Editorials

1914 2004 1956 1978 1982 1989 1993 For more covers, see the pdf version of this article. As the eyes are said to be the window to a person’s soul, so is a journal’s cover a window into the ethos of its editors and readers. Over the past 90 years, the cover of The Medical Journal of Australia has changed many times, reflecting the national and international events of the times, the perceived desires of its readers and, occasionally, the whims of its editors. The Journal’s first issue was published on 4 July 1914. The MJA arose from the amalgamation of the Australasian Medical Gazette (published by the NSW Branch of the British Medical Association since 1881) and the Australian Medical Journal (published by the Victorian Branch of the BMA since 1856). This union was not without some opposition, but there was a clear need for a national journal that would unite the six Australian branches of the BMA and reach the whole medical profession in Australia. The cover changed little in the first 40 or so years, featuring only the title, issue details and a large monochrome advertisement. This was a time of war (World War I, with Britain declaring war against Germany exactly a month after the first issue of the fledgling journal appeared), financial difficulties as the cost of paper and printing suddenly rose, the Great Depression, another war (World War II, when many of the Journal’s contributors were in the armed forces), and editors in for the long haul (Henry William Armit [featured on this issue’s cover] served 16 years [1914–1930], Mervyn Archdall served 27 years [1930–1957], and Ron Winton, whose obituary is published on page 26 of this issue, served 20 years [1957–1977]). In the post-war years, medicine experienced a technological explosion and the Journal took on a more modern layout with a bright blue cover, better-quality paper and some colour printing. The MJA’s content adopted a more global perspective, reflecting Editor Ron Winton’s Chairmanship of the Council of the World Medical Association for many years. The MJA also officially became the journal of the Australian Medical Association when the shackles of the BMA were cast off in 1962 and the Association became fully independent. At this time, the number of specialist journals increased greatly, with some fragmentation of the readership of the MJA. Winton countered this with an editorial policy of a mix in each issue to appeal to both generalists and specialists, a policy which continues today in recognition that our readership is almost equally divided between specialists and general practitioners. After Ron Winton, the Journal went through a turbulent time, with six editors in 10 years. These were also lean years, when the Journal changed from a weekly to a fortnightly publication (1978), and The Printing House in Glebe, Sydney, closed (after publishing and printing the Journal completely “in-house” for more than 60 years). During the late ’70s and early ’80s, the covers changed almost as often as the editors. Of particular note were Alan Blum (1982–1983), who came to the Journal from the United States and was responsible for some of its most controversial covers on topics such as smoking, nuclear war and AIDS, and Alistair Brass (1983–1985), described as a liberal thinker and an outspoken critic, who put Australian artworks on the cover. The Journal subsequently returned to its more conservative roots in the late ’80s under Kathleen King with, for the first time, the full contents displayed on a bright green cover. This was initially a space-saving device, but it proved popular with readers. In the early ’90s, joint editors Laurel Thomas and Jill Forrest continued to appease the scientific purists with the full contents on the cover, but softened it with a picture and a less stark grey–blue background. Martin Van Der Weyden took the helm in 1995 and the cover slowly evolved, with only minor changes in colour and typeface. With this issue, however, we present a major overhaul. We’ve aimed for cleaner lines, a less cluttered look and a Journal that’s generally easier on the eye. Our ideas are perhaps most succinctly stated by Joseph Pulitzer: “Put it before them briefly so they will read it, clearly so they will appreciate it, picturesquely so they will remember it and, above all, accurately so they will be guided by its light.” We hope you approve.

Bronwyn Gaut

Reducing error is an ongoing process, always in need of fine-tuning A crucial challenge in efforts to prevent or reduce the occurrence of medical error is obtaining information about the diverse types of medical mishaps. “Mishap” is a useful term — it is neutral and broad enough to encompass the wide range of things that can go wrong in clinical practice. The types of medical mishaps include the “near-miss”, the “incorrect procedure or treatment which does not harm the patient”, the “adverse event” (either anticipated or unanticipated), and, finally, the “sentinel event” (a blatant error, such as a blood transfusion error). All these forms of mishap have the potential to provide important information to help minimise or prevent patient harm and enhance standards of medical practice. The need for a flow of information far outweighs fingerpointing There are arguments about the definitions of medical error, and my assertion — that lessons can be learned from all forms of medical mishap — deliberately cuts a broad swath. Close examination of each of these types of mishap provides different learning opportunities. Near-misses, or errors that cause no harm, can trigger a re-evaluation of correct procedures to prevent these events; Adverse events, both “anticipated” and “unanticipated”, can help clinicians develop more rigorous thinking about evidence and standards; and Sentinel events can show how the protective systems put in place can be breached. Collecting extensive information in all these mishap categories not only leads to interventions to minimise and prevent harm, but also allows detection of patterns of error. For example, if an inordinate number of errors occur during night shifts, or when the change of shift occurs, organisational changes may be required. Information about mishaps also provides material for teaching medical students, residents and community practitioners, with the aim of preventing future errors. If the information prevents errors then there will be impressive cost savings for hospitals and healthcare systems, as well as for patients and their families.1 Finally, information about errors and patterns of errors forearms clinicians to avoid patient injury, thus reducing the stress involved in suspecting or knowing their actions may have caused harm. But there remains an ongoing impediment: can healthcare data systems provide timely information for risk management and reducing medical mishaps? In the book Medical mishaps. Pieces of the puzzle contributors from several countries identified “multiple overlapping and faulty mechanisms for the revelation, investigation and mitigation of errors”. There was “clearly considerable scope for greater collaboration, integration and coordination”.2 And the situation in Australia appears to be no exception. One of the key priorities of the Australian Council for Safety and Quality in Health Care (ACSQHC) is enhancing processes for measuring local quality improvement and aggregate-level reporting of performance and outcomes.3 A report in this issue of the Journal by Kingston and colleagues (page 36)4 explores the attitudes of the two main health-professional protagonists involved in reporting medical error. It analyses the differential use of incident reporting by doctors and nurses, and attributes this to the different cultures of the two professions. This finding has been well substantiated. Nurses work in a culture that responds to directives, including the directive to report incidents; doctors work in a culture that values intragroup action and professional–cultural definitions of error or mistake.5 Other, systems factors also influence the decision to report incidents: time constraints, dissatisfaction with the process, inadequate feedback, and failure to value the process.5 In addition, there may be confusion about what should be reported, feelings of fear of retribution and doubts about the possibility of remediation. Finally, what are the views of healthcare consumers? In a study published in the 7 June issue of the Journal,6 a random sample of Australians supported vigorous reporting of errors, and 68% of those surveyed also wanted disclosure of the identity of the healthcare worker involved. While this is understandable, it shows the need to educate the public about the importance of a “no-blame” culture to ensure that reports will be made in the first place. The need for a flow of information far outweighs fingerpointing. Clinicians want error reduction, and favour anonymity. Patients and the public want error reduction and are likely to accept anonymity in the name of this goal. The ACSQHC supports the principle of “no blame”, and has recently published a document Open disclosure standard: a national standard for open communication in public and private hospitals, following an adverse event in health care. This provides clear guidelines for patients, healthcare professionals and organisations confronting and dealing with medical error, and the legal issues attending such events. Its major message is an open, blame-free culture.7 Despite the human and systems factors impeding reporting of medical error, many of these can be overcome by adequate incident-reporting systems. These have the following characteristics:8 they are anonymous and easy to use (computerised); they acknowledge receipt of a report and confirm that it is being investigated; they report back the results of the investigation in a timely manner; they use the information for programs of reduction; they provide feedback about successful reduction efforts; and they receive continual public support from key physicians in leadership positions. The process of error reduction involves long-term effort. There needs to be consistent and persistent emphasis on a cycle of attention to information, patterns revealed by information, error-reduction efforts, evaluation, more information and more reduction efforts. These efforts now also include producing informed patients, who are coached to ask the questions that might avoid errors. We should think about this cyclic process to reduce error as an ongoing one, always in need of fine-tuning. Its effectiveness depends on clinical leadership providing a continuing example in error reporting.

Marilynn M Rosenthal PhD

The health service reforms fuelled by whistleblowing continue In 1995, the tragedy in paediatric cardiac surgery at the Bristol Royal Infirmary, exposed by a whistleblower, ended the laissez-faire approach to patient safety, management of clinical quality and professional self-regulation in the National Health Service (NHS). Indeed, the impending impact of the Bristol case was poignantly captured by an editorial in the British Medical Journal, entitled “All changed, changed utterly”.1 Britain may not be alone in whistleblowing. In this issue of the Journal, Faunce and Bolsin report on three such recent events in Australia2 (page 44). These show an uncanny commonality with the Bristol case. What has happened in the NHS since 1995? In the immediate aftermath of Bristol, the then Health Secretary, Frank Dobson, took urgent action to place a duty of quality of care on chief executives of NHS Trusts, effectively ending any doubt about where responsibility would lie. In 1998, the new Labour government introduced two white papers, The new NHS: modern, dependable3 and A first class service: quality in the NHS.4 Although these described the regulatory framework for a quality-oriented healthcare service in England, the principles were to apply across the UK. Subsequent policy papers have added many refinements — including some 42 quasi-autonomous regulatory bodies in healthcare. These have just been pruned after criticisms of overly oppressive regulation. The following are key elements of change in England: The National Institute for Clinical Excellence (NICE) is tasked to develop evidence-based clinical guidelines and to assess and evaluate new technologies and pharmaceuticals for the NHS. Complementing the clinical guidelines, National Service Frameworks were created to map out the essential ingredients of good clinical service provision. Originally, there were three — for coronary heart disease, cancer and mental health. Paediatric care was added after the report of the Bristol Inquiry.5 However, the focal process for the delivery of clinical care is clinical governance, which is defined as “a framework through which NHS organisations are accountable for continuously improving the quality of their services and safeguarding standardised care by creating an environment in which excellence in clinical care can flourish”.3 To monitor compliance, the government established the Commission for Health Improvement, which was superseded this year by the independent Commission for Health Audit and Inspection, to regulate institutional quality in both the public and private healthcare sectors. Adding to all this bureaucracy and control are bodies with more specific functions. For example, the National Patient Safety Agency manages the reporting and analysis of “near misses”. The National Clinical Assessment Authority advises NHS Trusts and complements the work of the General Medical Council (GMC) in assessing and retraining poorly performing doctors. In addition, there is a new, overarching body for coordinating the regulators of the individual health professions — the Council for the Regulation of Health Professionals. For the citizens, the Commission for Patient and Public Involvement in Health, together with local Patients’ Forums, is to champion and promote public participation in the direction of local health services. This is a breathtaking array that even the distant observer in Australia might find daunting. For doctors, the regulatory landscape has also changed dramatically. The recent consultant and general practitioner NHS contracts increase employers’ control over the organisation of medical work, incorporate performance incentives and strengthen accountability. But it is the GMC’s proposals for doctors’ registration, training and discipline that are potentially most far reaching. The GMC changes began in 1992 with a new approach to basic medical training — Tomorrow’s doctors.6 Even more radical was the publication, in 1995, of a patient-centred code of practice, Good medical practice.7 If embedded successfully in the medical culture, the code will lead to positive changes in attitude on matters such as communication with patients and colleagues, teamwork, risk management, transparency, and whistleblowing. To strengthen compliance, the GMC tied the code directly to registration in 1998. The full effect will begin to be felt in 2005, when all UK doctors in active practice will have to have a licence to practise that must be revalidated every 5 years. Revalidation will require doctors to submit evidence of their continuing competence and performance (assessed against the template of Good Medical Practice) regularly for review. So where do things stand now? Two recent reviews of the NHS show a picture of patchy performance through clinical governance, particularly in the workplace.8,9 Data quality and some other systems issues are still a serious problem. But the central questions are about the medical and healthcare culture, and therefore medical leadership. Have the GMC and the Royal Colleges the will to see revalidation — and with it clinical governance — implemented as rigorously as required to give patients the assurances of the quality and consistency of medical care they are entitled to expect? Such questions are likely to be aired publicly again later this autumn when the Shipman Inquiry reports. All these changes raise the question: will the need for whistleblowing ever pass away? I believe this will only happen if the medical profession is prepared to put the task of embedding, demonstrating and communicating patient-centred professionalism at the heart of its vision for the future.10 This task has to become central to our professional practice, our teaching and our research. It is the object on which our mutual leadership should be focused. The public expect no less.

Donald Irvine CBE, MD, FRCGP

There is currently no need to panic At a recent forum of the Australian Health Policy Institute in Sydney, the Editor of the Journal expressed concerns about Australia’s ability to cope with avian flu, and asked whether he could sleep soundly in his bed. We attempt to answer his concerns. Influenza is justifiably feared. In 1918–1919, 40 to 50 million people (2%–3% of the world’s population) died in the “Spanish” influenza pandemic.1 Subsequent influenza pandemics occurred in 1957 and 1968. Although the mortality of the later pandemics was far less, the potential for another major pandemic is ever present. Annual influenza outbreaks have caused more deaths overall than pandemics, but gentle antigenic “drift”, caused by minor mutations in the viral genome, allows the annual development of a new influenza vaccine, matched as closely as possible with predicted circulating strains. Pandemic strains caused by antigenic “shift” are, by definition, unpredictable, and unlikely to be prevented in the short term by vaccines. In 1999, stimulated by human infections caused by avian influenza in Hong Kong, the World Health Organization (WHO) published a pandemic preparedness plan, and urged countries to make their own plans.2 How well prepared is Australia? The origin of pandemics: The segmented genome of the influenza A virus favours genetic reassortment, which can lead to antigenic shift to a new, potentially pandemic, strain. Pandemic strains arise when a new type of haemagglutinin is introduced into humans. Pigs may act as a mixing vessel for reassortment by supporting growth of both avian and human viruses, or a human might be co-infected with both avian and human strains. Pandemic influenza spreads rapidly and affects children and young adults, causing enormous social disruption.1 Avian influenza: Birds, particularly aquatic and migratory species, are natural hosts of all 15 haemagglutinin subtypes of influenza A virus, whereas only a few of these viruses have established transmissible infections in humans, pigs and other mammals.1 Avian influenza strains readily infect domestic poultry and are highly pathogenic to birds.3 Since mid-December 2003, there has been a catastrophic outbreak of avian influenza in Asia, caused by a highly pathogenic H5N1 strain. Eight countries have confirmed outbreaks, mostly in commercial poultry, although wild birds have been infected. In 2 months, over 100 million birds in Asia died or were culled.3 There was great alarm when human infections with this avian strain were reported, with high mortality in both adults and children. However, despite the extent of the outbreak in birds, very few human cases have been reported. By 24 March 2004, 57 cases had been notified from Vietnam (37) and Thailand (20), of which 23 (40%) were fatal. All cases followed exposure to infected poultry. The number of unreported human cases is uncertain, but the absence of documented human-to-human spread is reassuring.3 The greatest concern is that there will be reassortment between the current avian H5N1 strain and circulating human or porcine influenza viruses, producing a novel, virulent human strain. Pandemic planning: Australia has been actively planning action to cope with an influenza pandemic since 1997. The framework for a pandemic plan was published in 1999,4 and an action plan was published in 2003.5 A National Influenza Pandemic Action Committee (NIPAC), formed in 2003, continues to plan for future pandemics and has closely monitored the avian influenza situation. Although NIPAC is an anagram of “panic”, the message so far is that there is no need to panic. A major concern of the audience at the health policy forum was the large number of different agencies involved in planning for a pandemic — a veritable “spaghetti junction”. Who should coordinate these agencies? Given the complexity of pandemic planning, we believe it is entirely appropriate that there are many different players, coordinated, as is now the case, by the Australian Department of Health and Ageing.6 Planning for pandemic influenza overlaps to an extent with planning for outbreaks of other viral infections. Australian pandemic planning has benefited from the need to develop plans to cope with a potential epidemic of SARS (severe acute respiratory syndrome)7 and possible bioterrorist attack with smallpox virus.8 NIPAC is addressing many facets of planning, including: Border protection. Although Australia is an island, modern air travel and the high infectivity of influenza preclude total exclusion of a pandemic. Because influenza can be transmitted before symptoms appear, screening incoming passengers for reported symptoms, as was done for SARS, would be less effective, but might delay widespread introduction of influenza. Even weeks of delay could be invaluable for vaccine development and distribution. Immunisation. It would probably take at least 6 months after the onset of a pandemic for significant quantities of vaccines specific to the pandemic strain to become available.9 WHO is currently developing H5N1 viruses suitable for vaccine production as rapidly as possible. Antivirals. The H5N1 virus is resistant to amantadine, but sensitive to the neuraminidase inhibitors oseltamivir and zanamavir, which can be used for both treatment and prophylaxis. It has been suggested that countries should stockpile antivirals.10 There was some evidence of their benefit in humans during the 2003 outbreak of highly pathogenic avian H7N7 influenza A in Dutch poultry farms.1 However, antivirals are very expensive and in short supply, and realistically could only be used as a stop-gap measure to “buy time” by treating early cases and protecting essential staff. Laboratory diagnosis. Influenza is difficult to differentiate clinically from “influenza-like illnesses”, necessitating laboratory testing of appropriate respiratory samples for confirmation. However, testing is not often done routinely (at least in adults). SARS and the threat of avian influenza suggest testing should be more widely available to facilitate decisions about infection control, but few laboratories provide rapid viral diagnosis. The network of WHO influenza and other public-health laboratories in Australia is actively developing rapid tests to detect H5N1 influenza. Infection control measures to limit spread. Children are at high risk of contracting and dying of influenza,1 and are an important source of infection for the elderly.11 In a pandemic, it would almost certainly be necessary to close schools, childcare centres and public gatherings to reduce spread. Respiratory hygiene. Simple respiratory hygiene, such as covering the nose and mouth when sneezing, and disposing of used tissues promptly in “no-touch” receptacles, is as important as the use of masks.12 Communication. The level of public concern and, in many countries, panic during the SARS outbreak vividly illustrates the importance of effective public communication. It is vital that authorities do not leave the dissemination of information about outbreaks to the popular press. There is currently no need to panic about avian influenza, as human cases are extremely rare and have followed close exposure to birds. Human-to-human spread of avian influenza has not been described. While Australia is well prepared to cope if an influenza pandemic started tomorrow, the unpredictability of these pandemics, their rapid spread and high attack rates mean it is impossible to be totally reassuring. Like the rest of us, the Editor of the Journal, if he wants to sleep soundly, will just have to cope with uncertainty.

