Volume 182 Issue 3

Congenital heart disease is often regarded as a chance occurrence affecting only a small number of children. In fact, it affects nearly 1 in 100 newborn infants1,2 and is the leading non-infectious cause of death in this age group. A third of those affected will need surgical or catheter-based intervention in the first year of life. In 2002, congenital heart disease accounted for 224 deaths in Australian children.2 In the United States there are more than 35 000 new cases each year and over 1 million survivors of congenital heart disease in the community.3 Studies of gene expression in animal models have provided a window into how the human heart is constructed . . . Diagnosis and treatment of congenital heart disease has improved dramatically over the past 15 years. The mortality rate for surgical repair of some common conditions, such as tetralogy of Fallot, is currently less than 3%,4 and innovative catheter-based therapies, including closure of certain septal defects, have been developed. Preservation of ventricular function, avoidance of repeat surgery and freedom from arrhythmias are the next goals to be achieved. The first question affected families usually ask is: “What is the risk of having an affected offspring or another affected sibling?”. Population studies suggest that the risk is relatively small (2%, or double the background risk). The reason the risk is relatively modest may be that most congenital heart disease is the result of multiple gene defects and/or an interaction between single or multiple defective genes and the fetal environment. As the genotype and experience of each individual is unique, the occurrence of congenital heart disease in most individuals will not be in the context of a strong familial trait. However, there are many rare examples of families in which congenital heart disease is strongly inherited, and apparently caused by single-gene defects. Even in these families, cardiologic phenotypes can vary enormously, presumably because of the effects of modifier genes and/or influences other than genetic. Such families, if large enough, can be studied using classical genetic techniques (such as linkage analysis), but so far only a small number of clinical cases can be matched to a specific mutation. Thus, family genetic studies are currently not indicated for isolated, non-syndromal cases of congenital heart disease. With the advent of high-throughput genetic screening technology and improved cost benefit, indications for screening may be extended in the future. Recently, cardiac developmental and molecular biologists and geneticists have started to unravel the molecular circuitry underpinning heart formation. Significant progress has come about partly because we can now dissect the morphological and genetic basis of human congenital heart disease in animal models from zebra fish to mice. Aspects of cardiac development are, in fact, highly conserved through evolution, and many of the regulators that transform embryonic mesoderm to myocardium are similar across species. One example is the cardiac regulatory gene NKX2.5, which was first isolated because of its similarity to a gene present in the fruit fly, a laboratory model for genetic studies. The developmental approach has defined a number of key cardiac regulatory genes subsequently found by conventional linkage studies to underpin familial congenital heart disease.5 Mutations in NKX2.5 itself cause atrial septal defect and conduction abnormalities, while TBX5 mutations underpin heart and hand malformations of the Holt–Oram syndrome, and mutations in GATA4 cause atrial septal defect and more complex congenital heart disease. In clear cases of familial inheritance, genetic screening for mutations in these genes may be beneficial. Studies of gene expression in animal models have provided a window into how the human heart is constructed, and recent insights have led to a revision of traditional concepts of how cardiac chambers and valves develop. The heart begins as a rudimentary vascular tube,6 which, cardiologists are taught, is composed of anatomical segments that develop into chambers. Yet mapping of the cardiac precursor cell populations in the embryo has revealed a more complex picture. Gene expression patterns now show us that chambers arise from discrete zones, not segments, and that non-chamber myocardium gives rise to the central conduction system.7,8 Another significant advance is the discovery of a second distinct pool of cardiac precursor cells in the embryo that migrate into the forming heart tube from the region of the developing pharyngeal arches. These cells, the so-called “secondary heart field”, contribute importantly to the right ventricle, outflow tracts and atria.9 Characterisation of the secondary heart field has unified genetic, developmental and clinical observations in congenital heart disease. Abnormal development and/or deployment of the secondary heart field cells causes underdevelopment and malpositioning of the outflow tracts over the ventricles. This occurs in velocardiofacial syndrome (VCFS, incorporating DiGeorge syndrome), which is caused by microdeletions in chromosome 22q11.10 The TBX1 transcription factor gene is expressed in the secondary heart field and is deleted in VCFS. Its loss in mice has been causally related to abnormalities of the outflow tract that can arise in VCFS. One such abnormality is tetralogy of Fallot, in which unequal partitioning of the rudimentary outflow vessel produces a large aorta and a right ventricular outflow tract obstruction, with subsequent complications. Malalignment of the outflow vessels over the interventricular septum causes a large ventricular septal defect. Although fewer than a third of cases of tetralogy of Fallot are associated with the 22q11 microdeletion, single-gene mutations may prove to be a significant cause. In the case of interrupted aortic arch type B and truncus arteriosus, however, more than 50% of cases are associated with the 22q11 microdeletion. Recent developments in genome-wide screening technology have the power to detect microdeletions in individual patients on an unprecedented scale. This may revolutionise the detection of congenital heart disease genes. Pathological circumstances also provide deep insights into development. In the fetus, even simple primary structural disease (eg, a pulmonary valve that fails to develop) can cause complex secondary disorders as a result of disturbed blood-flow patterns. In heart development, function (flow) dictates form, and loss of normal blood-flow patterns can contribute to underdevelopment of chambers. In these circumstances, it is often difficult to predict from primary lesions the extent to which abnormal development and remodelling will occur as the fetus grows — this is one of the challenges of fetal echocardiography. Now, surgical correction during fetal life, long taboo, is being explored experimentally for valve correction,11 as this would allow more time for normal ventricular development. While only a small proportion of congenital heart lesions currently have identifiable gene markers, the number is growing rapidly. The next decade of research into congenital heart disease will see an exciting convergence of the disciplines of developmental biology, genetics and paediatric cardiology, and, we hope, will not only go further towards answering the question “Why did this happen to us?”, but also provide more secure grounds for genetic counselling and intervention.

