Volume 188 Issue 12

Scientific evidence and the relationship between the medical profession, politics and the public are dynamic and inter-related In 1848, Rudolf Virchow asserted that “medicine is a social science, and politics nothing but medicine on a grand scale”.1 Regarded by many to be the father of modern pathology, Virchow saw clear responsibilities for doctors to engage with the broader social concerns that cause illness and harm. A century and a half later, human health faces threats ranging in scale from terrorism and climate change to the consequences of violence, substance misuse, poverty and environmental hazards that we deal with every day in our emergency departments and our clinics. On a handful of issues, such as smoking, health care professionals have been instrumental in changing public policy. But, with many ongoing social ills, is civic action a duty of modern clinicians? Following the September 11 terrorist attacks in the United States, the world’s leading medical journals expressed opposing views on this question. The editors of the New England Journal of Medicine implored doctors not to react directly to terrorism, but instead to treat injured patients, continue with medical research and ensure that the medical community is prepared for future terrorist attacks.2 In response, the Lancet’s Richard Horton argued that anyone working in the health professions is concerned with prevention as well as healing, that medicine cannot escape politics, and to reduce the burden of harm caused by violence, doctors must address how the political determines the clinical.3 Putting aside legitimate practical concerns — after all, few doctors think they have the time or skills to be effective political agents — the real question is whether or not we should nurture interest in addressing the health of communities among health care professionals, arming them with appropriate skills and promoting opportunities for engagement. If we examine the dual historical trajectories of scientific medicine and the place of professionals in society, we realise that this is not just a question of individual political or moral persuasion. Instead, it is one that depends on prevailing culture and circumstances of the time. In the 19th century, for example, doctors found professional distinction difficult to attain, largely because the scientific basis of medical practice was rudimentary and their treatments were often harmful. Public health activism was one way in which doctors could achieve status and authority. While not all doctors embraced it, public health was at least deemed to be complementary to the work of medicine.4 This changed rapidly early in the 20th century as scientific and clinical evidence evolved, and, in mastering this body of evidence, doctors became valuable to the public.5 Based on new understanding of bacteriology, germ theory and specific disease-based treatments, the biomedical model of disease triumphed. The new medical schools focused on diseases more than on people or populations, and on cures rather than on the social, behavioural and environmental forces that maintain health or produce disease. Unlike efforts to change social conditions, which were seen to be tainted by politics, advocacy and social diversity, the reductionism, objectivity and certainty of the biomedical model had great appeal. By the 1950s, the income, professional status and authority of doctors far exceeded that of public health professionals, and deep antipathies had evolved between them. In the most recent 50 years, this relationship has become less polarised, due especially to three scientific and sociological developments. The first was the birth of modern epidemiology and multivariate analysis. They demonstrated that most major illnesses were not random occurrences and that peoples’ overall health status was not only a consequence of the care they received. We now know that they are influenced by a range of social factors, including income and social status, social support networks, education and literacy, employment and working conditions, and social and physical environments.6,7 Second, business and government replaced the individual as the principal purchasers of health care, and have been increasingly interested in research that reveals disparities in health status, unequal access to treatment and variable quality of care. Managers and policymakers have challenged the view that entrenched health problems can be solved simply by more doctors, more medicines or faster discharge times. Third, fuelled by the repercussions of high-profile cases such as the Bristol Royal Infirmary8 and Bundaberg Hospital9 cases, cynicism grew about the medical profession’s ability to put aside its own interests and to self-regulate standards of performance. In light of such developments, it is no accident that doctors have been concerned with issues of professionalism. In February 2002, a transatlantic team of physicians published a Charter of Medical Professionalism, which was a bold restatement of the responsibilities of doctors as professionals — a sort of modern Hippocratic Oath.10,11 From July 2003, the American Council of Graduate Medical Education and the American Board of Medical Specialties required that all American medical and specialist training programs teach and assess “professionalism” as a core competency. The concept of professionalism rapidly gained traction, and the Charter provided a road map. It offered three fundamental principles: primacy of patient welfare, patient autonomy and social justice. The first two were uncontroversial. Social justice, however, with its implied responsibilities for public roles that redress social inequalities, was greeted with some ambivalence and much confusion, and needed clarification. With colleagues at Harvard I developed a conceptual and operational model based on our qualitative research with a range of professionals, academics, consumers and social commentators.12 Finding the label “social justice” generally unhelpful, we preferred the term “public roles”, which we defined as advocacy for and participation in improving the aspects of communities that affect the health of individual patients. We justified doctors’ public roles on the premise that doctors and the public expect discipline-based expertise to encompass all aspects of diagnosis, prevention and treatment; patients expect the medical profession to do what it can to promote their health; and doctors can be effective advocates for societal change through changes in legislation, advertising, public awareness and so on. We set reasonable limits on these obligations, based on the strength of evidence and the feasibility of doctor-promoted change. We identified three strategies for action by busy clinicians: community participation, individual political involvement, and collective advocacy through professional organisations. We made the case that individuals could choose activities — small or large — that suit their own situation and disposition. In the US the model generated considerable debate, became required reading for many medical training programs, and has been used in a variety of policy documents. In a survey of 1662 American doctors in six specialties, over 90% rated each of community participation, political involvement and collective advocacy as important roles, although fewer than half reported being involved in such activities in the previous 3 years.13 Dr John Furler and his team from the University of Melbourne Department of General Practice then explored the usefulness of the model for the Royal Australian College of General Practitioners’ policy on health inequalities. They conducted 80 interviews and two focus groups with a range of internal and external stakeholders.14 To some degree, Australian responses echoed the ambivalence to the concept of social justice observed in the US — public roles were supported when expressed within a familiar framework centred on care and compassion, but contested when expressed as matters of justice and fairness, particularly if any personal sacrifice was perceived. Their findings highlighted the tensions between the dual responsibilities of professional bodies to the public and to their members, and the importance of leadership from professional organisations in promoting public engagement. So what can we conclude? First, that both scientific evidence and the relationship between the medical profession, politics and the public are dynamic and inter-related. Second, most doctors now seem to accept that their expertise should include knowledge about social determinants of illness and access to care and that, even when they are not personally involved, it is important that the profession provides a responsible expert voice on such determinants in public debate. Third, public roles are most likely to gain traction among doctors when conceptualised as issues of care and compassion rather than as actions of justice and redistribution. Clinicians want their expertise put to good use in the public sphere in a way that complements rather than detracts from their core responsibility of being expert in the traditional doctor–patient relationship, and the rewards reaped from it. Fourth, a double challenge lies ahead because, while contemporary professional standing may partly depend on public engagement, the effectiveness of such engagement depends, in turn, on how convinced the public is that the profession has its own house in order.15 And finally, conceptual clarity, realistic expectations and good role models are needed if clinicians are to engage effectively with important public concerns. Teaching about social determinants of health alone is insufficient. To use this information and be effective political agents, future health care professionals will need skills in advocacy and public participation. Virchow led an extraordinarily civic-oriented life, as a participant in the 1848 Berlin uprisings and later as a Berlin city counsellor, cofounder of the German Progressive Radical Party, and member of parliament. With public-spiritedness and the right tools, modern health care professionals could be both active clinicians and evidence-based advocates on important health-related matters in their communities. Virchow would be pleased — medicine would once again be a social science.