David Isaacs MD, FRACP, FRCPCH · Dominic E Dwyer MD, FRACP, FRCPA · Alan W Hampson MSc, MASM

Now we know these services are widely used, we need to know how best to support them The Australian government has recently released the report of the independent National Review of Tele Counselling and Web Counselling Services.1 Initiated by the Office of the Prime Minister in 2001, the review aimed to “take stock of the expanding and dynamic sector” and to describe the use, management, financing and role of web and telecounselling services. The report was commissioned in response to the recognition that the rapid expansion of these services created ethical, legal, funding, service delivery and education issues. The main findings of the review are summarised in the Box. In Australia, telecounselling (communication by telephone between a counsellor and a caller) is a large, diverse industry provided by 131 not-for-profit organisations and an unknown number of commercial organisations or individuals. The largest provider, Lifeline, consists of a federation of 42 centres, employs 5000 volunteers and provides 24-hour service 7 days a week. Web counselling (synchronous and asynchronous communication online or through email between a counsellor and a user) is a smaller, newer industry, with 17 not-for-profit agencies providing services mostly directed at youth. Two key points emerged from the review. First, many Australians use telecounselling services, although the benefits of the services have not been evaluated. Two of the largest service providers answer a combined total of about 850 000 telephone calls annually. (Precise estimates of numbers of users cannot be provided because individuals do not identify themselves, and may visit many times to the same or other agencies.) Despite this extensive use, the review confirmed that no randomised controlled trials (RCTs) have been conducted of the efficacy of web or telecounselling either in Australia or internationally.2 However, telecounselling as an adjunct to professional care has demonstrated effectiveness in RCTs3,4 and has been associated with changes in suicidality and mental health in uncontrolled evaluations.5 A second finding was that mainstream healthcare professionals, including general practitioners, refer patients to web and telecounselling services, although these services are not a formal part of the healthcare system. More than 20% of web and telecounselling agencies estimated that at least half their caseload was referred by healthcare providers, and reported that many calls relating to mental health were answered in the evenings or at weekends. Moreover, although crisis intervention is a component of the caseload, telecounselling agencies report that they are increasingly responding to a core group of individuals with ongoing mental health needs and loneliness. For Lifeline, less than 25% of callers were first-time callers, and across all of the agencies that were surveyed nearly 40% of callers had rung 20 times or more. Different counsellors in different locations talk to these individuals and are not privy to their concurrent medical service use. These key findings suggest three directions for action. First, better integration of telecounselling within mainstream mental health services may be desirable. A core group of users will be better served by being linked to healthcare and other services (for example, accommodation) and by information being shared about concurrent service use. Although telecounselling and mainstream services may have different locations, one solution is to link Lifeline web or telecounselling directly to telepsychiatry services. Telepsychiatry provides consultations with formal healthcare services (either face-to-face using technology, or through email). Although telepsychiatry may be costly and difficult to implement in practice, the advantages are the potential for geographical reach, accessibility, responsiveness, Medicare cover for users, the provider’s attention to evidence-based care and the provider’s duty of care. Software that records user contacts with major community agencies and the healthcare system would be a great step forward, although issues of anonymity, consent, privacy and, importantly, user preference and acceptance need consideration. Access for rural users to affordable telephone and internet services also requires attention. A second direction to consider involves implementing strategies for improving mental healthcare delivery within a web or telecounselling framework. There is a range of educational initiatives that allow high quality, evidence-based interventions to be delivered by non-specialists.6,7 This direction may involve integrating web or telecounselling with internet therapy and psychoeducation. A third clear direction is the need to evaluate the effectiveness of web and telecounselling. Fee-based web counselling with specialists and non-specialists is readily available to users, and these services are likely to accelerate, driven by a body of consumers who use internet resources. There is now the opportunity to test the usefulness and effectiveness of web counselling before this proliferates further. The emerging managed-care models delivered by an engaged and organised workforce of experienced telecounsellors is an exciting research opportunity not to be missed. Before the web and telecounselling review, no one knew the extent, quality or standards of delivery of these services, or even who used them. Now we know that these services are used frequently, both by the community and by healthcare agencies, and that they play a major role in managing vulnerable individuals with mental health problems. If telecounselling services are found to be effective, there is an urgent need to adequately support the sector and improve continuity of care between the systems. To date, telecounselling has been seen as non-core — a poor cousin to mental health services. However, given the development of communication technology, consumer empowerment, and the infrastructure, workforce, and capacity in the web and telecounselling sector, we foresee a central role for these services in delivering flexible, evidence-based, cost-effective help to the community. The National Review of Tele Counselling and Web Counselling Services Method Survey of 131 agencies in July 2002. Analysis of caller data from Lifeline, Kids Help Line and Care Ring, using statistics collected since 1999. Surveys of 80 interviews with web and telecounsellors and allied service providers. 20 focus groups of industry stakeholders. Telephone surveys of 125 users of web and telecounselling. Results Few national services exist, although there is a proliferation of state and regional services. Between 62% and 90% of calls are not answered because of under-resourcing and poor routeing of calls among centres. Nearly 80% of services relate to a specialist issue, such as sexual assault, domestic violence or cancer. Most calls concern mental health. Major telecounselling providers perceive themselves to be increasingly supporting highly vulnerable people rather than offering crisis intervention. Many callers ring repeatedly. More than 20% of services estimated that more than half their caseload was referred by main sector healthcare providers. Most telecounsellors are formally trained, with almost two-thirds being paid professional rates. Research team Urbis Keys Young. Advisors to Urbis Keys Young: Professor Trevor Waring and Dr Nick Kowalenko. Reference group Mr Dermot Casey, Mr Conrad Gershevitch, Professor Matt Sanders, Dr Margaret Tobin, Dr Bronwen Harvey, Mr Gordon Gregory, Professor Helen Christensen, Mr Des Graham, Ms Dawn Smith, Mr Trevor Carlyon, Ms Barbara Hocking, Mr Jack Heath.

Helen Christensen PhD · Barbara M Hocking BSc (Hons), DipEd, Dip H Eed, GAICD · Dawn Smith MBA

Only when spirometry is performed in a uniform way can we expect its widespread use in primary care Spirometry appears to be an undervalued investigation in general practice, despite its capacity to inform clinicians about diagnosis, severity assessment, and optimal treatment for airways disease. The omission of spirometry from a thorough assessment of patients with breathlessness seems just as inappropriate as failing to measure the blood sugar level in a patient with thirst, polyuria and blurred vision. There are substantial individual and community risks in not performing a simple diagnostic test such as spirometry. In Australia, underdiagnosis of chronic obstructive pulmonary disease (COPD) and asthma is a documented consequence of this.1,2 Yet, anecdotal reports from general practitioners suggest that it is difficult to incorporate spirometry into the consultation, and there have been variable outcomes after systematic efforts to teach optimal performance of the test.3,4 There are many reasons for this, including the complexity of properly performing the test, the cost of equipment, the time taken to perform bronchodilator reversibility testing, and controversy regarding interpretation of results. Although Australian guidelines for the diagnosis and management of asthma and COPD5,6 clearly define the central role of spirometry in making a diagnosis and assessing severity, the practical implementation of the test remains a challenge. Bronchodilator reversibility testing should inform the clinician about the presence and severity of airway obstruction and its reversibility in response to a standard dose of bronchodilator. Once this information is reported, the clinician can determine — in combination with the other information available — whether asthma or COPD is likely. There is considerable overlap in the bronchodilator responsiveness of these two diseases, so that spirometry may not be diagnostic. However, the consistent performance and interpretation of any test is essential to maximise its value, allow comparison of results and to ensure its sensitivity and specificity are maintained. In this issue of the Journal (page 610), Borg et al report the results of a survey of 60 lung-function laboratories in Australia and New Zealand, and highlight marked differences between laboratories in performance and interpretation of bronchodilator reversibility testing.7 These variations, in a setting where rigorous quality assurance and standardisation would be expected, indicate that substantial work is needed to bring uniformity to spirometry and establish commonly agreed criteria for assessing reversibility of airway obstruction. Do such criteria exist? There are international guidelines for the performance and interpretation of lung-function tests,8,9 and respiratory laboratories would generally aim to achieve these standards, although they may be more difficult to attain in primary care. Recommendations for assessing reversibility are given in a Thoracic Society of Australia and New Zealand (TSANZ) position paper.10 These are similar to the American Thoracic Society (ATS) standards, which indicate that a 12% increase in forced expiratory volume in 1 second (FEV1) over baseline and a minimum 200 mL improvement in FEV1 or forced vital capacity (FVC) constitute a positive response to bronchodilator. However, the TSANZ guidelines lack detail, particularly with regard to the type, dose and timing of bronchodilator administration, the factors that varied most between laboratories. By contrast, the ATS guidelines indicate that bronchodilator reversibility should be assessed by use of a short-acting β2-agonist, equivalent to 200 μg salbutamol or 500 μg terbutaline by a metered-dose inhaler. Although laboratories may choose to enhance the sensitivity of the test and optimise delivery of β-agonist by using spacers, it does not appear appropriate to administer high doses of combination bronchodilators by nebuliser for conventional reversibility testing.11 It is also outside current ATS guidelines for standardisation of reversibility testing. Is this variability between respiratory function laboratories of concern, and what are the implications? Firstly, comparisons between results from different laboratories should not be made with the assumption that the test has been performed under identical conditions. Secondly, it is essential for clinicians referring patients to respiratory laboratories to know the local features of spirometry testing to be able to interpret the results appropriately. Thirdly, it would be most desirable, and many would argue essential, for Australian laboratories to agree to a set of standards and apply them universally for spirometry and reversibility testing. Fourthly, implementing spirometry testing in primary care and educating and up-skilling GPs is unlikely to succeed without an agreed position on acceptable standards for performance and interpretation. Among respiratory scientists and thoracic physicians, there is a range of views on the feasibility of implementing more widespread use of spirometry in primary care. Although it is a highly desirable goal, expressly supported by the peak bodies in asthma and COPD care, there are major challenges. Many argue that accurate performance and interpretation of bronchodilator reversibility testing is difficult and that GPs should be offered a range of options, which should include greater access to laboratories and pathology services for spirometry. There is a plethora of articles which provide background information to assist in implementing quality control procedures to standardise equipment and test performance, and provide reference values and guidelines for interpretation of results. Despite these specifics, the ATS guidelines frankly acknowledge “There is no clear consensus on what constitutes reversibility in subjects with airflow obstruction”. Nevertheless, agreement should be reached regarding the way in which a standard test is performed, even if reaching agreement on its interpretation is difficult. The article by Borg et al highlights the urgent need for agreed standards in Australia for spirometry. The TSANZ and the Australian and New Zealand Society of Respiratory Scientists are in the best position to take up this urgent task. Transferring this expertise into community practice, either in specialist or in primary care, remains a challenge that must be met if we are to maximise the possibilities for diagnosing and managing airways disease.12 One of the perceived hurdles to this process is the Medicare Benefits Schedule descriptor for office spirometry (Item 11506), which specifies that the test should be done before and after administration of bronchodilator to attract payment. The TSANZ and the Royal Australian College of General Practitioners have prepared a submission to have this descriptor changed to allow payment for testing before or after administration of bronchodilator. The availability of a wide range of affordable, electronic spirometers with built-in software for determining reference values, along with a “Buyers guide to spirometry”, currently being written, will add to the educational resources needed to help GPs in their use of spirometry for assessing patients with breathlessness. Standardised guidelines should greatly assist the implementation of spirometry in primary care and result in more appropriate treatment and better outcomes for patients.