David S Winlaw MB BS, MD, FRACS · Gary F Sholler MB BS, FRACP · Richard P Harvey PhD

We need restrictions on night driving and peer passenger numbers for novice drivers Road trauma remains one of the leading causes of death for young Australians.1 Of particular concern is the fact that more than a quarter of all fatal road injuries (27%) and hospitalisations (26%) are in the age group 17 to 25 years,2 and yet this age group comprises only 15% of licensed drivers.3 As well, despite continued funding and the implementation of effective road safety strategies, road fatalities in this age group have remained relatively constant since 1998. To achieve the national road safety strategy target of reducing the population-based road fatality rate by 40% (from 9.3 to 5.6 per 100 000) by 2010,4 various road safety strategies must receive priority. These include greater investment in the road infrastructure and adoption of further standards for motor vehicle safety, as well as enhancements to existing programs such as speed management and random breath testing. Importantly, implementation of promising new road safety initiatives that target the over-representation of newly licensed young drivers in the road crash statistics is necessary. Newly licensed or novice drivers are at increased risk of crashing, especially in the first months of licensing, with a recent study finding 14% of young drivers crash within the first 12 months of driving.5 The risk remains whether the drivers are licensed at 16 years of age (as in many states of the United States6) or at age 17 or 18 years (as in Australia7). The disproportionately high number of newly licensed drivers in the crash statistics has been attributed to factors such as inexperience, an inability to identify hazards, night-time driving, carrying same-age or peer passengers, and risky driving behaviour such as speeding.8,9 A response that has achieved some success in reducing the disproportionate number of crashes of young drivers has been the introduction of graduated licensing systems throughout Australia. The aim of graduated licensing systems is to moderate the effect of risk taking and inexperience, and thereby reduce a young driver’s risk of crashing and the concomitant risk of trauma to the passengers of young drivers and associated third parties. Graduated licensing can be described as a process whereby novice drivers begin their driving careers with significant restrictions, which are removed in stages depending on driving experience or successful test results. An elementary graduated licensing system exists in all Australian states and territories — Learner drivers are required to drive only under the supervision of an experienced driver, and Probationary/Provisional drivers have significant restrictions placed on blood alcohol content and, in some states, maximum speed. Integral to the effectiveness of the graduated licensing system is late night driving and peer passenger restrictions during the early probationary period of licensing. To date, no Australian jurisdiction has incorporated these restrictions into the system, although, in the first half of 2005, NSW will introduce passenger restrictions for provisional drivers who have previously lost their licence.10 Graduated licensing systems that include the three stages and the late night and peer passenger restrictions have shown significant reductions in fatal and injurious crashes involving young drivers. In New Zealand, where the licensing system has included these restrictions, reductions of between 7% and 23% in serious injury have been observed.11 Importantly, evaluations of graduated licensing systems that include late night driving restrictions have shown crash reductions of up to 60% during the late night hours.6 Discussions surrounding whether late night and peer passenger restrictions should be introduced in Australia have met with a number of objections: law enforcement officials perceive the restrictions would be difficult to enforce; politicians perceive a potential backlash from constituents; and young drivers (particularly rural drivers) believe the restrictions would place an undue burden on them given the absence of alternative transport. Despite these concerns, studies in countries that have implemented the restrictions have reported overwhelming support. For example, enforcement appears not to be onerous, as many parents play a significant role in policing the restrictions.12 With reductions in road trauma due, in part, to the comprehensive graduated licensing system, politicians in these countries have seen support rather than retribution. Finally, and most significantly, feedback from young rural drivers in the United States following the introduction of restrictions shows overwhelming support — young rural drivers either strongly agreed (10%) or agreed (53%) with the restrictions.13 A road safety policy that attempts to identify at-risk young drivers and to impose restrictions only on those drivers is unlikely to succeed, because there is no reliable screening test for at-risk drivers. Identifying at-risk young drivers on the basis of prior traffic violations (as proposed by the NSW government10) would not be useful, as most fatally injured young drivers have no prior traffic violations.6 Instead, a whole-population approach such as graduated licensing, which targets all newly licensed drivers, is likely to achieve reductions in young driver fatalities and serious injury. Of importance, however, is the unequivocal evidence that graduated licensing systems that incorporate late night and peer passenger restrictions reduce road fatalities and serious injury and convey a benefit to cost ratio of 74 to 1.6 It is evident that our current graduated licensing systems have been steering young drivers in the right direction. However, until night driving and peer passenger restrictions are incorporated into the graduated licensing system throughout Australia, it is unlikely that the national road safety strategy target for 2010 — to reduce the road fatality rate by 40% — will be achieved.