Russell L Gruen MB BS, PhD, FRACS

To decrease overall mortality, we need to focus on maximising appropriate medical therapies Increasing attention is being given to assessing and improving the quality of care of patients presenting with acute coronary syndromes (ACS).1,2 In this issue of the Journal, Chew and colleagues report on the use and survival impact of early invasive management (coronary angiography and revascularisation) in 3393 patients with ACS enrolled in the Australian prospective ACACIA (Acute Coronary Syndrome Prospective Audit) registry.3 They used propensity-adjusted regression modelling to quantify effects of invasive care independently of other confounders such as patient characteristics, contraindications to invasive care and use of pharmacological treatments. While rates of invasive care appeared near to optimal (90%) in patients with ST-segment-elevation myocardial infarction (STEMI), rates were purported to be less optimal in those with non-STEMI (71%) and unstable angina (45%). The study is unique in showing a 47% reduction in all-cause death at 1 year as a result of early invasive care, a finding used to argue for a greater use of this approach across the spectrum of ACS. The magnitude of this treatment effect is at odds with systematic reviews of randomised trials which report that survival benefits are restricted to patients with STEMI undergoing primary angioplasty, with relative risk reduction of death (compared with thrombolysis) no more than 32%.4 Such patients represented just over a fifth of the patients evaluated in ACACIA. In contrast, contemporary trials of routine invasive care versus medical therapy in patients with non-ST-segment elevation ACS (NSTEACS), who comprised three-quarters of the cohort, show no conclusive mortality benefit, although reinfarction and anginal burden are significantly reduced.5 Separate analyses for patients with STEMI versus those with NSTEACS were not reported, which brings into question the validity of implying that greater use of an invasive strategy among all patients with ACS would translate into proportionately more survival benefit. The authors argue that their cohort included many high-risk patients who tend to be excluded from trials, and among whom they infer a survival benefit was achieved. Several issues warrant consideration. Can observational studies validly show treatment benefits not seen in randomised trials? How replicable are these effects? If such an effect is real, would the number of lives saved from optimising invasive care exceed that achieved from optimising other forms of care, thus serving as a quality improvement priority? If so, what might be the most effective optimisation strategies? Even the best observational design can be biased by prognostically important baseline differences among patients, often because of unobserved or unreported treatment selection biases. Chew et al did their best to minimise such bias by estimating the likelihood (or propensity) of patients to receive invasive care on the basis of patient characteristics ascertained before such treatment was given. The association between invasive care and 12-month mortality was then assessed with regression modelling that adjusted for variables known or thought highly likely to influence mortality, including medical therapies such as statins and angiotensin-converting enzyme (ACE) inhibitors — although antiplatelet agents and β-blockers were notably absent. This association was then further adjusted after inserting the propensity score as a continuous variable. Unfortunately, methodological concerns persist for several reasons. First, the literature is replete with high-profile examples of well performed observational studies (eg, hormone replacement therapy and cardiovascular mortality, β-carotene and cancer prevention) suggesting favourable treatment effects that were later dismissed or reversed in large, pragmatic randomised trials. Second, different observational studies, which have included analytical methods other than propensity scoring, give very different results. An American study showed that early coronary angiography for acute myocardial infarction (AMI) was associated with a 50% reduction in mortality at 7 years using propensity analysis (designed to control for overt bias), but this fell to a 16% decrease when instrumental variable analysis was used (designed to control for hidden bias as well).6 A propensity-adjusted analysis of French patients with STEMI presenting to interventional versus non-interventional hospitals (the former highly correlated with higher rates of invasive care) revealed only a 24% decrease in mortality at 1 year.7 Third, the most appropriate design for observational studies remains unclear, with some arguing propensity scoring is no better than traditional multivariate regression adjustment.8 Fourth, as propensity analysis cannot adjust for unmeasured characteristics, sensitivity analyses are recommended to gauge effects of potential confounders which, for invasive care in ACS, may include patients’ socioeconomic status.9 Finally, trials of invasive care may actually overestimate treatment effects achievable in routine practice given the expertise, logistical support and rapid institution required for the optimal results available in high-volume research centres. With regard to prioritising efforts at improving quality of care, the use of early invasive care in patients with STEMI in the study by Chew et al was in accordance with trials and guidelines. In contrast, within the total cohort, there was considerable underuse of key drugs at discharge and at 12 months, respectively: β-blockers, 68% and 57%; aspirin, 87% and 74%; statins, 82% and 72%; ACE inhibitors or angiotensin receptor antagonists, 67% and 64%. This underuse was most pronounced in patients not receiving invasive care and, by association, not admitted to a metropolitan centre. Of all AMI-related deaths that are prevented by therapeutic interventions, both acutely and as secondary prevention, medical treatments account for 80% of these (35% acutely, 45% secondarily) compared with only 6% for early invasive management.10 If all indicated drugs are prescribed to eligible patients, risk-adjusted mortality at 6 months is reduced by 90% compared with patients who receive none of these drugs.11 Routine use of more costly invasive care is not associated with population survival benefit beyond that seen with optimal medical management.12 Thus, if decreasing overall mortality is the aim, a focus on maximising administration of appropriate medical therapies across all hospitals should take precedence over extending invasive care to all or most patients with ACS, especially as there are low-cost interventions that can increase rates of prescribing at discharge up to 90%.13 This is not to say the delivery of timely invasive intervention, particularly to patients presenting to non-interventional hospitals, is unimportant given its mortality benefit in STEMI4 and morbidity reduction in high-risk NSTEACS.5 There are actionable strategies for improving region-wide access to intervention14 and reducing door-to-balloon times15 for patients with acute STEMI, and these deserve consideration in Australian settings. Risk stratification methods for identifying patients with NSTEACS who are most in need of referral to interventional centres16 require universal implementation. More globally, quality improvement strategies — comprising use of opinion leaders and educational outreach, guideline-based decision support tools, regular audit and feedback, and clinical process redesign — have been validated in the management of patients with ACS,17 and innovative, multidisciplinary programs that integrate multiple strategies need to be maintained. What is critical is the continuance of well designed prospective registries like ACACIA, which provide standardised and representative data that allow us to monitor the quality of care and the effects of whatever actions we may take towards improving it.

Ian A Scott FRACP, MHA, MEd

Long (or short) QT syndrome is life-threatening, not as rare as once thought, and treatable if diagnosed “The fault dear Brutus is not in our stars, but in ourselves”. Through the lens of molecular medicine we are now beginning to see those faults more clearly. We can now increasingly understand why some apparently healthy children and young adults die without warning. The long-QT syndrome is foremost among responsible causes, and is known to be the consequence of mutations in genes encoding ion channel function.1 Originally an esoteric condition of great rarity, its prevalence is now estimated as one in 2000.2 Life depends on the continuous sequence of depolarisation and repolarisation in our heart cells. The QT interval is the time from the onset of depolarisation (the q wave) to the end of repolarisation (completion of the T wave) and is best measured over several R-R intervals in leads II or V5. It is not a value physicians ordinarily pay much attention to when they read an electrocardiogram (ECG; Box). Nor is it always easy to measure. Exactly where the T wave merges with the isoelectric baseline is subject to individual interpretation and hence error.3 It also varies with heart rate, requiring normalisation for comparison, and is longer in women than men. But it is important. The long-QT syndrome is essentially an autosomal dominant condition in which sudden death is commonly linked to situations of increased adrenergic activity, such as exercise and emotion, but also occurs at rest and during sleep.4 Seizures are common and easily lead to misdiagnosis. Although mutations in at least 10 genes have been found, long-QT syndromes 1 (LQT1), 2 (LQT2) and 3 (LQT3) constitute 95% of genotyped cases. LQT1 and LQT2 involve decreased function and hence diminished current flow in the slow and fast repolarising potassium currents, IKs and IKr, respectively, while LQT3 involves an increase in slow sodium current during the plateau phase of the action potential. The net effect is prolongation of the action potential and, most importantly, an increased dispersion of recovery times in different myocardial cells. This increased dispersion allows re-entry to occur with potentially fatal ventricular tachycardia and fibrillation, which manifests clinically as fainting and sudden death. LQT1 is the most common type, and events are typically triggered by exercise, including swimming, and emotion.5 The child found unconscious at the bottom of the swimming pool may well have LQT1.6 Events may occur with exercise or at rest in LQT2 and also, characteristically, with loud noises such as being awakened by a telephone call.7 LQT3 has been linked to death during sleep or inactivity, with a lower likelihood of events, but increased mortality. What are the implications for physicans and general practitioners? Fainting is common, most often vasovagally mediated, and benign. How do we decide otherwise? The key is to be mindful of possible long-QT syndrome when checking the history; fainting or a seizure during exercise, or when upset or angry, and premature death (including drownings or accidents) in family members should ring alarm bells and trigger detailed exploration of the family history, close scrutiny of ECGs and appropriate referral. In such settings, a corrected QT (QTc) interval > 0.45 seconds in males and > 0.47 seconds in females makes the diagnosis virtually certain. With diagnosis comes the dual responsibility of triaging individual patient risk and screening the wider family. The most important factor determining individual risk is the length of the QT interval — long intervals (QTc ≥ 0.5 seconds) equal high risk.8 Knowledge of the genotype is also predictive. β-Blockers are generally first-line treatment, although in genotyped individuals, evidence is lacking for a protective action in LQT3. Modifying risk by avoidance of competitive sport and QT-prolonging drugs (see http://www.qtdrugs.org) is important. Implantable defibrillators are appropriate in high-risk patients, but decisions about prophylactic implantation in intermediate-risk patients must balance the reduction in probability of sudden death against the not inconsiderable morbidity of life-long device therapy in young people. As well as personal history and ECG, family screening should include genetic testing if it is available. When a functionally important mutation is uncovered, testing of family members will disclose up to a third of individuals whose QT intervals are normal, and yet who carry the mutation.9 However, a genotypic diagnosis is possible in only two-thirds of clinically certain cases. Continuing research may diminish this gap. The establishment of registries, such as presently exist in New Zealand (http://www.cidg.org), facilitates surveillance of widely dispersed families and aids ongoing research. While the risks of QT prolongation are now well established, attention has recently been drawn to excessively short QT intervals. In a small number of families identified to date, a QTc interval of < 340 milliseconds has been also associated with a family history of sudden death.10 The first two syndromes described (short-QT syndromes 1 and 2), show a gain of channel function for IKr and IKs, the mirror opposite of the corresponding LQT2 and LQT1 with loss of function in those same channels. Although five short-QT syndromes have been recognised already, it nonetheless seems unlikely that they will rival the long-QT syndrome in prevalence. In conclusion, cardiac repolarisation is a complex interplay of ionic currents precariously maintaining stability. Dramatic progress has been made over the past 50 years in recognising, deciphering and predicting the clinical risk of the long-QT syndrome. Yet this knowledge counts for little if we fail to identify and protect at-risk individuals. Perhaps you will take a closer look at the QT interval in your next patient presenting with “just” another fainting attack. Electrocardiogram showing a markedly prolonged QT interval. The long ST segment is suggestive of long-QT syndrome 3.

