantly in Australia over the past 20 years.

Gabor T Kovacs MD, FRACOG, FRCOG · Gary Morgan BComm · E Carl Wood AC, CBE, FRCS, FRACOG · Donna Howlett BSc, MBA · Catherine Forbes BSc, MSc, PhD

State health departments bear considerable expenditure due to tobacco-related hospitalisations. We present a straightforward formula, based on aetiological fractions (attributable risks), with which to estimate tobacco-related expenditure in a way relevant and meaningful to state health departments and hospital managers. Tobacco was responsible for 43 350 hospitalisations in New South Wales in 1999–2000 alone, incurring $176 096 323 in hospital costs (nearly $482 456 per day). If the equivalent of a specified percentage of expenditure as calculated for one year were “invested” in tobacco control in the next year, then commitments to a substantive suite of health promotion programs could be made. For example, using our formula, a contribution of 3% would secure an annual tobacco control budget of $5 282 890 in NSW. Once securely funded, evidence-based tobacco control would reap dividends by reducing hospital expenditure and enhancing population health.

Seham T Girgis MB BCh, MPH · Jeanette E Ward MHPEd, PhD, FAFPHM

The current “Pharmaceutical Benefits Scheme (PBS) community awareness campaign” explicitly links the difficulties facing the PBS to patient behaviour and “waste”. The campaign suggests that patients are taking advantage of affordable access to prescription medicines, and emphasises that patient responsibility is “the prescription for a healthy PBS”. By neglecting to inform the public that the pressures facing the PBS also include doctors’ prescribing habits and intensive pharmaceutical industry marketing, the campaign has missed an opportunity to initiate a balanced and constructive debate about the future viability of the PBS. It has become something of an axiom that increasing cost is endangering the Pharmaceutical Benefits Scheme (PBS), and that something must be done about it. Typically, policy responses have been to target the prescription end-user — the patient. Successive governments have increased patients’ out-of-pocket charges as a means of containing drug costs. The present federal Government, thwarted thus far by the Senate in its attempt to increase the patient co-payment, is trying an alternative — appealing to patients’ moral sensibilities rather than their hip-pocket nerve. The current “PBS community awareness campaign”,1 an initiative of the National Strategy for Quality Use of Medicines (QUM)2 has been launched at a reputed cost of $27 million through a nationwide advertising strategy.3 The objective of informing the Australian public about the operation, strengths and costs of the PBS is laudable. However, the tone of the campaign is morally charged, with the suggestion that many Australian patients are not acting responsibly in their use of prescription medicines. The two main mediums of the campaign — a series of television advertisements and an information booklet — emphasise an association between patient behaviour, “waste”, and the increasing financial pressure on the PBS, a pressure which imperils the future viability of the scheme. It appears that patient responsibility is “the prescription for a healthy PBS”. As part of the National Medicines Policy, the strategy for QUM is underpinned by a set of principles, the first of which is “the primacy of consumers”. The strategy claims to recognise “the wisdom of consumers” and states “consumer involvement in all aspects of the Strategy is critical”.2 Far from incorporating the wisdom of patients, the present campaign appears to selectively choose more extreme examples of misuse of medicines to establish a moral position and place the responsibility for increasing prescription demand on patients. The campaign booklet states “some people like to get a prescription every time they visit a doctor”. This statement implies that patients drive the demand for prescriptions and that the low cost of prescription medicines promotes wasteful behaviour. The campaign repeatedly advises patients to take note of the full cost of the prescription that is borne by the Scheme (this is now highlighted on prescription labels). With such information, patients can “use the PBS responsibly” and minimise “waste”. Patients are also exhorted to consider their need for repeat prescriptions, but are not advised of the dangers of stopping treatment for some serious disorders (eg, diabetes and heart failure). The National Medicines Policy document raises the concern that “easy access can work against the quality use of medicines”, offering the common anecdote of patients’ stocking up unnecessarily on prescription medicines “. . . because they are available free or at low cost”. While patients probably do initiate a certain amount of unnecessary prescription demand, the relationship of this to the cost of a prescription is not clear in the available evidence.4 Further, there is no substantial evidence to show that such behaviour is common enough to be a major contributor to rising drug expenditure. The emphasis on patient responsibility reveals a conviction that prescription subsidy through the PBS results in significant “moral hazard”. In other words, low out-of-pocket cost generates unnecessary prescription demand or “waste”. Arguments for the operation of a “moral hazard” rest not on direct observations of patient behaviour, but on studies of aggregate prescribing data.5 Rather than drawing on the wisdom of patients, fluctuations in use of prescription medicines after changes to out-of-pocket costs are used to make inferences about patients’ motivations. Differences in rates of use of “essential” therapies compared with “discretionary” therapies are taken as proxies for “necessary” and “unnecessary” patient behaviours.6 However, prescribing data cannot show whether the changes in pharmaceutical use reflect appropriate or inappropriate patient responses to increased cost; nor can they reveal the motives of patients who have received prescriptions. Increased demand when drugs are affordable does not itself mean that patients are using medicines unnecessarily.7 The increasing cost of the PBS does, however, mean that Australians are being given more prescriptions, often for newer or novel therapies. Australians, like the citizens of other developed nations, live in a society where prescription medicines are central to the provision of healthcare and increasingly prominent in how we prevent and manage illness. The pharmaceutical industry devotes considerable expense and effort to promoting drugs directly to doctors and less directly to patients.8 Australian doctors’ preferences for prescribing newly released medicines, often neglecting older cheaper alternatives, have long been noted.9-13 Patients may sometimes ask their doctor to prescribe the latest available drug for their condition; however, there is no evidence to indicate that low cost is a prime motivator in this demand. The diminishing numbers of general practitioners willing to “bulk-bill” their patients means that seeing a doctor requires an increasing out-of-pocket expense for many patients.14 Most Australian patients do not undertake the cost and inconvenience of consulting a doctor lightly. It is unlikely that many visit their doctor to unnecessarily access affordable medicines. Even with affordable access, the underuse of prescription medicines is a commonly acknowledged problem. While some patients may “like to get a medicine every time they visit the doctor” (quote from the Strategy), other patients don’t seek a medicine when it is necessary, do not always accept a necessary prescription, nor do they always adhere to their prescribed therapy. Despite the PBS providing affordable access, medicine costs can still present a barrier for some Australian medicine users, particularly the chronically ill and those on lower incomes but not eligible for government concessions.15 While the strategy has parallel initiatives aimed at enhancing QUM among health professionals and the pharmaceutical industry, the notion of pharmaceutical “waste” is not a prominent feature of these. In contrast to the message about “waste” that is communicated to consumers, health professionals and industry staff who visit the PBS Web home-page receive a brief outline of the PBS drug-listing process. The strategy and its current awareness campaign give the impression that whatever waste exists is largely driven by consumers taking advantage of affordable access. Related phenomena such as prescription “drift” (the tendency to prescribe newer more expensive medicines for common conditions) and “leakage” (prescribing to a broader population than was intended in the subsidy decision) and aggressive industry marketing are left out of the public gaze.13,16 This restricts the community’s awareness about the PBS, the pressures it faces and its future viability. An opportunity has been missed to provide the public with a comprehensive and balanced view of the problems facing the PBS. The Strategy, as presented to the public, has selectively focused on the role of affordable access in creating “waste” and in contributing to the pressure on the PBS. Because of the complexities of prescription drug use in the community, this will have little impact on quality use of medicines overall. Further, this focus potentially alienates patients from information on the other important factors contributing to increasing PBS expenditure, such as intensive promotion by pharmaceutical companies and doctors neglecting to prescribe older, cheaper therapies. Accepting that most prescription use is necessary begs the question of what proportion of medicine use is unnecessary and what factors combine to generate such use. These questions are still to be coherently answered, and what current knowledge exists is insufficient to justify elevating “moral hazard” to a primary cause of difficulties facing the PBS. A more balanced approach to informing the community about these problems would be to acknowledge the role of patients, health professionals and the pharmaceutical industry in creating demand, and to initiate an informed debate on how to sustain the PBS.

