Volume 181 Issue 4

One function of such services is to help clinicians ask the “right” questions The article by Gill and colleagues in this issue of the Journal (page 204)1 raises the issue of the ethics of clinical ethics services and, secondarily, their potential legal liability. Expressly or by implication, the article points to many difficulties and pitfalls of such services, and certainly raises more questions than it answers. But, in doing so, it reflects a necessary and valid function of ethics services: to help those who should make the decisions ask as many of the “right” (ie, ethically relevant) questions as possible. It is not the function of ethics services to make those decisions. The authors make some important points. Variability in decisions or failure to reach consensus does not mean ethics consultations are pointless — it is as important to highlight moral differences as to resolve them. When conducted well, clinical ethics services can be a valuable hospital resource and a powerful, critical voice contributing to ethical practice. “Doing ethics” is an exercise of power, and power must be exercised ethically. But simply a desire to do good is not sufficient to ensure that. Our goal of doing good can blind us to the harm that is also unavoidably inflicted, and sometimes that infliction is unethical. Doing ethics is a matter of both substance and process. Questions that help to provide insights about process ethics include: Who should decide? On what basis? Using which procedures? For what purposes? One of my “process” concerns about the Acute Clinical Ethics Service (ACES) described by Gill et al is that the ACES team does not necessarily include a person trained in applied or practical ethics and, moreover, that the authors do not recognise the need for doing so. I also have substantive or principle-based ethical concerns. For example, their “organisational principles” do not make it clear that, when values conflict, the basic ethical and legal presumption governing decision-making is that the patient’s values should take priority, and therefore that contravening them must be fully justified. Rather, these principles instruct the ACES to consider “the facts of the case and the values and preferences of all stakeholders”. Most ethical issues involve a conflict of values, which means values must be prioritised when not all can be honoured. Justifying the breaches of values that result is the essence of doing ethics. An important function of a clinical ethics service is to provide such justification or to comment on that provided by others. This allows the clinical ethics service to fulfil its advisory role in individual cases, to establish precedents that can guide future decisions and to serve a teaching function within the healthcare institution as a whole. However, my purpose here is to address the broader ethical issues underlying an ethics service rather than the ethical issues raised by the cases presented by Gill et al, with whose analysis and conclusions I do not necessarily agree. Committee decisions, as compared with individual ones, can spread the responsibility. A committee can make a decision that no one person — in particular, no committee member — acting alone would make. In all the cases described by Gill et al, the issue was that of shortening life (by either withholding treatment or aborting a fetus), and the physicians doing that were morally reassured by the ACES’s involvement. Might that have allowed the “caring team” to implement decisions that their moral intuitions were indicating were unethical? While these decisions may have been ethical, we must always be aware that we ignore such intuitions at our ethical peril. Could the ACES be legally liable for its advice?A clinical ethics service could be held legally liable if it failed to act as a reasonably competent committee. In a Quebec Superior Court case,2 the court held the ethics committee of a McGill teaching hospital liable for negligence in its review of the informed consent forms for a research protocol. The very remote risk of death was not disclosed. A subject in the research trial died from an anaphylactic shock reaction to the injection of a dye. If the membership of an ethics service or committee is not reasonably constituted, it could give rise to a claim based on systems negligence for failure to establish a reasonably safe system for ethics review. Not having a trained ethicist as part of a service or committee, or at least available for ad-hoc consultation, raises this issue, although that absence may be able to be justified. Moreover, an ethics committee and a “single ethics expert” are not mutually exclusive alternatives, as often both are needed. Ethics services or committees may have an obligation to report unethical and illegal actions. If they do not intervene at all, there may be no liability, but, having intervened, they may be liable for failure to take reasonable care when it is clear that that failure could result in harm to others. Patient consentThe basic presumption concerning patients’ medical records is that they are subject to strict duties of privacy and confidentiality. Therefore, obtaining informed consent from the patient (or the legal representative of an incompetent patient) to consult the ethics committee is necessary. Acting without such consent would need to be justified. As presently drafted, the organisational principles outlined by Gill and colleagues could cause some confusion as to whether these rules apply. Once again, it should be made clear that, in situations in which values conflict, the basic presumption is that the patient’s values should take priority. Characteristics of the members of the ethics consultation teamThe relationship between an ethics consultation team and the hospital administration raises the issue of conflict of interest in those people who are both members of the ethics service and part of the hospital organisation. If their obligations or goals as members of a clinical ethics service could conflict with their duties as people holding hospital appointments, then there is such a conflict, whether or not in the particular circumstance a conflict arises in practice. Strong ethical sensitivity is required to identify and deal with such conflicts. An assumption that people of good intention acting in good faith are competent ethics committee members — in particular, that they are, by virtue of those characteristics, sufficiently educated in ethics — is not valid. A recent US Institute of Medicine report3 has recommended that substantial resources be devoted to such education. Schools of ethicsGill and colleagues mention various schools of ethics that “may assist with the resolution of ethical conflicts”. These schools can be looked at as different “lenses” through which one can view a situation that raises ethical dilemmas. When all reflect back the same response, one can be reasonably certain that acting in that way is ethical. But when conflicting responses show up, difficulties arise. These difficulties usually reflect an irresolvable conflict of values. In such cases, it is very important to give the reasons (ie, justification) for giving priority to one value or set of values and thereby contravening another value or set of values. Indeed, providing such justification is the essence of “doing ethics”. ConclusionThe article by Gill and colleagues raises some very important issues, and the cases they describe may raise substantial controversy in relation to healthcare ethics services. Certainly, if North American experience holds true in Australia, many doctors may feel, at least initially, that their professional autonomy is threatened by an ethics committee or even an ethicist. Many nurses, however, will see ethics committees and ethicists as empowering them to challenge doctors’ decisions that they believe are unethical. Junior members of the medical profession, especially students and residents, and a few of its leaders, will be the first to accept the benefits of properly constructed ethics consultation services and to promote their integration into the healthcare setting. As ethics services become more familiar, more people will recognise both their benefits and (as we should always keep in mind) their dangers. Like democracy, ethics committees and ethics consultations are not a perfect system, but they are better than the alternative of having no ethics consultation process at all.

Margaret A Somerville AM, FRSC, LLD

Should we do it, is it worthwhile, and who should decide? In the Western world, the number of people living beyond 80 years is increasing. In the United States, it is expected that 43% of the population will reach the age of 80.1 In Australia, men and women who reach 80 years may expect a further 7 and 10 years of life, respectively, the majority being disability free.2 Cardiac surgery in Australia has entered its fifth decade, and is now commonly performed (18 000 cases/year). The total cost (including salaries, equipment, building depreciation, etc) of having coronary artery bypass grafting (CABG) (which constitutes 75% of all cardiac surgery) at Western Australian teaching hospitals is about $12 000 per case (WA Department of Health, 1994, unpublished data). Over the past decade, the proportion of cardiac surgery patients aged 80 years or more has risen from negligible to 7% in selected centres.2-4 Surgical outcomes are encouraging: a 2002–03 report from six Victorian public hospitals revealed mortality rates of 2%–4% for elective CABG and 10%–12% for aortic valve replacement.4 However, follow-up assessment by direct patient contact has not been universal — commonly, outcome analyses rely solely on physicians’ perceptions.2 In a series of 64 octogenarians having cardiac surgery over a 5-year period at three Australian hospitals, our research group prospectively assessed outcomes and directly spoke to patients at several time intervals.2 The need for surgery was compelling — all had class III/IV symptoms of angina and/or dyspnoea. The total in-hospital mortality was 6.3% (nil in those having elective surgery and 10.5% in those requiring urgent surgery). The incidence of significant complications was low (perioperative myocardial infarction, 1.6%; stroke, 1.6%). At a mean follow-up time of 2.8 years, 44 patients were still alive, 42 (95%) were free of cardiovascular symptoms, and 42 remained independent, with a significantly improved quality of life. Kaplan–Meier actuarial survival for hospital survivors at 4 years was 74%. Interestingly, 8 patients (18%) had remarried and 8 had commenced on sildenafil. Not surprisingly, 43 (98%) of the patients said they would recommend cardiac surgery. Despite these favourable outcomes, one in five of the study participants had been originally advised by their general practitioner and/or physician not to proceed with surgery because of their age. Discrimination based on age alone is not uncommon.1,5 Performing surgery in these octogenarians was on a needs basis — other patients on waiting lists were not disadvantaged. If people over a certain age are to be barred access to healthcare, it is for society to debate and for governments to legislate. In Australia, Katrina Bramstedt (a bioethicist at the Department of Community Medicine and General Practice, Monash University) has cogently argued that age discrimination is common. Yet there is no ethical justification for denying cardiac surgery to octogenarians,5,6 particularly as empirical evidence validates the potential benefit of this treatment.5 It has been stated that “survival is not the most important outcome in the elderly”.7 Not so. Of the 102 patients on whom we have now operated, all wished to continue to live independently. So what have we learnt? Firstly, that surgery can be safely performed in octogenarians. The best people to make the decision whether to operate are the surgeon and the cardiologist, working in conjunction with one another. Secondly, that the success of surgery is critically dependent on the quality of anaesthesia and postoperative intensive care. There must be ongoing clinical governance so that expected outcomes match actual results.8 Not only are more and more octogenarians choosing to have cardiac surgery, but the chances of a good outcome are improving. Advances in surgical techniques in recent years mean that the risks of cardiac surgery, for all patients but especially those over 80 years, have been substantially reduced. The availability of “off-pump” technology (ie, doing coronary artery anastomoses without the use of cardiopulmonary bypass [CPB]), including mechanical aortocoronary anastomotic devices, allows CABG to be done not only without CPB, but also without manipulating the aorta, thus reducing atheroembolic risk.9 Furthermore, the duration of CPB and global myocardial ischaemia can be minimised by combining off-pump techniques with CPB (eg, valve replacement with CABG). Also, selective use of ventricular fibrillation (rather than cardioplegic arrest) when repairing a mitral valve avoids global myocardial ischaemia. Surgeons have several options for the technical performance of these operations. While there may be no surgical consensus on the optimal technique for a given patient, in my view a “one shoe fits all” surgical approach may prove hazardous. It is important to prepare the patient optimally before surgery. This includes universal carotid screening and judicious use of prophylactic carotid endarterectomy, together with preoperative optimisation of renal function and maintenance of perioperative enforced diuresis.10 Although none of these innovations has been tested in randomised controlled trials, myocardial, cerebrovascular and renal complication rates are now low. A critical factor determining surgical outcomes is whether the patient is in need of urgent surgery (ie, surgery required as a hospital inpatient because the patient cannot be satisfactorily stabilised with medical treatment).2-4 Delays in referring symptomatic patients are invariably associated with rapid clinical deterioration and poor results. The role of percutaneous coronary intervention (PCI) versus surgery for coronary artery disease requires comment. Neither surgery nor PCI is benign.11 For comparable patients of any age in experienced hands, the risks of inducing death, myocardial infarction, stroke or neurocognitive deficits are the same with either approach.12,13 With surgery, the failure rate is lower and there is less need for repeat interventions. However, surgery requires a sternotomy and graft harvest incisions on the leg. A number of clinical factors are associated with increased risk of PCI failure (eg, left main coronary artery or multivessel disease, diabetes).14 Before PCI is undertaken, it is essential that the cardiologist and the surgeon carefully assess which procedure is optimal for a particular patient. If PCI fails, performing emergency surgery (ie, within 24 hours of hospital admission) is associated with markedly increased risks, particularly in octogenarians. Which octogenarians should be offered cardiac surgery? Many, if not the majority, should be readily identifiable as unsuitable because of advanced comorbidities. However, the 20% of patients in our series who were advised not to proceed with surgery had no clear features distinguishing them from the 80% advised to proceed. It is impossible to provide unambiguous criteria for refusing surgery. Nor am I suggesting that all octogenarians be offered this treatment. What I am advocating is that age alone must not be a barrier to accessing cardiac surgery. We can be heartened that careful evaluation allows us to pick the right patients and that these patients are achieving acceptable outcomes. Patients should be offered a choice. Those who have had cardiac surgery believe it is worthwhile and are very grateful.2