Mark R Stevenson PhD, MPH

Considering the clinical implications of new research data on migraine and brain lesions Migraine has received considerable attention in the past 15 years as it has come to be better understood as a brain disorder with new and efficient treatment strategies.1 The World Health Organization considers a day with severe migraine to be in the highest category of disability, comparable to quadriplegia.2 Migraine is classically described and defined as an episodic disturbance manifest primarily as head pain and sensitivity to afferent stimuli, such as light (photophobia), sound (phonophobia) and head movement.3 Against this background, new data have emerged that open the issue of whether migraine may be progressive in some way. Kruit and colleagues recently published a cross-sectional, population-based study of Dutch adults aged 30–60 years. They compared the prevalence of brain infarctions and white-matter lesions between people with migraine and control subjects matched for age, sex, place of residence and potential risk factors for cerebrovascular disease.4 Overall, there was no difference between people with migraine and controls in prevalence of infarction. There was an increase in posterior circulation lesions in patients with migraine with aura, and more deep white-matter lesions in women with migraine. The authors concluded that some patients with migraine are at increased risk for subclinical lesions in certain brain areas. These data come at a time when others have suggested a link between migraine and right-to-left cardiac shunts5 (which may predispose to stroke), and when there are known risks for stroke in women under 35 years with migraine.6 It has been suggested that these data may mark migraine as a progressive, rather than simply episodic, disorder.7 This is not a trivial question for migraineurs or their physicians. A progressive disorder is one where there is a continuous increase in severity or extent (Oxford English Dictionary). This may relate to symptoms or some objective measure, such as brain imaging. Migraine certainly does not, in general terms, increase in severity with time, as the natural history is to abate and disappear in later life.8 So, with very few exceptions, it could not be called progressive on the basis of increasing severity with time. This does not negate the fact that some migraine sufferers go through enormously disabling periods of frequent attacks — chronic migraine. 9 This smaller group10 needs attention, but progression should not be ascribed to the vast majority of sufferers. Whether migraine causes permanent, progressive brain lesions is also not established. The relationship between migraine and cardiac right-to-left shunts is at best cloudy. These shunts may arise from a patent foramen ovale (found in about a quarter of the population), atrial septal defects and arteriovenous malformations; they have been implicated in stroke and decompression illness as a result of paradoxical embolism. However, studies of the association with migraine were not population-based, and case definitions were very poor, mixing migraine with aura with isolated aura. The latter makes it impossible to be sure whether the events described were migrainous or ischaemic in nature. Stroke risk is certainly increased for women under 35 with migraine with aura, but the increase is small, and one wonders if this highlights a prothrombotic or vasculopathic comorbidity in a particular subset, rather than a general pathophysiological principle for all patients. The new study by Kruit and colleagues4 gives pause for thought, but, as it is cross-sectional, it provides a hypothesis, not proof. It certainly does not provide evidence that lesions in the brain produce chronic migraine. Only a longitudinal study would give information on accumulation of lesion load that would provide evidence for a progressive course. While the authors of a recent meta-analysis of observational studies of ischaemic stroke risk in migraine conclude that there is an association,11 their review, unfortunately, adds nothing to our understanding. Most studies show an association, and half of the 14 studies in the meta-analysis did not divide their patients with migraine into those with and without aura. Thus, the really interesting possibility suggested by Kruit and colleagues4 of patients with migraine with aura being at increased risk of subclinical brain lesions could not be explored. What are the clinical implications of the new data? First, we can assure patients with migraine without aura that there seems little risk of any progressive or serious problem in terms of brain lesions. Unfortunately, we can also assure them that they will suffer, losing time from work and their personal life, year on year, unless we can help them manage their attacks properly by appropriate advice and use of acute attack and preventive medicines. For patients with migraine with aura, I explain that the risk of stroke is small. Indeed, it is smaller, even for those taking oral contraceptives, than the risk of stroke during pregnancy itself. The available data do not, in my view, justify antiplatelet agents in patients with migraine with aura, nor do they provide intellectual justification for paternalistic limitations on patient choice in, for example, contraceptive use. As a rule, I investigate the unusual: one might target those with prolonged aura (ie, over an hour3) with standard stroke investigations. Migraine is a horrible, disabling, biologically determined, inherited brain disorder rendering life much less tolerable, but for the moment there is no sustainable position that it is progressive for most patients. We can look forward to new data with which to qualify and quantify the issue.