Christine Jenkins MB BS, MD, FRACP · Iven Young MB BS, PhD, FRACP

Health policy decisions are based on more than evidence Benjamin Franklin’s 18th-century slice of wisdom that “In this world nothing can be said to be certain except death and taxes” still rings true today. But, in these modern times, adding “and rising health costs” would not be inappropriate. The inexorable increase in public spending on healthcare is a political issue for much of the developed world, and Australia is no exception. Our healthcare expenditure rose from 7.5% of GDP in 1989 to 8.5% in 1999, and it shows no sign of abating.1 Indeed, the federal treasurer recently observed that “When we look across the next forty years we find that the largest area of pressure in relation to Government spending is going to be in the health area.”2 So what are we to do? Commenting on a North American view of the United Kingdom’s National Health Service,3 the President of the Royal College of Physicians recently wrote: To contain the costs of growing needs and expectations for health and care services, there is an increasing emphasis on the clinical and cost effectiveness of health care, with evaluation of procedures and technologies, targeting of resources to services and interventions of proven effectiveness . . .4 This endorsement of evaluation of evidence, effectiveness and efficacy is the stuff of which evidence-based medicine (EBM) is made, and must be a godsend for governments, health ministers and their public servants. For, as noted by a UK social scientist, “EBM offers the vision . . . of solving all health care funding problems by eliminating unnecessary and unproven health care.”5 In short, stringent evidence is required if the public purse is to pay for new drugs, medical technology or other interventions. Policing bodies exist to effect this policy. For decisions regarding government funding support in Australia, the Federal Minister for Health seeks the advice of the Pharmaceutical Benefits Advisory Committee (PBAC) for new drugs and the Medical Services Advisory Committee (MSAC) for emerging medical technologies or procedures. How do these committees arrive at their advice? What are their modi operandi and tensions? Answers to these questions have not been readily forthcoming, as these bodies work behind closed doors, the details of their deliberations are confidential, and participants are bound by a code of silence. In this issue of the Journal (page 627), the door of a bureaucratic conclave is opened slightly as Ware and his colleagues examine the government’s deliberations regarding public funding of positron emission tomography (PET) services.6 Much of their information was obtained through freedom of information requests and, despite its inherent limitations, their account was of sufficient interest to the Journal for us to pursue the long road to publication. Each story has two sides and we also sought the views of the Australian Government Department of Health and Ageing (page 633).7 The “exposé” by Ware and colleagues raises issues about the political pressures that come to bear on potential “big ticket” medical technology roll-outs, the processes involved in technology assessment and the values attending this exercise. As certain as death and taxes is that new technology spawned by research and commercial concerns will increase pressure on the already runaway cost of healthcare. PET is one such technology. It is the latest in a stream of imaging modalities, following computed tomography and magnetic resonance imaging. PET capitalises on the differential metabolism of glucose by malignant cells and is of significant clinical utility in cancer diagnosis and staging, and for following the effects of treatment. But it is expensive, and not readily seen as cost-effective if judged exclusively through standard outcomes such as survival or mortality. PET fell victim to the health bureaucracy doctrine that new technology should not be comprehensively funded by the public purse in the absence of high levels of evidence of both clinical and cost effectiveness. Supposedly because of this, and much to the disappointment of Ware and colleagues, the current Commonwealth government funding arrangements for PET limit the number and location of publicly funded PET services8 and the clinical indications for its use.9 Ware’s qualms about MSAC’s deliberations raise questions about the hype of EBM in health policy. Nobody would disagree with the then Health Minister’s ideal that with the establishment of MSAC “the gap between research knowledge and clinical practice will narrow and patients will benefit earlier from the most advanced procedures drawing on the best scientific medical evidence”10 — in short, EBM. But it appears that the rhetoric surrounding EBM has led to a misunderstanding of policymaking. Indeed, the certainty value of EBM in this setting is more fanciful than real, as other considerations are involved.5,11 These include: competing goals other than clinical effectiveness (social, financial and political); beliefs that some of the research is irrelevant to circumstances in which assessments are taking place; lack of consensus in understanding, interpretation and applicability of the research; other types of competing evidence (personal experience, local information, eminent opinions and evidence provided by advocacy groups); a social or political environment that is not conducive to policy change; and scientific information being poorly presented to the policymakers. Ware et al’s critique of MSAC’s deliberations is not unique. Similar concerns have been raised about Britain’s National Institute of Clinical Excellence in its regulatory role for the introduction of new technology, interventions and pharmaceuticals in the NHS.12 Finally, the experience of Ware et al in extracting information through freedom of information provisions raises the issue of transparency and accountability of health-policy formulation. Most Australians would accept that even healthcare resources are finite. Most would expect our governments to make the tough decisions about how public funds are spent, however unpalatable the decisions may be to sections of the community. But the public is not impressed by the secret milieu in which this occurs. It leads to mistrust and suspicion. Professional disquiet can also arise when expert opinions proferred in committees are not reflected in the final outcome. Onora O’Neill, in the 2002 BBC Reith Lectures, counselled that, to confront society’s burgeoning culture of suspicion, “We need genuine rights, genuine accountability, genuine efforts to reduce deception and genuine communication”.13 More transparency in decision-making that affects the public is not unreasonable. Meanwhile, for the foreseeable future, rising healthcare costs will remain one of life’s certainties. Evidence-based medicine alone will not contain this.

Martin B Van Der Weyden MD, FRACP, FRCPA · Ruth M Armstrong BMed

Although the risk from medical radiation is small, we should not become complacent Ionising radiation is one of the most extensively researched agents in our society. Indeed, more is known about its effects than the effects of most other things in our environment. High doses are known to be harmful, with the main long-term adverse effect being cancer induction. The best evidence for this comes from survivors of the atomic bomb explosions in Japan, where models have been developed relating increased cancer induction to the dose of radiation received. Although the magnitude of the effect is small, the link is well established. When people are exposed to radiation, its use must be justified by ensuring that it does more good than harm. Diagnostic x-rays are the largest man-made source of exposure of the general population to radiation. Even if the risk from radiation to an individual is very small, exposure of a large number of people over time could translate into a considerable number of cancer cases. A recent report in The Lancet attempts to quantify the risk of cancer induction from diagnostic x-ray procedures, averaged over the population.1 From surveys of medical radiation use in a number of countries, the authors obtained information on the average annual frequency of various x-ray procedures and estimated the doses to various organs from those procedures. They then applied a model of radiation-induced cancer cumulative risk to the doses received by the various organs to derive an estimate of the attributable risk of developing cancer. Their analysis suggests that in Australia about 431 cancers per year (1.3% of all cancers) could be attributable to diagnostic x-rays. The corresponding percentages for 14 other countries considered ranged from 0.6% in the United Kingdom and Poland to 3.2% in Japan. Their study does not provide any new evidence that radiation from diagnostic medical procedures causes cancer. Rather, the researchers rigorously applied an existing model to medical diagnostic radiation exposure of the population to derive the best estimate to date of the magnitude of the risk of cancer induction. They acknowledge that there is considerable uncertainty attached to this estimate and that a number of assumptions had to be made in performing the analysis. There is uncertainty about the number and types of radiological procedures, the derivation from these data of doses to individual organs, and the applicability of the cancer induction model at the low doses used in diagnostic radiology. Nevertheless, it is probable that medical radiation procedures do lead to a small increase in cancer incidence in the population. The lowest dose of x-radiation for which there is epidemiological evidence of increased cancer risk is 10–50 mSv for an acute whole-body exposure.2 Some of the higher-dose diagnostic radiological procedures such as computed tomography (CT) produce effective doses at the lower end of this range.3 At lower radiation dose levels, in the absence of epidemiological evidence, there is some uncertainty as to whether there is any effect. However, a linear relationship between risk and dose with no threshold is commonly accepted and is supported by some laboratory data.2 Radiation protection agencies have adopted this linear-no-threshold hypothesis in their approach to risk management.4 The total population dose of radiation from medical diagnostic procedures is increasing worldwide, mainly due to the increase in CT scanning. CT entails the use of higher radiation doses than other common radiological procedures.3 In Australia, Medicare data indicate that CT use has increased 140% over the decade 1992–2002. The reason for the increased use of CT is that it is now able to provide much better and more valuable clinical information, and to do so more easily, than in the past. As the technology has improved, the image quality has improved and scanning times have been reduced to just a few seconds. CT can now image fine detail, even in mobile organs, and hence the indications for its use have expanded. It is easy to overlook the possible side effects of radiation, particularly if the risk is very low and the effect may not become apparent for years. Cancer may not develop until 20 to 30 years after radiation exposure, and so the group most at risk are people with a long life expectancy. Children are also more susceptible to the carcinogenic effects of radiation than adults. When people are exposed to radiation, its use must be justified by ensuring that it does more good than harm. If radiological investigations are done for a specific clinical problem, the potential benefit significantly outweighs the very small risk. However, if there is no valid clinical reason for a procedure, the risk is still present for no tangible benefit. One area in which risk is considered to outweigh benefit is whole-body CT screening of healthy asymptomatic people. The Royal Australian and New Zealand College of Radiologists has produced imaging guidelines on the appropriate use of diagnostic radiological procedures.5 The Australian Radiation Protection and Nuclear Safety Agency is in the process of drafting guidelines on radiation safety in medicine.6 Modern radiological equipment has the potential to reduce the radiation dose compared with older equipment. Radiologists also need to optimise their procedures to obtain the required diagnostic information using the lowest radiation dose.7 The Lancet article serves as a reminder that the potential dangers of radiation need to be respected.

Graeme J Dickie FRANZCR, FRACP, MBA · Robert S Fitchew MSc, MACPSEM, MAIP

Randomised trials suggest that ximelagatran is “non-inferior” to warfarin for preventing stroke in patients with non-valvular atrial fibrillation, but important questions remain Atrial fibrillation is a strong and independent risk factor for stroke because it predisposes to thrombus formation in the left atrial appendage, and subsequent embolism to the brain.1 Each year, at least 6000 cardioembolic ischaemic strokes occur among an estimated 150 000 Australians with atrial fibrillation,2,3 and these numbers are expected to rise substantially with the ageing of the Australian population and associated increase in the prevalence of atrial fibrillation. The only two treatments proven to reduce the risk of stroke among patients with atrial fibrillation are aspirin and adjusted-dose warfarin.4 However, both have limitations. Aspirin is only modestly effective, reducing the risk of stroke by about a fifth compared with placebo (absolute risk reduction [ARR], 1.7% per year; number of patients needed to treat for one year to prevent one stroke [NNT], 59). Warfarin reduces the risk of stroke by about two-thirds compared with placebo (ARR, 3.1% per year; NNT, 32) and by about a third compared with aspirin (ARR, 0.8% per year; NNT, 125), but causes at least twice as many intracranial and extracranial bleeds as aspirin, particularly in patients at increased risk of bleeding (eg, those aged over 75 years, those with a history of bleeding; see Box 1).4 Warfarin is also inconvenient to use because it has a narrow therapeutic index, interacts with numerous drugs and food, and requires close laboratory monitoring (Box 2).5 Consequently, only a third to a half of patients with atrial fibrillation who are appropriate candidates for warfarin therapy actually receive it.6 Reducing the intensity of warfarin therapy to an international normalised ratio (INR) of less than 2.0 lowers the risk of bleeding, but is associated with an increased incidence of ischaemic stroke and worse stroke outcomes compared with standard-intensity warfarin therapy (INR ≥ 2.0).7 Direct thrombin inhibitors are a new class of anticoagulant drugs that bind directly to thrombin and block its interaction with substrates, thus inhibiting fibrin formation, thrombin-mediated activation of coagulation, and thrombin-induced platelet aggregation. Hirudin is the only direct thrombin inhibitor currently available for use in Australia, but must be given parenterally and is approved only for the treatment of heparin-induced thrombocytopenia. Ximelagatran, a pro-drug of melagatran, is an orally administered direct thrombin inhibitor and the newest drug in this class. It is rapidly absorbed from the gut and converted to its active form, melagatran. Melagatran is not metabolised or bound to plasma proteins. It is cleared predominantly (about 80%) by the kidneys, and has a half-life of 4–5 hours, which means ximelagatran needs to be administered twice daily (Box 2). Two large phase III randomised trials have recently evaluated ximelagatran as a replacement for warfarin to prevent thrombotic complications in patients with non-valvular atrial fibrillation.8,9 The primary objective of the Stroke Prevention using the ORal direct Thrombin Inhibitor ximelagatran in patients with non-valvular atrial Fibrillation (SPORTIF) III and V trials was to determine whether ximelagatran given in a fixed dose of 36 mg twice daily without laboratory monitoring was non-inferior to adjusted-dose warfarin (INR, 2.0–3.0) for the prevention of stroke or systemic embolism in patients with non-valvular atrial fibrillation and at least one additional major risk factor for stroke. The prespecified criterion for non-inferiority required that the lower confidence interval for the difference in the rate of stroke or systemic embolism between ximelagatran and warfarin did not exceed the prespecified threshold of 2% per year.10 Establishment of non-inferiority would imply that ximelagatran has either equivalent or superior effectiveness to warfarin and would allow clinicians to select ximelagatran over warfarin for convenience or safety. The design of the two SPORTIF trials was identical, except that SPORTIF III (3407 patients) was conducted in Europe, Asia, Australia and New Zealand and treatment allocation was open label, while SPORTIF V (3922 patients) was conducted in North America and treatment allocation was double blinded. The pooled results of the SPORTIF III and V trials (which had mean follow-up periods of 17 or 20 months, respectively) showed no significant difference in the risk of stroke or systemic embolism between ximelagatran (2.5%) and warfarin (2.5%; Box 1). In both trials, findings for ximelagatran fulfilled the criterion for non-inferiority. However, the pooled results of the SPORTIF trials also showed that ximelagatran significantly reduced the risk of major bleeding compared with warfarin (2.5% for ximelagatran; 3.4% for warfarin; estimated annualised ARR, 0.6%; NNT for 1 year to avoid one major bleed, 167) and increased the risk of transiently elevated levels of liver alanine aminotransferase (ALT) enzymes (6.1% for ximelagatran; 0.8% for warfarin; absolute risk increase [ARI], 5.3%; number of patients needed to treat with ximelagatran to harm [NNH] with increased ALT, 19). Raised ALT levels typically occurred 2–6 months after initiation of ximelagatran therapy, but produced no symptoms, were transient (returning to baseline spontaneously or after cessation of treatment), and without sequelae in all cases reported in the SPORTIF trials. These results suggest the beginning of the end of warfarin, because ximelagatran is not only associated with less major bleeding than warfarin, but it also has a predictable pharmacokinetic profile (uninfluenced by the patient’s age, sex, weight, ethnicity or diet). Therefore, it is not necessary to monitor anticoagulation activity or adjust the dose of ximelagatran (except in patients with renal dysfunction, in whom a decrease in dose or longer dosing interval is likely to be required). Furthermore, ximelagatran has a wider therapeutic margin than warfarin, and a low potential for drug interactions (Box 2). Although the cost of ximelagatran is likely to be substantially higher than the cost of warfarin, it may prove to be more cost effective because of its lower risk of bleeding and superior convenience (eg, no laboratory monitoring). Yet, important questions remain. First, there was significant heterogeneity between the two SPORTIF trials (P = 0.02). In the SPORTIF III trial, random allocation to open-label ximelagatran was associated with an absolute reduction in stroke or systemic embolism of 0.7% per year compared with warfarin, whereas in the SPORTIF V trial allocation to double-blinded ximelagatran was associated with an absolute increase in stroke or systemic embolism of 0.4% per year compared with warfarin. The cause of this heterogeneity remains uncertain, but might, at least in part, be accounted for by diagnostic suspicion or reporting bias in the open-label SPORTIF III trial. Second, the 2% per year threshold that was chosen as the criterion for non-inferiority does not reliably exclude even a near doubling of risk of stroke or systemic embolism with ximelagatran compared with warfarin. Third, unexpected hepatic side-effects of ximelagatran are an important concern given their high incidence in the short-term (6%), the large population potentially eligible for ximelagatran, and the likely long-term exposures to ximelagatran (and possibility of other long-term adverse effects). Monitoring of liver function is likely to be required during the first 6 months of treatment, and additional long term outcome data are required. The SPORTIF data signal the emergence of ximelagatran as an effective, safe and more convenient long-term alternative to warfarin for preventing stroke in patients with non-valvular atrial fibrillation. Safety concerns and cost issues are likely to delay its approval and eventual uptake by clinicians in Australia. In the meantime a range of other new antithrombotic drugs are also being evaluated for this indication. Both idraparinux (a selective clotting factor Xa inhibitor administered by once-weekly subcutaneous injection) and the combination of aspirin and clopidogrel are being tested in clinical trials, and novel oral preparations of direct-thrombin inhibitor and factor Xa inhibitors are in clinical development. This is heartening news for patients with atrial fibrillation, their doctors, and also public health professionals and governments faced with a looming epidemic of morbidity caused by atrial fibrillation in the ageing Australian community. 1: Estimated benefits and risks of treating a typical cohort of 1000 patients with non-valvular atrial fibrillation with aspirin, adjusted-dose warfarin, or ximelagatran* Aspirin (v placebo) Warfarin (v placebo) Warfarin (v aspirin) Ximelagatran (v warfarin)† Stroke‡ ARR ↓ 17 NNT 59 ARR ↓ 31 NNT 32 ARR ↓ 8 NNT 125 ARR§ 0 NNT§ — Major extracranial bleeds¶ ARI ↑ 1 NNH 1000 ARI ↑ 3 NNH 333 ARI ↑ 2 NNH 500 ARR ↓ 6 NNT 167 ALT ≥ 3 times upper limit of normal — — — — — — ARI ↑ 53 NNH 19 ARR =absolute risk reduction. ARI = absolute risk increase. NNT = number of patients needed to treat for one year to prevent or avoid one event. NNH = number of patients needed to treat for one year to harm by causing one event. ALT = alanine aminotransferase. * Data for aspirin v placebo, warfarin v placebo, and warfarin v aspirin are adapted from Hart et al.4 † ARR and NNT in the SPORTIF trials were calculated by dividing the pooled event rate by the mean duration of follow-up in years (approximately 1.5 years). ‡ Includes haemorrhagic stroke. § Includes stroke and systemic embolism. ¶ Event rates are likely to be substantially higher outside clinical trial settings, in the elderly, and in those with major comorbid conditions. 2: Comparison of the pharmacology and costs of aspirin, adjusted-dose warfarin and ximelagatran to prevent stroke in patients with non-valvular atrial fibrillation Aspirin Warfarin Ximelagatran Route Oral Oral Oral Dose 150–325 mg Variable* 36 mg Frequency Once daily Once daily Twice daily Half-life 20 minutes 40 hours 4–5 hours Clearance Systemic Hepatic Renal† Laboratory monitoring Not required INR Liver function tests‡ Antidote No Yes — Vitamin K No Reversal of antithrombotic effect Platelet transfusion Vitamin K Fresh frozen plasma Prothrombinex Discontinue ximelagatran Maintain diuresis Haemodialysis Food interactions Nil Multiple Nil known Drug interactions Uncommon Multiple Nil known Major side-effects Gastrointestinal bleeding Bleeding Bleeding Abnormal liver function test results Precautions and contraindications Bleeding diathesis Peptic ulcer Allergy Bleeding diathesis Alcoholism Dementia Impaired liver function Bleeding diathesis Impaired renal function Impaired liver function Approximate costs $2 per month§ $10 per month§ Unknown¶ INR = international normalised ratio. * Dose adjusted according to the results of the INR. † Trials of ximelagatran in atrial fibrillation have been restricted to patients with a creatinine clearance rate of ≥ 30 mL/min. ‡ Monitoring of liver function is likely to be required for the first 6 months. § Pharmaceutical Benefits Scheme November 2003: aspirin, $6.13 for 112 100 mg enteric-coated tablets; warfarin, $8.40 for 50 5 mg tablets (does not include the cost of laboratory monitoring). ¶ Cost of ximelagatran is not known but is likely to be at least $100 per month for a private prescription.