Evan Doran PhD · David A Henry FRCP

Human fetal tissue is a scarce resource that has been used in Australia for biomedical research since 1980. From 1994 to 2002, it has been used for research by 19 biomedical researchers at 12 separate Australian institutions (four universities, six major teaching hospitals and two research institutes). With an average of 265 samples distributed annually, researchers have conducted experiments in biomedical research with the approval of their Human Ethics Committees, and published 74 manuscripts in peer reviewed journals over the past decade. The tissue is obtained from therapeutic termination of pregnancies at 8–20 weeks’, but mostly 14–18 weeks’, gestation. The average number of fetuses obtained over the past 10 years was 108 per annum. Our understanding of the pathogenesis of human diseases such as diabetes, multiple sclerosis, retinopathy of prematurity and osteoporosis has been advanced because of such experiments, and better drug treatment of disorders such as osteoarthritis has been made possible with the use of human fetal tissue. The benefits of human fetal tissue research need greater recognition.

Bernard E Tuch FRACP, PhD · Hayley Scott BScAg · Muhammad T Tabiin PhD · Liping P Wang MSc · Patricia J Armati PhD

Clinical records Patient 1 A 51-year-old woman was transferred to the Royal Brisbane Hospital from a country hospital, where she had presented with fever, sweats and an increasingly painful swelling of the jaw 5 days after removal of a wisdom tooth. The tooth had been removed by a general dentist, after a complaint of pain and swelling associated with it. The following day she had noticed an intraoral swelling that progressed over the week to become apparent extraorally. At presentation, she had difficulty swallowing and speaking. Although alert and oriented, she was febrile, had a “husky” voice and was starting to drool. Examination revealed a large sublingual, brawny mass extending bilaterally, bilateral submandibular swelling, and a swollen, protruded tongue. An emergency nasal fibreoptic intubation was performed in the operating theatre, where incision and drainage produced a large amount of purulent material. Cultures of this material grew Streptococcus milleri sensitive to penicillin, and the patient continued to receive intravenous ampicillin. An orthopantomogram (OPG) revealed a tooth root in situ after the extraction. The woman was discharged on Day 7 postoperatively with a diagnosis of Ludwig’s angina secondary to an infected extraction socket. Patient 2 A 48-year-old woman presented to the emergency department (ED) with headache and left-sided weakness, initially diagnosed from a computed tomography (CT) scan as a right parietal stroke. Magnetic resonance imaging (MRI) showed a parietal mass consistent with a tumour (Box 1, A). Using stereotactic craniotomy, purulent material was drained from the lesion, and S. milleri and Actinobacillus actinomycetemcomitans were grown on culture. Further investigation by the maxillofacial surgery team revealed two right maxillary premolars that were tender to percussion and radiolucencies at the root apexes on the OPG. The two teeth were removed and the sockets were cleaned by curettage and irrigation. Transthoracic and transoesophageal echocardiography excluded infective endocarditis as a complication. After 8 weeks’ treatment with intravenous benzylpenicillin, ceftriaxone and metronidazole, the woman’s neurological deficits resolved and an MRI scan showed scar tissue in the right parietal lobe without reaccumulation of pus. Patient 3 A 42-year-old woman presented to the ED with a 3-day history of constant right submental pain (no worse with eating) and swelling. She was given analgesia and sent home, but returned the next day with worsening symptoms. She was referred to the oral and maxillofacial surgery service. The patient gave a history of a “partial” right submandibular gland removal 10 years previously after recurrent sialoadenitis. She looked well, had no dysphagia or difficulty breathing, was afebrile and had no respiratory distress. There was a right submandibular scar consistent with her past history, moderate submandibular swelling and submandibular and deep cervical lymphadenopathy. A hard lump was felt in the floor of the mouth, but the tongue and floor of the mouth were not elevated. An OPG demonstrated a right-sided oval-shaped radio-opaque structure, confirmed on axial CT to be in soft tissue on the lingual side of the mandible. No odontogenic lesions were seen. The patient was diagnosed with infection secondary to a retained submandibular duct stone. She was admitted and given intravenous ampicillin and metronidazole. While she was awaiting surgery for removal of the stone, the swelling rapidly progressed over 12 hours, resulting in elevation of the tongue and difficulty in swallowing. Emergency awake fibreoptic nasal intubation and surgery were performed. No abscess was found, but two calculi were removed from the remaining portion of the submandibular duct. The patient, still intubated to protect her airway, was transferred to the intensive care unit. As the swelling of the tongue and floor of the mouth worsened postoperatively, she remained intubated for 3 days. When she became febrile (38.2°C), ampicillin and metronidazole were discontinued and she began treatment with intravenous ticarcillin and clavulanic acid. She was discharged on postoperative Day 4, with instructions to take oral amoxicillin 750 mg with clavulanic acid twice daily for 5 days. She made an uneventful recovery. Patient 4 A 28-year-old man presented to the ED of a regional hospital with left submandibular pain and swelling after having a dental filling 10 days previously in the lower left second molar. The patient was given analgesia and sent home. After a few days, the patient presented to another regional hospital with worsening symptoms. He was given oral amoxycillin and metronidazole and discharged. But the swelling and pain progressed until an inability to swallow saliva prompted him to return to the second hospital. On examination, the patient had difficulty breathing through the mouth. Marked left submandibular swelling, severe trismus and halitosis were noted. He was afebrile, but had a white cell count of 16.3 x 109/L (normal range, 4.0–11.0 x 109/L), neutrophilia of 13.1 x 106/L (normal range, 2.0–7.5 x 109/L) and a serum C-reactive protein level of 207 mg/L (normal range, < 10 mg/L). An OPG revealed a deep dental filling of the lower left second molar and a carious lower left wisdom tooth. He was admitted for airway observation and given intravenous benzylpenicillin and metronidazole. The next day he was unable to completely open his mouth. After awake fibreoptic intubation, the two teeth were removed and the abscess drained. (The clinical and radiological findings for a patient with a similar diagnosis are shown in Box 1, B–D.) Still intubated for airway protection, the patient was transferred to an intensive care unit at a tertiary hospital. His condition deteriorated and pericarditis and mediastinitis were diagnosed, necessitating transfer to an intensive care unit at a specialist chest hospital. After intensive medical treatment, the patient made a complete recovery. Numerous complications are attributed to maxillofacial infections, including Ludwig’s angina, mediastinitis, cerebral abscess, maxillary sinusitis, chronic fistulous tracts and infective endocarditis. These may result from a delay in adequate treatment of the original focus of infection, and may turn a minor problem into one with dangerous complications. Infections in the sublingual or submandibular space are not contained by any anatomical barriers and may spread to the mediastinum or diaphragm via the contiguous fascial spaces of the neck.1 Ludwig’s angina is defined as bilateral cellulitis of the submandibular and sublingual spaces.2 The adult mortality rate from the disease is reported to be between 4% and 10%.3 Ludwig’s angina has the potential to spread rapidly, resulting in mediastinitis and airway obstruction.2,4 Common clinical features of odontogenic infections (which may progress to cause significant maxillofacial infections) are summarised in Box 2. An OPG may reveal evidence of odontogenic infection. Other investigations, such as CT scans of the jaws and neck and blood investigations (eg, full blood count, electrolytes/urea/creatinine levels, procalcitonin level [an indicator of infectious processes] and blood cultures), may be ordered if clinically indicated. Clinical signs warranting prompt hospital referral include dysphagia, difficulty with or pain on moving the tongue, stridor, trismus, elevation of the tongue, and fever. It is inadvisable to treat these patients only with analgesia and antibiotics, as surgical drainage of the abscess or removal of the focus of infection is also required.5 An otherwise well patient with no systemic signs of infection, cellulitis or airway compromise does not require antibiotics once the source of the infection has been eliminated. With respect to odontogenic abscesses, this may involve extraction of the offending tooth or teeth, with drainage via the extraction socket, or may require intraoral and/or extraoral drainage. If the patient’s medical condition allows it, and if dentally suitable, the responsible tooth or teeth may be endodontically treated, allowing the patient to retain the tooth. Options for airway management include awake fibreoptic intubation, creating a surgical airway (tracheostomy or cricothyroidotomy), inhalational induction with blind nasal intubation under deep anaesthesia, and awake blind nasal intubation.6 When indicated, antibiotics that cover the expected mixed anaerobic and aerobic nature of oral infections should be chosen. Suitable choices include intravenous ampicillin (1 g four times a day) together with metronidazole (500 mg three times a day).5 For patients allergic to penicillin, clindamycin is a possible alternative. The regimen should be modified in response to culture and sensitivity results. Suppurative salivary gland infections are often caused by Staphylococcus aureus, for which treatment with dicloxacillin or flucloxacillin is appropriate. Lessons from practice Early management of odontogenic/maxillofacial infections may prevent serious complications Signs of severe infection include fever, stridor, protrusion or elevation of the tongue, dysphagia and trismus. These warrant prompt referral to an oral and maxillofacial surgeon In advanced presentations, airway control is imperative to prevent airway obstruction by soft-tissue swelling Surgical drainage of any collection of pus is mandatory Antibiotics are not indicated unless systemic signs, cellulitis or airway compromise are present, and should be viewed as an adjunct to treatment 1: Manifestations and complications of maxillofacial infections A: Magnetic resonance image (coronal view) of right parietal abscess (Patient 2). B: Right submandibular swelling secondary to an abscess of the lower right second molar tooth (case not described here but similar to Patient 4). C: Computed tomography scan (coronal view) of Patient in B, showing a collection (thick arrow) adjacent to the medial surface of the right mandible (a gas bubble [thin arrow] is also visible). D: Aspiration of pus from Patient in B. 2: Clinical features of odontogenic infections Toothache Dental pain exacerbated by hot or cold foods Intraoral or extraoral swelling Erythematous or inflamed gingiva Carious or broken tooth/teeth Intraoral or extraoral seepage of purulent material