Peter J Goadsby MD, PhD, DSc FRACP, FRCP

Indigenous Australians with cancer are twice as likely to die from the disease than non-Indigenous Australians. Because of this stark imbalance, the Cancer Council Australia recently convened the first-ever national discussion forum to address the issue. About 120 people from around Australia gathered in Darwin in August 2004 for the forum, “Reducing the impact of cancer in Indigenous communities: ways forward”. Originally conceived by the Cancer Council Australia as an internal event, planning for the forum tapped into a ground swell of concern about the poor outcomes for Indigenous Australians with cancer. This interest, combined with financial support from the Australian and Northern Territory governments, the National Cancer Control Initiative and the Cancer Council Northern Territory, turned the meeting into a major national event. Why a discussion forum?The past two decades have seen a 30% reduction in cancer mortality rates in Australia. However, at a meeting in late 2003, the board of the Cancer Council Australia reflected on the fact that recent successes in cancer control were not shared by Indigenous Australians and that we did not fully understand why. We were familiar with the rhetoric about limited access to services, cultural barriers and coexisting health problems, but, before we could work towards improving Indigenous cancer outcomes, the problems needed to be better understood. To this end, we invited Australia’s leading oncologists and epidemiologists with an Indigenous focus, academics, Aboriginal health workers and Indigenous cancer survivors to the forum. Organisational support from the National Aboriginal Community Controlled Health Organisation (NACCHO) helped us reach Aboriginal health workers from Australia’s most remote communities. The result was an unprecedented sharing of epidemiological, cultural and anecdotal Indigenous cancer data, with consensus on ways in which stakeholders could work together to effect measurable improvements. EpidemiologyThere is no simple answer to the question of why Indigenous people with cancer die at twice the rate of other Australians with cancer, nor is there a national dataset from which to draw. The inadequacy of data itself demonstrates the extent to which the problem has been overlooked. However, information gathering on a state and territory basis is improving significantly, particularly in South Australia and the Northern Territory. David Roder (Head of Epidemiology, Cancer Council South Australia) and John Condon (Senior Research Fellow, Menzies School of Health Research) explained that the comparatively high mortality rate is partly the result of Indigenous Australians getting “more than their share” of cancers with poorer survival outcomes, such as cancers of the lung, oropharynx, oesophagus, liver, gallbladder and pancreas. Conversely, Indigenous Australians have lower rates of some of the more curable cancers, such as breast, prostate, bowel and skin cancers. Delayed diagnoses in Indigenous people also contribute to poor survival rates, along with a reduced likelihood of completing treatment. These problems may explain why Indigenous Australians die at higher rates than other Australians, even when afflicted with the same cancer type. However, the forum also revealed other, less apparent factors. Penetrating insightsNgiare Brown (an Aboriginal medical educator and child health specialist with the NT Government) cited institutionalised racism, bureaucratic inaction, and a disconnect between Indigenous and non-Indigenous Australians as the underlying reasons behind the so-called “double burden” of disease suffered by Indigenous people. Brown also reminded the forum of other statistical inequities: twice the rate of low birthweight, and an overall life expectancy 20 years less than that of non-Indigenous Australians. A penetrating cultural insight came from Jeremy Baker Balung (an Indigenous man who works as a counsellor for Aboriginal and Torres Strait Islander cancer patients at Royal Darwin Hospital). Among Baker Balung’s Yolgnu people, each part of the body represents a spiritual link to individual members of the extended family; to have a cancer in a certain organ may be the result of offending the relative whom that part of the body represents. He emphasised the need to respect such beliefs, which are underscored by a deep regard for kin. A person who believes his or her cancer is “payback” for offending a family member may not pursue treatment. Respect and understanding must be reciprocal for people with such strong spiritual convictions; medical practitioners dismissive of time-honoured traditions may be unable to gain their patients’ trust. Cultural differences go hand in hand with communication barriers. For many Indigenous people, English is the second, third or fourth language, with multiple native dialects predominating in more remote communities. NT epidemiological data show that treatment outcomes are consistently poorer for all cancers in people whose first language is an Indigenous language. Access and distanceCancer is a difficult disease to treat remotely, and many Indigenous people live vast distances from urban centres. Sid Selva (Oncologist, Royal Darwin Hospital) described treating patients for whom arduous travel exacerbated the disorientation already induced by their diagnosis. The fact that Selva is the only resident medical oncologist in the “Top End” underscores a general problem with service provision in regional Australia. Michael Barton (Deputy Director of Radiation Oncology, Liverpool Hospital), who is author of a study of radiation services in the Northern Territory, expanded on the problems of distance, a reminder about the immobile and high-maintenance nature of radiotherapy hardware. Such problems reflect overall challenges for healthcare delivery in rural and remote Australia, which are compounded by the cultural, linguistic and socioeconomic barriers unique to Indigenous communities. Jacinta Elston (Associate Professor of Indigenous Health, James Cook University), herself an Aboriginal woman undergoing cancer chemotherapy, described the practical hurdles for anyone on the cancer journey and explained how they are considerably greater for most Indigenous people: no health insurance or income protection, limited understanding of prognosis and treatment options, the absence of an informed community, unfamiliarity with a hospital environment — all of it bewildering, particularly for people already at the margins of Australian society. Ways forwardThe forum sought “ways forward”, and the discussions and workshops mapped out paths towards improving the poor cancer outcomes for Indigenous people. Consistent throughout was the need for allied health agencies to form collaborative partnerships with Indigenous organisations and individuals. Our ignorance of complex yet imperative cultural and linguistic issues was laid bare at the forum and supported by the latest data. Only by engaging with people like Jacinta Elston and Jeremy Baker Balung in interface roles will we be able to break down these barriers. In response, the Cancer Council Australia is inviting Indigenous representatives to join its principal committees, is seeking to co-opt an Indigenous Australian onto its board, and is discussing a memorandum of understanding with NACCHO. Options will be examined to boost research on cancer in Indigenous people, ensuring it is undertaken with liaison officers and developed in ways that will give ownership of the data to Indigenous people, many of whom have reason to be sceptical about research given the history of European paternalism. Increased collaboration should be enhanced by efforts to build the capacity of the Aboriginal health workforce. Much will depend on government funding, and improved cancer control in Indigenous communities has now become a key cancer council advocacy goal. The signs are encouraging: the Coalition’s pre-election cancer policy included a national bowel cancer screening program, targeting Australians aged from 55 and Indigenous Australians aged from 45, indicating a shift towards policy adjustments consistent with the poorer health outcomes of Indigenous people. Cancer councils and their allies will also work towards factoring Indigenous issues into policy development and promotion at every step in the cancer journey, from prevention to palliation. There is no better example of the challenges of cancer prevention than smoking prevalence: 50% of the Indigenous population smoke, compared with about 20% of non-Indigenous Australians. To reduce this figure, again we must connect with Indigenous people and involve their organisations and communities in spreading the public health messages. The need to formally involve Indigenous people in service design and delivery also applies to cancer screening programs. Already there are signs of improvement, with targeted Pap smears contributing to a 50% fall in Indigenous cervical cancer mortality in the late 1990s. Palliation is also critical, particularly among people with such high rates of mortality and premature death. The Cancer Council Australia will look at educational tools to assist in the management of pain, dying and death among Indigenous communities. Our commitment is already well supported at state and territory level. The Cancer Council New South Wales’ recent employment of an Aboriginal liaison officer based in Dubbo and the release of a cancer information kit for Aboriginal health workers are excellent initiatives that could be applied nationally. These are all small steps towards a distant destination. But only through setting and achieving shorter-term goals will we be able to make an impact on the appallingly poor state of cancer outcomes for Indigenous Australians. The discussion forum reiterated the overarching themes of dispossession, hopelessness, grieving, racism, paternalism and abject socioeconomic status — seemingly insurmountable problems, but not when addressed with the sense of purpose, cooperation and strategic thinking evident at the recent national forum.

Ray M Lowenthal MD, FRCP, FRACP · Paul B Grogan · Ellen T Kerrins BNur

Aim: To ascertain the incidence of autism spectrum disorders in Australian children.Setting: New South Wales (NSW) and Western Australia (WA), July 1999 to December 2000.Design: Data were obtained for WA from a prospective register and for NSW by active surveillance.Main outcome measures: Newly recognised cases of autism spectrum disorders (defined as autistic disorder, Asperger disorder and pervasive developmental disorder not otherwise specified [PDD-NOS]) in children aged 0–14 years; incidence was estimated in 5-year age bands (0–4 years, 5–9 years, 10–14 years).Results: In WA, 252 children aged 0–14 years were identified with autism spectrum disorder (169 with autistic disorder and 83 with Asperger disorder or PDD-NOS). Comparable figures in NSW were 532, 400 and 132, respectively. Most children were recognised with autistic disorder before school age (median age, 4 years in WA and 3 years in NSW). Incidence of autistic disorder in the 0–4-years age group was 5.5 per 10 000 in WA (95% CI, 4.5–6.7) and 4.3 per 10 000 in NSW (95% CI, 3.8–4.8). Incidence was lower in older age groups. The ratio of all autism spectrum disorders to autistic disorder alone was 1.5:1 in WA and 1.3:1 in NSW, and rose with age (1.8:1 and 2.9:1 in 10–14-year-olds in WA and NSW, respectively).Conclusions: These are the first reported incidence rates for autism for a large Australian population and are similar to rates reported from the United Kingdom. Ongoing information gathering in WA and repeat active surveillance in NSW will help to monitor any future changes.