Warren M Smith MB BS, FRACP

Objective: To describe the impact of invasive management on 12-month survival among patients with suspected acute coronary syndrome (ACS) in Australia.Design and setting: Prospective nationwide multicentre registry.Patients: Patients presenting to 24 metropolitan and 15 non-metropolitan hospitals with ST-segment-elevation myocardial infarction (STEMI), and high-risk and intermediate-risk non-ST-segment-elevation ACS (NSTEACS) between 1 November 2005 and 31 July 2007.Main outcome measures: Death, myocardial infarction (MI) or recurrent MI, revascularisation and stroke at 12 months.Results: Among 3402 patients originally enrolled, vital status at 12 months was available for 3393 (99.7%). Patients from non-metropolitan areas (810) constituted 23.9% of patients. Early invasive management was more commonly undertaken among patients with STEMI (STEMI, 89.7% v non-STEMI, 70.8% v unstable angina, 44.8% v stable angina, 35.8%; P < 0.001). Factors most associated with receiving invasive management included admission with suspected STEMI or high-risk NSTEACS, being male and the hospital having an onsite cardiac surgical service. Overall mortality by 12 months among patients with STEMI, non-STEMI, unstable angina and stable angina was 8.0%, 10.5%, 3.3%, and 3.7% (P < 0.001), respectively. After adjusting for a propensity model predicting early invasive management and other known confounders, early invasive management was associated with a 12-month mortality hazard ratio of 0.53 (95% CI, 0.34–0.84, P = 0.007).Conclusions: A substantial burden of late morbidity and mortality persists among patients with ACS within contemporary Australian clinical practice. Under-use of invasive management may be associated with an excess in 12-month mortality, suggesting the need for more use of invasive management among these patients.

on behalf of the ACACIA investigators

Objective: To determine the causes of death in Australians with type 1 diabetes mellitus who died aged 40 years or younger.Design and setting: Retrospective review of autopsy reports at the Department of Forensic Medicine, Sydney, New South Wales, 1 January 1994 – 31 December 2006.Main outcome measure: Causes of mortality in people with type 1 diabetes aged ≤ 40 years.Results: Of the 26 682 autopsy reports, 1914 were for individuals with diabetes (type 1, 400; type 2, 1514). Cardiovascular disease accounted for 51% of deaths (169/333) in people with type 1 diabetes aged > 40 years, versus 13% among those aged ≤ 40 years (9/67; P = 0.001). Acute complications of diabetes (27%; 18/67), unnatural deaths (28%; 19/67), and sudden unexpected deaths (22%; 15/67) were the predominant causes of death in young individuals with diabetes. Sudden unexpected death was more common in those with type 1 diabetes compared with a sex-matched control population in the same age range (22% v 5%; χ2 P < 0.001). Of the sudden unexpected deaths, 10 people were found dead in an undisturbed bed with no cause of death found at autopsy (“dead-in-bed” syndrome; mean age [SD], 30.2 [9.4] years; males : females = 4 :1).Conclusions: In deceased young people with type 1 diabetes examined by the Coroner, acute diabetic complications, unnatural causes, and sudden unexpected deaths were the predominant causes of death. The relatively high frequency of sudden unexpected deaths, such as dead-in-bed syndrome, requires further investigation.

Emily Tu BSc · Stephen M Twigg PhD, FRACP · Johan Duflou FRCPA · Christopher Semsarian PhD, FRACP

Objectives: To evaluate whether introduction of an emergency department (ED) telemedicine system changed patient management and outcome indicators and to investigate clinicians’ perceptions of the impact of the system on care provided and on their work.Design: Before-and-after study of use of the Virtual Critical Care Unit (ViCCU), which uses an ultrabroadband connection allowing real-time audiovisual communication between clinicians at distant sites. Semi-structured interviews were conducted with medical and nursing staff at the end of the study.Participants and setting: The ViCCU intervention commenced on 1 January 2004. Our study was conducted in the EDs of an 85-bed district hospital and a 420-bed metropolitan tertiary hospital. It involved all acutely ill patients requiring urgent care (defined by triage category and grouped into critical care, major trauma and moderate trauma) who were treated during the 12 months before (n = 169) and 18 months after (n = 181) the intervention at the district hospital. Thirty-one of 33 clinicians (doctors and nurses) participating at the two hospitals took part in interviews at the end of the study.Main outcome measures: Changes in patterns of management (disposition [admission, discharge or transfer], treatment times, number of procedures) and outcomes (rapid acute physiology scores, hours on ventilation or in intensive care, length of stay).Results: Patient disposition remained unaltered for major trauma patients. For critical care patients, admissions fell significantly (54% to 30%), transfers increased (21% to 39%), and more procedures were performed. For moderate trauma patients, discharges increased significantly (45% to 63%), transfers decreased (48% to 25%) and treatment times were longer. No significant changes were found in outcome indicators. Clinicians reported that the ViCCU allowed greater support to remote clinicians. Specialists reported increased workloads and feelings of greater responsibility for patients at the district hospital. Nurses at the district site reported reduced stress, but district doctors reported some loss of autonomy.Conclusions: The ViCCU appears most effective for moderate trauma patients, with associated reductions in admissions and transfers. Large-scale trials of telemedicine systems that include measurements of both patient care and impact on clinicians’ work are required.

Johanna I Westbrook BAppSc, MHA, PhD · Enrico W Coiera MB BS, PhD · Michelle Brear BAppScEnvHlth · Stuart Stapleton MB BS, FACEM · Marilyn I Rob MA, CStat, PhD · Monique Murphy BNurs, MHM · Patrick Cregan MB BS, FRACS

Objective: To examine the nature and extent of ambulance attendances involving γ-hydroxybutyrate (GHB) and to compare these with heroin-related attendances in Melbourne, Victoria.Design: Retrospective analysis of a database of ambulance service records on attendances at non-fatal drug overdoses, March 2001 – October 2005.Participants and setting: Patients who took GHB and were attended to by an ambulance, as recorded by Metropolitan Ambulance Service (Melbourne) paramedics.Main outcome measures: Transportation to hospital by ambulance; other outcomes included number, age, sex and Glasgow Coma Score (GCS) of patients, characteristics of attendances (in public or private space, others present, police co-attendance).Results: There were 618 GHB-related ambulance attendances across the 46 months of data collection; 362 involving GHB only and 256 involving the concurrent use of GHB and other drugs. These figures compare to 3723 heroin overdoses observed during the same period. The number of GHB-related attendances increased by around 4% per month, which was a higher rate of increase than that found for heroin overdose attendances. Most patients were younger than 25 years, were attended in public spaces, and had a GCS < 10. Around 90% of patients were transported to hospital, compared with 21% of heroin overdose attendances.Conclusions: Ambulance attendance data can be used to index GHB-associated harms. The clear increases in GHB-related ambulance attendances over time highlights the need for further research on how best to respond to this emergent drug-related harm.