Peter J Aquilina MB BS(Hons), BDS(Hons), FRACDS · Anthony Lynham BMed(Hons), FRACDS(OMS), FRCS

A 62-year-old woman with longstanding, well controlled type 2 diabetes mellitus and hypertension initially presented with a 2-day history of acute, partial right-sided facial weakness. The facial paralysis was not accompanied by hyperacusis, and taste sensation was preserved. The patient presented again 2 weeks later with complete paralysis of the left facial nerve and only partially resolved right-sided symptoms. No other central or peripheral neurological signs or symptoms were elicited during either presentation. As bilaterality makes facial neuropathy a more ominous sign of various known conditions,1,2 we carried out prompt further investigation. Results of haematological and biochemical assays, including liver function tests, were unremarkable. Specifically, the serum angiotensin-converting enzyme (ACE) level was 42 U/L (normal range, 30–50 U/L). Results of urinalysis and cerebrospinal fluid examination were also normal (although the latter did not include oligoclonal IgG and ACE assays). Nerve conduction studies and electromyography findings were consistent with denervation of the facial nerves. Electroneurography of lower limb nerves showed normal nerve conduction bilaterally. No abnormality was detected on chest x-ray or brain magnetic resonance imaging. However, a computed tomography scan of the chest showed bilateral hilar lymphadenopathy with bilateral basilar lung infiltrates (Box, A). A transbronchial biopsy revealed a single, non-caseating granuloma (Box, B). The patient was discharged from hospital with instructions to take 30 mg prednisone daily for a month (because of her diabetes, she was given half the ideal dose of 1 mg/kg per day). After 1 month of treatment she showed marked improvement, and the dose was gradually reduced over the following month. DiscussionThis is an unusual case of sequential or “consecutive” bilateral facial paralysis — in which unilateral facial palsy was followed by contralateral facial palsy before the side affected first had recovered — in association with biopsy-proven pulmonary sarcoidosis. This case makes the point that a normal chest x-ray does not, unequivocally, exclude hilar lymphadenopathy. Although sarcoidosis is known for its unusual and protean manifestations, including neurosarcoidosis, we are aware of only two other case reports of bilateral facial paralysis as the sole presenting feature of sarcoidosis.3,4 However, we cannot exclude the possibility that the facial weakness seen in this case was related to type 2 diabetes or another aetiology, such as Bell’s palsy. A: Computed tomography scan of the chest, showing hilar lymphadenopathy. B: Transbronchial biopsy, showing a single, non-caseating granuloma (haematoxylin–eosin stain).