Katrina Williams PhD, FRACP, FAFPHM · Megan Helmer MHlthSc(CDM) · Craig M Mellis MPH, MD, FRACP · Marshall Tuck MPH · Emma J Glasson PhD · Carol I Bower MSc, PhD, FAFPHM · John Wray FRACP

Objective: To assess differences in trends for prostate cancer mortality, radical prostatectomy and prostate-specific antigen (PSA) testing for Australian men aged 50–79 years living in capital cities compared with regional and rural areas.Design: Descriptive, population-based study based on data from official sources from 1985 to the 2002/03 financial year (depending on data availability).Main outcome measures: Age-standardised rates per 100 000 men aged 50–79 years of mortality from prostate cancer, incidence of prostate cancer, PSA tests and radical prostatectomy.Results: We found a statistically significant and increasing (age-standardised) mortality excess for prostate cancer in regional and rural areas. In 2000–2002 the excess (compared with capital cities) was 21% (95% CI, 14%–29%). Rates of radical prostatectomy in rural and regional Australia were 29% lower (95% CI, 23% lower to 35% lower) than in capital cities. Although PSA testing is common across the whole of Australia, age-standardised rates in 2002/03 were 16% lower (95% CI, 15% lower to 17% lower) in regional and rural areas than in capital cities.Conclusions: Our results show that the probability of a man having a PSA test and the management of his prostate cancer depend on where he lives. The cause or causes of the prostate cancer mortality excess in regional/rural areas cannot be established in a descriptive study, but fewer radical prostatectomies in regional and rural areas, perhaps associated with less PSA screening, remain among the several competing hypotheses. Other possibilities are related to other differences in management, perhaps associated with access to urologists. Governments and other budget holders need good evidence about the effectiveness of prostate cancer screening and early treatment, but also about the best strategies for providing equitable access to cancer services in both urban and rural areas.

Michael D Coory MB BS, PhD, FAFPHM · Peter D Baade BSc, MMedSc, PhD

Objectives: To assess whether healthcare professionals correctly incorporate the relevance of a favourable test outcome in a close relative when determining the level of risk for individuals at risk for Huntington’s disease.Design and setting: Survey of clinical geneticists and genetic counsellors from 12 centres of clinical genetics (United Kingdom, 6; The Netherlands, 4; Italy, 1; Australia, 1) in May–June 2002. Participants were asked to assess risk of specific individuals in 10 pedigrees, three of which required use of Bayes’ theorem.Participants: 71 clinical geneticists and 41 other healthcare professionals involved in genetic counselling.Main outcome measures: Proportion of respondents correctly assessing risk in the three target pedigrees; proportion of respondents who were confident of their estimate.Results: 50%–64% of respondents (for the three targets separately) did not include the favourable test information and incorrectly estimated the risks as being about equal to the prior risks; 77%–91% of these respondents were “sure” or “completely sure” that their estimations were correct. Twenty of the 112 respondents correctly estimated the risks for all three target pedigrees.Conclusions: Clinical geneticists and genetic counsellors frequently use prior risks in situations where Bayes’ theorem should be applied, leading to overestimations of the risk for an individual.

Benno Bonke PhD · Theo Stijnen PhD · Aad Tibben PhD · Dick Lindhout MD · Angus J Clarke MD

Change for the sake of change is not real improvement, and distracts from providing consistent high-quality care Who could possibly question the value of continuous improvement in any service or other collective human endeavour? It is not surprising, then, that modern management across the developed world has taken up continuous improvement as a central theme and turned it into a management strategy, which I refer to below as “Continuous ImprovementMS”. Here, I wish to compare continuous improvement, as a generic entity, with the newer Continuous ImprovementMS. Continuous improvement has been around since prehistoric times. In its best form, it flowed from a particular attitude, shared by many people, ordinary and otherwise. Such people went about their work or other activities with a mind open enough to recognise better ways of doing things, or ways of doing better things, and they were prepared to try them out. Their improvements were mostly minor, but added together over time to transform tasks. These people listened to others — especially the young, who often had a fresh, new approach, and the old, who could remember changes which had not been good, and who had seen useless fashions come and go. Occasionally, an open mind, inventiveness and serendipity would coincide to produce a spectacular advance, but the continuous improvement was generally evolutionary, not revolutionary. It took its time; it came in “fits and starts”. Old continuous improvement had the wisdom to distinguish real improvement from change for the sake of change. It valued and retained the traditional and the “tried and tested”, at least until the “new” was truly proven to be better. I believe Continuous ImprovementMS, on the other hand, is a corporate, multinational systems approach. It is a management tool, aimed at achieving specific targets and outcomes. It has become a mantra, a fundamentalist plank of modern managerialism. To me, it is a stick, not a carrot. It is like a clanking military tank set on autopilot. It assumes that improvement can be introduced by “force-feeding”. Continuous ImprovementMS is supported by Strategies and Action Plans — if you don’t have these in place, then you aren’t ImprovingMS. Modern management believes there is no activity that cannot benefit from Continuous ImprovementMS. It insists if change is not happening continuously then something is wrong. I believe Continuous ImprovementMS is particularly frustrating and disheartening when it is required to be applied to standard clinical practice, where the ongoing challenge is to maintain a high standard, day after day, patient after patient, often with limited resources; history-taking and physical examination, for instance, don’t require continuous improvement — they just need to be done to the best standards that were taught and performed decades ago. Continuous ImprovementMS ascribes no value to the substantial achievement of maintaining a high standard, and, as far as I am aware, modern managerialism has no category to recognise it. Needing to repeatedly demonstrate compliance with Continuous ImprovementMS is additionally problematic for busy clinical services, because it fails to recognise the essential, central work of such units. Continuous ImprovementMS, by its very own words, implies that this essential, central work is not good enough — no wonder that it demeans hard-working, earnest people, damaging their morale. Critics have said to me: “You just don’t understand Continuous ImprovementMS and quality management generally.” But they do not seem to be aware of the extent and depth of adverse feelings to these systems approaches experienced by the people doing the work. What of the future? Continuous ImprovementMS — itself a sort of reincarnation of Total Quality Management — will disappear, only to be reincarnated as another corporatised, systematised, jargonised entity — perhaps “Non-Selective Non-Stop Upgradance (NSNSU)”? Notwithstanding this, it would be good if modern managerialists could consider adding “Working Systems Maintenance Tracking (WSMT)” to their systems approach, if only to recognise the importance of the need to acknowledge and value good work done well, irrespective of further improvement. And clinicians will continue to dream of a system that recognises the best of what we do at the same time as questioning everything — from what people really need through to how that can be provided — then making changes with due care. In line with current global trends, I expect reactions to what I have written will be polarised. So I will put out some challenges: To those who feel some empathy with what I have said — speak up! Express your concerns, and make suggestions for some real continuous improvement in quality and other management. To those who object to what I have written — pilot and perfect new management strategies on a small scale to show they have the potential to produce substantial, real benefits for real people. Only then, “roll them out”. Additionally, accept the same standards of evidence and accountability that you demand of others.