John MP Alvarez FRACS

More accurate food labelling would assist consumers and the food industry alike “We . . . can . . . not be held responsible for its content or any side-effects resulting from exposure to same. Your statutory rights are not affected. May contain traces of nuts” [website disclaimer].1 Conceived as a warning for allergic consumers, born and nurtured as a statement to dissuade potential litigation, the phrase “May contain traces of . . .” now threatens to become immortal as it enters the lexicon as a proxy for a blanket disclaimer. This situation developed as a response to the problem of hidden food allergens. Immediate hypersensitivity to certain foods, with the potential for anaphylaxis and death, affects about 6% of children and 2% of adults.2 Characterised by sudden allergic symptoms on ingestion and confirmed by positive skin and/or radioallergosorbent tests, inadvertent ingestion of a food allergen may require self-injection with adrenaline using an EpiPen (self-injectable adrenaline device) and/or medical resuscitation. Food allergy causes about 25% of anaphylactic deaths in the United Kingdom.3 There is also the distressing scenario of administering and/or witnessing emergency treatment that affects everyone, including parents, friends, carers and schools. “Hidden” allergens are hidden in the sense of being unrecognisable, such as egg in a pudding. In December 2002, Food Standards Australia New Zealand introduced changes to the Food Standards Code, making it mandatory that common food allergens and products derived from those allergens be labelled on packaged foods.4 Foods that are not labelled must have ingredient information available at the consumer’s request. Food allergens that must be declared include egg, milk, peanut, tree nuts, sesame, crustaceans, fish, soy, and cereals containing gluten. There are rare sensitivities for which mandatory labelling does not apply, including anaphylaxis to certain spices5 or fruits.6 In this issue of the Journal, the article by Smith et al7 (page 219) describes the first reported Australian cases of anaphylaxis to lupin, and the authors submit that foods containing lupins, used increasingly in manufactured food products, should be subject to mandatory labelling. Follow-up strategies after anaphylaxis include assessment in a specialist clinic, immunological and food analysis, provision of an EpiPen (now listed under the Pharmaceutical Benefits Scheme), practice with an EpiPen trainer, a written anaphylaxis action plan, a personal allergen identification medallion, access to useful websites (Box), and involvement of carers and schools. Education of children as well as their carers is crucial so that teenagers can walk away from childhood with skills to help keep them safe. There are simple principles to emphasise: Always carry an EpiPen Always read food labels Ask questions about food preparation (be aware of the risk of cross-contamination) No label/no eat No EpiPen/no eat Tell friends about a serious food allergy Tell friends if feeling unwell, especially after eating. How are we to interpret the disclaimer “May contain traces of . . .”? “May contain” means the allergen is stored or processed close to the food product, and/or added to other food lines, but not purposely included in the product. We don’t know the chances of accidental contamination, which may be measurable if the same production line is used, but remote if the allergen is restricted to a separate building. The word “traces” implies extremely small amounts, but defining the allergenic potential of foods, and thus obtaining a threshold dose that triggers reactions in the majority of sensitised subjects, has proved difficult.8 While people with allergies welcomed the 2002 changes to the Food Standards Code, their diet is now more restricted because of the proliferation of these “may contain” precautionary statements. Manufacturers argue that the risks associated with cross-contamination of food ingredients “from paddock to plate”, despite good manufacturing practice, have led to the many variations of “may contain” warnings. This has reduced the already limited food choices of consumers with allergies and has led to a rise in unnecessary avoidance of many foods that may in fact be safe. Since January 2003, Australia has had more than 50 food recalls for undeclared allergens.9 While many of the recalls have involved imported products, an alarming number have related to Australian-made foods recalled as a result of consumer complaints or government testing. How can we improve the current situation? Recently published Australian guidelines recommend that allergen minimisation, rather than banning certain foods, is the appropriate strategy in schools.10 If a school “thinks” it has banned an allergen, a level of complacency may develop among teachers and childcare workers. But if one focuses on allergen minimisation, then it follows that foods that have peanut, for example, in the ingredient list should be left for consumption at home and not sold in the school canteen, but foods that are labelled “May contain traces of . . .” can be allowed at school for the non-allergic school population. We must be alert to newly recognised hidden food allergens, such as the lupins identified by Smith et al.7 Consensus protocols are being developed to determine threshold doses of food allergens,11 and, in time, these may serve as a guide to more accurate labelling. Food manufacturers, food scientists, health professionals and consumer organisations must work towards reducing the number of precautionary statements. The Australian Food and Grocery Council now facilitates an Allergen Working Group, which draws together relevant stakeholders to focus on the needs of consumers with allergies. As Australia imports and exports both food ingredients and packaged foods, steps toward uniform regulations will assist consumers and the food industry alike. In time, with a cooperative approach, we may even find a smarter way of saying “May contain traces of . . .”. Useful websites for information about food allergy Anaphylaxis Australia Inc (www.allergyfacts.org.au) Australasian Society of Clinical Immunology and Allergy (www.allergy.org.au) Food Allergy and Anaphylaxis Network (www.foodallergy.org) Food Allergy and Anaphylaxis Alliance (www.foodallergyalliance.org)

Maria Said RN · John M Weiner MBBS,FRACP, FRCPA

Objective: To assess the effect of home-based health assessments for older Australians on health-related quality of life, hospital and nursing home admissions, and death.Design: Randomised controlled trial of the effect of health assessments over 3 years.Participants and setting: 1569 community-living veterans and war widows receiving full benefits from the Department of Veterans’ Affairs and aged 70 years or over were randomly selected in 1997 from 10 regions of New South Wales and Queensland and randomly allocated to receive either usual care (n = 627) or health assessments (n = 942).Intervention: Annual or 6-monthly home-based health assessments by health professionals, with telephone follow-up, and written report to a nominated general practitioner.Main outcome measures: Differences in health-related quality of life, admission to hospital and nursing home, and death over 3 years of follow-up.Results: 3-year follow-up interviews were conducted for 1031 participants. Intervention-group participants who remained in the study reported higher quality of life than control-group participants (difference in Physical Component Summary score, 0.90; 95% CI, 0.05–1.76; difference in Mental Component Summary score, 1.36; 95% CI, 0.40–2.32). There was no significant difference in the probability of hospital admission or death between intervention and control groups over the study period. Significantly more participants in the intervention group were admitted to nursing homes compared with the control group (30 v 7; P < 0.01).Conclusions: Health assessments for older people may have small positive effects on quality of life for those who remain resident in the community, but do not prevent deaths. Assessments may increase the probability of nursing-home placement.

Julie E Byles PhD · Meredith Tavener BAppSci(Hons), MMedSci · Nick H Higginbotham PhD · Lyn Francis BN, MHM · John E Marley MD · Rachel L O’Connell BMath, MMedStat · Balakrishnan R Nair FRCP, FRACP · Brendan G Goodger PhD · Claire L Jackson MB BS, MPH · Mary E McKernon DipAppSci(Commun Nurs), GradDip(Nurs Admin) · Richard F Heller MD, FRACP · Jonathan Newbury MD

Objective: To examine whether hospital patients with cancer who were identified as Indigenous were as likely to receive surgery for the cancer as non-Indigenous patients.Design, setting and patients: Epidemiological survey of all Western Australian (WA) patients who had a cancer registration in the state-based WA Record Linkage Project that mentioned cancer of the breast (1982–2000) or cancer of the lung or prostate (1982–2001).Main outcome measures: The likelihoods of receiving breast-conserving surgery or mastectomy for breast cancer, lung surgery for lung cancer, or radical or non-radical prostatectomy for prostate cancer were compared between the Indigenous and non-Indigenous populations using adjusted logistic regression analyses.Results: Indigenous people were less likely to receive surgery for their lung cancer (odds ratio [OR], 0.64; 95% CI, 0.41–0.98). Indigenous men were as likely as non-Indigenous men to receive non-radical prostatectomy (OR, 0.69; 95% CI, 0.40–1.17); only one Indigenous man out of 64 received radical prostatectomy. Indigenous women were as likely as non-Indigenous women to undergo breast-conserving surgery (OR, 0.86; 95% CI, 0.60–1.21).Conclusions: These results indicate a different pattern of surgical care for Indigenous patients in relation to lung and prostate, but not breast, cancer. Reasons for these disparities, such as treatment choice and barriers to care, require further investigation.

Sonja E Hall BA, MPH, RN · Caroline E Bulsara BA(Hons), GradDipEdStudies · Max K Bulsara BSc(Hons), MSc · Delia Hendrie BSc, MA · C D'Arcy J Holman MPH, PhD, FAFPHM · Timothy G Leahy FRACGP, MFM · Margaret R Culbong

Objective: To examine the trends in processes of diabetes care and in participant outcomes after an intervention in two remote regions of Australia.Design: Follow-up study over 3 years.Setting: Seven health centres in the Tiwi Islands and the Katherine West region of the Northern Territory.Participants: 137 Aboriginal people with type 2 diabetes.Intervention: Implementation of a multifaceted trial, including transfer of purchasing and planning responsibility to local health boards, the development and dissemination of clinical guidelines supported by electronic registers, recall and reminder systems and associated staff training, and audit and feedback.Main outcome measures: Trends in the proportion of Aboriginal people receiving services in accordance with clinical guidelines and in the proportion for whom specified levels of blood pressure and glycosylated haemoglobin (HbA1c) were achieved; health staff perceptions of barriers to effective service delivery.Results: An initial improvement in overall service levels from 40% to 49% was not fully sustained over the 3-year period. The overall proportion of services delivered varied from 22% to 64% between communities and over time. The proportion of participants whose most recent HbA1c level was less than 7% improved from 19% to 32%, but there was little change in blood pressure control. Perceived barriers to service delivery included discontinuities in staffing, lack of work-practice support and patients’ acceptance of services.Conclusions: Multifaceted interventions can improve quality of care in this environment, but achieving sustainable, high-quality care in a range of services and local conditions presents particular challenges. Developing and testing strategies for consistent and sustained improvement should be a priority for service providers and researchers.