John W Eikelboom MSc, FRACP, FRCPA · Graeme J Hankey MD, FRCP, FRACP

Announcing the Dr Ross Ingram Memorial Essay Competition (entry details below) Not so long ago, we at The Medical Journal of Australia realised that, when it came to Indigenous health, we were great at publicising the problems. Most of the articles we publish are observational studies confirming that, yes, in health, as well as in almost every other area, Indigenous Australians are worse off than other Australians and, indeed, Indigenous populations worldwide. Ross Ingram (16 Feb 1967 – 15 May 2003) Ross Ingram was an Indigenous doctor who died last year, aged 36, of cardiovascular disease. At the time of his sudden death he was working as a GP in the New South Wales rural town of Leeton. Ross grew up in the Leeton area, where he was educated at the local primary and high schools. In 1984 he was named Young Citizen of the Year for Leeton, and in 1985, while vice-captain of Leeton High School, he received a Rotary Citizenship Award. In 1987 he was awarded a National Aboriginal Islander Day Observance Committee (NAIDOC) Award for Aboriginal Youth of the Year. Ross was the first Indigenous person from NSW to be accepted into the University of Newcastle’s Medical School. He enrolled in 1986 and graduated in 1993, the first Wiradjuri person to become a doctor. Life and medicine took him to an internship and residency in Gosford, then general practice on the NSW central coast and in Tasmania, and finally back to practise in Wiradjuri Country (central western New South Wales). His death is the first among the small community of Indigenous doctors who have been graduating from Australian medical schools since 1984. A keen practitioner of softball, football and cricket, as well as medicine, Ross was proud of his achievements both as a man and an Indigenous man. He is remembered by a loving family, including his wife, Julie, three children and three stepchildren. We also realised that the Journal was missing an important “voice”, telling us the story of Indigenous health. Many of the people working in Indigenous healthcare do not publish in academic journals. Also, more than in some other sectors of the population, social, cultural, political and economic issues influence the health and wholeness of Indigenous people. Some of these factors cannot be explored in strict academic style. Essays, on the other hand, leave room for the writer to analyse and interpret, often from a personal perspective and possibly including some form of narrative — “telling a story”. With this in mind, we are delighted to announce the annual Dr Ross Ingram Memorial Essay Competition for the best essay relating to Indigenous health. The competition is open to any Indigenous person who is working, researching or training in a health-related field; we are looking for essays that present original and positive ideas aimed at promoting health gains and health equity for Australia’s Indigenous peoples. After all, real insights and solutions come from within, not from without. The essays should be no more than 2000 words long, and must be submitted by Monday, 10 January 2005. A panel, including external experts and MJA editorial staff, will judge finalist essays, and judges will be blinded to the identities of the authors. The judges’ decision will be final. The winning entry will be published in the 2005 Indigenous Health issue of the Journal (the second issue in May), and the author will receive $5000. Other essays of high merit may also be published. We asked the members of the Australian Indigenous Doctors’ Association (AIDA) to help us name the prize and they chose to name it after Dr Ross Ingram (see Box). Ross’s story of premature death from natural causes is not an unusual one. More than half the deaths in Indigenous men occur before they reach the age of 50, compared with 13% of deaths among non-Indigenous men. The members of AIDA chose Ross not just because he was the first known Indigenous doctor to die, but because his plight typified that of many of the people currently working in Indigenous health. The human reality of statistics like those mentioned above is that Indigenous Australians inhabit a world of sickness, death and tragedy. Many of the seeds of future ill health are present from before birth. To a greater extent than most of their non-Indigenous colleagues, Indigenous doctors risk becoming a part of the problem they are trying to treat. “As Indigenous doctors, the fraternity of medicine has always accepted us wholly, and without question, and yet we are very different from so many of our non-Indigenous colleagues. Many doctors, when they look into the eyes of an Indigenous child, get a glimpse of a world they never knew existed; when we look into the eyes of that child, we see ourselves, and are reminded of the toll taken by unending stress and anxiety, and cycles of grief. For Indigenous doctors, the loss of our dear brother Ross reminds us that the privilege we enjoy as doctors does not remove our responsibilities to our people.” — Louis Peachey, President, AIDA We are hoping that the Dr Ross Ingram Memorial Essay Competition will provide a forum for some of the stories and ideas of Indigenous people working in Indigenous healthcare. Ross Ingram will not be able to contribute in this way, but he is a silent reminder of both the problem and the struggle of those who are working to find a solution. We look forward to receiving your entries.

Ruth M Armstrong BMed · Martin B Van Der Weyden MD, FRACP, FRCPA

Consensus is yet to be reached on the optimal approach to screening Australians have a 1 in 21 lifetime risk of developing colorectal cancer.1 The incidence of the disease and mortality resulting from it can be reduced by population-based screening programs, as has been demonstrated in several large randomised controlled trials of faecal occult blood testing (FOBT).2 The Bowel Cancer Screening Pilot Program currently under way in Queensland, South Australia and Victoria is assessing the practical application of FOBT. While screening of asymptomatic, average-risk individuals for colorectal cancer is advocated by many authorities worldwide (including the National Health and Medical Research Council [NHMRC] in Australia1), uncertainty remains as to the screening test of choice. The numerous publications on the subject are indeed like jigsaw pieces waiting to be put together to reveal the complete picture. In addition to FOBT, the NHMRC-recommended screening options for asymptomatic, average-risk individuals include flexible sigmoidoscopy (FS), and it is timely to review its role here. Colonoscopic studies on asymptomatic people show that 60% of adenomas and cancers occur in the distal colon and are potentially detectable by sigmoidoscopy. Case–control studies have shown that sigmoidoscopy can reduce the risk of subsequent fatal distal colorectal cancer by up to 60%, translating to an approximate 30% reduction in overall colon cancer mortality.3 Direct evidence of the magnitude of benefit from randomised controlled trials that are currently under way is awaited. A 5-yearly screening interval is recommended, based on data from these ongoing studies (which suggest that benefit from sigmoidoscopy extends up to 10 years) and on studies of repeat colonoscopy (which show that significant neoplasia is very uncommon 5 years after polypectomy or a normal examination). What are the performance characteristics of FS? The procedure is typically done in an unsedated patient after administration of an enema and takes 5–10 minutes to perform. At our institution, generally eight procedures are done by one operator over 2 hours. The instrument is advanced as far as is tolerated with reasonable comfort (mean insertion depth, 60 cm; range, 30–110 cm4) with biopsy or removal of polyps performed at the time. The finding of any adenomatous polyp or other suspicious lesion prompts further evaluation with colonoscopy. Fifteen percent of such screenings result in referral for colonoscopy.5 However, some have suggested that diminutive adenomas may not require follow-up — a policy that might reduce colonoscopy referrals to 5% of screenings.6 FS is a safe procedure, with a reported colonic perforation rate of about 1 in 50 000.7 Outpatient colonoscopy, which includes therapeutic procedures, has a perforation rate of about 1 in 1000.8 Concerns are commonly raised about the potential miss rate of FS for lesions in the proximal colon beyond the reach of the instrument and of small lesions that are overlooked in the areas examined. Many heterogeneous studies have addressed the issues of missed proximal colonic lesions and of what distal colonic findings should trigger colonoscopic follow-up. The likelihood of a proximal advanced polyp (ie, one with pathological features that increase malignant potential, such as size or villous architecture) increases with a more advanced distal finding. In the absence of any distal adenoma, 2%–5% of asymptomatic people screened will have isolated proximal advanced lesions.9 Whether this is acceptable in the context of cancer screening may become clear from prospective studies. The fact that sigmoidoscopy may also miss lesions within the area of colon that is examined may have implications for the screening intervals used. It has been shown on repeat FS that polyps may be missed in up to 20% of cases,10 while with colonoscopy a 6% miss rate for adenomas larger than 1 cm has been reported.11 Schoen et al12 recently reported a 0.8% advanced adenoma or cancer rate (there were 6 cancers in 9317 repeat examinations) in patients having a repeat examination 3 years after an apparently normal examination; 80% of advanced lesions were in regions thought to have been adequately examined previously, indicating missed or newly evolved lesions. However, other studies have shown that after 5 years the rate of new findings is low enough to consider lengthening the screening interval.5 The technical aspects of FS are sufficiently clear to enable us to define what FS can and cannot do. From the point of view of screening, FS clearly cannot completely exclude the presence of colon cancer in all asymptomatic people. A distinction must be made between screening the general population and testing the individual seeking screening. For the former, obtaining the greatest mortality benefit safely and at an acceptable cost to the nation is the crux of the matter. Recently published data indicate that FS is a cost-effective screening strategy, although colonoscopy and annual FOBT avert a greater number of cancer deaths.13 The results of randomised controlled trials of screening FS and colonoscopy, currently being conducted, will allow us to make a more accurate comparison with the established data regarding FOBT. Participation rates in sigmoidoscopy screening (23% in initial screening and 54% in follow-up screening at our institution) are encouraging given the invasive nature of FS screening.4,5 The ability of Australian gastroenterologists to accommodate increased demand for colonoscopy, whether as a follow-up to FOBT or FS, remains to be seen. Pieces of the jigsaw continue to fall into place, although it is likely to be some years before a clearly superior screening modality is determined. The emergence of new technologies such as virtual colonoscopy14 and faecal genetic testing will continue to add to the available armamentarium.

Charlie H Viiala MB BS, FRACP · John K Olynyk MB BS, FRACP, MD

Although some vaccines new to the childhood schedule are not free, they are strongly recommended In September 2003, the National Health and Medical Research Council (NHMRC) approved the new Australian Standard Vaccination Schedule recommended by the Australian Technical Advisory Group on Immunisation (ATAGI) (Box). The schedule includes inactivated poliomyelitis vaccine (IPV), varicella vaccine and seven-valent pneumococcal conjugate vaccine (7vPCV) for infants and young children. Earlier, in late 2002, routine meningococcal C conjugate vaccine was approved and funded for children aged 12 months, together with a cross-sectional catch-up program for young people to the age of 19 years (media release, Senator Kay Patterson, 24 November 2002). For the first time since 1994 — when all vaccines recommended on the schedule were funded for children vaccinated by both private and public providers under the National Immunisation Strategy1 — the childhood schedule recommended by NHMRC contains vaccines (IPV, varicella and 7vPCV) not available free of charge to parents. As well as adding these four vaccines to the childhood program, the NHMRC also approved changes to the pertussis vaccination schedule. Since the diphtheria–tetanus vaccine was replaced by a combined diphtheria–tetanus–acellular pertussis (DTPa) vaccine at 4–5 years in 1995, the peak age of pertussis has progressively risen to 13–18 years.2 Based on recent evidence that three doses of DTPa in the first year of life provide good protection until the age of 6 years,3 it was decided to adjust the schedule so that the fifth dose is now given to adolescents at 15–17 years, using an adult-formulated vaccine (dTpa). This was done by removing the 18-month dose, thus making the 4-year dose the fourth dose. This is not expected to lower preschoolers’ protection from pertussis,4 but should help reduce the number of large local reactions seen when the dose was given at 18 months.5 Inactivated poliomyelitis vaccine was recommended because it does not cause the extremely rare (1 in 2.4 million doses) live-vaccine-associated paralytic polio. The United States has already changed to inactivated vaccine,6 and other countries are considering doing so. The change to this vaccine in Australia may take time, as it is many times more costly than the oral vaccine and has had limited availability. Although various combinations of IPV with diphtheria, tetanus, acellular pertussis, Haemophilus influenzae type b and hepatitis B vaccines are licensed in Australia,7 they are not yet available, as the companies producing them are uncertain of the potential market. In the interim, the Australian Government’s National Immunisation Program will continue to provide free oral live-attenuated poliomyelitis vaccine. In making recommendations about the inclusion of each new vaccine in the childhood vaccination schedule, ATAGI took into account a wide range of factors. These included: vaccine safety and efficacy; the preventable burden of the disease targeted by the vaccine; the ease with which the vaccine could be integrated into the existing schedule; any likely effects on herd immunity, reduction in antibiotic resistance or impact on disease epidemiology; and cost-effectiveness and equity issues. Some of the information used by ATAGI as the basis for its recommendations is contained in the The Australian immunisation handbook (8th edition), while the levels of evidence for the new recommendations are available on the Internet and on CD-ROM.7 NHMRC resolved that the benefits of these vaccines were sufficient for them to be included in the schedule, irrespective of the provision of public funding. These new vaccines are more costly than any previous additions to the vaccination schedule. In the private market, three doses of conjugated pneumococcal vaccine cost far more than $300, one dose of varicella vaccine more than $40 and combinations with IPV more than an extra $18 for the IPV component. At the government level, the total annual cost of adding IPV, varicella vaccine and 7vPCV to the schedule would be about $100 million, and would almost double the current cost of all other childhood vaccines. This is a large expenditure. The cost-effectiveness of these three vaccines in Australia is therefore important.8-10 Changing to IPV (at $14 per dose) is estimated to prevent one case of vaccine-associated paralytic polio every 2–3 years, a cost of $17 million per case averted.8 This must be considered in the context of the maintenance of public confidence in immunisation programs. For varicella vaccine (at $53 per dose), universal vaccination of infants could prevent 450 hospitalisations each year, at a cost of $21 000 per hospitalisation averted, and one death per year, at a cost of $10 million per death averted, over a 30-year period.9 This does not include the out-of-pocket costs to families of a child having varicella, which make vaccination cost-effective in the United States.11 Universal use of 7vPCV (at $90 per dose) could prevent two to three deaths, 13 cases of meningitis, 110 cases of invasive pneumococcal disease, 800 cases of pneumonia and 14 600 cases of otitis media which would otherwise occur annually in each birth cohort of about 240 000 non-Indigenous Australian children by their fifth birthday.10 The cost per death averted and the cost per life-year saved by 7vPCV is estimated to be $5 million and $230 000, respectively.10 This does not take into account the impact of universal 7vPCV on adult pneumococcal disease or pneumococcal antibiotic resistance, as documented in the United States.12 However, these economic data were only part of the many reasons that ATAGI and NHMRC recommended that all children receive these vaccines (see above). Parents should be strongly encouraged by their physicians to have their children vaccinated. Conjugated pneumococcal vaccine is funded for a small group of children with medical conditions placing them at high risk of disease, as well as for Aboriginal and Torres Strait Islander children.7 For some parents the NHMRC recommendation will be sufficient; for others further discussion of the vaccine costs and benefits will be needed. Detailed fact sheets to assist providers and parents are available on the website of the National Centre for Immunisation Research and Surveillance of Vaccine Preventable Diseases <www.ncirs.usyd.edu.au>. Until all recommended vaccines are available free at the point of service, there is a dilemma for the community and for policy makers. The objectives of high childhood vaccine coverage and of equity for children could be at stake. This will be a continuing issue over the next 5–10 years as more new vaccines become available. These include rotavirus vaccine, live attenuated intranasal influenza vaccine, and other live vaccines targeting viral respiratory pathogens. Until now, vaccines have had a very high cost–benefit ratio, often being cost-saving,13 in contrast to many other prophylactic and most curative treatments. We can no longer expect vaccines to be cost-saving, with the increasing cost of the large clinical trials now needed to measure impact on rare diseases and to exclude rare adverse effects. Nevertheless, despite the fall in cost–benefit ratio in absolute terms, the economic benefits of vaccines relative to pharmaceuticals will persist.13 We now need greater public awareness of the current and potential benefits of disease prevention from vaccines, leading to greater public advocacy. Maximal benefit from vaccines can only be obtained by ensuring their availability and use across all age-eligible members of the population. Australian standard vaccination schedule7