Henry A Kilham FRACP

We describe a patient with myasthenia gravis and thymoma who developed recurrent severe myasthenic crises associated with the use of combination chemotherapy. Myasthenia gravis (MG) is an uncommon immunological disorder of the neuromuscular junction that is characterised by abnormal weakness and fatigability of some or all striated voluntary muscles. It is the most common autoimmune disorder in patients with thymoma, in whom the incidence is 30%–50%. 1 In patients with MG, up to 90% of their acetylcholine receptors may be destroyed by autoantibodies, predisposing them to disease exacerbation by any agent that impedes neuromuscular transmission.2 Clinical recordIn February, a 49-year-old self-employed builder developed MG and was subsequently found to have invasive thymoma. This was incompletely excised. The surgical procedure was complicated by left phrenic nerve palsy. In May, the patient commenced his first cycle of chemotherapy, which was to comprise doxorubicin 50 mg/m2 Day 1, cisplatin 100 mg/m2 Day 1 and etoposide 120 mg/m2 Days 1, 3 and 5, with dexamethasone 20 mg, ondansetron 8 mg and metoclopramide 10 mg administered before chemotherapy to control nausea. His MG had been well controlled on pyridostigmine 60 mg twice daily. However, within 24 hours of the first dose of chemotherapy, he developed a severe myasthenic crisis with respiratory failure requiring intubation. This was managed with dexamethasone 8 mg daily and plasmapheresis, and was thought to be due to the high-dose dexamethasone given prior to chemotherapy. In addition, he had developed a chest infection a couple of days before starting chemotherapy, which may have contributed to the respiratory failure. A methicillin-sensitive Staphyloccus aureus was isolated from sputum cultures. This was managed upon hospitalisation with intravenous ceftriaxone 1 g daily for 7 days. In June, the patient received his second cycle of chemotherapy, this time without dexamethasone. Within several hours, he developed increasing breathlessness with bulbar dysfunction and generalised weakness. Despite treatment with steroids and intravenous neostigmine, his respiratory state continued to deteriorate, necessitating intubation and subsequent plasmapheresis. No further cycles of chemotherapy were administered. A restaging computed tomography scan at the time revealed minimal residual tumour and mediastinal lymphadenopathy. In August, he completed a course of mediastinal radiotherapy that was complicated by mild radiation pneumonitis. DiscussionA review of the literature revealed no previous report of MG unmasked or aggravated by chemotherapeutic agents. However, several other classes of drugs have been associated with exacerbation of pre-existing MG. Aminoglycosides have been most frequently associated with drug-induced neuromuscular blockade. However, agents most likely to cause aggravation of MG when overused are anticholinesterase drugs, high-dose prednisolone, anaesthetic agents and neuromuscular blockers. Immunosuppressive drugs have also been implicated,3 and transient worsening of MG by high-dose corticosteroids is commonly encountered.4 Miller and colleagues5 found a positive correlation between serum methylprednisolone sodium succinate concentrations and deterioration in neuromuscular transmission. No effect on acetylcholine-receptor antibodies was noted. They speculated that the effects of steroids on MG arise from dissociation of nerve excitation and muscle contraction. Our patient developed recurrent severe myasthenic crises despite the omission of steroids in his second cycle of chemotherapy. It is highly likely that at least one of the three chemotherapeutic agents used had a direct inhibitory effect on neuromuscular transmission, aggravating pre-existing MG. The adverse drug reaction was assessed as “probable” based on a score of 5 on the Naranjo Adverse Drug Reaction Probability Scale.6 The exact mechanism for the neuromuscular blockade is uncertain, but may be due to disrupted calcium entry into the presynaptic nerve terminal, inhibiting presynaptic acetylcholine release. Alternatively, it may be due to postsynaptic blockade, the drugs may bind competitively to the acetylcholine, or may interfere with ionic conductance across the muscle membrane.7 A combination of pre- and post-synaptic blockade may also occur.