Paul M Dietze PhD · Stefan Cvetkovski MPH · Monica J Barratt BSc(Hons) · Susan Clemens MPH

Objective: To investigate rates and predictors of cardiac rehabilitation (CR) attendance after coronary artery bypass graft surgery (CABGS) at Royal Melbourne Hospital (RMH), Victoria, where current best practice referral and recruitment strategies have been adopted.Design, setting and participants: Prospective cohort study of 184 patients who underwent CABGS at RMH between July 2001 and April 2004. Patients completed questionnaires pre-operatively, and 170 patients (92%) had their CR attendance tracked after referral to CR either at RMH or elsewhere.Main outcome measures: Rates of CR attendance among RMH patients referred to CR either at RMH or elsewhere; sociodemographic, medical, cognitive, psychosocial and geographical predictors of CR non-attendance.Results: The CR attendance rate was 72%. Patients referred to CR at RMH were more than four times more likely to attend than patients referred elsewhere (odds ratio [OR], 4.36; P = 0.024). Travel time significantly predicted CR attendance (OR, 0.86; P = 0.039).Conclusions: CR attendance rates were found to be higher than previously reported for CABGS patients, suggesting that best practice referral and recruitment procedures minimise common barriers to CR attendance.

Rosemary O Higgins GradDipBehavHealthCare, BBSc · Barbara M Murphy PhD · Alan J Goble MD, FRCP, FRACP · Michael R Le Grande BSc(Hons), MPH · Peter C Elliott PhD · Marian U C Worcester PhD

A revitalised public health strategy offers the most sustainable way to address current health inequalities and prevent chronic non-communicable diseases. Success in these goals requires a whole-of-government approach and long-term investments. A sizeable proportion of this investment must be outside the health sector, in the social, economic and environmental fabric of our society. The benefits of the federal government’s proposed prevention agenda will only be realised if there is greater clarity about what constitutes preventive health activity, who is responsible for carrying out the preventive agenda, how it is integrated and funded within the health care system, and how prevention outcomes will be measured and evaluated.

Lesley M Russell BSc(Hons), BA, PhD · George L Rubin MB BS, FRACP, FAFHM · Stephen R Leeder MD, PhD, FRACP

At the time of the 2006 Census, there were 3154 centenarians in Australia, 797 men (25%) and 2357 women (75%). This number is expected to increase to 12 000 by 2020. In Australia we are experiencing a demographic transition in which the proportions of people in the oldest age groups are increasing while the proportions in the youngest age groups are decreasing. Centenarians are the fastest growing age segment of the Australian population. Their numbers have increased by 8.5% per year over the past 25 years. In 2006, they represented 0.12% (3154/2 644 469) of the population aged 65 years and over. More than half of centenarians live in private dwellings, with 27% of men and 14% of women living on their own. Government policies are starting to address the issues of an ageing population, including provisions for financial support, improved access to medical services, and appropriate housing and transport facilities. However, we need specific social, medical and financial estimates of the impact of living to 100 years and beyond.

Robyn L Richmond MA, PhD, MHEd

Takotsubo cardiomyopathy is an increasingly recognised syndrome characterised by transient apical left ventricular dysfunction in the absence of significant coronary artery disease. We describe a case of Takotsubo cardiomyopathy complicated by Dressler’s syndrome. To our knowledge, these two conditions have not previously been reported in combination. Clinical recordA 75-year-old woman presented with acute onset of discomfort in the chest, left scapula, neck and arm after being informed of the unexpected death of her son, and 2 days after undergoing an uncomplicated laparoscopic cholecystectomy. Her medical history included Graves’ disease and a hysterectomy. She had no modifiable risk factors for coronary artery disease. Examination revealed a heart rate of 90 beats per minute and a blood pressure of 120/80 mmHg, with no evidence of acute pulmonary oedema. At presentation, an electrocardiogram demonstrated 1–2 mm ST elevation in leads V1–V6, I and aVL (Box 1). The patient was immediately transferred to the cardiac catheter laboratory, where angiography revealed angiographically normal coronary arteries but extensive anteroapical and inferoapical ballooning consistent with Takotsubo cardiomyopathy.1-9 Peak creatinine kinase and troponin I levels were 245 μg/L (reference range [RR], < 200 μg/L) and 6.62 μg/L (RR, < 0.1 μg/L), respectively. The patient’s in-hospital course was complicated by heart failure, necessitating treatment with intravenous diuretics. The patient also developed pleuritic-type chest pain, but computed tomographic pulmonary angiography (CTPA) excluded pulmonary embolism. The patient was discharged 3 days after admission on a medication schedule of metoprolol 25 mg twice a day, and perindopril 2.5 mg, frusemide 40 mg and aspirin 150 mg once a day. A follow-up echocardiogram 6 weeks later showed normal left ventricular function and size, with a calculated ejection fraction of 72%. A trivial pericardial effusion measuring less than 0.2 cm was noted. All cardiac medications were ceased at that point. About a week after the follow-up echocardiogram, the patient presented again with severe pleuritic chest pain that was relieved by sitting forward. The pain was associated with low-grade fever, shortness of breath and a dry cough. She did not report any other symptoms suggestive of an upper respiratory tract infection. Examination revealed signs of a pericardial friction rub and bilateral pleural effusions but no evidence of cardiac tamponade. In view of the recent cholecystectomy, the patient underwent repeat CTPA, which excluded a pulmonary embolus but revealed a moderate pericardial effusion measuring up to 2.1 cm laterally and small bilateral pleural effusions (Box 2). An echocardiogram confirmed the pericardial effusion but showed no evidence of cardiac tamponade. Inflammatory markers were markedly elevated, with a C-reactive protein level of 290 mg/L (RR, < 12 mg/L) and an erythrocyte sedimentation rate of 103 mm/h (RR, < 21 mm/h). The patient had low-grade anaemia (haemoglobin level, 96 g/L; RR, 115–165 g/L), but this improved to 116 g/L without treatment. Her white cell count was elevated at 16 × 109/L (RR, 4–11 × 109/L), with predominant neutrophilia, and her platelet count was significantly elevated at 800 × 109/L (RR, 150–400 × 109/L). Renal function, urinalysis, autoimmune markers and a repeat troponin I measurement were normal. These findings were consistent with a diagnosis of Dressler’s syndrome. Treatment with ibuprofen 400 mg three times daily resulted in a rapid reduction in pain and levels of inflammatory markers. Inflammatory marker levels normalised within 3 months. DiscussionTakotsubo cardiomyopathy was first described in Japan in 1991. It is characterised by transient apical left ventricular ballooning in the absence of significant coronary artery disease.1 Our patient’s initial presentation was consistent with a diagnosis of Takotsubo cardiomyopathy. The pathogenesis of this condition is not well understood but is postulated to be caused by coronary artery vasospasm in association with intense emotional or physical stress, leading to apical myocardial stunning.2-4 As a result there is often minimal myocardial necrosis, as reflected by the minor cardiac enzyme rise in this case.5 Left ventricular function usually returns to normal within 1–4 weeks, as seen in our patient.6-8 The role of catecholamines in the pathogenesis of Takotsubo cardiomyopathy has been documented in numerous studies.9-12 Dressler’s syndrome was first described by Dressler in 1956.13 It is characterised by a late-presentation pericarditis, presenting weeks to months after a myocardial infarction. Six weeks after the diagnosis of Takotsubo cardiomyopathy, our patient displayed typical features of Dressler’s syndrome: pleuritic chest pain, pericardial friction rub with associated effusion, fever, leukocytosis, pleural effusions and elevated levels of inflammatory markers.13 The pathogenesis of Dressler’s syndrome is thought to be immune-mediated, as evidenced by late onset of the syndrome. The putative pathogenetic sequence begins with myocardial injury that releases cardiac antigens and stimulates antibody formation. The immune complexes that are generated then deposit onto the pericardium, pleura and lungs, eliciting an inflammatory response.14-16 Earlier studies quoted the incidence of Dressler’s syndrome to be as high as 3.3%–4.8% after myocardial infarction,17-18 but more recent estimates have been significantly lower, possibly as a result of reperfusion strategies that limit the size of the infarct and the release of cardiac antigens that stimulate an immune response.19 Our patient presented with Takotsubo cardiomyopathy and developed Dressler’s syndrome 6 weeks later. To our knowledge, Dressler’s syndrome following Takotsubo cardiomyopathy has not been previously described in the literature. This may be because the extent of biochemical myocardial damage demonstrated is often small in Takotsubo cardiomyopathy, whereas Dressler’s syndrome is often associated with significant myocardial necrosis. For this reason, the diagnosis of Dressler’s syndrome in our patient was unexpected and the mechanism is unclear. 1 Electrocardiogram showing 1–2 mm ST elevation in leads V1–V6, I and aVL ST elevation was noted anterolaterally, with reciprocal changes inferiorly. 2 Pericardial effusion seen on computed tomographic pulmonary angiography The pericardial effusion (white arrow) measured up to 2.1 cm laterally. A small pleural effusion (black arrow) is also visible.