Ali A Haydar MD · Nabil M Hujairi MD · Aiman Tawil MD · Raja A Sawaya MD

William J Glasson,* Robert A Bain† * Federal President, † Secretary General, Australian Medical Association, PO Box E115, Kingston, ACT 2604. To the Editor: The workforce article by Brooks et al1 identifies key factors causing the medical workforce shortage and notes, correctly in our view, that: “The full impact of these factors is yet to be felt, but might occur very rapidly”. However, the authors fail to address why this has occurred and what should be done. The answer as to why is quite simple. In the 1990s, the Labor and Coalition federal governments introduced a series of measures to ration the supply of doctors and the provision of services in order to restrain the health budget. Measures such as restrictions on medical student places, reduced training places, restricted provider numbers, failure to properly index the Medicare Benefits Schedule or introduce the Relative Value Study, and the move away from fee-for-service with the rapid expansion of red tape, were all designed to restrict services that cost the government money. The current doctor shortage, falling participation rates (the trend to doctors retiring early or working part-time) and demoralisation of significant sections of general practice are a tribute to the success of these policies. As the recent Australian Medical Workforce Advisory Committee careers study shows, the much-discussed feminisation of the GP workforce is as much a consequence of a declining number of young male doctors considering general practice to be a rewarding career as it is the result of a need by both male and female doctors for an occupation that allows a flexible work and family lifestyle.2 Nevertheless, the outcome — the falling participation rate among current and future general practitioners — is at the heart of the problem. The solution will require a total shift in policy direction from sticks to carrots. It will need to cover Medicare, training, working conditions, and the removal of red tape and all forms of restrictions not required to ensure good clinical practice. Attempts to use regulations or commercial levers to enforce bulk-billing in an already depleted workforce will only serve to exacerbate the current situation.

William J Glasson · Robert A Bain

Francisco J Ruiz-Ruiz,* Fernando J Ruiz-Laiglesia,† Juan I Perez-Calvo,‡ Carmen B Torrubia-Perez§ * Home Doctor; †,‡ Associate Professor of Medicine; § Staff Doctor, Servicio de Medicina Interna “B”, Hospital Clínico Universitario “Lozano Blesa”, Avenida San Juan Bosco 15, Zaragoza 50009, Spain. fjruiz1ATterra.es To the Editor: Sarcoid arthritis is often underdiagnosed because it may mimic reactive or rheumatoid arthritis. We report a case which was initially misdiagnosed. A 38-year-old white woman was admitted to hospital because of pain and swelling of her hands and feet. Two years earlier, she had been admitted because of joint pain and erythematous, painful round lesions on her shins. A chest x-ray at that time was normal. She was diagnosed with reactive polyarthritis based on positive serological tests for Rickettsia conorii and Coxiella burnettii. Doxycycline and indomethacin were given and her condition improved. Three days before the current admission her fingers, wrists and ankles had become painful and swollen. There was tenderness and swelling of the metacarpophalangeal, wrist and ankle joints. She was afebrile. Chest x-rays showed an enlarged left hilum. Computed tomography (CT) of the chest (Box) showed lymphadenopathy in the mediastinum and both hila. Her erythrocyte sedimentation rate was 104 mm/h (normal, 3–12 mm/h). Laboratory test results were normal, except for an elevated serum level of angiotensin-converting-enzyme (ACE). A mediastinoscopy was performed, and specimens obtained for biopsy revealed sarcoidosis. Prednisone (30 mg/day) was prescribed and she was discharged 7 days later with no symptoms. “Sarcoid arthritis” is a sarcoid process whose main or unique manifestation is joint disease. Some of its characteristics are seasonal clustering (typically in spring), higher incidence among non-smoking patients, and the presence of the human leukocyte antigen DQ2 (DQB1*0201) and DR3 (DRB1*0301) haplotypes. It occurs slightly more frequently in women. The median age of affected patients is 40 years. The process affects mainly ankle and knee joints symmetrically. Acute sarcoid arthritis is a self-limiting joint disease with a benign prognosis, but some patients can develop chronic sarcoidosis of the lungs, specially those who suffer recurrent episodes of arthritis.1,2 In our patient, the first episode, with associated erythema nodosum, was misdiagnosed as a reactive arthritis as there were false positive serological test results for Rickettsia and Coxiella secondary to an immune polyclonal response. In the second episode, the patient had mediastinal and hilar lymphadenopathy and an elevated ACE level. Although sarcoid arthritis is very often associated with lymphadenopathy and erythema nodosum (Löfgren syndrome), we should keep in mind other forms of joint involvement in sarcoidosis.3 Doctors should consider sarcoid arthritis in the differential diagnosis of seronegative arthritis. Chest x-ray and ACE assay are useful in identifying sarcoidosis. Computed tomography scan showing mediastinal and hilar lymphadenopathy

Francisco J Ruiz-Ruiz · Fernando J Ruiz-Laiglesia · Juan I Perez-Calvo · Carmen B Torrubia-Perez

Zhiqiang Wang,* Wendy E Hoy† * Senior Research Fellow, † Professor, Centre for Chronic Disease, School of Medicine, University of Queensland, Herston, QLD. zwangATccs.uq.edu.au To the Editor: In a recent article, Thompson and colleagues provided useful information on the prevalence of cardiovascular risk factors in urban Aboriginal people.1 Using the Sheffield table of absolute risk,2 the authors estimated that “15% men and 6% women had an absolute risk > 15% of a cardiovascular event within 10 years”. The Sheffield risk table was developed for assessing the risk of coronary deaths rather than the risk of cardiovascular events.2 Moreover, the validity of applying the Sheffield table and other risk assessment tools based on the Framingham risk functions to Aboriginal people is yet to be assessed. The lower risk estimate in women reported by Thompson and colleagues may simply reflect the higher cholesterol concentration cut-offs for women in the Sheffield table. The true risk difference between sexes in Aboriginal people may not be as dramatic as Thompson and colleagues suggest. Firstly, data in Box 1 of their article show that there was little difference between men and women as regards past history of cardiovascular disease. Secondly, Aboriginal women experience a higher prevalence than men of some cardiovascular risk factors such as diabetes,1,3 abnormal HDL cholesterol level and overweight.3 Thirdly, our own research suggests that there may be a substantial difference between estimated and observed risks. Using data from a cross-sectional study of 681 Australian Aboriginal people in a remote community,3 we performed a similar analysis to that of Thompson et al. Based on the Framingham functions,4 we estimated that 10-year risks of coronary heart disease for women were much lower than those for men in all age groups (a finding similar to that of Thompson and colleagues). However, in a related study of the same Aboriginal community (as yet unpublished), when we analysed cohort data from 838 participants with 13 years of follow-up, the observed coronary disease rates for women were as high as those for men (Box). The discrepancy we found between estimated and observed risks is a warning that researchers and clinicians need to be cautious when applying existing risk assessment tools to Aboriginal people. Incidence rates per 1000 person-years of coronary heart disease (95% CI), by age and sex (based on a cohort study of 838 Aboriginal people in a remote community) Age (years) Women Men 20–34 4.1 (1.8–9.1) 3.2 (1.4–7.0) 35–44 15.6 (9.4–25.9) 8.6 (4.5–16.5) 45–54 19.3 (10.9–33.9) 26.5 (15.0–46.7) ≥ 55 50.2 (32.4–77.9) 31.9 (16.6–61.2)