Ross S Bailie MPhil(MCH), MD · Damin Si MMed · Samantha J Togni MA · Gary W Robinson PhD · Peter H N d’Abbs PhD

Australian criminal law is a matter for states and territories. In relation to abortion, many laws are unclear and outdated, and are inconsistent between states and territories. Doctors practise under time constraints and on a case-by-case basis. Most current laws have grey areas that leave doctors vulnerable to accusations, negative publicity and career damage, especially in the case of late abortions. All jurisdictions should follow the Australian Capital Territory’s lead in allowing women to access abortion without fear of criminal prosecution. Federal, state and territory governments should introduce a single clear national law on abortion, both in early and late pregnancy.

Lachlan J de Crespigny MD, FRANZCOG, COGU · Julian Savulescu MB BS, BMedSci

In Australia there has been only limited experience with ethics consultation, and there are no reports of practical details. In 1999, the Institutional Clinical Ethics Committee at John Hunter Hospital, Newcastle, initiated an Acute Clinical Ethics Service (ACES) to formalise a perceived need within the hospital for ethics consultation. This need had previously been met by ad-hoc councils of “wise men”. The ACES approach uses a team of people with different perspectives to provide an ethics consultation in a timely manner. Our initial experience of ACES has shown that a formal process of ethics consultation may be preferable to informal approaches in many circumstances; even when genuine consensus is not possible, an ethics consultation nevertheless provides an opportunity to share different points of view and helps to avoid practices that may be unacceptable. The specific implications of acute ethics consultations are not yet fully elucidated.

Andrew W Gill FRACP · Peter Saul MRCP, FRCA, FFICANZCA · John McPhee BCom(Hons) (LegStud) · Ian Kerridge MPhil(Cantab), FRACP, FRCPA

There have been major advances in clinical understanding and treatment of bipolar disorder over the past decade. Randomised controlled trials of pharmacological treatments and psychological interventions have shown that there are effective short-term and long-term treatments for the disorder. Despite advances in treatment, diagnosis is often delayed or mistaken, and many people who could benefit are not using the treatments available. Functional and symptomatic recovery from episodes of bipolar disorder is frequently less complete than previously considered, and disability is often profound. Although manic episodes are the distinguishing feature of bipolar disorder, it appears that depression is the predominant mood disturbance and that much of the functional impairment associated with bipolar disorder results from this. Comorbidity with anxiety disorders or substance misuse is common. Advances in genetics, brain imaging and basic pharmacology are starting to provide understanding of the complex causative processes.

Philip B Mitchell MD, FRANZCP, FRCPsych · Gin S Malhi MB ChB, FRANZCP, FRCPsych · Jillian R Ball BA, MA (ClinPsych), PhD

Despite it being confusing, inherently inequitable, and subject to excessive federal government control, Australia provides good healthcare My career has spanned three decades, two of these as a specialist oncologist, and I have been directly involved in delivering healthcare at a variety of levels on three continents. Over the years, I have been the sometimes innocent, but often active, participant in innumerable healthcare changes. Many resulted in outcome improvements. However, on balance, I believe there have been far too many changes in the organisation of the systems of care, not all of which have been for the better. Examples of this include internal markets being developed and then partially removed in the British National Health Service (NHS) because of inequalities in funding and access; and here, in Victoria, the governance structure affecting the Alfred Hospital where I worked changing four times from 1992–2003, returning eventually almost to the second-generation format. One of my blessings has been direct experience of working and observing in four diverse social and medical cultures: Edinburgh (somewhat pretentious and aloof), Houston, Texas (brash and pushy), Melbourne (relatively conservative) and Glasgow (friendly, but impoverished). My roles in healthcare have included scrubbing surgeons’ boots, in an era when the average length of stay after a myocardial infarction was four weeks and surgeons did not clean their own clogs. Highlights have been working with dedicated clinicians (doctors, nurses and other healthcare professionals), patients and others to deliver, improve, manage and otherwise organise patient-centred care. My personal philosophy of healthcare was moulded and refined by observing, as a child, a “Dr Finlay-type” family general practitioner in a fledgling NHS and by “salt of the earth” working-class parents. They raised me not in poverty, but in a Scots “but ’n ben” (a two-room house common to many families in postwar Britain) where there could be no savings or excess — and certainly no money for “choice” of education or healthcare. But then, in 1950s and 1960s Britain, there was no need for choice, as both were good and often excellent. That personal ethos has also been honed and influenced by mentors to whom I owe a great deal. They include teachers at Edinburgh Medical School, and in hospitals in Houston, Texas and, in the last decade, in Australia. Encountering Australia’s healthcare systemWith that background, for which I give thanks and make no apologies, I embarked in 1992 on the most exciting part of my career — emigration to Melbourne, Victoria. The difference at that time between the NHS — showing its age and beginning to reel from the dogmatic attacks of Mrs Thatcher — and Australia’s complex healthcare system was profound. For a start, Australia is not an offshoot of the “old country”. It is foreign. The light is different, and even the hospital buildings seemed brighter and lighter than the soot-begrimed heritage collection that still makes up much of the NHS estate. Of course, a close inspection of Australia’s younger hospitals reveals the inevitable flaws, cracks and problems. However, to be asked to direct a new radiation oncology centre, the William Buckland Radiotherapy Centre at The Alfred in Melbourne, kitted out with the best equipment of the times, and with space and an ambience to please both patients and staff, was an opportunity that had to be grasped and enjoyed. The challenge permitted me to show that a public hospital such as The Alfred in Melbourne could house a facility the equal in appearance and service quality to any private hospital. Somewhat curiously, there were some in the profession who disapproved. An initial impression of those early days was that some clinicians and many patients felt the public system was for the indigent; that facilities should reflect that; and that the process of care — public clinics, denial of any right to see a particular clinician — should also emphasise the difference. My background would not allow me to concede that. The team I was fortunate to gather and mentor at The Alfred proved over and over (if proof were needed) that quality care could be delivered in the public system and be the equal of that in the private system. It seemed to me, in 1992, that some clinicians believed they were still “honoraries”, donating their time and skills to those who could not afford to see them in private. Yet any observer would not take long to realise that that “private” system was underpinned and subsidised significantly by the federal health service’s Medicare system. The mysteries of MedicareMedicare confused me from Day 1. When, in early 1992, I innocently asked a committee of Victoria’s healthcare service managers and senior clinicians (who were intent on yet another review of radiotherapy services) to explain Medicare, I was regaled with laughter. Eleven years on, as I departed, it was patently clear that neither the press, nor television journalists, nor politicians of any hue, understand Medicare. Clinicians who bill the Medicare Benefits Schedule (MBS), however, do know it in infinite detail, because they need to. That media and politicians debate as though Medicare only applies to general practice is nonsensical. Argument centred on bulk billing belittles the complex and essential nature of the Australian “NHS”. Because Medicare is misunderstood by patients, media, politicians, government and public servants, healthcare managers at all levels have been able to play the game of cost shifting. It appears to be enjoyed by both federal and state officials and public servants and their ministers and shadow ministers. Add hospital managers to that equation and the situation is ripe for confusion and gamesmanship. Is it reasonable to manage a multibillion-dollar healthcare system on the basis of confusion and shifting costs, often in breach of the Act governing it? Healthcare professionals in Australia have to adapt to this confusing conspiracy. Usually this is done for the benefit of patients. Otherwise, the built-in inequity of the Australian systems would be more obvious to all, and hence presumably less acceptable. Such inequity is confusing to a newly arrived migrant, particularly one brought up to believe that healthcare should and can be delivered free at the point of care on the basis of need. In addition, is Australia not renowned for being classless and for mateship? The financial contribution of patients in Australia to their healthcare is significant and does not clearly and fairly take into account their ability to pay. It is also the secret part of the cost/payment equation. It is rarely quantified in easily available public information, although the Australian Institute of Health and Welfare and the Health Insurance Commission do publish reports on out-of-pocket costs for healthcare. Legislation over recent years to cajole citizens into private health insurance has increased that contribution. It can also be argued that the federal subsidy that supports private health insurance contributions compensates for this increased personal copayment. It appears that, politically, on both sides of the House, Medicare cannot be dismantled. Compulsion by carrots (the 30% subsidy on insurance premiums) and sticks (increased Medicare levy for those who refuse to be insured) gives money to the private insurers. It is to be hoped that the previously reported ludicrous use of subsidised private health insurance to fund lifestyle improvements (with compact discs and suchlike for the overly stressed) have ceased. The health insurance industry’s policies are, however, themselves overly complex and confusing and far from ideal, constrained as the insurers are by legislation as to what is insurable. Two systems, two tiersThe premium subsidy will rise relentlessly because premiums will rise relentlessly. That subsidy is not available to improve the public hospitals. With two health systems managed by the state and federal governments the process of healthcare management and improvement is not joined up. The result is two systems offering two tiers of care. To access the “top”, or private, tier a patient must generally pay — insurance, “gap” contribution, and over-gap charges. By exercising that much-vaunted “choice”, the patient who can elect and who can pay may not be choosing a better outcome. He or she may only be choosing a better place or a more convenient time. While these may be the drivers of such choice, those who cannot so choose should, in my view, not be penalised by needing to rely on underfunded services. There is, I believe, no inherent or ethical problem with exercising such a choice. The problems I had with the systems were the inbuilt unfairness of one arm of government manipulating the situation at so many levels. The federal government decides on the major subsidy to each state for, inter alia, healthcare. It also legislates over private health insurance — not only what can be covered, but also how the people may be persuaded to buy it. In addition, that same government manages a significant double subsidy for private healthcare — the insurance premium subsidy and MBS fees. One result is that those too poor to afford insurance or gap payments rely on a public system which has been progressively underfunded and too often denigrated. One proof of underfunding is the significant waiting times in the public system compared with those in the private system. The bright sideIn spite of these challenges and differences and inequities, the public sector, at least in cancer care in most of Victoria, was good. It was possible to deliver personal, patient-centred care of the highest quality and with the latest technology. It was pleasing to see patients return to a public hospital that had access to a new, but expensive, cytotoxic drug before that drug received a PBS subsidy. Of course, the reverse occurred when that subsidy was approved. It was sad when the public hospital budget ran dry and public patients had to scrimp and save for the same drug in the private sector. Fortunately, recent pilot changes to this unfair categorisation of and access to expensive drugs will address this inequity. The driver for this was pressure from oncologists, particularly in Victoria and its Cancer Council and the Victorian Cooperative Oncology Group, and it resulted in a pilot study that allowed some public hospitals like The Alfred to prescribe medication to outpatients and, on discharge, on the PBS. It was also a privilege to work closely with inspired and dedicated colleagues in the “private” sector who established patient-centred services with full support personnel and multidisciplinary-team care. Medicare could not fund that directly in the private sector. The public sector hospitals led the way and did fund, for example, breast care nurses. Enlightened practitioners in private practice followed suit at their own expense. Now, a year after returning to the real NHS, I recognise that the complex, blurry-edged, two-level system that is Australian healthcare delivers, one way or another, high-quality care to most patients. I still do not think it is equitable or totally fair, but, for the time being, the standard of care is better than much that is available in the UK. Perhaps it is because the UK system has fallen behind badly that, across Britain, there is an enormous critical reappraisal of the service at all levels. Modernisation agencies, targets, extra funding — even a cancer “czar” and “czarina” — have found their way into a creaking system. It seemed to me that, until very recently, Australia has been slow to ask questions beyond the large political issue of Medicare — bulk billing. Perhaps a glow of self-satisfaction tinged the healthcare community. There also seemed to be a reluctance to rock the boat of subsidised private medicine. Yet, in recent months there has been a healthy questioning in the medical community1,2 and medical press,3,4 matched by reasoned critiques in the press.5,6 Sadly, the federal government’s response is akin to Hollywood’s approach to the movies, and so we had “MedicarePlus” then “Strengthening Medicare” — or is it just Medicare II? At least the debate continues, if somewhat quietly. I hope that debate will not go silent once the new Medicare has been dragged through Parliament. The issues of equity, quality and cost of care have not yet been fully addressed. The Australian healthcare system is good. It offered me the opportunity to learn much, from both patients and colleagues. It allowed me to practise good medicine with a superb team in an excellent environment. This good system can still be improved for everyone, if the issues of intergovernmental argument over an unnecessarily duplex, but two-tiered, system could be resolved.