Edmund J Lee MB BS(Hons) · Randall Hendriks MB BS, FRACP, FCSANZ · Alan P Whelan MB BS, MRCP, FRACP

The burden of atherosclerosis has triggered intense interest in the study of “vulnerable” plaques at high risk of rupture. Optical coherence tomography (OCT) has recently contributed to the in-vivo visualisation of plaque, providing unique insights into the atherosclerotic process, previously only attainable through postmortem examination. This technique uses near infrared light and an optical imaging wire attached to a patient interface unit with a pullback speed of up to 3.0 mm/s. In this patient, a 62-year-old man with treatment-resistant dyslipidaemia and stable angina, coronary angiography revealed possible non-flow-limiting plaque in the proximal left anterior descending coronary artery (arrow; Figure, A). OCT images confirmed extensive non-flow-limiting plaque (Figure, B–D), consisting of lipid (L)-rich areas with characteristic low reflectivity and homogenous appearance (Figure, B and C), and a fibrous (F) plaque with a high reflective and homogenous appearance (Figure, B). The images revealed almost circumferential thin cap fibroatheroma (TCFA; Figure, D), a marker of plaque vulnerability, as well as the plaque’s necrotic core (NC; Figure D). This case demonstrates the potential of OCT to visualise plaque and detect TCFA. This is particularly useful in stable patients in whom aggressive management of risk factors might prevent future adverse events.

Peter Barlis · Giuseppe Ferrante · Francesca Del Furia · Carlo Di Mario

To the Editor: The Rural Doctors Association (RDA) of New South Wales, of which I am President, has been involved in desperately trying to keep maternity units close to people’s homes. The conclusion formed by Ford and colleagues in their recent report,1 that women with a previous postpartum haemorrhage should only deliver in units with a blood transfusion service, appears extraordinary and contradictory to their own findings. The authors based this conclusion on their finding that 5.8% of women had a postpartum haemorrhage in their first pregnancy, even though their definition of this was remarkably subjective and largely unscientific. They recognised in their study that the incidence of postpartum haemorrhage requiring transfusion is only 0.7%. Therefore, 88% of women defined as having a postpartum haemorrhage do not require a blood transfusion. I am bemused why the authors think 88% of women who did not require a blood transfusion but had a “postpartum haemorrhage” should only deliver in a unit with blood transfusion services. I doubt any of my colleagues would wish to deliver women who required a blood transfusion for a previous postpartum haemorrhage in a small unit. I refer Ford and colleagues, and readers, to a study by Tracy et al reported in January 2006.2 This was a much larger study of 750 491 women giving birth during 1999–2001. This study concluded that “In Australia lower hospital volume is not associated with increased adverse outcomes for low risk women”. In the past 10 years, we have seen the loss of 50% of our maternity units in NSW, and the rest are under severe stress due to the lack of staffing. I doubt that the sort of extraordinary conclusion made by Ford and colleagues will help us maintain services in rural NSW.

Leslie A Woollard

In reply: Safety and appropriateness are important principles underlying the provision of health care. Maternity care in Australia requires that women are offered care in an environment that is appropriate to their level of risk. Such a risk-management approach requires accurate data to inform the process, including accurate identification of women who may access local services as well as those who may benefit from higher levels of care. The aim of our study was to present risk estimates of recurrent postpartum haemorrhage (PPH) to better inform decision making by both clinicians and women about subsequent pregnancies. While we are aware of the struggles faced by rural maternity units, we estimated that only 0.2% of women giving birth in New South Wales would be affected by our suggestion that women with a history of PPH consider delivering at a hospital with onsite cross-match facilities. The definition of PPH that we used is consistent with that of the International classification of diseases1 and the NSW Department of Health’s PPH policy;2 this policy resulted from a review of hospital PPH policies sparked by a coronial inquest into a maternal death.3 In contrast to Tracy et al’s study, which only considered low-risk women and had no maternal morbidity outcomes,4 our study calculated risk among all women. Women with a PPH are at increased risk of transfusion, intensive care unit admission, unplanned procedure in the operating theatre, hysterectomy and major maternal morbidity.3 Where we have information about an increased risk of a potentially life-threatening event, surely we should communicate and act on this knowledge to achieve the best possible outcome for women and babies. In Canada, which has similar geographical challenges to those in Australia, it is recommended that where risk factors for PPH are identified, additional precautions such as intravenous access, coagulation studies, and availability of anaesthesia should also be considered.5 The key to successful regionalised maternity care is ensuring that women give birth in risk-appropriate settings.

Jane B Ford · Christine L Roberts · Jane C Bell · Charles S Algert · Jonathan M Morris

To the Editor: Pesce’s criticism of midwifery practice at Mareeba District Hospital1 requires rebuttal. His implication that the service is inefficient or pandering to “the powerful sway of maternity care politics” is incorrect and insults those who struggle to provide woman-centred care in a system focused on doctors. A private obstetrician in Sydney cannot understand midwifery workloads in a rural hospital without knowing the local environment and other impacts on the way clinicians work. The small group of midwives in Mareeba provide a highly valued service in their community, with few of the ancillary services taken for granted in metropolitan areas. In routine antenatal care, Dr Pesce presumably orders blood tests and then reviews the results filed in the chart or placed on his desk. A Mareeba midwife providing the same service will also perform the venepuncture, prepare a slide and spin the blood, arrange transport to the laboratory, make the next appointment, and file the results in the chart. A Mareeba midwife’s workload includes, among other things: Comprehensive perinatal care of inpatient midwifery clients; Postnatal and neonatal transfers from Cairns Base Hospital (CBH) (eg, to establish breastfeeding for low birthweight babies); 35–40 paediatric admissions per month; Emergency stabilisation and transfer of high-risk presentations (eg, a woman planning delivery with a private obstetrician in Cairns will nevertheless present to Mareeba when in labour at 32 weeks); Follow-up of high-risk or disadvantaged women who should attend CBH, but won’t for various social reasons; Lactation and parenting support for Mareeba women, regardless of where their deliveries occur; Pap smears and vaccinations; and Indirect care, including policy development, data collection, compilation of reports, professional development, inservice training and education. Pesce also criticised the low level of epidural use at Mareeba, which he says reflects a lack of access. However, models that provide one-to-one care in labour and promote continuity of care have been shown to decrease all interventions and increase maternal satisfaction.2,3 Perhaps the high use of epidurals and other interventions in modern tertiary units reflects a lack of access to such beneficial, woman-centred models of care.

L Gay Hawksworth

In reply: I am surprised that Hawksworth feels my editorial1 was critical of the Mareeba birth unit. There is no criticism of midwifery practice at Mareeba contained in the editorial. Several midwives have commended me for my support of the need for rural maternity units to evolve sustainable models of care based on the local workforce and infrastructure. Conversely, I received a few snide remarks from some obstetricians who felt that I had been too supportive. I have usually felt that when one is criticised by both sides in a controversial debate, one’s view is likely to be reasonable. I stand by my comments that the resourcing of the unit, based on staff–patient ratios and the availability of a nearby alternative service, would be the envy of many rural medical, surgical or community health teams. I also stand by my comments that a 1% rate of epidural use is more likely to reflect lack of access to an epidural service, rather than true patient preference. Reviews by a well known midwife of birth centre care and continuity of care confirm that these models of care decrease the use of epidural anaesthesia but are still associated with a 15% epidural rate.2,3 I am certain that if an epidural service were available, at least some of the Mareeba women would be grateful to have access to it.