Zhiqiang Wang · Wendy E Hoy

Peter L Thompson,* Pamela J Bradshaw,† Margherita Veroni,‡ Edward T Wilkes§ * Cardiologist, † Clinical Research Coordinator, ‡ Epidemiologist, Western Australian Heart Research Institute, Sir Charles Gairdner Hospital, Nedlands, WA 6009; § Senior Research Fellow, Centre for Developmental Health, Telethon Institute for Child Health Research, Subiaco, WA. peter.thompsonAThealth.wa.gov.au In reply: We appreciate the commentary by Wang and Hoy on the problems of the use of risk scores for assessing cardiovascular risk in Aboriginal people. In general, we agree that caution is essential in using tables that predict absolute risk of cardiovascular events. However, despite their limitations, absolute risk estimates are being encouraged by Australian, European, New Zealand and US authorities as a practical aid to targeting coronary disease preventive measures.1 An estimated risk of > 15% of a fatal cardiovascular event within 10 years, based on the Sheffield or Framingham scores, is now recommended as an indication for active treatment. Our prime purpose in providing an estimate of absolute risk in the Perth urban Aboriginal population was to demonstrate that a program of cardiovascular risk assessment with strong Aboriginal community support is capable of detecting high-risk people who will benefit from intensive risk-lowering strategies. Wang and Hoy’s caution about applying absolute risk estimates based on the Framingham population to unrelated populations is of particular importance in the case of Australian Indigenous people, in whom diabetes and the related metabolic syndrome may be the predominant risk factors. We have recently completed an analysis of the determinants of carotid atherosclerosis in the same population described in our earlier study.2 Our results confirm that, while the Framingham estimates (based on sex, age, LDL cholesterol and blood pressure) are indeed predictors of carotid atherosclerosis, their predictive value is significantly enhanced by the addition of markers of diabetes status and obesity. The 13-year follow-up study of the Aboriginal cohort referred to by Wang and Hoy will provide unique data to help identify reliable risk predictors specific to Aboriginal people, and we look forward to its publication.

Peter L Thompson · Pamela J Bradshaw · Margherita Veroni · Edward T Wilkes

John R M Caplehorn Senior Lecturer, Clinical Epidemiology, School of Public Health, University of Sydney, Sydney, NSW 2006. johncAThealth.usyd.edu.au To the Editor: The trial of buprenorphine-assisted heroin detoxification in primary care and a specialist clinic by Gibson et al1 was intended to compare the effectiveness and cost-effectiveness of buprenorphine-assisted withdrawal in a specialist clinic with treatment by general practitioners. However, of the average $191 for primary care staff costs, $69 was incurred at the clinic. As at least a third of interactions between patients and staff actually took place in the clinic, the primary care arm of the trial was really a combination of specialist clinic and primary care. Another design problem was the study’s lack of statistical power. A study would need 550 participants to have an 80% chance of identifying (at the 0.05 level of statistical significance) a difference of 50% in self-reported abstinence during the 8-day detoxification (ie, improving the percentage reporting abstinence from 22% to 33%). The trial by Gibson and colleagues had only 115 participants. As expected, the trial produced statistically non-significant results. Yet, the authors highlight the finding that 23% of primary care patients reported being abstinent during the 8-day detoxification, compared with 22% of the clinic patients, (95% CI risk difference, –14.1% to 16.5%; P = 0.9 [χ2]). Moreover, the clinic group performed better on an objective and more reliable measure of abstinence: 20% of clinic patients versus 14% of primary care patients gave morphine-free 8th day urine specimens, (95% CI risk difference, –7.7% to 19.8%; P = 0.4 [χ2]). As the confidence intervals for these risk differences include zero, the confidence interval for any estimate of incremental cost-effectiveness includes infinity. It is quite misleading for Gibson and colleagues to claim that “it costs $20 to achieve a 1% improvement in outcome in primary care”, as this ignores both the conflict and the variability in their clinical outcomes.1 Moreover, the statement ignores the variability in the estimated costs of treatment (eg, mean cost per clinic patient, $332; SD, $70). Surprisingly, Gibson and colleagues did not collect any information on continuing abstinence at the 13-week follow-up. Rather, they collected information on patients’ current treatment. While patients in whom detoxification therapy fails should be offered other treatment, post-withdrawal engagement in maintenance treatment is not a meaningful measure of the effectiveness of detoxification. If anything, it is a measure of failure. The trial needed sufficient statistical power to identify clinically meaningful differences in abstinence at the end of the 8-day detoxification and at 13 weeks. Staff working in the specialist clinic should not have been extensively involved in the delivery of primary care. Gibson and colleagues should have summarised their findings using appropriate estimates of clinical effect and cost-effectiveness with 95% confidence intervals.2

John R M Caplehorn

Amy E Gibson Senior Research Officer, The National Drug and Alcohol Research Centre, University of New South Wales, Sydney, NSW 2052. amy.gibsonATunsw.edu.au In reply: The primary focus of our study1 was retention in treatment, and not differences in abstinence. Caplehorn has previously argued compellingly that an orientation to abstinence can have an adverse impact on treatment outcomes in opioid dependence.2 We were using buprenorphine to redefine detoxification, not as a treatment producing lasting abstinence but as a way of promoting engagement in ongoing treatment. The power of our study was calculated on the basis of the proportion of subjects entering post-detoxification treatment, not on their self-reported abstinence levels. During the detoxification stage in the primary care setting, we used a shared-care dosing arrangement. This was primarily because of the need to give an initial research assessment to all participants before they were randomly allocated to treatment arms — something that would only occur in the context of a research study, and noted in the discussion. Further details of the health economic analysis are soon to be published.3 Ours was a study of the setting for buprenorphine treatment. Its critical finding was that patients were equally as likely to be engaged in maintenance treatment with practitioners in primary care as in specialist clinics.

Amy E Gibson

Paul M Bailey Emergency Physician, Joondalup Health Campus, Shenton Avenue, Joondalup, WA 6027. pbaileyATiinet.net.au To the Editor: In the article by Davey1 no evidence other than deviation from a protocol published months before the study is produced to document the implied inappropriateness of single troponin assays. Emergency physicians are experienced in assessing undifferentiated chest pain. Acute coronary syndromes are but one cause of presentation to emergency departments (EDs) of patients with chest pain, and indeed are but one cause of elevated serum troponin levels. Many reasons may justify the “appropriate” ordering of single troponin assays. Some patients present to EDs many hours after their episode of chest pain. A single troponin test may be a very useful and sensitive test for a patient whose chest pain occurred yesterday. How many patients in the study group had their single troponin test done more than 12 hours after their episode of pain? How many patients discharged themselves against medical advice as they were unwilling to wait 6–8 hours for a second blood test to triage their risk for an acute coronary syndrome? How many patients died or were transferred to another hospital? How many patients had their single troponin test ordered in the investigation of a primarily non-cardiac illness, such as sepsis or pulmonary embolism? I have no doubt that many troponin assays ordered in the study population were inappropriate. But, by failing to conduct an explicit medical record review of those patients whose tests were deemed inappropriate, the author has failed to answer his stated aim of determining if the troponin assay is used appropriately when chest pain is encountered. We are left with no knowledge of whether this problem is small or large. Finally, does it matter? Are two consecutive negative troponin assays required to triage patients with chest pain? Recently, the Journal published a clinical outcome study that examined the implementation of a chest pain assessment protocol at a metropolitan university teaching hospital in Bankstown, Sydney.2 Patients presenting to the ED with “possibly cardiac” non-traumatic chest pain who were deemed to be low risk did not receive a second, late troponin assay, and yet this approach appeared to be safe. Those of us who have an interest in the rational use of diagnostic testing for patients with acute coronary syndromes eagerly await the publication of further evidence on this important matter.