Margaret A Burgess MD, FRACP, FAFPHM · Peter B McIntyre FRACP, FAFPHM, PhD

Unravelling the uncertainties The antiphospholipid antibody syndrome is an autoimmune disease that commonly presents with either venous thromboembolism (VTE) (deep vein thrombosis, pulmonary embolism), arterial thrombosis (ischaemic stroke, coronary thrombosis, peripheral arterial occlusion) or unexplained fetal loss. A high index of suspicion for the diagnosis is raised in patients with unusual thrombosis, those without obvious risk factors, or those who experience recurrent events. The diagnosis is based on presentation with one of the above clinical criteria and detection in the laboratory of persistent antiphospholipid antibodies. Clinically relevant antiphospholipid antibodies are identified by either functional coagulation assays (lupus anticoagulant) or immunoassays (anticardiolipin antibody, β2-glycoprotein-1 antibody).1,2 When considering the diagnosis of the antiphospholipid antibody syndrome, it is important to perform both clotting and serological tests, as they are concurrently positive in 50% of unequivocal cases.3 The detection of a lupus anticoagulant and/or medium- to high-titre IgG antiphospholipid antibodies is associated with an approximately 10-fold increase in risk of VTE.4,5 Unlike the treatment for other autoimmune disorders, anticoagulation rather than immunosuppression is the mainstay of treatment.1-3 About 40 000 tests for thrombophilia are performed in Australia each year . . . Why are we performing these tests? Significantly elevated levels of antiphospholipid antibodies are detected in up to 20% of patients with VTE, compared with only 2% of healthy adults.6 This means that clinicians will be frequently asked to make decisions based on positive antibody test results. With about 40 000 tests for thrombophilia performed in Australia each year,7 the question arises as to the impact of testing for antiphospholipid antibodies in clinical practice. Why are we performing these tests? Up to now the reason has been twofold. Firstly, there is a perception that there is a high risk of recurrent thrombotic episodes, and even death, when anticoagulation treatment is stopped in people with antiphospholipid antibodies. Several retrospective studies have suggested that treatment with warfarin should be continued for at least 12 months, if not longer or lifelong, as up to 70% of patients will have recurrent events without ongoing treatment.8,9 For patients with arterial occlusion, particularly those without other atherosclerotic risk factors (eg, smoking, diabetes, hyperlipidaemia, hypertension), recurrence of thrombosis from significant levels of antiphospholipid antibodies would be catastrophic. For such patients, anticoagulation is usually continued. For patients with VTE and no obvious risk factors, testing of antibody levels may help to resolve the current uncertainty about the optimal duration of anticoagulation treatment and may even help to determine whether anticoagulation should be stopped at all. In a multicentre study, 412 patients were prospectively followed after a first episode of VTE: within 4 years after ceasing warfarin, 29% of patients with IgG anticardiolipin antibodies had experienced further events, compared with 14% without antibodies.6 However, maintaining people on long-term warfarin therapy carries the inevitable risk of serious haemorrhage (1.1 events/100 patient-years) and anticoagulant-related death (0.25 deaths/100 patient years).10 If we had further data on the optimal duration of anticoagulation treatment, we would be in a better position to discuss with patients the risk versus benefit of ongoing treatment. The second reason for determining the presence of antiphospholipid antibodies is that it assists in deciding the optimal intensity of anticoagulation treatment. There is evidence from retrospective case series that recurrence of thrombotic episodes can occur even with moderate-intensity warfarin therapy (target international normalised ratio [INR], 2.0–3.0) when compared with higher-intensity therapy (target INR, 3.0–4.5).8,9 However, this information comes from specialised expert clinics for high-risk patients, and to generalise the findings to a large number of VTE patients without better evidence is problematic. The cost of having a higher INR (3.0–4.4 rather than 2.0–2.9) is the doubling of the risk of any bleeding event.10 A recent prospective randomised controlled trial on the efficacy and safety of high-intensity warfarin treatment (target INR, 3.0–4.0) versus standard-intensity treatment (target INR, 2.0–3.0) in 114 patients with arterial thrombosis and VTE with antiphospholipid antibodies attempted to address this uncertainty.11 The results of the trial showed that there was no difference in the rates of recurrent thrombosis and bleeding between the two groups. Although the confidence intervals were wide because the number of events was small, the study does give some guidance regarding treatment decisions for the majority of patients with thrombosis and antiphospholipid antibodies. However, there are several caveats: Patients were included after already receiving warfarin for variable periods of time, and only a third of patients were allocated to one of the trial groups within 6 months of thromboembolism. This means that patients who were at highest risk of recurrence or bleeding while on warfarin were excluded; Patients who already had recurrent thrombosis while receiving warfarin with a target INR > 2.0 were specifically excluded; Control of INR range was supervised by expert clinic staff, who kept INRs within range 70% of the time for the standard-intensity arm and 40% of the time for the high-intensity arm. Most of the patients out of the INR target range in the high-intensity group were below the therapeutic range. Whether this degree of control for a given target INR is achieved in everyday practice is uncertain and needs further validation. It highlights the difficulty of maintaining a narrow therapeutic target INR range with warfarin despite the best intentions. Given the limitations of the published studies, the clinician is still faced with uncertainty in dealing with patients with thrombosis and antiphospholipid antibodies. For most people with thrombosis and antiphospholipid antibodies, long-term standard-intensity warfarin with a target range INR 2.0–3.0 may be appropriate. However, there will still be patients with extensive or unusual thrombosis for whom higher-intensity anticoagulation treatment could be considered. This situation applies particularly to people in whom recurrence may be threatening to life, limb or organ, particularly when no other recognised risk factor for either VTE or atherothrombosis can be removed or modified. To reliably answer the question of how to manage patients with thrombosis and a significant level of antiphospholipid antibodies would require an inception cohort study, with patients randomised at diagnosis to different intensities of anticoagulation treatment.

Ross I Baker MB BS, FRACP, FRCPA

Graded physical exercise is no panacea, but is beneficial Much remains unknown about the enigmatic clinical disorder chronic fatigue syndrome (CFS). Apart from clear evidence implicating certain infections as a trigger, and reproducible evidence of increased rates of comorbid depression, the aetiology remains obscure.1 Similarly, despite numerous tantalising hypotheses of pathogenesis, including immunological, neuroendocrine and metabolic disturbances, all remain unproven.1 On the positive side, the criteria for diagnosis are well accepted internationally,2 and have been the subject of recent refinements to improve reliability.3 The disorder is well recognised, and about 0.5% of patients attending general practice are identified as having CFS.4 What, then, of treatment for a disorder with so many unknowns? About 40 controlled trials of treatment interventions for patients with CFS have been published to date.1,5 The most striking features of these studies are, firstly, that no curative treatment has been found, and secondly, there has been a remarkable lack of benefit demonstrated from any of the broad array of antiviral, immunological, hormonal, antidepressant and other treatments evaluated. The sole exception lies in the relief of symptoms and improvement in functional capacity provided by programs incorporating graded physical exercise. Several studies have incorporated physical exercise as a component of cognitive–behavioural therapy (CBT). The CBT approach in treatment for patients with CFS is based upon the premise that cognitive attributions and behavioural patterns act as perpetuating factors for symptoms. In particular, given that the cardinal phenomenon of fatigue in CFS is characterised by a marked and prolonged exacerbation of symptoms following minor physical activity, patients may reach the conclusion that it is best to avoid exercise. Thus, patients may develop an understandable cognitive attribution that exercise is harmful in the short term (as symptoms are worsened) and detrimental in the longer term. This leads to altered behaviour in the form of reduced physical activity with consequent deconditioning. Similarly, as sleep typically takes on a characteristic unrefreshing quality, and fatigue is dominant in the symptom complex, patients may consider that increased sleep holds promise for symptom relief and for rapid recovery. This attribution commonly leads to a behavioural pattern of phase-shifted sleep (late night to late morning) and frequent daytime naps. Accordingly, the CBT approach generally seeks to alter these cognitive attributions and modify the associated behavioural patterns. Having established CBT as a beneficial treatment approach, subsequent studies have sought to identify the “active” components of the CBT package. In this regard, graded physical exercise therapy has been found in several studies to be significantly better than comparators such as relaxation therapy, notably in reducing symptom severity and gaining improved function.6-8 In particular, Fulcher and White6 reported that 16 of the 29 patients who completed exercise treatment rated themselves as “much” or “very much” better, compared with eight of the 30 patients in the “flexibility” control group. Similarly, Powell et al7 found that 84% of a selected patient group had significantly improved functional capacity and reduced fatigue 12 months after graded exercise therapy when compared with standard medical care. The report by Wallman et al (page 444) adds to this evidence with a systematic and well-controlled evaluation of graded exercise versus relaxation over 12 weeks.9 Importantly, these authors have incorporated the notion of “pacing” into the exercise program. This concept recognises that individual patients with CFS differ significantly from each other in the amount of physical activity they can achieve before symptoms become exacerbated. In addition, this “threshold” beyond which symptoms worsen may vary over time. Hence, the graded exercise program allowed patients who experienced worsened symptoms to temporarily reduce exercise duration and then to resume once symptoms subsided. Their findings are noteworthy in that multiple parameters of exercise performance, such as resting systolic blood pressure and work capacity, were improved in the active group, indicating that the reconditioning component of the program was indeed effective. In addition, measures of mood and cognitive performance also showed improvement. Interestingly, the proportion of patients who rated themselves as significantly better was not different in the two groups. Unfortunately, no commonly used measure of disability (such as the SF-36)10 was included as a primary outcome measure, as would be typical in studies of chronic medical illness. In addition, the durability of the effects was not examined after the completion of the intervention. Finally, although “pacing” was an important component of the exercise intervention, this approach was not formally evaluated against “unpaced” exercise. Nevertheless, one can safely conclude from these studies that graded physical exercise should become a cornerstone of the management approach for patients with CFS. When applied astutely, including via “pacing”, it may not be realistic to anticipate cure, but it is realistic to expect that patients will feel better and will improve their functional capacity. In combination with appropriate interventions to improve sleep hygiene and to treat any comorbid mood disturbance,11 patients with CFS managed in this way often achieve a substantially better quality of life while awaiting recovery.

Andrew R Lloyd MB BS, MD, FRACP

In diagnosis and prognosis, we should avoid intuitive “guesstimates” and seek a validated numerical aid One of the axioms of clinical practice is that, in medicine, there are few, if any, certainties. When assessing the likelihood of a specific disease in a particular patient, or the chance of a future adverse event in a patient with known disease, clinicians are estimating probabilities or risk. These estimates derive from a clinical gestalt — the process of interpreting findings from history, examination and simple investigations (diagnosis), or of disease-specific correlates of complications or death (prognosis). Clinicians use these estimates of probability or risk to decide whether they should intervene immediately, particularly if effective treatments are available. Alternatively, if the disease likelihood is low, or treatments toxic or only marginally effective, these estimates are used to decide whether to defer treatment and either observe expectantly or conduct more sophisticated tests whose results may substantially alter pre-test likelihood estimates. If the estimate is too high, patients may incur unnecessary treatments or confirmatory investigations, or, if the estimate is too low, they may suffer the consequences of delayed intervention. Thus, a fair bit is riding on how accurately we can judge the likelihood of current or future disease. Available research suggests that, for various reasons, we are not that good at it.2-4 Common pitfalls include: framing a clinical problem in a way that may exaggerate risk; overweighting or underweighting certain clinical features; erroneously extrapolating past, vividly recalled cases to current patients; or manipulating risk subliminally to better fit with a preferred course of action (or inaction). Overall, most of us, not surprisingly, are risk averse and will commit to action to avoid personal regret at witnessing an unfavourable but possibly preventable event, even if our perception of risk of such an occurrence seems low.5 In this issue of the Journal, Attia and colleagues (page 449) evaluate the extent to which clinicians’ estimates of probability or risk for commonly encountered case scenarios vary from the “correct” estimate, and which clinician-related factors may influence such variation.6 They distributed three hypothetical case scenarios to groups of general practitioners and physicians in Australia and the United Kingdom, and compared respondents’ estimated probabilities of angina (in a patient with chest pain), deep vein thrombosis (DVT) (in a patient with a swollen leg), and future stroke (in a patient with chronic atrial fibrillation) with the “correct” estimates derived from statistically validated clinical-decision rules. Two cautions come to mind: were the clinicians given sufficient information on which to base a reasoned judgement (keeping in mind that they could not examine the patients); and how accurate was the rule-based estimate as the reference standard? One could argue that, in the chest-pain scenario, few experienced clinicians would be comfortable estimating the likelihood of angina simply on being told of a 65-year-old man presenting with exertional chest pain, without more detail about the character of the pain, the existence of coronary risk factors, and any signs of vascular disease seen on physical examination. The decision rule applied to the same case is also suspect, as it includes, for example, rapid relief with nitrogylcerine as being positively predictive of angina, which recent evidence would challenge.7 In the other two scenarios, the clinical details provided were more complete, and the decision rules more robust. Another concern is that the “correct” estimate was stated as a single percentage, which clinicians were expected, perhaps unfairly, to closely approximate. This ignored the fact that, in developing the rule, the “correct” estimate is actually a mean within a range of observed frequencies, all of which would probably lead to the same clinical action. On the positive side, the strengths of the study were its large, representative samples of clinicians, use of three different scenarios, and use of logistic regression to identify clinician-specific predictors of accuracy. Setting aside methodological limitations, how did the respondents fare? Only slightly more than half of the whole group were within 20 percentage points of the “correct” probability estimate for the angina and stroke scenarios, and less than one in 10 achieved a similar result with the DVT scenario. In keeping with my earlier comments, most respondents overestimated rather than underestimated the risk, with estimates spread over a huge range, from 10% to 100% at least, for all cases. There was a notable lack of association between accuracy and experience as measured by age, years of practice, or field of specialty, with GPs performing as well as physicians. Unfortunately, the study by Attia et al did not have the power to determine whether graduating from a medical course that used problem-based learning — with emphasis on evidence appraisal — predisposed to better performance. The implications of this study and others are several. First, all clinicians, irrespective of experience, appear to have problems quantifying probability or risk of disease, and, while there may be exceptions, this difficulty is independent of the clinical circumstances. Consequently, we should avoid intuitive “guesstimates” and seek instead a validated decision-rule, scoring scheme or other numerical aid that gets us closer to the mark. Fortunately, an increasing number of such tools are becoming available8 and in a form compatible with hand-held computers. Second, if we are to choose the best rules and use them appropriately, we need to understand how such rules should be constructed and tested.9 Third, we may need to “unlearn” some of our cherished clinical “rules of thumb” if evidence arises that questions their validity.10 Finally, we should advocate for more research into decision aids that will help us to more accurately estimate and communicate likelihood of disease in individual patients. The results of such efforts should facilitate a more rational use of investigations and treatments and lead to better patient outcomes.