Andrew F Pesce

To the Editor: Millar and colleagues recently described their comparison of the national inpatient medication chart (NIMC) with 14 other medication charts.1 They concluded that the NIMC contained design features that were adverse and therefore inferior to the medication chart previously used in their hospital. They also stated that the advantages expected by the Western Australian Director-General of Health in introducing the national chart were not experienced at their hospital. Millar et al failed to mention that the NIMC underwent an extensive process of piloting and evaluation in over 30 sites across the country in a structured before-and-after study.2 Failure to recognise (i) the benefits of standardisation as medical, nursing and pharmacy staff move between sites, (ii) the opportunities for structured safe medication practice training,3 and (iii) the value of the collaborative methods used will inhibit the possibility of overcoming problems like those identified by Millar et al in future redesign processes. Millar and colleagues themselves noted that “marked heterogeneity of chart design has been abolished by the NIMC”. The national pilot study considered the entire medication management cycle using a broad definition of medication error (“A prescribing decision or prescription writing process that results in an unintentional, significant reduction in the probability of treatment being timely and effective or increases the risk of harm, when compared with generally accepted practice”4). The NIMC was designed to reduce the risk of errors that prescribers have identified with previous charts.5 The NIMC also reduced the need for all staff to interpret unclear or incomplete prescriptions, thereby further reducing the risk of medication errors.2 We support the comments by Millar and colleagues that the process of implementing clinical practice change must involve significant buy-in and championing by clinicians. The implementation of the NIMC in Queensland recognised the importance of top-down support from senior health officials, combined with the need to increase clinicians’ awareness of risks of current systems and the need for a clear demonstration of the benefits of a revised system to bring about any substantial change in behaviour. We understand that the Australian Commission on Safety and Quality in Health Care has established a quality assurance process which operates at jurisdictional and national levels to adjust the NIMC on the basis of issues raised. This important platform will succeed in addressing the issues raised by Millar et al provided clinicians participate in this collaborative approach to medication safety. We have a rare opportunity, in which Australia is taking a leading role, to address one of the critical safety risks facing patients today. Let us all work together and criticise constructively within a framework of collaboration.

Ian D Coombes · Danielle A Stowasser · Carol M Reid · Charles A Mitchell

In reply: It is understandable that the designers of the national inpatient medication chart (NIMC) should wish to defend it against criticism, especially after 5 or more years of hard work and the major administrative achievement represented by the “top-down” implementation. It is regrettable that the chart at the centre of this otherwise admirable activity turns out to have significant weaknesses compared with the previous medication chart used at Royal Perth Hospital, and that the designers acknowledge this only obliquely by allowing for “future redesign”. Rather, they emphasise secondary outputs such as cross-border familiarity (which we discussed in our article1), “training in structured safe medication practice”, and “collaborative methods”. These supposed advantages are but small crumbs of comfort compared with the imposition of an unsatisfactory chart, loss of local autonomy and increased hazard for patients. There is no evidence that the NIMC has decreased medication errors, defined in relation to patient harm. There was indeed a pilot study, and we referred to it in two different contexts in our paper, but it assessed the chart on the basis of unsatisfactory process-based criteria similar to those employed after the chart was implemented. Perhaps a better indication of the problems of the pilot chart lies in the hundreds of suggested changes made from pilot sites to the NIMC Oversight Committee.2 We note that Coombes and colleagues do not dispute our scientific findings or the design faults we described. Their response repeats unverified claims of benefit that we discussed in our article, and seeks to reassure readers that a process is in place to “adjust the NIMC on the basis of issues raised”, thus acknowledging that “issues” exist. However, readers should be aware that the process referred to is subject to a set of ground-rules which prohibit changes to several design aspects of the chart that we criticised (eg, the block design of the pro re nata [PRN] section).3 Thus, the possibility that the NIMC will be substantially improved is remote. A more likely outcome is that Australia will be left with a chart that satisfies the superficial attraction of national standardisation but contains significant design flaws which represent a hazard to patients. A better approach would be to agree on binding national standard design elements and to restore to individual hospitals or health areas the right to design their own charts within these constraints — “think globally, act locally”.4

J Alasdair Millar · Robyn C Silla · Glenda E Lee · Ann Berwick

To the Editor: I wish to comment on Collignon’s recent editorial on methicillin-resistant Staphylococcus aureus (MRSA).1 The crux of the piece is his argument that what we need is interventional studies, not more studies documenting the extent of environmental contamination. This echoes the sentiment held by me and other colleagues working in the areas of infectious disease, microbiology and infection control. We do need more research and we need good data to evaluate interventions. However, we need to go one step further — a step that can and should be taken now, across the country. In 2006, I was part of a small team that reviewed the infection control program of a major teaching hospital in New South Wales. It became very clear that what is needed in infection control is a change in governance. At present, there is little ownership of nosocomial infections by clinicians or hospital administrators. Infection control intervention is perceived as belonging to the infection control practitioners, and not really the business of the doctors, nurses and other health workers who are caring for the individual patient. At worst, this attitude regards the necessary barrier precautions as an annoying, meddlesome burden imposed by some external agency. Clearly, such an attitude is unlikely to result in good compliance with containment measures. Infection control units have a very important role in terms of providing advice, consultancy and monitoring. But as long as there remains a general perception that nosocomial infections are solely the province of these units, progress in control is likely to be slow. One of the recommendations of our review was to change the governance structure as it relates to nosocomial infection. Elements of this included the following: Introducing infection control into the job descriptions of senior hospital executives and heads of departments; Conducting performance appraisals of these personnel to include infection control indicators; Seeking explicit agreement from all senior medical staff regarding compliance with infection control interventions; Requiring all departments to regularly and frequently review infection control indicators; and Requiring all departments to have regular, formal education sessions in infection control for all medical and nursing staff, including junior staff. We need a change in the mindset of clinicians. They must accept responsibility for what happens to their patients, including MRSA infections. These complications are no different from any others their patients may experience during their encounter with the hospital system.

Raymond C Chan

In reply: I heartily endorse Chan’s comments. To control infections in our hospitals, we desperately need not only a change in governance, but also a change in attitude. Chief executives of all hospitals, as well as all clinicians (nurses and doctors), need to take personal responsibility for serious infections that occur frequently in our hospitals. To do so, they also need to know how often these infections occur. We need robust and transparent measures — for example, data on health care-associated Staphylococcus aureus bloodstream infections, including methicillin-resistant S. aureus (MRSA),1 and deep-seated prosthetic joint infections. In recent years, faced with rising numbers of health care-associated infections, especially MRSA infections, the United Kingdom embraced necessary changes in governance. These included the promotion and use of seven key actions,2 with active surveillance and investigation being the first on the list. One of these mandatory surveillance measures was of all bloodstream infections caused by S. aureus (including MRSA)2,3 and the investigation of all episodes caused by MRSA with a “root-cause analysis”.2,4 There are early indications that the changes have successfully reduced the number of MRSA infections: from a peak of 3955 episodes of MRSA bloodstream infection occurring between October 2003 and March 2004, the number had fallen by over 40% to 2376 episodes in the period April 2007 to September 2007.3 Prevention and control of health care-associated infections must be a core part of clinical governance and patient safety programs in all hospitals. Chief executives and all clinical directors need to be aware of the numerous factors that must be given careful attention in order to reduce health care-associated infections. More importantly, they need to ensure that all appropriate steps are taken to prevent infection. This includes basic issues such as making sure that surfaces in clinical areas are adequately cleaned5 and that hand hygiene protocols are complied with — not just some of the time, but all of the time.