Paul M Bailey

Richard X Davey Chemical Pathologist, Melbourne Health Shared Pathology Service, Western Hospital, Footscray, VIC 3011. Richard. DaveyATwh.org.au In reply: In acute myocardial infarction (AMI) diagnosis, the sensitivity and specificity of troponin rise with time after symptom onset. The sensitivity of troponin-I testing was shown to increase from 35% at 0–4 hours to 97% at 12–24 hours after an infarct.1 Similarly, a meta-analysis found that “multiple testing of individual biomarkers over time substantially improves sensitivity, while retaining high specificity” for AMI diagnosis.2 This position is taken by the National Academy of Clinical Biochemistry3 and European and American cardiologists.4 Furthermore, the diagnostic clock starts from a patient’s emergency department presentation if there is any unreliability suspected in the patient’s assessment of pain onset. Pain onset may have been stuttering, indeterminate, simply forgotten, some combination of these, or even absent. Bailey describes several situations such as these, thought to justify, or to explain, singlicate troponin testing, and suggests that, as I did not audit records, I was not able to quantify the true extent of inappropriate ordering. I acknowledged this shortcoming, but believe it does not detract from the endpoint found. The Bankstown low-risk patients5 are only a confounder here. In our protocol they probably would not have been thought to have cardiac pain, and all the remaining Bankstown patients had serial biomarker testing. In my audit,6 93% of singlicate troponin test orders did not diagnose an AMI, and if AMI were still considered, then the tests contravened the protocols.3,4 This is why they were called “inappropriate” — no arbitrary whim. I assumed, moreover, that no clinician ordered a troponin test unless seeking a cause for chest pain. Our protocol begins with chest pain, recognises uncertainty, and leads through to treating an AMI or reconsidering the diagnosis. Obliquely invoking Ockham’s principle is also dangerous here. Illnesses such as sepsis may “provoke” an AMI, but this must then be investigated independently, and according to its own rules of engagement, which do not alter solely because of the primary (co-)morbidity. In short, we did know what is appropriate troponin use, and surveyed it. Like Bailey, we look forward to seeing further evidence.

Richard X Davey

Lloyd K Morgan Retired General Practitioner, PO Box 150, Lorne, VIC 3232. To the Editor: New imaging and pathology investigations continually improve diagnostic accuracy. But tests must be used because they supplement clinical deduction, not because they are available, and the constellation of clinical features should not be ignored. The case report by Chatterjee and colleagues is valuable for describing delayed diagnosis of meningitis, based on imaging which suggested subarachnoid haemorrhage and aspiration pneumonia.1 The 4-day history, examination (raised respiratory and heart rates, high fever) and results of initial investigations (neutrophilia, raised C-reactive protein level, lung consolidation) suggested a primary respiratory infection. The absence of a typical history of onset of subarachnoid haemorrhage is excused by the 5.5- hour hiatus before the patient was found semicomatose. Subarachnoid haemorrhage was diagnosed because of density in the subarachnoid space on computed tomography (CT). The authors noted a 1980 report of this appearance in a patient with bacterial meningitis.2 They also noted only one previous report of purulent meningitis mimicking subarachnoid haemorrhage on CT scan (in 1994),3 but there is reluctance to publish “negative” outcomes. Aspiration as the cause of upper-lobe consolidation was unlikely. Bacterial pneumonia and chemical pneumonitis affect the lower lobe.4 Clinical findings were not consistent with subarachnoid haemorrhage, and meningitis was the differential diagnosis, so only the overweighted CT results prevented lumbar puncture on Day 0, which would have resulted in earlier, broader antibiotic therapy and possibly resumption of warfarin. By Day 1, it was too late to prevent permanent blindness (it was possibly too late on Day 0, but pupils were reactive at that time). Even on Day 1, repeat cranial CT showed infarction but less evidence of bleeding; “a disparity between the amount of [alleged] subarachnoid blood and the patient’s clinical condition” was followed by magnetic resonance imaging then angiography and venography, instead of lumbar puncture as suggested by hindsight in the last sentence of the report. Shadows do not always equate with pathology. Compare an article on the clinical diagnosis of meningococcaemia.5 Holistic care of Chatterjee et al’s patient included anticoagulation therapy. “It probably could have recommenced earlier” than after “a large pulmonary embolus” on Day 13 — perhaps, given the presence of long-term indications (lupus inhibitor, anticardiolipin antibody and previous thrombosis) and cerebral vessel inflammation causing infarction, on Day 1. The main lesson, which we were all taught as students but needs career-long reinforcement, is in the penultimate sentence of the case report: “Investigations should not be interpreted in isolation from the clinical picture”.

Lloyd K Morgan

Tony D Merritt,* Carolyn Herlihy† * Epidemiologist/Biostatistitian, † Environmental Health Officer, Hunter Public Health Unit, Hunter Area Health Service, LMB 119, Wallsend, NSW 2287. tmerrittATdoh.health.nsw.gov.au To the Editor: Travelling animal shows, with animals such as young poultry, rabbits and reptiles, commonly visit childcare centres in Australia. Transmission of Salmonella infection to children from ducklings and chickens is well documented in the United States1,2 and United Kingdom,3 but not in Australia. We investigated a cluster of Salmonella agona cases in children, identified through routine laboratory surveillance. Initial investigations identified a potential association with visits to childcare centres by a single local hatchery. At each show, children saw an egg hatching, watched day-old ducklings swim and had the opportunity to hold a day-old chick or duckling, and to touch an adult chicken. Details of gastrointestinal illness were sought from childcare centres that had hosted visits from the hatchery. This identified laboratory-confirmed cases with onsets between 14 April and 6 May 2002 in seven people. All attended one of four childcare centres; six were children and one was a staff member. Onset of illness occurred 2–12 days after the hatchery visit. A total of 316 children attended shows by the hatchery between 9 April and 8 May. Environmental sampling at the hatchery recovered Salmonella agona from multiple sites over repeated visits. These included the egg incubator, faeces from day-old hatchlings returning from a show with children, faeces from young chicks and ducklings in the brooder cage, duck faeces from their yard, corn meal used in the preparation of feed for all poultry, and rat droppings in the feed preparation and storage areas. No Salmonella were detected in samples collected from the corn meal supplier. New procedures based on guidelines from South Australia4 and the Centers for Disease Control and Prevention5 were introduced for all shows from 8 May. These included supervised handwashing after handling animals, avoiding carpeted areas for the show, adequate cleaning of macroscopic faecal contamination and disposal of the water used by swimming ducklings into the sewerage system. No further cases were identified among the 251 children who attended shows over the subsequent two weeks until the hatchery cancelled all further visits. We conclude that infection was acquired through contact with chicks and ducklings from a single hatchery, and that the outbreak was halted by the introduction of measures emphasising handwashing after animal contact. Contact between young children and young animals, both of whom have naïve immune systems, represents a special ecological niche. Young poultry are particularly vulnerable to salmonella infection and subsequent high level excretion, and young children are similarly vulnerable. As animal visits to childcare centres are highly valued by children and carers, appropriate guidelines should be widely promoted to the childcare sector and the petting zoo industry to reduce the risks these visits pose. The petting zoo guidelines developed in South Australia4 are an excellent resource and NSW Health is currently developing a fact sheet on the topic.