Alan Rodger FRCSEd, FRCR, FRANZCR, FAChPM

QuestionDoes early detection (by prostate-specific antigen [PSA] testing and digital rectal examination) and treatment of prostate cancer reduce the risk of death from prostate cancer among men aged 45–80 years invited to screening? Trial details Design: Randomised controlled trial. Setting: Population-based study in Quebec City, Canada. Participants: 46 193 men aged 45–80 years registered on the electoral roll of Quebec City and metropolitan area. Interventions: Invitation to attend annual PSA testing and digital rectal examination to screen for prostate cancer from November 1988 to December 1996. Main outcome measure: Deaths from prostate cancer. Main results: Death rates from prostate cancer over 8 years were 48.7 per 100 000 man-years for unscreened men and 15 per 100 000 man-years for screened men; the death rate was 69% lower in screened men. Conclusions: The authors concluded that “. . . this approach demonstrates, for the first time, that early diagnosis and treatment permits a dramatic decrease in deaths from prostate cancer.” CommentaryRationale for the trialScreening for prostate cancer could be done by means of PSA testing, but whether this would reduce mortality from the disease was not known. No randomised trials on the question had been undertaken when the study began in 1988. Trial methodsBenefit from cancer screening can only be validly assessed by randomised trials which compare mortality rates over the same time period among people randomly allocated to early detection and treatment or to usual care. This is necessary because studies of cancer screening can show an apparent benefit even if screening is completely ineffective, because: Survival may appear better among screen-detected cases simply because the diagnosis was made earlier (“lead-time bias”) — if the time of death is not altered, cases detected by screening may be getting more “disease time” rather than more life time; Screening preferentially detects slower, less aggressive cancers which have a longer preclinical (but screen-detectable) phase — fast-growing cancers are more likely to be missed by screening because they are more likely to develop and progress in the interval between screenings, giving the appearance of better outcomes among screened people (“length-time bias”); and People who attend for screening are generally healthier and more health conscious, so their risk of death from any cause is lower.1 The major strength of this study is that it was designed as a randomised trial and therefore could potentially validly answer the question. Important methodological features of good randomised trials are: high-quality randomisation with allocation concealment; blinded assessment of outcomes; high follow-up rates; and analysis by intention to treat.2 The major (and fatal) weakness of this study is that the primary analysis was not as a randomised trial (ie, by intention to screen). The authors compared the prostate cancer mortality rate among men who were screened (15 deaths/100 000 man-years) with that among men who were not screened (48.7 deaths/100 000 man-years). However, they included in the screened group men who had not been allocated to screening, but who sought screening anyway. They also included in the non-screened group men who were allocated to screening but did not attend. They thus destroyed their randomisation, reducing the study to an observational one. Their analysis yields a statistically significant, and apparently impressive, 69% relative reduction in prostate cancer mortality. However, this analysis is almost certainly biased (by one or more of the biases listed above). The authors also report what they originally set out to do — an intention-to-screen analysis which preserves the randomisation — as a secondary analysis. They report a 6% relative reduction in prostate cancer mortality (relative risk, 0.94) but provide no significance test or confidence interval. We have estimated these from the article’s data and found the result to be non-significant, with a 95% confidence interval of about 0.71–1.25. This means the true effect could be anywhere between about a 30% reduction to a 25% increase in prostate cancer mortality. The null result may be attributed to the poor participation in screening in the study. In the group invited to screening, only 23.1% actually attended for screening. In the control group, 6.5% of uninvited men attended for screening. While these “drop-out” and “drop-in” rates do not invalidate the study if it is analysed correctly, they inevitably cause a substantial attenuation of the intervention if it is effective. It is possible to adjust for this attenuation (due to poor participation) by methods previously described.3,4 However, in the case of this trial, adjustment will not be useful, as the adjusted estimate will also be non-significant, with a wide confidence interval. New informationNone — this trial contributes no new valid information. Implications for clinical practiceNone — we still have no evidence from good-quality, randomised trials about whether screening for prostate cancer reduces prostate cancer mortality. Two large trials are in progress, but are not expected to report results for some years yet.

Alexandra L Barratt MPH, FAFPHM, PhD · Alan S Coates AM, MD, FRACP, AStat

When decisions about a new intervention are being made, the “net clinical benefit” of the intervention needs to be assessed. This requires balancing all the reported benefits and side effects of the intervention. The adverse events experienced in a trial must be known in sufficient detail for their severity and relationship to treatment allocation to be judged. Reporting of such events is the subject of item 19 of the CONSORT statement (Box 1).1 What is an adverse event?The definition of adverse events (AEs) adopted by the International Conference on Harmonization (ICH) is shown in Box 2; it is designed to document all untoward events occurring in a clinical trial.2,3 AEs are thus both those events for which there is a known or plausible association with treatment and those for which there is none. Adverse drug reactions (ADRs) are those AEs that may reasonably be attributed to the medication (Box 2), distinguishing between medications that are used in accordance with their marketing approval (eg, in the approved dose, patient population and indication) or not.2,3 AEs are also classified as being serious or non-serious (Box 2 and Box 3). Standard schemes used to classify AEs, usually by body system, allow for easier comparison between different trial results and between different treatment options. Examples include the International classification of diseases,4 and the Medical dictionary for regulatory activities.5 Some classifications also grade severity of AEs, such as the Common terminology criteria for adverse events (CTCAE) system of the United States National Cancer Institute,6 which has five grades of severity, ranging from 1 (mild) to 5 (death). Regulatory requirements for reporting adverse eventsTo reliably report on AEs, procedures must be in place from the beginning of a trial for systematically recording and reporting them.2 All investigators participating in a clinical study, and their respective human research ethics committees (HRECs), must have been provided with an investigator’s brochure which includes all relevant information known about the safety, efficacy and pharmacodynamics of the investigational drug, and a description of the possible risks and adverse drug reactions associated with the drug and similar products.2 Good clinical practice guidelines require investigators to report immediately to the trial sponsor any serious AEs that occur during the conduct of a trial.2 In turn, many countries require the study sponsor to then report these to national regulatory authorities. An AE which is considered to be a serious unexpected adverse drug reaction7 must be notified by the sponsor to relevant regulatory authorities as an “expedited” SAE within 7 days of awareness for events that were fatal or life-threatening, and within 15 days for others.3 ICH guidelines for good clinical practice, as adopted internationally, also specify that all serious unexpected adverse drug reactions should be reported to the relevant HRECs.7 It is not possible to assess the significance of AEs from reports in which the treatment allocation remains blinded and the number of participants exposed to the trial medications is unknown. Hence, Data and Safety Monitoring Boards (with the ability to review events and their frequencies unblinded, if preferred) are an important (although insufficiently used8) mechanism for protecting the safety of trial participants9 and for ensuring that studies are stopped as soon as it becomes clear that the trial intervention is beneficial or harmful.10,11 Australian requirements for adverse event reportingIn Australia, the Therapeutic Goods Administration (TGA) only requires reports on serious unexpected adverse drug reactions that occur in Australia, and that it be informed of any significant safety concerns that arise from the sponsor’s monitoring of overseas safety reports and of any action undertaken by overseas regulatory agencies.3 In Australia, the section of the ICH good clinical practice guidelines on reporting to HRECs has been overridden by the National statement on ethical conduct in research involving humans.12 This mandates that investigators inform the TGA and HRECs of “all serious or unexpected AEs that occur during the trial and may affect the conduct of the trial or the safety of the participants or their willingness to continue participation in the trial”. One consequence of this directive is that HRECs in Australia are being inundated with large numbers of essentially uninformative AE reports.8 Presentation of adverse event reportsPatient selection can influence the rates of AEs. It is important that the trial population is described adequately so that clinicians can assess the risk of a particular treatment for an individual patient. It is also important that the mechanisms used to elicit reporting of AEs are documented. Volunteered reports of AEs can give incidences of AE markedly different from those ascertained through checklists or diaries.13,14 Counts of adverse eventsThe numbers of patients who had each type of AE should be clearly detailed in the study report. If some patients experience more than one type of AE, the numbers of each event type should also be documented.1 Both the number of patients experiencing at least one occurrence of the event of interest (for statistical analyses) and the total number of such events observed (for cost–benefit analysis) help interpretation (Box 4). Types of adverse eventsThe types of events chosen for reporting must be prespecified and may be selected on the basis of absolute numbers of events (ie, the most common events), biological relevance to the drug or study question, clinical relevance, or safety (ie, serious or severe events are reported). Adverse events by treatmentPresentation and comparisons of AEs are generally reported by allocated treatment (ie, the intention-to-treat [ITT] principle), but reporting by “treatment actually received” can also be useful in some settings. For example, where non-compliance rates with allocated treatment are substantial, ITT analyses will under-report treatment-related AEs. However, analyses by “treatment actually received” will provide only non-randomised comparisons and therefore contain a varying degree of selection bias.16 Therefore, ITT methods should be routinely reported, and data for treatment actually received should be added, with an explanation as to why, if there are high rates of non-compliance. Treatment withdrawal after adverse eventsAdverse events resulting in withdrawals from treatment should also be adequately described, as they reflect tolerability of treatment, and will be useful for both patients and clinicians to better assess the importance of particular reported AEs. Abstracts and keywordsFinally, when the study is published, the abstract and keywords should mention the term “adverse events”, even if none occurred in the study, to facilitate retrieval of AE data from databases such as MEDLINE.17 Current deficiencies in trial reportsA statement in the results section of a publication that “no adverse events were observed on the trial medication” without details in the methods section of the steps taken to ascertain AEs is difficult to interpret. What is less apparent is how difficult it really is to convey useful information on the types, severity and incidences of the AEs observed. Even large, multicentre studies published in first-rate journals can fail to report the number of patients who withdrew because of side effects of the trial medication. For example, a large study on the efficacy of irbesartan in preventing the development of nephropathy in patients with type 2 diabetes and microalbuminuria has the following description of the AEs observed: “Serious adverse events during treatment and up to two weeks after treatment were recorded in 22.8 percent of the patients in the placebo group and 15.4 percent of those in the combined irbesartan groups (P = 0.02). Nonfatal cardiovascular events were slighty more frequent in the placebo group (8.7 percent, vs. 4.5 percent in the 300 mg group; P = 0.11). The study medication was permanently discontinued in 18.9 percent of the patients in the placebo group, as compared with 14.9 percent of those in the combined irbesartan groups (P = 0.21).”18 In the report, the AEs that led to discontinuation were not described. Furthermore, it was unclear whether they were related to the condition being treated, to the trial medication, or to intercurrent illnesses. Guidelines have been developed to help researchers give useful information about AEs for reporting, both in general1 and for particular classes of trial, such as chemotherapy19 or postoperative analgesia.13 The need for such guidelines is evident from studies of adequacy of AE reporting. In one evaluation of reporting of safety data from clinical trials of HIV treatment, the severity of AEs was regarded as adequately defined in only a third of trials.20 In a subsequent study in other clinical areas, only 39% of trials adequately reported clinical adverse effects and only 29% adequately reported laboratory-determined toxicity.21 Other studies show similar rates of deficiencies in AE reporting in a variety of circumstances.22-25 These deficiencies are serious, as they can prevent clinicians from being able to provide patients with balanced information about the scale and scope of risks associated with different treatment strategies. Even when AEs have been well described, retrieving data about them can be problematic — of a sample of 37 trials indexed on MEDLINE or EMBASE known to present AE data, only 49% could be found by searching for text words such as “adverse event”, “side effect” or “h(a)emorrhage”, while adding indexing terms relevant to AEs only improved retrieval to 78%.17 ConclusionLarge randomised controlled trials and meta-analyses of randomised controlled trials are very effective in distinguishing AEs that are caused by the underlying condition from those that are related to the intervention. They can provide clinicians with unbiased information about the frequency and severity of adverse effects at a time when a drug or procedure is new. While other mechanisms for obtaining safety data are needed to detect AEs that are too rare to be detected by even the largest studies (Box 5), or that occur in groups of patients who would normally be excluded from trials (eg, because of illness severity, comorbid conditions or the need for potentially confounding therapies), these do not allow clinicians to quantify the risk of a treatment26 and can give markedly different impressions of the incidence of adverse drug reactions compared with those obtained from randomised clinical trials.27 Only proper reporting of AEs from randomised controlled trials allows adequate assessment of the potential net clinical benefits of interventions. 1 CONSORT checklist of items to report when reporting a randomised trial1 Section and topic Item no. Descriptor Results Adverse events 19 All important adverse events or side effects in each intervention group. 2 Definitions adopted by the International Conference on Harmonization, and adopted by Australia’s Therapeutic Goods Administration2 Adverse event An adverse event is any untoward medical occurrence in a patient or clinical investigation subject administered a pharmaceutical product and which does not necessarily have a causal relationship with this treatment. An adverse event can therefore be any unfavourable and unintended sign (including an abnormal laboratory finding), symptom, or disease temporally associated with the use of a medicinal (investigational) product, whether or not related to the medical (investigational) product. Adverse drug reaction Before marketing approval: all noxious and unintended responses to a medicinal product related to any dose should be considered adverse drug reactions. The phrase “responses to a medicinal product” means that a causal relationship between a medicinal product and an adverse event is at least a reasonable possibility. After marketing approval: a response to a drug which is noxious and unintended, and which occurs at doses normally used in man for prophylaxis, diagnosis, or therapy of diseases or for modification of physiological function. Unexpected drug reaction An adverse drug reaction, the nature or severity of which is not consistent with the applicable product information (eg, investigators’ brochure for an unapproved investigational medication). Serious adverse event or reaction Any untoward medical occurrence that at any dose: Results in death Is life-threatening Requires inpatient hospitalisation or prolongation of existing hospitalisation Results in persistent or significant disability or incapacity Causes a congenital anomaly or birth defect 3 Severity and causality of adverse events (AEs) * Or more severe than previously known. NSAE = non-serious adverse event; SAE = serious adverse event; SADR = serious adverse drug reaction. 4 Checklist for presenting adverse event (AE) reports Describe methods used to ascertain AEs (eg, reported by physician or patient) Show events which are unexpected in the context of the treatment given Categorise the seriousness of events where relevant Report AEs by the number of patients affected and by the number of events Report AEs by intention-to-treat methods (may additionally be shown by treatment actually received) Highlight AEs whose severity causes withdrawal or modification of treatment Highlight substantial differences in the risk of an AE for different subgroups of participants Use time-to-event (Kaplan–Meier survival) methods to avoid inflated estimates, where discontinuation rates have been high in long-term trials15 Mention key AE findings in the abstract and keywords of the report 5 Numbers of patients that need to be exposed to a medication to ensure that an adverse drug reaction has a 95% probability of being observed at least once Frequency of adverse drug reaction Minimum no. of patients required* Very common (≥ 10%) 29 Common (1%– < 10%) 299 Uncommon (0.1%– < 1%) 2 994 Rare (0.01%–< 0.1%) 29 956 * Number is based on the lower boundary of each category of frequency.