Peter J Collignon

To the Editor: Parasitic infections of the respiratory tract are rare causes of haemoptysis in Western communities, and are often clinically indistinguishable from pulmonary tuberculosis.1 We report a case of a 19-year-old Burmese factory worker who presented to our outpatients department with a history of haemoptysis for 4 years. He was born in Myanmar (Burma) and lived in Malaysia for 2 years before migrating to Australia. He had no past history of significance, and denied having any contacts with tuberculosis. He was a non-smoker and was taking no regular medications. His haemoptysis started in Myanmar, but increased in frequency after he migrated to Australia. He coughed up both fresh and old blood mixed with some sputum, and complained of weight loss of 6 kg, intermittent chest pain and headaches. He had no fever, night sweats, shortness of breath, dysuria, or gastrointestinal or neurological symptoms. He appeared well, and findings of a general physical examination were unremarkable. Chest x-rays from before this presentation, which included migrant screening x-rays, were normal, but his most recent chest x-ray revealed a round lesion posteriorly. A computed tomography scan organised by the patient’s general practitioner showed an area of consolidation at the base of his left lung, not typical of tuberculosis which was the primary suspect in this case. Blood tests showed a raised white cell count of 14. 5 × 109/L (reference range [RR], 4.0–11.0 × 109/L) with a neutrophil count of 11.33 × 109/L (RR, 2.0–7.5 × 109/L) and an eosinophil count of 0.51 × 109/L (RR, 0.04–0.4 × 109/L), an erythrocyte sedimentation rate of 44 mm/h (RR, 1–10 mm/h) and C-reactive protein level of 20 mg/mL (RR, < 5 mg/mL). The result of a QuantiFERON-TB Gold test for tuberculosis was negative. Attempts to obtain sputum samples were unsuccessful, and the patient underwent a bronchoscopy that revealed white milky mucous secretions within the lower lobe of the left lung, where a bronchial lavage was performed. Microscopy of bronchial washings revealed the presence of parasitic structures consistent with Paragonimus westermani (Box 1). Therapy with praziquantel was initiated at a dose of 1200 mg orally, twice daily for 2 days. His condition improved quickly and, on review in the outpatients department 4 weeks later, he had no clinically or radiologically evident recurrence of infection. Paragonimiasis is a common endemic infection in South-East and East Asia, particularly in India, China, Japan and the Philippines. Humans acquire the infection by eating raw or undercooked crayfish and freshwater crab, in which the metacercariae encyst. Once the organisms reach the duodenum, they excyst, penetrate the gut wall, and travel through the peritoneal cavity as immature flukes. They then migrate through the diaphragm and pleural space to reach the lungs, where they form adult worms.2 Early after infection, pleuritic chest pain may develop, in some cases accompanied by a pneumothorax or pleural effusion. Later, with invasion of the lung parenchyma, low-grade fever, cough or streaky haemoptysis may develop. Once the adult worms inhabit the lungs, usually after 2 months, recurrent haemoptysis becomes the cardinal symptom.3 Pulmonary paragonimiasis is most commonly misdiagnosed as tuberculosis, owing to many similarities in the clinical pictures of the two infections (Box 2).4,5 In a patient from a known endemic area, differential diagnoses should be considered and every effort should be made to obtain sputum samples or bronchial washings to distinguish between these two conditions. Serological tests are available if sputum or washings cannot be obtained. 1 Paragonimus westermani eggs detected on microscopy of bronchial washings 2 Similarities in the clinical pictures of paragonimiasis and tuberculosis Both are endemic in the same areas Neither responds to standard antibiotics Both produce chronic symptoms Symptoms of both include: Haemoptysis Weight loss Pleural effusion Chest pain

Murad G Ibrahim · Richard Bunter · Stanley Rajasooriar · Francis Thien

To the Editor: In recent years, solaria have multiplied across Australia. Solaria can emit higher concentrations of ultraviolet radiation than the midday summer sun.1 As exposure to ultraviolet radiation is a risk factor for skin cancer, including melanoma,2 it is not surprising that there is mounting evidence that solarium use increases melanoma risk.1,3-4 Public attention to this issue increased following coverage of Clare Oliver’s story in August 2007.5 Clare was dying from melanoma, which she attributed to her use of solaria. In the last weeks before her death, Clare publicly warned of the dangers of solaria. She featured in a television advertisement promoting the message “No tan is worth dying for”, launched nationally in February 2008. There is evidence that public awareness of the cancer risk of solaria increased after this media coverage. We surveyed adult Western Australians in September 2006, and again in 2007, about their perceptions of cancer risk factors. The survey was conducted by computer-assisted telephone interviewing using random-digit dialling from the Perth White Pages (2006, n = 196; 2007, n = 250). Ethical approval was granted by the Curtin University of Technology Human Research Ethics Committee. Participants were read a list of 16 factors (including solaria) and asked how each factor affected cancer risk (response categories: increase a lot; increase a little; decrease a little; decrease a lot; no effect). While risk perceptions for the other 15 factors remained constant, there was a substantial increase in the proportion of “increase a lot” responses for solaria (40% in 2006 v 72% in 2007; P = 0.001). Total “increase” responses were 71% in 2006 and 92% in 2007 (P < 0.001). In addition, Clare’s advocacy may have been a factor in increased regulation of the solarium industry. Until recently, the Australian solarium industry was unregulated, but operated under a voluntary code of practice. There is evidence that compliance with this code was lacking.6 The Australian Government has explored making the code of practice mandatory. As of 1 February 2008, the Victorian Government enacted regulations to tighten the control of solaria under the Radiation Act 2005 (Vic). Similar regulations were introduced in South Australia on 14 March 2008 and in Western Australia on 4 April 2008. There have been no campaigns about the dangers of solarium use in the general population, so it is very likely that this increase is due to the media coverage of Clare’s story. This and responses to other individuals’ personal stories7 provide evidence of how such stories can increase the community’s awareness of a health issue and gain support for legislative change.

Geoffrey Jalleh · Robert J Donovan · Chad Lin · Terry Slevin

To the Editor: We were interested to read the article on health services research (HSR) in Australia,1 and the previous editorial and articles on health technology assessment (HTA).2-5 In contrast to Australia’s prominent role in applying HSR and HTA to new pharmaceuticals, there has been very little local development of these techniques in evaluating new diagnostic technologies. The Quality Use of Diagnostic Imaging program of the Royal Australian and New Zealand College of Radiologists recently examined the introduction of new imaging technologies in Australia, with particular attention to Medicare Benefits Schedule funding. The major findings were: Delays of up to 7 years between the emergence of evidence for benefit from a new technology and Medicare listing. A large part of this delay was in the period before application to the Medical Services Advisory Committee (MSAC). A lack of significant permanent infrastructure for evidence-based assessment and prioritisation of new imaging technologies. This is in stark contrast to the situation for new pharmaceuticals and surgical procedures. Where some published evidence of clinical efficacy exists, but does not meet MSAC requirements, there is no mechanism to trigger targeted trials on questions of safety, efficacy, and cost-effectiveness. The generation of such evidence is costly, but, arguably, cost-effective in the longer term. Data collection by the Australian and New Zealand Association of Physicians in Nuclear Medicine during the interim funding of positron emission tomography has cost $2.5 million. This “coverage with evidence” approach is used in other countries, like the United States and the United Kingdom, to generate relevant evidence about the performance of emerging technologies when this does not exist in the published literature The current restriction of MSAC reviews to examining existing evidence, rather than sponsoring projects designed to provide specific relevant evidence, ensures continuing delays in the approval of new technologies for Medicare funding.