Tony D Merritt · Carolyn Herlihy

Taposh Chatterjee,* John R Gowardman,† Tony D Goh‡ * Registrar, † Intensivist (corresponding author), ‡ Radiologist, The Canberra Hospital, PO Box 11, Woden, ACT 2605. John.gowardmanATact.gov.au In reply: We agree with Morgan that the symptoms, signs and laboratory investigations in our case report, although non-specific, supported a diagnosis of infection.1 The C-reactive protein level was not available for 24 hours. The unwitnessed drop in level of consciousness that occurred between 09:00 and 14:30 could have been secondary to meningitis or an acute cerebral event, and, while it is true that the lower lobes are predominantly involved in aspiration, they are not solely involved. Consolidation in other gravity-dependent segments, including the posterior segments of the upper lobes, can occur.2 The suggestion that “permanent blindness” could have been prevented is not supported. Fortuitously, an appropriate antibiotic to which the organism was fully sensitive was given from Day 0 (ceftriaxone). Adjunctive supportive care was quickly provided. In retrospect, anti-coagulation therapy could have recommenced earlier, but this remained a difficult decision in the context of the computed tomography findings. It remains unclear how this would have modulated the meningeal process, but it possibly contributed to the complication of pulmonary embolism. We agree that there is a reluctance to publish what may be perceived as “negative” outcomes, but, educationally, these may be the most rewarding. This case was an uncommon presentation of a common disease, and we considered it sufficiently important to notify other practitioners. Of most importance in this era when technology in medicine advances exponentially, any investigation must be considered only an adjunct to, and not a replacement for, thorough clinical evaluation.

Taposh Chatterjee · John R Gowardman · Tony D Goh

Amanda J Caswell Managing Editor, MIMS Australia, Locked Bag 3000, St Leonards, NSW 1590. amanda.caswellATmims.com.au To the Editor: Tan et al outline deficiencies in product information documents (PIs) as published in MIMS.1 It needs to be clarified that MIMS Australia is not responsible for the content of PIs — this is specified and approved by the Therapeutic Goods Administration in consultation with the sponsoring company. The conclusion by the authors that the “PIs for many prescription products listed . . . do not adequately detail paediatric doses” should not be specifically attributed to MIMS, as all published medicines information that relies on approved PIs will suffer from the same deficiencies.

Amanda J Caswell

Re: "1: Epidemiology and prevention of type 2 diabetes and the metabolic syndrome", by Shaw JE and Chisholm DJ in the 6 October 2003 issue of the Journal (Med J Aust 2003; 179: 379-383). In the section "Who should be screened?" the reference number should be 14 rather than 13 and the year of publication of reference 14 is 2002 not 1992. The second paragraph of this section, should read "Screening should also be offered to people aged 45-54 years with one or more of the following: obesity (body mass index ≥30 kg/m2); a first-degree relative with type 2 diabetes; or hypertension" The authors also wish to add an Acknowledgement: readers are referred to the NHMRC Evidence Based Guidelines for Type 2 Diabetes on case detection and diagnosis (from which the information in reference 14 is derived) and primary prevention, at www.diabetesaustralia.com.au or www.health.gov.au/nhmrc/publications/synopses/cp86syn.htm The html and pdf versions of this article published on the eMJA website were corrected on 30 October 2003.

Jonathan E Shaw · Donald J Chisholm

An atlas of surface microscopy of pigmented skin lesions: dermoscopy. Scott W Menzies, Kerry A Crotty, Christian Ingvar, William H McCarthy. Sydney: McGraw-Hill, 2003 (vii + 175pp). ISBN 0 07 471102 4. All medical practitioners who examine patients should be able to diagnose early melanoma. The diagnostic algorithm involves ascertaining how long the lesion has been present and whether it has been undergoing change. Examination includes not only observation of the specific morphology of the pigmented lesion in question, but also considering the lesion in the context of other skin lesions that the patient may have. This book on surface microscopy focuses specifically on the diagnosis of pigmented skin lesions based upon their morphology and, in particular, their morphology when examined with a hand held surface microscope. The authors have data to show that general practitioners achieve a 39% improvement in the sensitivity for the diagnosis of melanoma when using this Atlas. This cannot be specifically interpreted as meaning that fewer melanomas are missed when using this book, but it may translate to fewer benign naevi being excised unnecessarily. Nevertheless, any book that improves diagnostic accuracy has to be welcomed, and this book certainly does that. Examination of pigmented lesions using surface microscopy is a double-edged sword. To the uninitiated, hand held microscopes are confusing and may actually diminish diagnostic accuracy. As such, no general practitioner should pick up a hand held surface microscope without first having read this book. This excellent book is simply written and beautifully illustrated. It is the best of its type in the discipline and the first edition has been widely used by dermatologists and dermatology trainees. The steps to diagnosis are clear and constructive, and the quiz on the CD-ROM that accompanies the book is also very useful. At $94.95, including a CD-ROM, it is excellent value and I recommend it to all general practitioners contemplating the use of a hand held surface microscope. Rodney D SinclairDermatologistMelbourne, VIC Invasive melanoma - clinical view (a) and surface microscopy (b). Reproduced with permission. Order this book