Anthony C Keech FRACP, MClinEpi · Susan M Wonders BDS · Val J Gebski BA, MStat · David I Cook FAA, FRACP

Clinical records Patient 1 A 42-year-old woman developed acute urticaria and angioedema, with throat tightness and cough, after a meal including a bread roll. A more severe anaphylactic reaction, including marked breathlessness requiring oxygen and adrenaline, followed ingestion of the same type of bread roll on another occasion. The only unusual ingredient in this type of bread roll is lupin bran. Skinprick tests with saline extracts of the raw lupin bran and the baked bread roll were strongly positive (Box 1). Tests for allergy to soy and peanut were negative. The patient’s history included seasonal rhinitis with positive skin tests to aeroallergens, but no previous food allergy. She was advised to avoid products containing lupin, as far as possible. She decided not to carry an EpiPen (a self-injectable adrenaline device). A subsequent mild generalised reaction followed ingestion of a specialty bread that was later found to contain lupin bran. Patient 2 A 42-year-old woman developed acute abdominal discomfort, urticaria, facial oedema, cough and shortness of breath 10–15 minutes after eating a bread roll that contained lupin bran (the same type as Patient 1). She was treated at a hospital emergency department with oxygen, salbutamol, promethazine and hydrocortisone. Skin testing was positive to a saline extract of lupin bran (Box 1). Her history included seasonal rhinitis with pollen allergy on skin testing. She was provided with an EpiPen. Patient 3 A 26-year-old woman with a Mediterranean family background had often eaten lupini (boiled/dried lupin in the form of a snack food). On one occasion, after eating commercially prepared lupini from a jar, she developed urticaria, angioedema and respiratory difficulty, requiring hospital treatment with adrenaline. She subsequently tried a small portion of home-prepared, boiled and salted lupini, and had a similar but less severe reaction. She reported experiencing urticaria and angioedema after eating a bread roll (she was unable to find out the ingredients of the roll) and after eating imported European ginger biscuits, which were subsequently noted to contain lupin flour as a labelled ingredient. Skin testing was strongly positive to a saline extract of lupin bran (Box 1). Specific IgE to lupin (12.9 kUA/L; reference range, < 0.35 kUA/L) was identified in her blood by the UniCAP test (Pharmacia Diagnostics, Uppsala, Sweden). She was provided with an EpiPen. Two of the three patients described here were atopic and thus had an increased propensity to develop food allergy, although one of them had no previous food allergies and the third had no previous allergies at all. None was allergic to peanut. None had exercised after eating the implicated foods, and none reacted to normal bread, other wheat sources, or pea. DiscussionIgE-mediated food allergy is an important cause of acute anaphylaxis1 and anaphylaxis-related death.2 The major allergenic foods are well known: peanuts and tree nuts (in people of all ages), milk and egg (mainly in children), and crustaceans and fish (mainly in adults). A variety of other foods are less commonly responsible for anaphylaxis. Peanut-allergic individuals are sometimes allergic to other foods from the legume family, such as soy. Lupin, another legume related to pea, peanut and soy, has been recognised in Europe as a cause of allergic reactions and anaphylaxis.3-5 Lupin flour in food has been reported to produce urticaria and anaphylaxis,3 and may also produce rhinitis and asthma in an occupational setting, through inhalation.6,7 Moneret-Vautrin et al reported that 44% of children allergic to peanut showed positive skinprick responses to lupin, and 7 of 8 who were challenged reacted to lupin flour.8 It seems that lupin allergy may arise by cross-reactivity in people who are already allergic to peanut, or de novo, by primary sensitisation, as in the cases reported here. Lupinus albus (of the genus Lupinus, which has about 500 members, including ornamentals) is the species most widely cultivated for food (Box 2). Dried lupini, prepared by boiling — a traditional snack in some Mediterranean countries (and, in Australia, among migrants from these areas) — have been reported to cause anaphylaxis.5 Lupin flour and bran are widely used in Europe in bread, pasta, biscuits and other baked products, confectionery, and soya substitutes. Inclusion of lupin in wheat flour was officially authorised in France in 1997. It has been identified as a target for allergy surveillance in that country.8 It was introduced in the United Kingdom in 1996 and has been recognised as a new or novel food. A form of “postmarketing surveillance”, analogous to that employed by pharmaceutical companies for new drugs, has been suggested.9 Until recently, lupin was not common in Australian foods, but lupin flour and bran are now entering into food manufacturing, where they contribute protein content, fibre, and some textural properties. Currently, lupin is not covered by mandatory labelling regulations such as are in place for peanut, soy and several other allergenic foods. It is of some concern that, despite relatively restricted use, lupin sensitisation has already become clinically apparent in Australia. According to the current requirements of Food Standards Australia New Zealand (Standard 1.2.4),10 lupin flour, as a separate ingredient or as a component of greater than 5% of a compound ingredient, must be included in the ingredient list on the product label. However, lupin is not part of the mandatory allergy warning system (Standard 1.2.3).10 We believe that it is currently justified to consider it a potentially “hidden” allergen, as bread rolls sold without labels or packaging may contain lupin bran, and indeed at least two and probably three of our patients reacted to an unlabelled food. We suggest that lupin should be considered in cases of unexplained food allergy and should be added to the list of ingredients requiring mandatory allergy warning labelling. 1 Skinprick test results* Average diameter of weal (mm)† Case 1 Case 2 Case 3 Lupin bran 9 12 9 Bread roll crust 10 ND ND Peanut 0 2 0 Pea ND 10 8 Soy 1 1 3 Wheat ND 3 3 Negative control 0 0 0 Histamine positive control 7 5 7 Aeroallergens Positive Positive Negative ND = not done. * Standard skinprick test methods were used. Standard extracts (Hollister-Stier, Wash, USA) were used for all foods except lupin. To test reactions to lupin-containing products, a crude saline extract was prepared by incubating the food in equal volumes of sterile isotonic saline for 10 minutes. This extract produced negative skin test results in 10 atopic (non-legume-allergic) and 10 non-atopic donors, ruling out non-specific irritant effects.† A weal > 3 mm diameter was taken as a positive reaction (note that not all positive reactions correlate with clinical symptoms). 2 Seeds of Lupinus albus, the lupin species most widely cultivated for food Lessons from practice Lupin, a legume, is either eaten whole as lupini or used in the form of flour or bran in food manufacturing. Lupin has the potential to cause anaphylaxis, which may occur by cross-reactivity in people with peanut allergy or may arise de novo in people with no previous food allergy. Currently, lupin may appear on the ingredient label of manufactured foods, but it may also be used as an unlabelled ingredient in some foods, such as bread rolls. Lupin allergy may be investigated by referral to an allergy specialist, and/or specific IgE blood testing (available by special request at some laboratories).