Christina V T Ng MB BS,FRACP

Clinical record A 35-year-old man presented to the emergency department complaining of right visual blurring and discomfort overnight. Over the previous 2 years, similar episodes had occurred, mostly at night or in dim lighting, affecting one eye at a time and resolving spontaneously each time. The patient was not using any type of medication at the time when the episodes began to occur. Although infrequent initially, these episodes had increased to two or three times a week after mirtazapine, a tetracyclic antidepressant, had been prescribed for depression and anxiety 5 months previously. Symptoms persisted despite treatment being changed to sertraline, a selective serotonin reuptake inhibitor (SSRI). Ten days before presentation, the sertraline was replaced by venlafaxine 75 mg once a day. Symptoms were occurring about every other day. There was no other significant ocular or family history. Spectacle correction revealed compound hypermetropic astigmatism (right eye, +1.00 + 1.50 × 75° left eye, +1.75 + 2.25 × 110°). On presentation, the patient’s visual acuity was 6/24, improving, with a pinhole before the eye, to 6/9 (right eye) and 6/6 (left eye). The right pupil was fixed and mid-dilated and the cornea was mildly oedematous. Both anterior chambers were axially shallow, with forward displacement of the iris–lens diaphragm (ie, the plane formed by the iris and the anterior surface of the lens at the pupil). Intraocular pressures were 69 mmHg (right eye) and 62 mmHg (left eye) (intraocular pressure > 21 mmHg is generally considered as being elevated). Gonioscopy revealed bilateral completely closed angles. The patient was given intravenous mannitol 100 g over 40 minutes, oral acetazolamide 500 mg, topical timolol 0.5%, apraclonidine 1% and pilocarpine 2%. Intraocular pressures fell to 13 mmHg and 5 mmHg in the right and left eyes, respectively. Gonioscopically, the angles could now be opened with indentation of the cornea; however, the anterior chambers remained shallow. Bilateral laser peripheral iridotomies were performed on the day of presentation (left eye) and on the next day (right eye) to eliminate pupil block. Post-iridotomy gonioscopy showed no change in the angle configuration or anterior chamber depth. The patient was sent home with instructions to take oral acetazolamide 250 mg three times a day, topical timolol 0.5% once a day, pilocarpine 2% four times a day, and brimonidine 2% twice a day. Venlafaxine was discontinued. The patient refused alternative antidepressant medication and requested referral to a psychiatrist or psychologist for counselling. On Day 4 after the patient presented with acute angle closure, ultrasound biomicroscopy showed bilateral supraciliary effusions and anterior chamber shallowing (Box 1). Manifest refraction (ie, manual subjective measurement of refractive error) at this time revealed a myopic shift of about 3 dioptres in each eye. Over several weeks, medications to lower intraocular pressure were withdrawn one by one. Follow-up ultrasound biomicroscopy showed gradual resolution of the supraciliary effusion, which was complete some 5 weeks after the acute attack. The anterior chambers deepened slightly and the patient’s usual hypermetropic refraction returned. Gonioscopy at this time still showed easily occludable angles. Bilateral laser peripheral iridoplasties were performed to reduce the risk of future angle closure. Venlafaxine is described as a safe and effective antidepressant that is chemically distinct from other antidepressants.1 It is a non-selective inhibitor of the reuptake of serotonin, norepinephrine and dopamine and has no anticholinergic activity in vitro. Because of their relative lack of anticholinergic effects, venlafaxine and similarly acting selective serotonin reuptake inhibitors (SSRIs) are preferred over tri- and tetracyclic antidepressants for patients who are at risk of angle closure. We report the case of a young patient taking venlafaxine who developed simultaneous bilateral acute angle closure secondary to supraciliary effusions. Angle closure and/or acute transient myopia possibly caused by supraciliary effusion has been reported for many drugs, including sulfonamides, tetracycline and some diuretics.2 Supraciliary effusions causing secondary angle closure in patients taking topiramate3-5 and sulfonamides6 have been documented by ultrasound biomicroscopy by various authors. The postulated mechanisms by which supraciliary effusions produce angle-closure glaucoma and transient myopia are illustrated in Box 2. There have been reports in the literature of angle closure or increased intraocular pressure in patients taking venlafaxine8,9 or SSRIs.5,10-15 We found one previous report of bilateral acute angle-closure glaucoma in a patient taking venlafaxine8 and one report of raised intraocular pressure in two known glaucoma patients with narrow angles taking venlafaxine.9 Eleven cases of raised intraocular pressure in patients taking SSRIs have been reported to the Australian Adverse Drug Reactions Advisory Committee.10 However, the mechanisms for the raised intraocular pressure in these cases are not mentioned. To our knowledge, ours is the first reported case of acute angle closure in a patient taking venlafaxine in which the presence of a supraciliary effusion precipitating the secondary angle closure has been identified by ultrasonography. Furthermore, our patient was taking only venlafaxine at the time of presentation. The patient in the abovementioned case of acute angle closure8 had taken four other medications immediately before starting or during treatment with venlafaxine. There is a case report of secondary angle closure due to supraciliary effusions in a patient taking topiramate who was also taking venlafaxine, but the authors attributed the effusions to the topiramate.4 It is possible that the mirtazapine and sertraline taken previously by our patient contributed to his condition, as did his underlying hypermetropic status. It may be that the weak anticholinergic or mydriatic effects of serotonergic drugs are sufficient to precipitate angle closure by a mechanism similar to that of the cyclic antidepressants.6,8 The serotonergic effects of these drugs may also have a role in angle closure.11,14,16 Serotonin and serotonin receptors have been found in the human ciliary body, and serotonin, its agonists and antagonists do affect intraocular pressure.17 The supraciliary effusions documented here are evidence of the serotonergic effects of venlafaxine causing angle closure, although the precise cause for the effusions is unknown. Lessons from practice Use venlafaxine (and antidepressants in general) with caution in patients who are at risk of angle-closure glaucoma. Patients at risk are those with hypermetropic refraction (ie, whose distance spectacles magnify objects) and those with symptoms of angle closure (intermittent blurring of vision associated with seeing coloured rings around lights, eye redness, or eye pain). Such symptoms should not be dismissed as “migrainous”. Patients at risk of angle closure should undergo ophthalmological screening, particularly gonioscopy, before starting antidepressant drugs. Because any patient could develop a supraciliary effusion in response to various drugs (especially antidepressants), it is prudent to include symptoms of angle closure when educating patients about possible side effects of these drugs. They should seek ophthalmological care if they experience symptoms of angle closure or a myopic shift in their vision. 1 Ultrasound biomicroscopy images, Day 4 after the patient presented with acute angle closure A: Supraciliary effusion, right eye (arrow). (C = cornea; CB = ciliary body; I = iris; S = sclera.) B: Shallow anterior chamber, left eye. The large area of iris–lens apposition indicates forward displacement of the lens. Pupil block has already been relieved by peripheral iridotomy (not shown). (AC = anterior chamber; C = cornea; I = iris; L = lens.) 2 Postulated mechanisms by which supraciliary effusions produce angle-closure glaucoma and transient myopia * Based on information from Craig et al.7

Maria Hannah Pia de Guzman MD, DPBO · Sureka Thiagalingam MPH, MB ChB · Poh Yan Ong MD, MS · Ivan Goldberg MB BS, FRANZCO, FRACS

A 66-year-old man presented with a 12-month history of progressive gait disturbance with cerebellar ataxia and extrapyramidal features. Computed tomography of the head showed calcification of the basal ganglia and dentate nuclei of the cerebellum, and periventricular calcification (Box). Biochemical testing showed serum level of calcium, 1.19 mmol/L (reference range [RR], 2.15–2.55 mmol/L); ionised calcium, 0.61 mmol/L (RR, 1.14–1.29 mmol/L); phosphate, 1.8 mmol/L (RR, 0.8–1.5 mmol/L); and parathyroid hormone, 0.9 pmol/L (RR, 1.5–8.0 pmol/L). The patient was diagnosed with hypocalcaemia caused by idiopathic hypoparathyroidism. He was treated with calcitriol (2 μg daily) and calcium carbonate (6.0 g daily). His gait showed some improvement, and serum calcium levels became normal over several weeks. The pathophysiology of intracerebral calcification in hypoparathyroidism, which appears paradoxical, is unknown. It is usually asymptomatic. When neurological effects occur, they are thought to be caused by microvascular degeneration from massive perivascular calcium deposition in high-metabolic areas. Computed tomography of the head, showing cerebral calcification A: Calcification of the basal ganglia. B: Calcification of the dentate nuclei of the cerebellum. C: Periventricular calcification.