Rodney D Sinclair

Therapeutic guidelines. Antibiotic. Version 12. Melbourne: Therapeutic Guidelines, 2003 (xv + 406 pp). ISSN 1329 5039. This edition of Australia's Therapeutic guidelines — Antibiotic marks 25 years of continuous publication for the Therapeutic guidelines series and this volume has certainly matured over time — now it really can call itself a book! Not only has it grown from 31 to 406 pages, it has also developed into a more considered and better quality text. Thankfully it is still not a Cochrane review — I shudder to think of its size if that had happened — but it contains clearly enunciated and authoritative guidelines on the management of a broad range of infections. Cardiovascular, gastroenterology and respiratory physician groups have collaborated in writing the relevant chapters, and endorsements have been obtained from infectious diseases, HIV medicine, dental, nursing, sexual health and general practitioner societies, the Royal Australasian College of Physicians, the National Prescribing Service and several state and territory health departments. There are major changes in the sections on bone and joint, genital, upper and lower respiratory tract infections, HIV/AIDS, hepatitis, and biological warfare. Community acquired pneumonia has been dealt with in a more methodical and sensible way than in the book’s widely quoted North American and European counterparts. The section outlining the principles of antimicrobial use should be compulsory reading for all students and doctors — with a refresher course every 3 years! The appendices contain an encyclopedia of valuable information on drug toxicity and interactions, doses for children, pregnant women and those with renal impairment, and on how to monitor drug levels, as well as much more. I was disappointed to find only a short, noncommittal section on prosthetic joint infections. A recommendation to refer such patients to an infectious diseases physician would be wise. Some of the print has become small, although it has not achieved anything close to the eye-straining properties of the Sanford guide to antimicrobial therapy. Very few of the chapters contain further reading suggestions. All these criticisms are minor — this is a great book! It is traditional to say that a book should be on everyone's shelf, but I would strongly recommend keeping this one in a more secure place, otherwise it may disappear! Joseph G McCormackDirector of Infectious Diseases Mater Misericordiae Hospital, Brisbane, QLD

Joseph G McCormack

Management of alcohol and drug problems. Gary K Hulse, Jason M White, Gavin Cape (editors). Melbourne: Oxford University Press, 2002 (xx + 404 pp). ISBN 019551331-2. Drug and alcohol dependent patients present a challenge to many doctors and medical students. Despite recent advances in medical education, there is still prejudice and fear to the extent that some medical practitioners will not treat addiction. This book goes a long way toward demystifying the treatment of drug dependence. This book is a comprehensive manual written by leaders in the field of addiction in both Australia and New Zealand. Despite its numerous contributors, the book flows seamlessly through the history of drug use, to opioids, cannabis, psychostimulants, alcohol and tobacco use. There are well written sections on Aboriginal Australians and Mäori, explaining the particular problems of each group. A strong clinical focus is present which describes assessment, diagnosis and treatments available. Graphic case studies illustrate chapters on women and substance abuse, adolescent drug use and coexisting mental disorders. I found the chapter on professional issues particularly interesting. It addresses the difficulties doctors have in treating this group of patients, in boundary setting and maintaining appropriate limits. In addition, there is advice on drug and alcohol abuse and impairment within the medical profession. Regarding detoxification from opioids, the book does not endorse the use of buprenorphine, stating that it has not yet been fully evaluated. My understanding is that this is no longer the case and that buprenorphine is now the preferred option for detoxification in Australia. Despite having a host of contributors, this book is easy to read, well set out, and has many illustrations and useful tables. At $55.00, this is excellent value for money. Having worked in addiction for 20 years, I wish this book had been available when I first started seeing drug and alcohol dependent patients. It would have made my life easier. Raymond SeidlerGeneral Practitioner Kings Cross, NSW Order this book

Raymond Seidler

Solar system Indian researchers have found a simple, very inexpensive way for health workers in developing countries to treat infectious material.1 They immersed simulated and real infectious medical-waste in water within a solar box-cooker. After 6 hours of solar exposure reaching temperatures of 68°-87°C, the viable population of a range of common pathogens decreased — by a 7 log reduction — to fewer than 10 colony-forming units or bacteria/mL. Commentators point out ways in which solar cookers can achieve even higher temperatures and faster inactivation times and another plus: solar cookers don't have the problems that come with electrical components or moving parts.2 1. Lancet 2003; 362: 1285-1286 2. Lancet 2003; 362: 1251-1252 Head first Moves are afoot in North America to obtain funding for a "term cephalic trial" — a randomised study that will compare primary elective caesarean section (ECS) with vaginal birth for uncomplicated pregnancies with a cephalic presentation at term, report Canberra authors. This follows an apparent narrowing of the difference in cost and outcome of either delivery mode in the uncomplicated setting, and increasing requests from women for ECS in the absence of any clear obstetric indication. In an opinion piece, the Canberra authors say that any such trial would add useful evidence for pregnant women and their carers to consider when choosing a preferred method of birth. Aust N Z J Obstet Gynaecol 2003; 43: 341-343 Adverse events: costly; not always preventable The financial burden of "medical injuries" in the USA can be high, say researchers.1 They examined costs associated with 18 specific injuries documented in 7.45 million discharge abstracts from acute-care hospitals across 28 states in 2000. Post-operative sepsis had the greatest impact (with hospital stays extended by nearly 11 days and charges increased by more than US $50 000 per patient) followed by postoperative wound dehiscence. Across the Pacific, NZ researchers found that for almost two-thirds of detected adverse events there was little or no evidence of preventability.2 Many of the non-preventable events occurred operatively. 1. JAMA 2003; 290: 1868-1874 2. www.nzma.org.nz/journal/116-1183/624/ Walk on US researchers report that, compared with placebo, a year’s treatment with the lipid-lowering agent atorvastatin increased pain-free walking time, if not maximal walking time. In their randomised, double-blind trial of 354 patients with intermittent claudication, they also noted a reduction in peripheral vascular events, such as worsening claudication and rest ischaemia, in the statin-treated groups. Circulation 2003; 108: 1481-1486 SIRIUS business With the advent of drug delivery from intravascular stents, endoluminal therapy for coronary artery disease is likely to produce similar or even better results than bypass surgery in most patients, according to a Swiss author in the Lancet.1 He was commenting on the European arm of the SIRIUS program (E-SIRIUS) which has found that sirolimus-eluting stents are markedly superior to bare-metal stents in preventing early restenosis in complex coronary lesions — relatively longer lesions in smaller arteries that may be managed with multiple stents.2 Further, the reduced need for repeat target-lesion revascularisation contributed to fewer major adverse cardiac events over 9 months of follow-up. The US arm of the program (SIRIUS) has also been published, with similar findings.3 1. Lancet 2003; 362: 1088-1089 2. Lancet 2003; 362: 1093-1099 3. N Engl J Med 2003; 349: 1315-1323 Ottawa rules When it comes to deciding whether to order a plain x-ray in suspected fracture of the knee, the Ottawa rules are the best of the available clinical prediction rules, say US reviewers. This finding is one of several reported from their systematic literature review of the usefulness of history, physical examination and imaging in assessing acute pain of the knee. The Ottawa knee rules are that, in acute knee injury, a plain film is needed to assess for fracture if the patient has at least one of four characteristics — age older than 55 years, tenderness at the head of the fibula or isolated to the patella, an inability to flex the knee to 90°, and an inability to weight-bear for at least four steps (some limping allowed). A well-documented follow-up plan is recommended for all patients, as these rules will miss the diagnosis in three of 1000 patients who have an initial negative x-ray and, rarely, in those patients who do not proceed to x-ray. Ann Intern Med 2003; 139: 575-588 — Dr Ann Gregory, MJA

Ann Gregory