William B Smith FRACP, FRCPA, PhD · David Gillis FRACP, FRCPA · Frank E Kette FRACP, FRCPA, PhD

The death of William McLaren (“Dr Will”) on 23 January 2004 ended a long and dedicated life of service to the people of Cowra. He was a Cowra person in the truest sense, being born at Cowra District Hospital on 25 May 1914, attending school in Cowra, and spending most of his working life there. He was the youngest child of Hugh McLaren, a physician. He studied medicine at the University of Sydney, graduating in 1940. After a period of training at the Royal North Shore Hospital, Sydney, Will left to join the Australian Army. He spent most of his wartime service in New Guinea on the Kokoda Track and with Z Force, working behind enemy lines on intelligence operations. His intrepid character, dedication and innovative ability saved many lives. His distinguished war service and contribution to wartime and postwar medical services in New Guinea are well documented in the official history of World War II. In 1947, Will joined the family medical practice in Kendal Street, Cowra, and in 1975 he was joined by his son John, thereby continuing the McLaren medical tradition into a third generation. Will was a practitioner with exceptional skills in all areas of medicine and surgery and had a wonderful ability to communicate with his patients. He was immensely loved for his great charm and roguish wit, which remained intact to the end. Will was also involved with many community organisations in Cowra, especially Alcoholics Anonymous and the Mentally Handicapped Association. He helped to set up the Lachvale School (now the Holman Place School) for students with intellectual disabilities. Although not a Rotarian, he had the honour of being awarded a Paul Harris Fellowship by the Cowra Rotary Club for his services to the community. In his spare time, he loved being with his grandchildren and pursuing his hobby of raising ducks. The Anglican priest, Susanne Pain, who had been delivered by Dr Will, officiated at his funeral service — surely a rare event. He is survived by his son John and daughter Ann.

William Muggridge

Most consumers consider complementary and alternative medicine (CAM) products inherently safe. The growing simultaneous use of CAM products and pharmaceutical drugs by Australian consumers increases the risk of CAM–drug interactions. The Therapeutic Goods Administration (TGA) has a two-tier, risk-based regulatory system for therapeutic goods — CAM products are regulated as low risk products and are assessed for quality and safety; and sponsors of products must hold the evidence for any claim of efficacy made about them. Adverse reactions to CAM products can be classified as intrinsic (innate to the product), or extrinsic (where the risk is not related to the product itself, but results from the failure of good manufacturing practice). Adverse reactions to CAM practices can be classified as risks of commission (which includes removal of medical therapy) and risks of omission (which includes failure to refer when appropriate). While few systematic studies of adverse events with CAM exist, and under-reporting is likely, most CAM products and practices do not appear to present a high risk; their safety needs to be put into the perspective of wider safety issues. A priority for research is to rigorously define the risks associated with both CAM products and practices so that their potential impact on public health can be assessed.

Stephen P Myers PhD, BMed, ND · Phillip A Cheras PhD, BAppSc

Michael C Kennedy Research Associate, Department of Clinical Pharmacology and Toxicology, St Vincent’s Hospital, Darlinghurst, NSW 2010. drmkennATozemail.com.au To the Editor: Since the Sydney Olympics in 2000, many developments have occurred in drug use and the rules regulating drugs in sport. The most significant regulatory development is the acceptance by the Olympic Federation, and many other sports bodies, of the World Anti-Drug Agency’s World Anti-Doping Code.1 Caffeine and pseudoephedrine have been removed from the Prohibited List, and an in-competition monitoring program is under way to detect any changes in the patterns of use of caffeine, pseudoephedrine and other drugs not on the banned list. Had this code been used in 2000, the Romanian gymnast Andreea Raducan would have retained her gold medal, lost after she inadvertently used a cold preparation containing pseudoephedrine. Precise in-competition limits on blood and breath alcohol have been introduced in sports such as archery and modern pentathlon. β-Blocking agents and diuretics are completely banned in specific sports. A new category of “specified substances” now exists: . . . the prohibited list may identify specified substances which are particularly susceptible to unintentional anti-doping rule violations because of their general availability in medicinal products or which are less likely to be successfully abused as doping agents. These substances include cannabinoids, probenecid, glucocorticosteroids and ephedrine. Doctors treating athletes should advise them to inform their relevant sporting authority of drugs prescribed. If necessary, athletes can apply to the Australian Sports Drug Advisory Committee for a therapeutic use exemption for a banned substance. Notifiable substances can be documented on an Abbreviated Therapeutic Use Exemption form held by the national sporting body. There can be no doubt of the need for drug testing to ensure a level playing field. Drug use to enhance performance is unabated since the Sydney games, with scandals occurring around the world. The Bay Area Laboratory Corporation scandal, involving the anabolic steroid tetrahydrogestrinone, is the most prominent. This has ruined several sporting careers and led to criminal charges against company directors.2 Other anabolic steroids continue to be widely used, including nandrolone, which causes problems because of contamination of dietary supplements and some foods.3 One of the “holy grails” for drug cheats over the past 4 years has been to enhance oxygen transport and delivery. RSR13 (efaproxiral), an allosteric modifier of haemoglobin, is in clinical trial as a radiosensitising agent. It has been shown to increase Vo2max in dogs and hence has been of interest to endurance athletes. The manufacturer’s collaboration with the Olympic Analytical Laboratory of the University of California (Los Angeles) resulted in an analytical method now being available for detection of the drug in sport.4 Haemoglobin- and non-haemoglobin-based oxygen carriers are now available commercially. There are few scientific data about their use in sport, but it is likely they are misused by some athletes.5 Recombinant human erythropoietin is widely used in cycling and other endurance sports. A detection method developed from Australian research will limit its use, at least at the Olympic venue.6 Genetic manipulation is unlikely in 2004, but its potential is foreseen. This technology is also prohibited in the new code.1 Unfortunately, drugs will continue to be misused. The opportunity for Olympic winners to gain huge financial rewards will fuel their use.

Michael C Kennedy

Ronan J Murray,* Kishore Sieunarine,† Peter B Ward,‡ John W Pearman§ * Senior Microbiology Registrar, § Clinical Microbiologist, † Vascular Surgeon, Royal Perth Hospital, Perth, WA; ‡ Senior Scientist, Department of Microbiology, Austin Repatriation Medical Centre, Heidelberg, VIC. ronan.murrayAThealth.wa.gov.au To the Editor: Previous articles in the Journal have described the emergence of Staphylococcus aureus with reduced susceptibility to vancomycin (also known as heteroresistant vancomycin-intermediate Staphylococcus aureus, or hVISA) in populations where methicillin-resistant S. aureus (MRSA) is endemic in healthcare settings.1,2 We describe a case of infection caused by hVISA from a region where healthcare-associated MRSA infection is relatively uncommon.3 A 79-year-old woman with an extensive medical history, including type 2 diabetes mellitus and multiple bypass procedures for lower-limb ischaemia, presented with critical ischaemia of the right lower leg. After above-knee amputation, she developed a discharge from the stump wound from which multiresistant MRSA was cultured. Despite receiving several courses of intravenous vancomycin (a total of 25 days of therapy over 5 months), the infection did not resolve. Extensive debridement surgery, with removal of multiple grossly infected vascular grafts, was performed, and MRSA was cultured from the graft material. Subsequently, the patient developed a discharging sinus from which MRSA with reduced susceptibility to glycopeptide antibiotics was cultured (vancomycin minimal inhibitory concentration [MIC], 8 mg/L; teicoplanin MIC, 24 mg/L). This isolate was shown to be hVISA by population analysis profiling (PAP). When the original MRSA isolate was subsequently tested by PAP, heterogenous subpopulations of bacteria with reduced susceptibility to vancomycin were present which had not been detected by routine susceptibility testing (ie, the isolate was already hVISA). Review of the patient’s medical records from other Perth healthcare institutions revealed no evidence of vancomycin administration before the initial isolation of MRSA, or contact with known MRSA-colonised patients or healthcare workers. Multilocus sequence typing and staphylococcal cassette chromosome mec allotyping identified the MRSA strain as ST239-MRSA-III, a multiresistant “international” MRSA clone frequently isolated in Australia, mainly on the east coast.4 Despite further surgery and institution of alternative antimicrobial therapy (initially rifampicin and fusidic acid and subsequently linezolid), the patient died of ongoing ischaemia and uncontrolled infection. Prolonged or repeated use of vancomycin in patients with implanted prostheses that are infected with MRSA should be discouraged, not only because it is commonly futile, but also because it may promote the emergence of subpopulations of S. aureus with reduced susceptibility to vancomycin, as occurred in this case. The fact that these resistant subpopulations were detected in an isolate before the commencement of vancomycin therapy (and then only with specialised testing) reinforces our recommendation.