Ian A Scott FRACP, MHA, MEd

We need a deep and broad international debate to begin The BMJ and a range of partners, including other journals published by the BMJ Publishing Group, The Lancet, the Canadian Medical Association Journal, the Dutch Journal of Medicine, the Medical Journal of Australia, the Croatian Medical Journal, the Academy of Medical Sciences, and many others, have initiated a project to bring people together to debate whether the existing structure of academic medicine is still fundamentally sound and, if not, to propose alternatives to it.1 I have taken on the challenge of coordinating this project, and I extend an invitation to readers all over the world to join me in this exciting enterprise. We are especially interested in the views of the “customers” of academic medicine — patients, politicians, the public, professionals. To achieve the project’s broad goals (Box 1) we begin from the position that “more of the same” is not enough. We need to be free to propose radical changes to the fundamental nature of academic medicine (is the balance between bench and applied research all wrong?); its name (should it become “academic healthcare” or should we drop “academic”?); its home base (are hospitals the wrong place to train doctors?); its relation to service (why are they so often far apart?); its methods of training and certification (should medical education be lecture based and far shorter?); and its responsibilities (should it be held accountable for inequities in healthcare at the global level?). Our approach will be inclusive and is designed to ensure a broad input of opinions. Rather than allowing the process to be taken over by a few experts with vested interests, we will build consensus by inviting an exhaustive range of global stakeholders to contribute their views. We are especially interested in the views of the “customers” of academic medicine — patients, politicians, the public, professionals. Anyone can contribute their views right now, today, as a rapid response to this article at bmj.com. In addition, our new project webpage is under development (www.bmj.com/academicmedicine), and this will contain regular campaign updates, news, and collected resources. The proposed structure is as follows. The pivotal group will be an international working party whose composition will include knowledge and competency across the dimensions of global health and basic to applied healthcare research, representing the range of constituents (medical students, postgraduates, junior faculty, established academics — especially women). Supported by four advisory groups (Box 2) and made up of about eight individuals, the working party will begin by answering four questions. Firstly, what are the roles of academic medicine? Secondly, how well is academic medicine carrying out these roles? Responses to the earlier BMJ editorial launching this initiative have already nominated a wide array of (but no clear consensus about) perceived failures, including failing to serve the public good, lack of a global perspective, an unnecessary dichotomy between education and research, various shortcomings in medical education, and inadequate numbers of and career paths for well-trained medical academics.2 Thirdly, why is academic medicine failing to fulfil its roles? Reasons might include inadequate leadership, a failure to translate basic discoveries into benefits for patients, inappropriate incentives to take up or maintain an academic career (especially among women), deficient mentoring for aspiring academics, lack of appreciation of the benefits of academic medicine by elected representatives, and poor integration with other health services. Many of the reasons will be economic — the salaries and resources needed for research and teaching make academic medicine currently unattractive — but we need to examine ethical and moral explanations as well. Finally, for each failure, what ought to be done about it? Given current economic constraints in countries with high and low income, special attention will go to strategies that call for no additional funding. We will, however, welcome strategies that call for the reallocation of current funding. At the policy level, we welcome strategies for how academic medicine can contribute to national and global health. These strategies will be combined and formulated into concrete proposals for action. We need your support and input. To nominate a member of the working party, join an advisory group, or register your experiences and views, send a rapid response to bmj.com or contact our project manager, Jocalyn Clark, at jclarkATbmj.com. 1: Goals of the project Development of strategy on the following issues: How should academic medicine look in the 21st century? How can we increase the impact of academic medicine on the rest of medicine and on health and healthcare? How should academic medicine be positioned internationally within medicine and also in the wider intellectual arena? How can recruitment to and job sati sfaction of those working in academic medicine be increased? 2: Four advisory groups Perspectives forum — patients, health professionals, government representatives, and medical unions. Ad hoc consultants — providing systematic reviews and other factual summaries about the efficacy of different educational, organisational, and administrative approaches, and trends in human resources in academic medicine. Communications consortium — disseminating surveys, drafts, and reports to everybody who is joined up to the campaign or may want to give input. International advisory panels — deans and chairs whose support could help establish funding, profile, and implementation; also used as an ongoing sounding board.

Peter Tugwell

Possible protection against cancer and improved immune function make supplementation with selenium attractive, but its toxicity and other unknown effects urge caution Selenium presents a nutritional conundrum because of its dual status as a highly toxic, but essential, trace element.1 The eightfold gap between the estimated average requirement2 and the upper limit of safe intake is relatively narrow, so questions of too much and too little are important. Additional key questions pertain to adequate versus optimal status, and reflect the shift in focus of nutrition from preventing deficiency towards promoting optimal health. As is the case for many micronutrients, the quest for protective effects of selenium (Se) intakes above requirements is rapidly gaining momentum. Ever since the biological role of Se in humans was first delineated less than 30 years ago, evidence for its increasing scope and importance to human health has been rapidly accumulating. Increasingly, Se depletion, as opposed to “deficiency”, is being associated with a range of health outcomes, including viral infection, reproduction, mood, thyroid function, cardiovascular disease, inflammatory conditions, immune function and cancer protection. 3,4 It is possible to advance a range of theoretical arguments that suboptimal Se status may have an effect on health, but evidence of a direct relationship to health outcomes is very limited. Se research is incipient and there is a paucity of data. For example, Se reference values that have been adopted in the United States2 are based on only two studies, one of which was a 1983 Chinese study of poor quality. Research is hampered by substantial difficulties in assessing and interpreting Se intakes and status, which become even more significant in the context of extreme global variations in the Se content of soil, food and human tissue.3,4 We do know that Se has key roles in redox regulation and antioxidant function, and hence in membrane integrity, energy metabolism and protection against DNA damage. 1,3,4 These and other functions are mediated through over 35 selenoproteins, which require adequate Se intake for synthesis and expression. Selenoproteins include several forms of the enzymes glutathione peroxidase (GPx), thioredoxin reductase and iodothyronine 5'-deiodinase. The number of known selenoproteins has almost trebled over the past 7 years,1,3 although the roles of several remain undefined. Plasma Se concentration is the most commonly used indicator of Se status.2 Low Se intakes, plasma Se concentrations and GPx activities have direct, linear associations up to a threshold plasma Se concentration (70–100 μg/L), beyond which GPx activity plateaus. This maximum GPx concentration is thought to represent repletion, and commensurate Se intake forms the basis of recommended dietary requirements.2,5 Concentrations of other selenoproteins are also influenced by Se intake and may have a role as functional indicators of Se status, 2,3,5 but assay methods and reference standards are at an early stage, and comparisons between studies are difficult. There is differential hierarchical expression of the selenoproteins, with relative preservation of the presumably more metabolically important at lower intakes of Se. 1,3 However, we do not clearly understand the health implications of submaximal expression of the selenoproteins. There are enormous geographical variations in the Se content of soil and food, and hence in Se intakes and concentrations in human blood and tissues.3,4,6 Thus, it is essential to use local data for monitoring and interpreting Se status.6 The 2000 US Recommended Dietary Allowance (RDA) is 55 μg/day.2 The 1987 Australian RDAs are 70 μg/day for women and 85 μg/day for men, but these are currently under review.7 Organic selenomethionine is the predominant form of Se in food. The most important dietary sources of Se are meat, poultry, fish and cereals (although brazil nuts are very high in Se and certain fish also have particularly high levels). Accurate assessment of intake is exceptionally difficult because the Se content of food is so variable. 2,3,6,8 Estimates of Se intakes include 106 μg/day in a large representative US sample,2 and a range of 29–70 μg/day in Europe.3 Extremely limited Australian data suggest intakes of around 90 μg/day,6 while more comprehensive New Zealand data show intakes as low as 28 μg/day, and indicate that conventional dietary intake methods are inadequate for estimating Se intake.8 Inorganic Se (selenite and selenate) is only available through supplementation, is generally less bioavailable and produces a different physiological response than organic forms of Se. 1,2 Environmental changes and agricultural practices may be reducing Se concentrations in soil.4 These factors, in conjunction with trade barriers (eg, the cessation of importing high-Se US wheat to the European Union), appear to be associated with a decline in the availability of Se through the food chain and in human Se status, particularly in Europe.3 Changes in food supply and habits, including the importation of Australian wheat, have improved the previously marginal Se status of New Zealanders.9 Twenty-six European studies since 1990 all reported mean plasma Se concentrations below 100 μg/L, the level postulated to be required for GPx saturation and cancer protection. 3,10 Ten of these studies reported plasma Se levels under 70 μg/L,3 postulated by others to be associated with GPx saturation.11 A representative US plasma Se level was 124 μg/L.2 In this issue of the Journal (page 383), Lyons and colleagues present evidence that although mean plasma Se concentrations of South Australians are relatively high by European standards, they may be declining, and over a third of their sample had levels below 100 μg/L.12 Overt human Se deficiency is rare. It is manifested as Keshan disease, an endemic fatal cardiomyopathy, which is virtually unknown outside areas of China, where the levels of Se in soil and dietary Se intake are extremely low. A few studies have reported Se deficiency as a result of long-term total parenteral nutrition.1 Despite myriad claims for potential relationships between a range of diseases and Se status, there are no clear population health outcomes that can be attributed to Se status in countries like New Zealand, where intakes are very low. 1,9 The evidence for an effect of Se on health outcomes is strongest in cancer prevention. Secondary findings from the 10-year US Nutritional Prevention of Cancer Trial demonstrated a protective effect of supplementation with 200 μg/day of organic Se (from yeast) on total cancer incidence and mortality, and on prostrate cancer incidence (relative risk, 0.75, 0.59, and 0.48, respectively).10 The effects were stronger in men and in those with lower baseline plasma Se levels (< 105 μg/L), and were not found for a range of other site-specific cancers. Of concern is that in the top tertile for baseline plasma Se level there may be an association between supplementation and increased risk of breast cancer and melanoma, as well as overall cancer incidence.10 There are numerous limitations to what was a small study, and the relatively high baseline plasma Se levels (114 μg/L) make it difficult to generalise the findings. It appears that protection from cancer may require supplementation beyond correction of depletion and maximal expression of the selenoproteins. Several large trials are under way to clarify the benefits and risks of Se supplementation with respect to tumorigenesis. More speculative and tantalising is the potential association between Se and immune function. Evidence suggests that reduced Se status may be associated with the incidence of clinical infection in adults,13 and supplementation of apparently Se-replete individuals potentially enhances immune function.3 Animal studies indicate that the Se status of the host can genetically alter invading viral pathogens, so that a normally benign strain may become virulent in an Se-deficient host.14 This is of interest given the emergence of new influenza virus strains from China, where there are significant areas of overt Se deficiency, and given the decline in Se status associated with progression of HIV infection.3 In summary, there has been an explosion of interest in the biological role of Se and the potential health implications of Se status. Much of the evidence in humans is descriptive, and the dearth of quality prospective trials means the links with many diseases are still controversial and, in many cases, speculative. There are very limited representative data on Se content of the food supply and Se status in many populous parts of the world, and no nationally representative Australian data. Lyons and colleagues provide the most comprehensive Australian plasma Se data to date,12 but they are neither prospective nor representative, and there may be variations according to states.6 Outcomes of research on Se in the next decade are likely to be important, and we urgently need more Australian data. Meanwhile, it is necessary to remember that selenium is toxic.1-3 Intakes below 400 μg/day are considered safe for almost all individuals.2 As illustrated by the Nutritional Prevention of Cancer Trial,10 outcomes of Se supplementation are variable and may not be without risk. Benefits and an appropriate dose for supplementation remain controversial. Until further evidence is available, supplementation should be recommended with caution, and overconsumption should be avoided.3

Lynne A Daniels PhD, APD

Can chemoprevention reduce the risk of progression to malignancy? Once a rare tumour, adenocarcinoma of the oesophagus has tripled in incidence in Australia over the past 20 years (Ian McDermid, Australian Institute of Health and Welfare, personal communication). This increase, together with the dismal 5-year survival of patients with this cancer, has focused attention on its risk factors. The strongest of these are symptomatic gastro-oesophageal reflux disease and Barrett’s oesophagus, a condition in which the squamous lining of the lower oesophagus is replaced by metaplastic columnar epithelium. Based on postmortem studies, Barrett’s oesophagus probably affects about 1% of the population in the United States and, at endoscopy, one in five to 10 patients with gastro-oesophageal reflux.1 Evidence of Barrett’s oesophagus (or at least intestinal metaplasia) is commonly found in resection specimens for oesophageal cancer.1 When Barrett’s oesophagus is found at endoscopy, the appropriateness of the patient entering a surveillance program may be considered, with the aim of reducing the risk of death from oesophageal adenocarcinoma. These programs involve regular endoscopy with multiple biopsies from the metaplastic epithelium and interpretation by a skilled pathologist. The rate at which malignancy develops in patients undergoing surveillance has been overestimated in the past because of publication bias; a reasonable estimate appears to be about 1 tumour in 200 patient-years of surveillance.2 The absolute lifetime risk of an individual with Barrett’s oesophagus developing oesophageal adenocarcinoma is probably about 1 in 20, which is comparable to the community risk for developing colorectal cancer. The average age for developing oesophageal adenocarcinoma is the mid to late 60s, but only a few patients with Barrett’s oesophagus die of oesophageal cancer, as comorbidities are common.3 Given these facts, and the problem of ensuring compliance with surveillance, it is not surprising that it has been difficult to demonstrate that surveillance programs reduce mortality, either overall or from oesophageal cancer. The only positive evidence that surveillance improves outcomes derives from the results of surgery on patients with surveillance-detected tumours. These patients generally fare better than those who are diagnosed after presenting with symptoms. Although individual patients may benefit from surveillance, the overall community benefit and cost-effectiveness of these programs is still debated (particularly for programs not conducted in well organised centres by enthusiasts with access to specialist pathologists).4 The use of biomarkers, such as aneuploidy or molecular markers, may help predict the risk of malignancy and may be useful in targeting surveillance programs.5 If surveillance of patients with Barrett’s oesophagus is unrewarding, are there ways to retard the neoplastic process? Recently, the pathobiology of Barrett’s oesophagus has come under intense scrutiny, and it is likely that repeated exposure of the lower oesophagus to reflux of acid and bile is a major factor resulting in metaplasia and subsequent dysplasia.6 Molecular changes in the pathway to malignancy have been identified, including upregulation of cyclo-oxygenase-2 (COX-2).7 The study reported by Hillman and colleagues in this issue of the Journal (page 387) examines the effect of acid suppression on the development of dysplasia in Barrett’s oesophagus.8 The authors analysed the pathology findings from a group of patients enrolled in a surveillance program over the period of time during which proton-pump inhibitors (PPIs) were introduced. The rates of development of dysplasia and malignancy were examined before and after patients started taking PPIs. Although the results must be interpreted in the light of the lack of randomisation, the time effects, and difficulties in distinguishing low-grade dysplasia from inflammatory atypia (problems which the authors recognised and corrected for as far as possible), the study does demonstrate an effect of acid suppression on the development of dysplasia and malignancy. Over 50% of patients (a somewhat high figure) developed low-grade dysplasia within 3 years while not taking PPIs, but this percentage was reduced by almost two-thirds in patients taking PPIs. Interestingly, the dysplasia-free survival curves diverged after only months, suggesting that the effect was rapid. If acid suppression were efficacious in reducing the risk of malignancy, it would be an attractive chemopreventive option, as: it is the cornerstone of therapy for gastro-oesophageal reflux disease, with which Barrett’s oesophagus is closely associated; powerful acid-suppressant drugs are available; and a reduction in gastric acid exposure leads to a concomitant reduction in bile exposure. Combining acid suppression with COX inhibitors (especially aspirin) has further attractions, as COX inhibition alone may reduce the incidence of oesophageal carcinoma by up to half,9 and some of its risks would be ameliorated by acid suppression. COX inhibitors may have an additional benefit on cardiovascular risk in this group of patients. Studies to investigate these issues are under way. So how will this information help us control oesophageal adenocarcinoma? In particular, if acid suppression does reduce the rate of progression of Barrett’s oesophagus to low-grade dysplasia, will this translate into a reduction in the incidence of oesophageal adenocarcinoma? The natural history of low-grade dysplasia is not well defined, while even that of high-grade dysplasia has been debated,10 with the estimated cumulative incidence of cancer varying dramatically between studies, from 56% at 3 years to only 9% at 5 years. The most efficacious method of preventing gastro-oesophageal reflux is good antireflux surgery, so, if control of acid and bile reflux alone were the answer, one might expect to see a dramatic reduction in the rate of oesophageal adenocarcinoma after fundoplication. Unfortunately, this has not been the case.11 One might also predict that the increasing use of proton-pump inhibitors in the past decade, and particularly in the past few years, would reduce the rate of oesophageal adenocarcinoma. However, this effect is not yet evident either in follow-up of patients prescribed omeprazole,12 or in national cancer monitoring (Ian McDermid, Australian Institute of Health and Welfare, personal communication). Even if chemoprevention using potent acid suppression, with or without COX inhibition, can be shown to slow development of malignancy, given the modest absolute risks (1 per 20 patients with Barrett’s oesophagus and perhaps 1 per 200 of those with gastro-oesophageal reflux), we must still identify and target appropriate groups for this or other interventions. We must also carefully examine strategies for efficacy and cost effectiveness. Low-risk strategies, such as chemoprevention, may be broadly applicable, whereas intensive strategies, such as endoscopic surveillance with examination of biopsy specimens for biomarkers of malignancy, will need to be targeted to high-risk groups.13 The jury is still out.