Nicholas J Ferris · Stacy K Goergen · Makhan S Khangure

Hypertension. A companion to Braunwald’s Heart Disease. Henry R Black and William J Elliott. Philadelphia: Elsevier Saunders, 2007 (xxii + 615 pp). ISBN 978 1 4160 3053 9. At the clinical interface little seems to be new in the area of hypertension. Non-pharmacological strategies have been unchanged for decades and there have been no new drug therapies since the advent of the angiotensin receptor blocker class in the mid to late 1990s. However, much has changed in the past few years with regard to our understanding of the genetics of hypertension, the underlying pathophysiology of the condition and recognition of hypertension as the main risk factor driving cardiovascular morbidity globally. Furthermore, a number of new classes of agents are being developed and indeed (the renin inhibitor class) have been approved in a number of countries outside Australia. For all of these reasons a comprehensive update on new developments in hypertension, anchored by sections on the fundamentals of knowledge regarding this condition, is clearly warranted. Is Black and Elliott’s Hypertension: a companion to Braunwald’s Heart Disease the definitive textbook in this regard? It is certainly a handsome volume with an easy-on-the-eye layout accompanied by appropriate figures, tables and drawings. Its chapters fall along classical lines comprising epidemiology, pathophysiology, diagnosis, risk stratification, treatment, concomitant diseases and management in special populations. Thus, it appears to provide a comprehensive overview of this condition. To test whether this is in fact the case I consulted a similar publication, Hypertension: a companion to Brenner and Rector’s The Kidney by Oparil and Weber (interestingly, put out by the same publishers, Elsevier Saunders). I would have to say that the Black and Elliott text suffers by comparison. One is struck by the much more comprehensive approach by Oparil and Weber in outlining the pathophysiology of the condition. As well, there is much greater attention to diet and nutrition, with six separate chapters on non-pharmacological management of the condition. There are also extremely thorough assessments of individual drug trials contributing to the evidence base of hypertension management. Drilling down into my own area of interest (the interface between hypertension and heart failure), again the Black and Elliott book came across as somewhat superficial with little discussion on left ventricular hypertrophy (an important disease entity in its own right) and essentially a restating of management strategies for heart failure per se, rather than as it specifically pertains to hypertension patients. Despite these reservations, there are particular areas of strength in Black and Elliott’s text. There are extremely important and sorely needed chapters on hypertension in special populations and across Third World geographic areas, which underscores the global epidemic we face (expected to reach almost 50% of the adult population by 2025). Furthermore, chapters on the drug development process in hypertension and a focus on guidelines and their differences across regions also give the text a comprehensive feel. Clearly, with sections and chapters of this type, this textbook will not be for everyone. For the busy general practitioner requiring guidance as to how best to manage the individual hypertension patient, this is not the book. For others requiring an in-depth review of the fundamentals of hypertension, pathophysiology, diagnosis and management, Black and Elliott is a worthy addition to one’s library (or that of one’s institution). Oparil and Weber may, however, be an even worthier addition!

Henry Krum

Who owns our health? Medical professionalism, law and leadership beyond the age of the market state. Thomas Faunce. Sydney: UNSW Press, 2007 (xi + 298 pp). ISBN 978 086840 821 7. Global warming, unsustainable global demands for fossil fuel as China and India come on line, threats to biodiversity, obesity, 1.1 billion people in extreme poverty, wars and rumours of wars — it’s enough to make you sick. How, in a world like this, can we find the strength to be a doctor? Faced with this mess, you might choose to retreat into silence, keep your own council, look after your family and plan for retirement. Not prepared to retreat or be silent, Thomas Faunce — doctor, lawyer, philosopher and ethicist at the Australian National University — writes passionately in pursuit of a future for medical professionalism. He is deeply worried about how market fundamentalism has come to dominate everything, including politics, and explores what might be a satisfactory foundational ethic, or basic moral commitment, for tomorrow’s doctor. He considers the market state will not last, but in the meantime, we need to keep the flame of professionalism alight. Of the market state, which Faunce finds so objectionable, he writes: Governments are controlled by the will not of the people, but of . . . corporate executives [who] espouse . . . socially and environmentally damaging, profit-laden values . . . creating a world where . . . individualistic consumers grow increasingly apathetic about the erosion of their rights and responsibilities as citizens. Faunce sees the progressive privatisation of health care as a manifestation of the growing dominance in politics, without a popular mandate, of the private health insurance funds, large pharmaceutical and device manufacturers, and those seeking to make huge profits on behalf of shareholders from the care of the sick. Here is market fundamentalism on full display. After extended excursions into philosophy and ethics, and multiple literary allusions, Faunce proposes that the foundational value — the base plate — for medical practice should be “loyalty to the relief of patient suffering”. He does not think that medicine should primarily be promoting communal welfare, nor promoting and maintaining health. These are worthy actions, but they lack the voltage to power the engine of dedicated medical practice. If we cut medicine off from a strong connection to individual human suffering, then we cut it off at the knees. The relief of patient suffering, Faunce argues, is a strong moral force that generates action that is externally and publicly focused. There are many good things that come from being a doctor, such as status, job satisfaction and money, that motivate us, but none of these internally directed, individualistic ambitions provides all the strength for medical practice that responds to the need of individual patients who come seeking help. This requires us to put suffering patients always ahead of ourselves. A primary moral commitment to the relief of patient suffering then allows us, Faunce argues, to build a structure of other ethical action that constitutes truly professional practice.

Stephen R Leeder

Mobile medico With three-quarters of the world’s population having no access to medical imaging, a group of US and Israeli researchers has set out to use mobile phone technology in the fight against disease in developing countries. Motivated by World Health Organization reports highlighting this alarming lack of access to affordable and reliable medical imaging technologies, researchers developed a system through which raw imaging data can be sent via mobile phone to a base where it can be processed and reconstructed to produce a medical image. The image can then be interpreted and reported back to the patient site. The potential feasibility of the system is promising, with the authors concluding that a standard commercial mobile phone can be used in both the data-collection phase and the display of results. They comment that this technology could decrease the complexity of operating imaging systems and make diagnostic and interventional imaging available in disadvantaged, non-industrialised countries. PLoS ONE 2008; 3: e2075 Biomarkers mark the way Multiple biomarkers from different diseases may be useful in predicting the risk of death from cardiovascular causes. Using data from a Swedish longitudinal study of older men, researchers determined levels of biomarkers such as troponin I, N-terminal pro-brain natriuretic peptide, cystatin C, and C-reactive protein. Measurement of these biomarkers appeared to improve the risk stratification for death from cardiovascular causes beyond assessment based on established risk factors for cardiac disease, such as cholesterol level, diabetes, smoking status, and body mass index. Moreover, the biomarkers remained useful for risk assessment in the subgroup of participants who did not have cardiovascular disease at baseline. N Engl J Med 2008; 358: 2107-2116 Blood pressure control — age is not an issue The benefits of reducing blood pressure are not limited to younger adults, according to the results of a large international meta-analysis of randomised trials. A total of 31 trials, involving over 190 000 participants, were included in the study. Researchers aimed to determine if a difference exists between age groups (< 65 v > 65 years) in the effects of a reduction in blood pressure on cardiovascular events such as stroke, coronary heart disease, and heart failure, and on the incidence of death from these causes. The meta-analysis also looked at the effects of different drug classes on the major cardiovascular events in the two age groups. In contrast to some other published studies, the analysis did not show evidence for the selective use of particular classes of drugs according to the age of the patient. The authors comment that, due to the nature of the statistical analysis, their findings do not completely exclude the possibility of differences in the effectiveness of drug regimes between age groups, though such variances are likely to be minor. BMJ 2008; 336: 1121-1123 Drugs in developing countries The relationship between pharmaceutical companies and developing countries may be set to change from a largely charitable and cost-cutting exercise to a more even and mutually profitable partnership, according to a commentary in The Economist. In the past, protecting patents in places such as India and Brazil has been difficult, and pharmaceutical firms have been slow to invest research dollars into treating diseases in developing countries. New drug companies are emerging that aim to make licensing deals for branded drugs in developing countries, and some firms are now opening research centres in these areas, hopefully leading to an increase in local skill and research funding. The Economist (online) 2008 ; 15 May Mesothelioma and chemo Patients with malignant pleural mesothelioma have traditionally been given few treatment options, with active symptom control (ASC) the main recommendation for management. The role of chemotherapy with ASC has been unclear, with little evidence of its benefit for survival or improved quality of life. In order to clarify the issue, British and Australian researchers have conducted a randomised controlled trial involving 409 patients with malignant pleural mesothelioma. Participants were randomly allocated to receive ASC alone (which could include steroids, bronchodilators, and palliative radiotherapy), or ASC plus a chemotherapy regime. The chemotherapy treatments consisted of either MVP (mitomycin, vinblastine, cisplatin) or vinorelbine alone. Results showed no apparent significant benefits in terms of survival or quality of life for the addition of chemotherapy to ASC. However, a small, non-significant increase in survival was noted in the group receiving vinorelbine, prompting the authors to suggest that this chemotherapeutic agent deserves further investigation in the treatment of this almost universally fatal malignancy. Lancet 2008; 371: 1685-1694

Tanya Grassi

Med J Aust 2008; 188 (12 Suppl).