Ronan J Murray · Kishore Sieunarine · Peter B Ward · John W Pearman

Anton Y Peleg,* Wendy J Munckhof† * Infectious Diseases Registrar, Alfred Hospital, Prahran, VIC 3181; † Specialist in Infectious Diseases and Microbiology, Infection Management Service, Princess Alexandra Hospital, Brisbane, QLD. A. PelegATalfred.org.au To the Editor: Infection with community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) is emerging in many countries, including Australia.1 We report the first case of fatal necrotising pneumonia caused by CA-MRSA in Australia. A previously well 21-year-old Aboriginal man presented to the emergency department with fever and a productive cough. He had no known risk factors for sepsis (such as immunosuppression, diabetes, HIV infection, alcoholism, asplenia or recent influenza) and no history of hospitalisation in the previous 12 months. Chest x-ray revealed left mid-zone consolidation. He was prescribed amoxycillin–clavulanate and discharged. Two days later, the patient re-presented, with rigors, haemoptysis and agitation. Examination revealed a respiratory rate of 38 breaths per minute, oxygen saturation of 79% breathing room air, temperature of 38.7°C, sinus tachycardia (135 beats per minute), and a systolic blood pressure of 80 mmHg. Respiratory examination revealed diffuse coarse crepitations. No other source of infection was identified. The patient required intubation, mechanical ventilation and inotropic support. Sputum and blood samples were taken for culture, and empirical treatment was begun with intravenous ceftriaxone, erythromycin and a single dose of gentamicin and rifampicin. Initial investigations showed leukopenia (2.3 × 109/L; reference range [RR], 3.9–12.7 × 109/L), acute renal failure with a serum creatinine level of 0.18 mmol/L (RR, 0.06–0.11 mmol/L), and severe metabolic and respiratory acidosis (pH, 7.19; RR, 7.38–7.43). The following day, blood and sputum cultures showed gram-positive cocci resembling staphylococci, and intravenous flucloxacillin was added to the antibiotic regimen. Repeat chest x-ray revealed bilateral necrotising pneumonia. Despite resuscitation efforts, the patient died 48 hours after admission. Susceptibility testing of blood and sputum isolates subsequently confirmed MRSA. The isolate was sensitive to erythromycin, clindamycin, gentamicin, ciprofloxacin, tetracycline, vancomycin, rifampicin and fusidic acid. Methicillin resistance was confirmed by detection of the mecA gene by polymerase chain reaction (PCR). Further PCR testing of the isolate revealed the Panton–Valentine leukocidin (pvl) gene, an important virulence factor that has been associated with necrotising pneumonia2 and death,3 and is rarely found in methicillin-susceptible S. aureus or hospital-acquired MRSA isolates.1,2,5 Typing of the isolate by pulsed-field gel electrophoresis showed that it was the recently described “R” pulsotype of CA-MRSA, or “Queensland clone”.4 This clone was first noted in the white population in south-east Queensland in 2000, and is uncommon in Aboriginal people.4 Most CA-MRSA infection in Aboriginal people is caused by WA-MRSA, which may be less virulent than the Queensland clone of CAMRSA as it lacks the Panton–Valentine leukocidin.5 This is the first reported case of fatal necrotising pneumonia caused by CA-MRSA in Australia and illustrates the invasive nature of this infection. Thus far, CA-MRSA has predominantly caused skin and soft tissue infections, but the incidence of life-threatening sepsis is increasing. The first case of severe pneumonia caused by CA-MRSA in Australia was reported in early 2003.6 Fatal cases of necrotising pneumonia caused by CA-MRSA have also been described in the United States3 and France,7 and this presentation is becoming a particular feature of this organism. Clinicians should consider the possibility of CA-MRSA in any patient presenting to hospital with severe staphylococcal sepsis or pneumonia and should consider including parenteral vancomycin in the initial empirical therapy, particularly in geographic locations where CA-MRSA has been reported and in ethnic groups at increased risk.

Anton Y Peleg · Wendy J Munckhof

Lloyd K Morgan General practitioner (retired), PO Box 150, Lorne, VIC 3232. lloydmorganATiprimus.com.au To the Editor: O’Leary et al1 are pessimistic about the value of antibiotic treatment for leptospirosis, based on an inconclusive Cochrane review2 and no proven mortality decrease. Yet we can be more optimistic, given the efficacy of prophylactic doxycycline (soldiers in Panama were 95% protected by 200 mg once-weekly3), the susceptibility of leptospira to various antibiotics in vitro (especially penicillin, but not erythromycin4), and the existence of a Herxheimer reaction with penicillin,5 which indicates in-vivo activity. The Cochrane review2 was of randomised controlled trials of confirmed cases. It included 75 patients given antibiotics and 75 given placebo. Penicillin (61 patients) and doxycycline were not compared. The time from symptom onset to starting antibiotics was stated in only two trials (9 and 2 days). Nevertheless, the review concluded that penicillin or doxycycline may do more good than harm. In the spirochetaemic phase of leptospirosis (Days 4–7), vasculitis causes multiorgan failure. Successful treatment with antibiotics seems likely if commenced within 2 days of symptom onset, before generalised vasculitis is irreversible. Unfortunately, early diagnosis and efficacy assessment is difficult because symptoms are protean and non-specific, no rapid laboratory test exists, the condition is mild and self-limited in most cases, and mortality varies from zero to 7%. A high index of suspicion is essential so that antibiotics can be commenced empirically. The consensus is that antibiotics should be commenced within 4 days. In one study, starting antibiotics within 7 days was associated with shorter illness, and if antibiotics were started within 2 days the shorter duration was highly significant (P = 0.006).6 Another trial showed penicillin commenced on Day 9 was beneficial, but antibiotics had been used before entry to the trial.2 Various penicillins and tetracyclines have seemed useful, but only oral doxycycline and intravenous benzylpenicillin are recommended. These are the first and second preferences, respectively, in Therapeutic guidelines antibiotic.7 In the case described by O’Leary et al,1 antibiotics were commenced on Day 3, but the penicillin dose was only half the recommended daily dose for leptospirosis. The vasculitis was probably terminal before the patient was transferred to Concord Hospital.

Lloyd K Morgan

Marianne E Jauncey,* Paul K Armstrong,† Emily L Morgan,‡ Jeremy M McAnulty§ NSW Public Health Officer, Public Health Training and Development Branch; † Medical Epidemiologist, § Director, Communicable Diseases Branch; NSW Health, North Sydney, NSW. ‡ General Practitioner, Ballina West Medical Centre, Ballina, NSW. Marianne.jaunceyATyahoo.com.au To the Editor: In 2003, severe acute respiratory syndrome (SARS) became the first pandemic of the 21st century. Despite spreading to 29 countries, a rapid and coordinated international effort led to its containment. Here, we examine Australia’s only laboratory-confirmed case, and the investigation of possible subsequent transmission. In June 2003, the World Health Organization (WHO) notified Australian health authorities of a 26-year-old tourist in whom SARS-coronavirus-specific antibodies had recently been detected. She was part of a retrospective serological survey of people who stayed at the Hotel Metropole, Hong Kong, on 21 February,1 the same time a SARS source case infected at least 14 other hotel guests.2 On 22 February, the 26-year-old tourist travelled to Australia and 4 days later developed myalgia, lethargy and cough. On 6 March, 6 days before the first WHO global alert on SARS, she saw a general practitioner (GP) in northern New South Wales, to whom she also reported nausea, vomiting, nocturnal fever and pronounced lethargy. On examination she was afebrile, pale, unwell, with a cough and clear chest on auscultation. She declined further investigations and hospital admission; her condition gradually improved, and she left Australia 6 days later. She reported close contact with only three people during her Australian visit — her partner, the GP, and the GP’s surgery nurse. None reported subsequent illness and all tested negative for SARS-coronavirus antibody by direct immunofluorescence, a highly sensitive and specific method.3 Australia was fortunate that the tourist was not particularly infectious. The Hotel Metropole case was identified as the source case for four national and international clusters of SARS.2 The resulting human and economic cost was substantial.4 Without specific treatments, basic public health measures proved the only effective means to contain SARS. These included rapid case detection and isolation, contact tracing, handwashing and the correct use of personal protective equipment.5 Many GP practices and some hospitals in Australia do not have isolation facilities or infection control resources to effectively contain diseases like SARS. In the event of local transmission of SARS, infection may well have occurred in Australian healthcare workers. In the wake of SARS and, more recently, avian influenza, GPs must develop infection control plans to protect their own health as well as that of their patients. These should include obtaining a history of travel to outbreak-affected areas, reserving an area for patient isolation, and using appropriate infection control precautions during such outbreaks. Clinicians in other healthcare settings also need to review current infection control practices. If Australia is to remain the “lucky country” with regard to communicable diseases, basic public health measures aimed at preventing transmission of infection in healthcare settings is essential.

Marianne E Jauncey · Paul K Armstrong · Emily L Morgan · Jeremy M McAnulty

Jennifer W Majoor,* Joseph E Ibrahim† * Associate Professor, Department of Psychiatry, Alfred Hospital, Prahran, VIC; † Monash University Professor of Aged Care Medicine, Peninsula Health, Frankston, VIC. J. MajoorATalfred.org.au To the Editor: We applaud the Journal’s new series to improve the standard of teaching within the medical profession.1,2 However, it seems ironic that a profession that relies so heavily on an experiential, apprentice-based model of learning should be running such a series. Since the early nineties, we have seen a paradigm shift with regard to improving the quality of healthcare. However, this recent managerial preoccupation with systems, processes and outcomes has largely ignored the relationship between effective teaching and patient care. Clinical service work is given priority over training and education activities, and it is likely that, if it weren’t for the clauses in our employment contracts, all training, conferences and educational activities would occur out of work hours. Although we have seen a number of structural interventions to promote ongoing education, such as the introduction of Continuing Medical Education programs, the idea that “any” education will do, and that “anyone” can teach, remains pervasive. The danger of promoting “teaching on the run” is to reinforce the view that teaching is not a specialised discipline that requires specific skills and training. It is astounding that no formal qualifications in education are required for teaching at the most senior level, whereas to be taken seriously as a researcher requires an MD or PhD. It is a rare gifted teacher who instinctively performs well without formal training. High-quality teaching requires formal training, just as high-quality research does. Do we allow anyone in medicine to simply do “research on the run”? Would we ever consider a series called “Research on the run”? In medicine, we recognise that people are drawn to particular specialties because of their different knowledge, skills, interests and temperaments. This is not always the case in teaching, and names on a tutorial roster are too often allocated without regard for the style or ability of the teacher. Lake points out that the majority of problems with teaching are related to the traditional culture of medical practice and health service delivery.2 Similarly, Quadrio has observed that “career advancement in medicine . . . depends primarily upon research productivity, less upon clinical work and teaching . . .”.3 In our view, medicine requires another paradigm shift towards competency assessment and promotion of our teachers in academic settings. Furthermore, the allocation of appropriate resources is paramount and is justified because of the likely spin-offs for improved quality of patient care. We look forward to the day when medical education is rewarded as a highly valued endeavour, rather than a burden for busy clinicians and academics. We eagerly await further instalments of this well intentioned series on teaching, and hope that it goes some way towards effecting a “Kuhnian revolution”.4 (US scientist Thomas Kuhn proposed that scientific knowledge proceeds according to popular paradigms that, every now and then, undergo “intellectually violent revolutions . . . in each of which one conceptual world view is replaced by another . . .”.)

Jennifer W Majoor · Joseph E Ibrahim

Fiona R Lake Associate Professor in Medicine and Medical Education, Faculty of Medicine and Dentistry, University of Western Australia, Nedlands, WA. flakeATcyllene.uwa.edu.au In reply: As noted by Majoor and Ibrahim, teaching and learning, as a mission, are not well regarded when compared with research. Not only that, but changes in healthcare are making it harder to teach. Shorter patient stays and more complex patients result in “survival” learning by junior staff, rather than in-depth learning.1,2 Experts in medical education will be increasingly important in teaching, guiding curricula, and assessing trainees.2 However, professional learning occurs while doctors immerse themselves in clinical practice. “On the run” teaching doesn’t mean substandard teaching, but relates to doing it while delivering patient care.3 Although there is room for improvement, many clinicians teach well. Most are keen to teach and would like to have formal training,4 and evidence suggests that, with support, they can improve.2,3 How much support? Short workshops have been shown to have an impact, as has the provision of a few simple educational ideas.5 By not supporting our clinicians/teachers in ways that could be very simply put into practice, we risk losing in-context learning and wasting an enormous resource. Along with focusing on the teacher, I believe we need an important shift in the way health services recognise (provide time for) and reward (see as important) the mission of teaching and supervision alongside their mission of excellence in delivery of care.