Geoffrey S Hebbard PhD, FRACP · Sanjay Nandurkar FRACP

Tips for teaching in tough times Patients, families, carers and our communities expect high-quality, safe, efficient, acceptable health services in which advice and interventions are based on evidence. The quality of undergraduate, postgraduate and continuing education is a key determinant of the capacity of clinicians to work with patients, administrators and other health professionals to fulfil such expectations. Successful teaching programs recognise and address the needs of students and teachers within particular educational settings. They use techniques that are likely to be effective, efficient and acceptable. This issue of the Journal features the beginning of a series called “Teaching on the run tips”. The first article, “Doctors as teachers”1 (page 415), outlines barriers to quality medical education and offers practical solutions. The title of the new series is particularly apt, as it highlights two causes of anguish among teachers: lack of time, because of expanding clinical and administrative workload, and lack of know-ledge of teaching techniques. Teachers’ anguish is increased by changes that have occurred within hospitals, such as reductions in junior-doctor working hours and shortened lengths of stay. These changes have resulted in fewer learning opportunities with inpatients and hence an even greater need for comprehensive and efficient teaching. To compound the problem, increasing specialisation means that a smaller pool of clinicians is both available and willing to teach across the breadth of clinical areas. Furthermore, clinician-teachers feel unsupported — a recent survey across US teaching hospitals reported that only a minority offer faculty development in teaching skills.2 Thirty years of research in medical education has provided some valuable insights.3 Much is now known about the attributes of effective clinical teachers,4 but knowledge of these advances is limited to a relatively small number of clinical teachers. The “Teaching on the run tips” series aims to improve dissemination of knowledge by providing practical tips on undergraduate and postgraduate clinical teaching. One barrier to the uptake of advice about teaching is the fact that some teachers are sceptical about the effectiveness of recommendations for changing teaching techniques. This is especially relevant for clinicians supporting evidence-based practice, who may seek the same standards for recommendations about teaching that they have learned to expect for recommendations about treatment and diagnosis. Unrealistic expectations for high “levels of evidence” may lead to disappointment, as there are fewer randomised trials and systematic reviews of educational interventions than there are of clinical interventions. Clinician teachers may also be concerned about the applicability of teaching recommendations derived from other settings to their own situation. The essential problem is that we have not yet developed “best practice” for assessing recommendations about teaching. The ultimate “outcomes” should be clinical and should reflect the needs of patients. These largely relate to the quality, safety, acceptability, appropriateness and accessibility of healthcare services. The problem is that such outcomes are all difficult to measure, and changes in them often reflect factors other than the uptake of teaching recommendations. Furthermore, the protracted time between uptake of educational initiatives and clinical outcomes makes it difficult to establish associations and causal relationships. Three developments might serve to reduce such scepticism. Firstly, in teaching, as in clinical areas, where outcomes prove too difficult to assess it may be possible to develop surrogate markers of process that reliably predict clinical outcomes of educational interventions. Secondly, pleas for more evidence in medical education5,6 are being heard. In recent years, several guides to “best evidence medical education” (BEME) have been published in Medical Teacher,7 BEME has become an established international collaboration of medical educationalists,8 research directions in medical education have been defined,3 and an educational section has been established in the BMJ.9 The third development offers great promise. The recognition of the limitations of randomised controlled trials in many educational areas10 is an incentive to switch the focus towards scientific evaluations of educational initiatives using studies specifically designed for this purpose. 11,12 Although “level-of-evidence” hierarchies are essential for assessing research quality, in themselves they are insufficient. They should be considered along with other dimensions of scientific quality, including the magnitude of the effect; applicability in different settings; and the extent to which bias, confounding and statistical error are minimised. Scientific rationality, educational reasonableness, resource implications and ethics13 should also be taken into account, and evidence across a range of research strategies must be sought.12 Good clinical teaching improves student performance.14 It clearly has the potential to improve clinical outcomes and to help satisfy the community’s expectations of a high-quality healthcare system. The recent recommendation for medical graduates in the United Kingdom to “understand the principles of education as they are applied to medicine”15 may help to enhance teaching skills in the United Kingdom and elsewhere. Along with other recently published resources for teachers, such as the BMJ’s “ABC of learning and teaching medicine” section, this MJA series is enthusiastically welcomed.

Peter B Greenberg MD, PhD, FRACP · Susan L Elliott MB BS, MD, FRACP

Adequate staffing and devices to impIement active strategies are the key Pressure ulcers significantly reduce the quality of life of patients and increase the costs of patient care, as well as length of hospital stay. The most notable feature of pressure ulcers is that most are preventable. Prevalence studies in Australian acute-care hospitals have found their prevalence to range from 4.5% to 27%.1 . . . The most notable feature of pressure ulcers is that most are preventable. Guidelines for preventing and treating pressure ulcers have been developed in many countries, beginning with the Netherlands2 and the United States.3 Guidelines specifically tailored to Australian healthcare were released in 2001 by the Australian Wound Management Association.4 A major limitation of all these guidelines is the level of evidence on which they are based. Using the evidence-grading system of the National Health and Medical Research Council,5 only one recommendation in the Australian guidelines achieved level 1 (evidence obtained from a systematic review of all relevant randomised controlled trials) — the recommendation that pressure-reducing or pressure-relieving mattresses or beds be used in place of standard hospital mattresses in high-risk patients. As is common with many guidelines for preventing pressure ulcers, much recommended practice is based only on consensus statements from experts in the field. In this issue of the Journal, Jolley and colleagues (page 324) report a randomised controlled trial of a newly developed pressure-reducing surface, the Australian Medical Sheepskin, compared with standard care in the prevention of pressure ulcers.6 The trial was in 441 hospital patients considered at low to moderate risk of developing pressure ulcers. Patients using the sheepskin developed new pressure ulcers at a rate half that of patients receiving standard care. Clearly, in this group of patients, the Australian Medical Sheepskin is better than standard care. However, it must be appreciated that standard care in this study was itself suboptimal. It consisted of “any other pressure-relieving device or prevention strategy deemed appropriate by ward nursing staff, comprising standard hospital mattress and sheet, with or without other low-technology constant pressure-relieving devices and repositioning as determined by nursing staff”. Standard care resulted in 16.6% of patients developing a pressure ulcer. The answer to reducing the prevalence of pressure ulcers lies not in implementing any one strategy, but in providing an institution-wide prevention program. Common to guidelines for preventing pressure ulcers is identification of patients at risk. It is imperative that some form of structured method to identify those at risk is applied to all hospital inpatients. Assessments need to be repeated regularly throughout a patient’s hospital stay and when there is a significant change in health status. A number of risk-assessment tools can be used, the most common being the Norton Risk Assessment Score,7 the Braden Scale8 and the Waterlow Risk Assessment card.9 The major risk factors for developing pressure ulcers are immobility, sensory loss, impaired cognitive state, urinary and faecal incontinence, age over 65 years, male sex, European background, chronic illness, poor nutritional status, impaired oxygen delivery to tissues, raised skin temperature, skin dryness and the presence of pressure, shear or friction forces. After establishing a patient’s risk of developing a pressure ulcer, the next step is to implement preventive strategies to reduce that risk. This requires the support of hospital administrations in providing both the necessary trained staff and pressure-reducing or pressure-relieving devices. It is also imperative that staffing levels are adequate to ensure that nurses have sufficient time to provide the “hands-on” care necessary for these high-risk patients. For patients at low to moderate risk of developing pressure ulcers, the ideal preventive strategy may include any one of a wide range of pressure-reducing or pressure-relieving surfaces, including the Australian Medical Sheepskin, combined with a repositioning strategy. The Australian Medical Sheepskin has yet to be compared with other surfaces and devices in this group of patients. A major challenge in many areas of medical practice is to successfully implement guidelines for clinical practice. A recent review of effective strategies for implementing pressure-ulcer guidelines concluded that active strategies were more successful in reducing ulcer prevalence.10 The most effective strategies used targeted educational sessions and, in particular, multiple approaches. Such a strategy was recently shown to reduce pressure-ulcer prevalence in a multicentre Australian study.11 This indicates that developing guidelines alone is not sufficient to influence outcomes, but that they need to be linked to educational strategies to ensure their successful implementation and subsequent influence on clinical outcomes.

Michael C Stacey DS, FRACS

Smokers who undergo surgery have higher risks and are a greater burden on healthcare resources. Is it acceptable to give them lower priority on surgical waiting lists? A wide range of elective surgical procedures should not be offered to smokers who do not try or do not succeed in quitting. There is no denying that this approach is controversial and overtly discriminatory, but it is also evidence-based. New concerns are not based on well-recognised cardiac and respiratory risks, but on increased risks of wound infection and the adverse complications that ensue. The extent of this evidence is such that it is no longer possible for surgeons and others in the healthcare system to ignore it. What, then, is the evidence? Wound infection rates are higher in smokers than in non-smokers who have had joint replacement surgery,1 breast reconstruction,2 “facelifts”, and a variety of other plastic surgery procedures.3 For example, with breast reconstruction, abdominal-wall site necrosis is seen in 7.9% of current smokers compared with 1% of non-smokers, and mastectomy-flap necrosis in 7.7% of smokers compared with 1.5% of non-smokers.2 Furthermore, after abdominoplasty, secondary surgery for dehiscence was necessary in 24% of smokers and 8.2% of non-smokers.4 In a randomised study examining smoking cessation intervention before joint replacement surgery, wound infection rates were reduced from 27% in continuing smokers to zero in those who quit smoking.1 Reduction rather than cessation in smoking is inadequate.1 Infection rates in parasacral incisions made to remove punch biopsy scars were reduced from 12% to 2% in those who abstained from smoking for 4 weeks, while, in the same study, wound ruptures occurred in 12% of smokers but in no non-smokers.5 The optimum period of smoking cessation is uncertain but it is probably at least 6 weeks. Periods of smoking cessation of less than 3 weeks before colorectal surgery are not associated with a benefit.6 The mechanism for the increased wound infection rate is not clear. Tobacco combustion produces more than 3000 products. Nicotine, the best known of these, is a potent vasoconstrictor and impairs revascularisation of bone.3 Reassuringly, nicotine replacement treatment, used to assist smoking cessation, does not increase infection rates in experimental incisions5 or after joint replacement surgery.1 Of the many other combustion products, carbon monoxide decreases tissue oxygenation and a range of other compounds impair the microcirculation. In surgical wounds, there is relative hypoxia in smokers to an extent that is known to impair wound healing in animals.7 Wound infections are never trivial, but in certain clinical situations they can have particular, deleterious sequelae. Immediate breast reconstruction may be desirable for some patients after mastectomy. An infected prosthesis, or necrosis of a flap or tissue donor site, can delay important adjuvant chemotherapy or radiotherapy. Wound infection after joint replacement surgery is associated with increased risk of infection in the prosthesis,8 delays in hospital discharge, increased time to effective rehabilitation and massively increased cost of hospital care. The extent to which doctors seek, and the wider community provides, permission for discrimination is an issue for serious community debate. An essential part of a surgeon’s role is to be selective in choosing who to operate on, and when, in line with current evidence. Policies and practices that flow from this may be regarded by the healthcare community as discriminating, but by smokers and the wider community as discriminatory. Continuing smokers must accept that some risks are simply unacceptable given the intent of the surgery. To put the smoking-related risk in context in orthopaedic surgery, the adverse effect of failing to quit smoking is similar to that of omitting antibiotic prophylaxis.9 The risk of adverse outcomes from wound infections alone is clear enough evidence to suggest that aesthetic plastic surgery should not be offered to current smokers, and that surgery should be delayed for 6 weeks after cessation. Doing otherwise would be simply foolish. Joint replacement surgery presents a different decision-making framework. Patients are likely to have had time to consider and address cessation of smoking. In relation to an individual, pain and limitation of mobility may be deemed sufficient to justify a procedure, despite an increased risk associated with continuing to smoke. However, public health systems are faced with overwhelming demand and must generate the greatest benefit from limited resources. If smokers, as a group, have a reversible factor that causes a longer hospital stay, incurs greater costs and leads to poorer outcomes, might it be reasonable to allocate them a lower priority? Given that the end of a joint replacement waiting list is likely never to be reached, allocating smokers a lower priority could be tantamount to an indefinite deferral of surgery for a smoker unable to quit. A recent Victorian study found that less than 10% of smokers having day-stay surgery recalled being advised by their surgeon or general practitioner to quit smoking.10 Clearly the medical community needs to do better. The message to the wider community is this: continued smoking in the face of elective surgery increases the risk to the individual and stretches the already stretched healthcare resources and expenditure unnecessarily. The community has to decide whether this waste is justified. Critically, if discriminatory policies are implemented, they must be matched by a commitment to fully and effectively support smokers in quitting, which is an altogether different challenge. This applies particularly to smokers who are already socioeconomically disadvantaged and those with mental illness. Failure to help these individuals risks exacerbating existing health and economic inequalities.