Fiona R Lake

Chin-Pin Yeo,* Melissa J Gillett,† Samuel D Vasikaran‡ * Chemical Pathologist, † Biochemistry Registrar, ‡ Head, Core Clinical Pathology and Biochemistry, Royal Perth Hospital, GPO Box X2213, Perth, WA 6847. gptycpATsgh.com.sg To the Editor: In about 2% to 5% of patients with subclinical hypothyroidism, the condition progresses to overt hypothyroidism each year.1 It is currently recommended that thyroid function tests should be repeated at 6- to 12-month intervals to monitor improvement or worsening in level of thyroid-stimulating hormone (TSH).1 Testing for thyroid peroxidase antibody (TPOAb) is also common practice in subclinical hypothyroidism, as it has been shown that individuals with raised TSH and TPOAb levels have a 40-fold increased risk of developing overt hypothyroidism.2,3 We audited the management of patients who had a result indicating subclinical hypothyroidism from our hospital laboratory, focusing on follow-up thyroid function and TPOAb tests. In December 2003, we retrospectively inspected clinical case notes of patients who had been reported in November 2002 with a TSH level of 4.1–9.9 mIU/L (normal reference interval, 0.4–4.0 mIU/L) and a free thyroxine (FT4) level within the reference range of 10–23 pmol/L (subclinical hypothyroidism). We also contacted the patients’ general practitioners (GPs) for further information when necessary. There were 72 patients with results suggesting subclinical hypothyroidism. Of these, we excluded 29 from other hospitals and three whose GPs were not able to be contacted. Of the remaining 43 patients, 18 had no previous history of thyroid disease (8 men and 10 women; age range, 24–90 years). Six patients were seen in the emergency department, four in the outpatient clinics, and eight in the wards. All the laboratory reports of subclinical hypothyroid results were accompanied by a comment advising repeat thyroid studies at a later date and thyroid antibody tests. However, only three of the 18 patients (17%) had TPOAb tested. Only seven of the 18 patients (39%) were followed up with repeat thyroid function tests, at intervals ranging from 3 days to 7 months. One patient, with a TSH level of 9.8 mIU/L, was started on thyroid replacement therapy. The GPs of 10 of the 11 patients who did not have follow-up testing were not informed of the initial TSH results. The low rate of follow-up of hospital patients with a first-time diagnosis of subclinical hypothyroidism is of concern. While the increase in TSH level in some of these patients may have been related to sick euthyroidism, this can only be confirmed by normalisation of TSH level on repeat testing. TPOAb testing can be deferred until confirmation of persistently raised TSH level. Better strategies, such as a computerised system for selective copying of results to GPs whenever relevant, and inclusion of treatment advice dependent on TPOAb status in the reports,4 may be needed to improve follow-up.

Chin-Pin Yeo · Melissa J Gillett · Samuel D Vasikaran

The doctors' tale. Professionalism and public trust. Donald Irvine. Oxford: Radcliffe Medical Press, 2003 (ix + 247 pp). ISBN 1 85775 977 X The doctors' tale is an insider's story of recent reforms affecting the British medical profession. Donald Irvine presided over the United Kingdom's General Medical Council (GMC) during this turbulent period (1995--2002) and his narrative explores the challenges he confronted in dragging an insular and imperial GMC into the new millennium. Irvine had been elected to the presidency on a reform agenda. Before his ascendancy, reform had been pursued through blueprints for medical education (Tomorrow's doctors: recommendations on undergraduate medical education. London: GMC, 1993) and for professionalism in practice (Duties of a doctor: good medical practice. London: GMC, 1995). But reform had moved at a snail's pace and remained impervious to societal changes. However, all this became history following the well-publicised events in paediatric cardiac surgery at the Bristol Royal Infirmary. Public trust in doctors' abilities to self-regulate and ensure clinical competence evaporated almost overnight. Politicians and the public perceived the GMC as no longer in control. Further shocks followed with the revelation of the medical murders by Harold Shipman; the gross professional misbehaviour of gynaecologists Rodney Ledward and Richard Neave; and the arrogance displayed in the Alder Hey affair. But the Bristol case, which is central to Irvine's theme, was to become the epicentre for reform and restoration of public trust. The second half of his book covers the post-Bristol efforts to advance revalidation of the profession and to achieve GMC change. There are other subplots: the politics involving the British Medical Association, the National Health Service and the Medical Colleges, and the measured relationship between Irvine and the UK Secretary of State for Health. In the details of these interactions lies the book's only drawback -- it all seems so gentlemanly, without passion or heat! The book is easy to read. It is divided into four parts: Irvine's formative years in general practice and its Royal College; his time as a member of the GMC; his seven years as GMC President; and finally his afterthoughts. It is well referenced, with helpful glossaries and appendices. All doctors interested in medical reform and politics should read The doctors' tale, especially those in our health departments and medical boards. I recommend it for anyone who enjoys a good political whodunit. Martin B Van Der WeydenEditor, The Medical Journal of Australia Sydney, NSW

Martin B Van Der Weyden

Medical management of acute and chronic low back pain. An evidence-based approach. Nikolai Bogduk, Brian McGuirk. Amsterdam: Elsevier, 2003 (viii + 224 pp). ISBN 0 444 50845 7. Low back pain is a topic that has not enjoyed the publicity that it deserves in medical circles. With its limited coverage in medical curricula, both in hospital and GP training programs, one would be forgiven for thinking it is an uncommon or unimportant complaint. Yet it is a popular topic in the media where cure claims abound. It is also the leading cause of disability in the workplace and a very common cause of presentation to healthcare providers, often non-medical practitioners. The authors are well qualified to write about this topic: Bogduk is Professor of Pain Medicine at Royal Newcastle Hospital and McGuirk is a specialist in musculoskeletal and occupational medicine for the Hunter Area Health Service. They seek to redress many of the common misconceptions about low back pain by presenting an approach to diagnosis and management firmly supported by the evidence. Many readers may be surprised to hear that the evidence base for low back pain is stronger than that for most other common conditions, but that this evidence gives little support for the traditional orthopaedic approach. The evidence is presented with great clarity and links very logically with the algorithms for diagnosis and management. These algorithms gravitate towards precision diagnosis and treatment of the anatomical sources of back pain when conservative therapy has failed. This book is essential reading for people involved in musculoskeletal medicine and medicolegal work, for rehabilitation providers, physical therapists, WorkCover and other insurance providers, and for independent medical assessors. It would also be a very useful reference text for general practitioners and supersedes most other books in this area. Especially useful are the sections on history, imaging and management. These sections will save a lot of nail-biting among practitioners who are nervous of missing dangerous conditions, or who think they need to routinely refer low back pain patients to orthopaedic surgeons or rheumatologists. Health economists may also find the concepts in this book informative, as cost savings abound in this billion-dollar heath expenditure pit. C Scott MastersPresident, Australian Association of Musculoskeletal Medicine, Caloundra, QLD Order this book

C Scott Masters

Transplanting rabies Three recipients of transplanted organs from a donor who died of a presumptive subarachnoid haemorrhage died a few weeks later themselves — from rabies.1 According to the US Centers for Disease Control (www.cdc.gov) these are the first reported cases of rabies transmission via solid organ transplantation; rabies has been transmitted previously via corneal transplants. Later, it was reported that a segment of iliac artery recovered from the donor had been used in another liver transplantation procedure; the recipient also died of rabies a few weeks after the procedure. Rabies testing is not part of the routine donor-screening process and rabies had not been suspected in the donor; however, a subsequent public health investigation determined that the donor had reported being bitten by a bat. As of 9 July, rabies postexposure prophylaxis had been initiated in about 20% of the 916 persons assessed for exposures to the organ recipients or the donor. BMJ 2004; 329: 68 Photos by mobile phone Mobile phone use may be eschewed in many medical environments, but for one surgical team at Sydney’s Nepean Hospital mobile phones with photo-messaging capabilities are proving a relatively inexpensive and effective means of enabling telemedicine. Lam and colleagues used two Nokia phones equipped with digital cameras to capture, store and send images of hand trauma from registrar bedside to consultant elsewhere. Over two months, images (including x-rays) for 27 various cases (including compound fractures [see photo], lacerations and tip amputations) were sent by phone, aiding communication and conventional clinical discussion between the team members. Aust N Z J Surg 2004; 74: 598-602 Joint strategy A multifaceted, intensive outpatient treatment strategy for active rheumatoid arthritis (RA) can lead to better clinical results than routine outpatient care, say Scottish researchers. They compared these two approaches in a randomised controlled trial involving more than 100 adult patients who had had RA for less than 5 years. The intensive strategy incorporated monthly review, intensive use of intra-articular steroid injections and a structured protocol for escalating disease-modifying drug treatment; neither strategy offered anti-tumour necrosis factor treatment. After 18 months, the intensive strategy resulted in greater improvements in disease activity (including more remissions), physical function and quality of life and less radiographic disease progression — all at no additional overall cost to the NHS. Lancet 2004; 364: 263-269 Outbreak While Toronto was coming to grips with the SARS epidemic, another Canadian city, Montreal, was experiencing an outbreak of Clostridium difficile-associated diarrhoea (CDAD), which may have been responsible for about twice as many deaths as SARS in that country, according to a series of articles in CMAJ.1 In recent years, cases of CDAD seem to have become more frequent and more severe, possibly due to a more virulent strain of the organism. One research team has identified proton pump inhibitor use as an independent risk factor for CDAD.2 1. CMAJ 2004; 171: 5; 19-21; 27-29; 45-48 2. CMAJ 2004; 171: 33-38 Soy story Soy protein supplements may not improve bone mineral density in healthy, older postmenopausal women, according to a Dutch double-blind, placebo-controlled trial. About 200 study participants aged 60 to 75 years were randomised to receive either 25.6 g of soy protein containing 99 mg of isoflavones or 25.6 g of placebo (total milk protein) on a daily basis. After a year of supplementation, not only bone mineral density but also cognitive function and plasma lipid levels did not differ significantly between the soy and placebo groups. However, the researchers acknowledged that findings in the study subgroups, formed according to years since the menopause, supported the idea that it may be easier to prevent than reverse changes or losses after menopause. In the most recently menopausal women, soy supplementation seemed to improve bone mineral density, whereas this effect was absent in late menopause. JAMA 2004; 292: 65-74 AIDS 2005 In 1995, 500 000 workers with AIDS around the world were too ill to work; by 2005, and without access to antiretroviral drugs, this figure will have grown to two million workers, according to an International Labour Organization report presented at the 15th International Aids Conference held in Bangkok from 11-16 July 2004.1 The resultant economic impact on developing countries is expected to be significant. Research from Tanzania offers some hope for those affected: a randomised trial of multivitamin supplements involving more than 1000 women infected with HIV conducted from 1995 to 2003 has found that daily oral supplementation with vitamin B complex, vitamin C, vitamin E and folic acid delayed the progression of disease compared with placebo.2 1. BMJ 2004; 329: 129 2. N Engl J Med 2004; 351: 23-32 Dr Ann Gregory, MJA

Ann Gregory