Matthew J Peters · Lucy C Morgan · Laurence Gluch

Practical contributions towards solving the medical workforce problems of rural Australia A viable practice is one that meets the particular medical needs of the community by providing appropriate services in a way that takes account of the financial and personal costs to both the practitioner and the community at large.1 Since 1978, there has been a plethora of inquiries, conferences and symposia on how best to recruit more rural doctors.2-6 These endeavours have resulted in a series of loosely articulated initiatives such as affirmative medical school entry for rural high school students, scholarships, decentralised medical education and other support mechanisms. It is envisaged that these initiatives will eventually ease the rural workforce shortage and diminish our reliance on overseas-trained locum doctors, many of whom are from underdeveloped countries with doctor shortages of their own. However, there is not much sense in recruiting and training rural doctors if the conditions under which they are expected to practise are not viable. In this context, two recent reports — Viable models of rural and remote practice and Easy entry, gracious exit — break new ground in defining the conditions necessary to build and ensure a viable rural medical practice.1,7 The reports are based on two separate studies. The larger study, the basis of the viable models report, was initiated and managed by the Rural Doctors Association of Australia, funded by the Australian Government Department of Health and Ageing and carried out under the guidance of the Bendigo branch of the Monash University School of Rural Health. The investigators used a rigorous, triangulated methodology, which included a national survey of all 4403 rural and remote general practitioners in Australia, focus groups and detailed site visits to a representative sample of 53 practices across Australia. There was a 34% response rate (1498 GPs), representing 53% of all practices. And what did the study find? Demographics: The major finding was the large proportion of ageing and overworked rural GPs, a matter of obvious concern to governments charged with providing healthcare for all people in Australia. Doctors over 50 years of age comprised 40% of the current workforce, and 61% of all rural doctors worked in areas with a shortage of GPs. A quarter of all doctors in the study were trained overseas, predominantly in the United Kingdom, Africa and Asia. Doctors in towns of 10 000–20 000 people need between two and three extra GPs, while those in towns of less than 10 000 people require an extra four to five GPs. Female doctors are now making an increasing contribution to the rural and remote workforce: they comprised 27% of the 1498 doctors responding to this study.8 Contrary to popular belief, they work the same number of hours as their male counterparts. This demographic picture has a fluid element, as a third of all rural and remote GPs intend to leave their current practice in the next 5 years. The proportion intending to leave ranged from 31% in the bigger towns to 66% in the more isolated communities. Capabilities: The ability to cope in depth with procedural presentations and emergencies, both in the consulting room and in the hospital, defines the rural and remote doctor. Over 50% of doctors working in population centres of between 5000 and 25 000 were involved in accident and emergency work outside of their surgery, 22% were doing obstetrics, 12% major surgery and 15% provided general anaesthesia. Work conditions: Rural and remote practitioners worked an average of 48 hours per week in patient-related activities and 8 hours in non-patient-related activities, mostly patient and practice administration. The weekly workload consisted of an average of 160 consultations per week, with a mean of 14 minutes per consultation. In addition, the practitioners were on-call one day and one weekend in three. Their vacation time averaged 24 days per year. Economics: A detailed economic and staffing analysis was performed for 91 of the participating practices. The average full-time rural doctor earned $266 000 per annum from all sources, including hospital work. Of this, 33% was consumed by staff costs and 19% by practice costs. The net taxable income was $127 680, which equates to $47.50 per hour net for a 56-hour week. Half of the GPs surveyed were practice principals and their yearly average profit was $201 000. From this, they paid for motor vehicles, medical indemnity, and continuing medical education. However, a quarter of all practice principals were financially unviable, with a net profit of less than $120 000 per year. Nearly all practices had a manager, and 72% had at least one practice nurse. In response to increasingly complex regulations and red tape, most managers had resorted to a reactive rather than a strategic approach to management. Dimensions of viability: Viable models of rural and remote practice identified a hierarchy of three core interrelated dimensions of viability that are amenable to systematic intervention. These are: A level of remuneration that reflects rural GPs’ skills, workload and commitment; A sufficient number of medical colleagues to limit after-hours workload to one night and one weekend in four, as well as adequately skilled locum support to enable annual recreation and study leave; and The physical facilities and administrative support to do their job. The habit of state governments of closing country hospital obstetric and anaesthetic facilities has been shown to be a major factor in procedural country doctors leaving their practice.9,10 Previously identified family, social and environmental factors were significant, but were found to be dependent on the above three dimensions and therefore less important in a doctor’s likelihood of remaining in rural practice.2-4 Benchmarks: These data have been used to derive benchmarks for models of viable practice. The authors of the report stress that these benchmarks are not a wish list, nor an ambit claim, and explain clearly how they have reached their conclusions. For example, income benchmarks of $110 per hour are derived from the median incomes of private GPs, government salaried GPs, rates for locum GPs, and the hourly rate paid to GPs engaged in divisional activities. Other benchmarks cover education, workforce numbers according to emergency and after-hours requirements, and various forms of leave. They also include purpose-built practice premises, a required number of support staff, and business systems which enhance practice management and include broadband internet access. The final chapter of the report illustrates the use of the viability framework in three different geographical locations. Easy entry, gracious exit complements the viable models report. It is a case study of an innovative model piloted in the towns of Brewarrina, Collarenebri, Lightning Ridge and Walgett in the far west of New South Wales.7 The unique feature of this model is a third-party provider as the owner and manager of the practice. This relieves doctors of the hassles of being a small-business owner, worried about a low return on infrastructure investment, and allows them to concentrate on practising medicine. In addition, this project is supported by the New South Wales Rural Doctors Network, which provides for safe working hours, regular holidays and promotes a guilt-free “walk-in, walk-out” approach by concentrating on continuity of the practice rather than continuity of the doctor. This model has proven to be an important factor in recruiting and retaining doctors. Both these reports make major conceptual and practical contributions towards solving the medical workforce problems of rural and remote Australia. They provide clear guidelines for health planners, consumers and medical stakeholder groups on what is required to give their particular geographical area the best chance of obtaining a viable and ongoing medical service.

Max Kamien MD, FRACP, FRACGP, FACRRM

National water-recycling guidelines will address both health and environmental risks Separating drinking water from sewage may seem obvious now, but the idea that sewage could affect health was not understood until the 19th century. Dr John Snow (1813–1858) was one of the first to make the connection when investigating a cholera outbreak in London. He noted that most of the people who were sick had consumed water from a pump in Broad Street, Soho, that was contaminated by sewage. When the pump’s handle was removed, the spread of cholera dramatically stopped. But it was not until the early 1900s that adequate separation of water supplies from sewage routes was achieved (at least in developed countries), resulting in substantially fewer cases of waterborne disease. . . . water is used for gardens, toilets and laundry, where water of lesser quality would suffice. In Australia, in 2004, we are 6 years into another drought, and water shortages and increasing climate variability are behind efforts to reduce water consumption and find other, sustainable ways of utilising all available water. While current efforts concentrate on reducing per-capita water use through more efficient appliances and water restrictions, other, longer-term strategies are also needed. These pressures are leading the community to consider alternative sources of water for some household uses. At present, potable-quality water is supplied for all household purposes. But more than 50% of this water is used for gardens, toilets and laundry, where water of lesser quality would suffice. The domestic use of alternative water sources — rainwater, stormwater, greywater and sewage — has the potential to expose large populations to pathogens and chemical contaminants unless the water is appropriately treated and managed. These treatments can be complex, and, to further confound the issue, permissible applications vary by jurisdiction. There are also many gaps in the regulations for urban domestic uses. Reports of health outcomes from reusing water predominately concern sewage reuse. These studies focus on the health of wastewater workers,1 farm workers and surrounding communities.2 Many of the studies are poorly designed and examine reuse of untreated sewage,3 which means they are of limited relevance to Australia. Because of the paucity of relevant studies on the health effects of other water sources, water quality is used as a proxy health-risk measure. Furthermore, much of the information on urban use of alternative water sources is in literature that is not readily accessible and often not peer reviewed. Thus, there is a pressing need for more rigorous scientific evidence to inform regulation. Rainwater collected from roofs is mixed with debris (eg, leaves and animal droppings) from the roof or from the guttering, and possibly contaminated by dead insects, trapped animals and leaf litter in the tank itself. Additionally, heavy metals from roofing materials, airborne pollutants from traffic emissions and industrial exhaust, or agricultural chemicals can contaminate rainwater supplies.4 It is widely accepted that rainwater can safely be used for bathing, laundering and watering the garden,5 and only in situations where a treated reticulated water supply is not available is it endorsed as a primary source of drinking water. Rainwater is generally considered safe to drink for most members of the community if it is clear, has low odour and taste, and the tank and roof are well maintained.5 Stormwater is rain that drains into the stormwater system from roofs, roads, footpaths and other ground surfaces and is channelled, untreated, directly to local waterways. The water carries rubbish, animal faeces, motor oil, petrol, tyre rubber, soil and debris. Use of this water has been limited to date, partly because of its seasonal variability in volume and the need for large-scale storages. However, in New South Wales, it has been proposed that stormwater from local residences be redirected to irrigate local sports fields, wetlands6 and parks.7 Greywater is sourced from kitchen, laundry and bathroom drains but excludes toilet water. Some guidelines exclude wastewater from the kitchen, as it can contain higher levels of wastes.8 Greywater may contain urine and faeces from nappy washing and showering, in addition to kitchen scraps, soil, hair, detergents, cleaning products and fats and oils. Greywater contaminants can include substances such as boron and phosphates, and the water is often alkaline and saline.9 Treated greywater may potentially be used for toilet flushing, laundering and subsurface garden watering. However, reusing greywater for gardens can detrimentally alter the properties of soil and gradually kill plants sensitive to phosphorus, including Australian native flora. Sewage is water entering the sewerage system. It has all the contaminants of greywater, in addition to high concentrations of faecal material. This water can be reclaimed after rigorous treatment at a sewage treatment plant and piped to individual households, as part of a dual-reticulated water-supply system (additional to and separate from normal tap water), for uses such as toilet flushing, garden watering and washing of cars and outdoor surfaces. It may also be used for irrigating sports fields and public parks, as well as for fire control, sewerage flushing, dust suppression, topping up of ornamental ponds or irrigating agricultural crops. A number of such systems are currently in place across Australia and are the focus of long-term assessment.10-14 Some new urban developments are planning to incorporate alternative water sources, such as reclaimed sewage water at Rouse Hill in Sydney,10 but there are questions about the potential impact on public health, particularly if long-term regulation and governance issues are not adequately addressed. With the exception of good-quality rainwater, all of the above water types are unsuitable for drinking. However, if they are supplied to thousands of individual households, incidents of accidental ingestion are bound to occur. In addition, errors in plumbing installation may result in the non-potable water being “cross-connected” to potable water taps. Regulatory oversight, awareness by health professionals of the potential for waterborne diseases, and continuing surveillance programs will be required to monitor and minimise these risks. Recognising the need for better guidance for regulators and water suppliers, the Environment Protection and Heritage Council and the Natural Resource Management Ministerial Council have initiated the development of national guidelines for water recycling. These guidelines are intended to provide a unified approach across Australia, and will address both health and environmental risks, and be developed in collaboration with the National Health and Medical Research Council. In keeping with recent revisions to the Australian Drinking Water Guidelines,15 a risk-management approach will be adopted, emphasising the multiple-barrier principle and ongoing monitoring of the effectiveness of systems to protect public health.

Teresa Z Mitakakis PhD, BSc(Hons) · Martha I Sinclair PhD, BSc(Hons) · Karin Leder MB BS(Hons), FRACP, MPH

RCT evidence for rehabilitation is strengthened by an observational cohort study The study by Sundararajan et al1 (page 268) is a novel data linkage study and is best described as a cohort study. The study showed 35% lower mortality in patients with cardiovascular disease who had undergone cardiac rehabilitation when compared with patients who had not undergone cardiac rehabilitation. However, even the best cohort studies can give only limited inference on treatment effects. For example, observational studies suggested that women who used hormone replacement therapy (HRT) had a lower incidence of cardiovascular events than did non-users.2 However, not only did prospective randomised controlled trials (RCTs) fail to confirm the protective effect of HRT,3 they suggested that such treatment might actually cause cardiovascular disease.4 The apparent impressive protection of HRT suggested by observational databases may have been accounted for by socioeconomic differences between the users and non-users of HRT. Thus, RCTs have assumed the strongest evidence in suggesting a relationship between treatment and outcome. So why does the database linkage study by Sundararajan et al1 appeal at all? Perhaps it is because the evidence base for cardiac rehabilitation programs fails to convince all medical practitioners, despite “level 1” evidence existing from other studies.5 Even the best RCTs have intrinsic limitations. The first is that most trials exclude older, sicker patients with multiple comorbidities and those who might not cooperate with the trial protocol. This often results in a clinical trial of low-risk patients, which may miss a beneficial effect of treatment. The second limitation of RCTs, more common in single-centre studies, is publication bias. It is hard work to prepare a study for publication — even harder for a negative study than for a positive one. As a result, investigators are less likely to submit negative studies and journal editors are less likely to accept them for publication. Publication bias is likely to exist in most, if not all, areas of published research. So, what are the limitations of the evidence specifically regarding cardiac rehabilitation? The Cochrane Library review of exercise-based rehabilitation for coronary heart disease reviewed 51 RCTs of 8440 patients.5 Total cardiac mortality was reduced by 31% (random effects model odds ratio [OR], 0.69; 95% CI, 0.51–0.94) and 26% (random effects model OR, 0.74; 95% CI, 0.57–0.96) in the exercise-only and comprehensive cardiac rehabilitation groups, respectively. Neither intervention had any effect on the occurrence of non-fatal myocardial infarction. In other words, exercise that did not affect cardiac risk factors was as effective in reducing cardiac mortality as a comprehensive program that included exercise and successfully reduced cardiac risk factors. The reasons for this are unclear given the level 1 evidence supporting the proven effects of lowering blood pressure6 or serum cholesterol7 in reducing cardiac mortality. Furthermore, one has to be currently active to experience the benefit of physical activity or fitness — loss of activity and fitness means loss of the protection of exercise. So, medical practitioners can have reasonable doubts about the protective effects of a 6- or 8-week cardiac rehabilitation program on cardiac mortality years after the event, despite the Cochrane evidence. And this is why the data linkage article by Sundararajan et al appeals.1 The clinical trial data in the Cochrane review were derived from selected patients who had undergone exercise training for periods varying from a few weeks to several years. Sundararajan et al show that Australian patients with coronary heart disease who had undergone cardiac rehabilitation for 6–8 weeks had a better survival rate than did patients not undergoing cardiac rehabilitation. Although the study may be fraught with problems similar to those described for the HRT studies, it is pleasing to note how similar is the magnitude of protection from death associated with cardiac rehabilitation in this Australian series compared with that described in the Cochrane review. This observational study lends strong support to the trial information. Patients surviving an acute coronary syndrome should be referred for cardiac rehabilitation, as the experience may save their life. There is another nugget in the article by Sundararajan et al.1 Patients with acute coronary syndromes not undergoing coronary artery bypass surgery are very much less likely to undergo cardiac rehabilitation than patients who have received surgery. Percutaneous cardiac intervention is now performed twice as often as cardiac surgery. Such patients are often younger and fitter and return to work and their usual life within days of their procedures. Alternative models of rehabilitation are required for these patients who have not been physically deconditioned. These were recently discussed in this journal by Scott et al.8 One such model is the COACH Program, which has been validated by two RCTs.9,10 The COACH Program is a training program for patients with coronary heart disease, in which a healthcare professional coach trains patients to aggressively pursue the target levels for their particular coronary risk factors while working in partnership with their own doctors. The COACH Program has been shown to have a favourable effect on many coronary risk factors, including total and low-density lipoprotein cholesterol, arterial blood pressure, dietary saturated fat intake, body weight, and the performance of regular walking.8,9 If patients do not attend cardiac rehabilitation, then alternative strategies for achieving secondary prevention are required. The COACH Program is one such effective method. In summary, the evidence supporting cardiac rehabilitation is less than convincing, particularly when the rehabilitation is confined to the period after an acute cardiac illness. The data linkage study by Sundararajan et al adds support to the Australian practice of convalescent-phase cardiac rehabilitation.

V Michael Jelinek MD, FRACP, FACC