Huong Van Nguyen MB BS · Seng Khee Gan FRACP

Setting When teaching in the clinical setting, you often quiz students, the junior medical officer and registrar on patients they present. Sometimes it works well, sometimes it makes the trainees clam up, sometimes you are not sure it is hitting the mark and wonder what they have learned. You wonder whether there are ways to make questioning more effective. Your students and trainees learn better when they are involved in the teaching episode,1-3 and an effective way to involve them is to ask questions. By using questions you are able to: stimulate and engage learners; find out their learning needs and knowledge level, so that what you teach them is relevant and pitched at an appropriate level; promote higher-order thinking (ie, clinical reasoning); monitor how learners are progressing; and encourage reflection. Types of questionsWhen using questions to test knowledge, we should recognise the concept of a hierarchy of knowledge,4 from low level (facts) to high level (synthesis and analysis) (Box).4,5 The kind of questions used — whether “closed” (ie, requiring a single correct answer) or “open” (requiring the learner to combine pieces of information and formulate an answer) — pitches the discussion at different levels.6 Questions used should be appropriate to the learner’s level of knowledge. However, we should be attempting to promote thinking in all, from the medical student to the registrar. Promoting higher-order thinking and reasoningWhen teaching, clinicians often ask questions aimed at elucidating low level knowledge. In 1933, John Dewey, one of the most influential thinkers on education in the 20th century, proposed that thinking and problem-solving occurred not when answering a question posed by a teacher, but when attempting to solve a problem important to the learner.7 We learn more from what we “don’t know” than what we “do know”. So shifting from asking “What is the cause of . . .?” to “What are you uncertain about?” moves away from simple factual recall and promotes thinking. A strategy to introduce this approach is SNAPPS, as described in “Tips 4”,8 in which the learner probes the teacher about the learner’s areas of uncertainty. Other types of questionsWhen questioning a student, involve others by deflecting back to the group to promote thinking (“What do the rest of you think?”). Use questions to clarify points (“Can you explain that again?”) and encourage students to elaborate (“Can you expand on that?”). Good habits when questioningUse the learner’s name. Use the “pose, pause, pounce” technique — pose a question to the group, pause long enough for all the group to consider the answer, then direct it to someone at random. Spread the questions around to involve everyone — don’t let a few dominate. Start at one end, then the other, and randomly move to the middle. It keeps learners engaged. Remember that questioning can be intimidating. Provide a supportive atmosphere by being friendly, by encouraging questions and making it clear that any response is acceptable (nothing is “too stupid”). When you ask a question, don’t get embarrassed by the silence that follows and rush to rephrase it or answer it yourself. Just pause, and they will get embarrassed before you do. Expect the unexpected. Brief the patient and learners first, because you don’t want to upset patients with an unexpected answer (“cancer”) or embarrass learners if they don’t know. Remember the principle espoused by David Pencheon, a UK public health doctor: the three most important words in education are “I don’t know”,9 whether they come from the teacher or the learner. Coping with different levels of learnersIn the clinical setting, groups often include students, junior doctors and registrars. The challenge is to involve them all, but teach each at his or her appropriate level. Set the ground rules first, so everyone knows what is expected of them. The most junior learners may be asked to focus on interpreting the history or clinical signs, the most senior on applying evidence-based therapy. Avoid asking a more junior person a question their senior couldn’t answer. Deflect questions from junior staff onto seniors. Get the registrar to explain to the students his or her reasoning. Take-home message When using questions: Be aware that the type of question asked (“open” or “closed”) pitches it at certain levels. Promote thinking and problem-solving by focusing on what learners don’t know (areas of uncertainty) rather than what they do know (factual recall). Use names, and then “pose, pause, pounce”. Clarify, elaborate and deflect. Establish a supportive environment in which everyone can say “I don’t know”, even the teacher. Remember that these principles also apply to other settings such as tutorials.10 Hierarchy of knowledge and examples of questions to determine the learner’s knowledge* * Adapted from Peyton and Allery5 and Douglas et al.6

Fiona R Lake MD, FRACP · Alistair W Vickery MB BS, FRACGP · Gerard Ryan MB BS, FRACP

Obesity in children and adolescents has reached alarming levels — 20%–25% of children and adolescents are overweight or obese, and 4.9% of boys and 5.4% of girls are obese. Rates of obesity have increased significantly in Australia from 1985 to 1995, with the prevalence of overweight doubling and obesity trebling. Body mass index (related to reference standards for age and sex) is recommended as a practical measure of overweight and obesity in children, and is used in monitoring individual progress in clinical practice. Obesity in childhood and adolescence may be associated with a range of medical and psychological complications, and can predispose individuals to serious health problems in adult life, including type 2 diabetes, hypertension, dyslipidaemia and non-alcoholic steatohepatitis. Obesity interventions for which there is some evidence include family support, a developmentally appropriate approach, long-term behaviour modification, dietary change, and increased physical activity and decreased sedentary behaviour. Prevention of obesity in children and adolescents requires a range of strategies involving changes in both the microenvironment (eg, housing, neighbourhoods, recreational opportunities) and the macroenvironment (eg, food marketing, transport systems, urban planning).

Jennifer A Batch MB BS, MD, FRACP · Louise A Baur MB BS, PhD, FRACP

Emma J Best,* Monica M Lahra,† Pam Palasanthiran‡ * Paediatric Infectious Diseases Fellow, † Microbiology Registrar, Neonatal Medicine, Royal Prince Alfred Hospital, Sydney, NSW. ‡ Infectious Diseases Physician, Sydney Children’s Hospital, Level 4, High Street, Randwick, NSW 2031; PalasanthiranpATsesahs.nsw.gov.au To the Editor: Pasteurella multocida is an oral commensal of domestic pets known to be an opportunistic human pathogen after traumatic animal contact. The most common infections in humans are skin and pulmonary infections. This report outlines a case of P. multocida meningitis, which has not previously been reported in Australia. A 19-day-old girl presented with a 12-hour history of fever and poor feeding. Her temperature was 39.5°C, and she was irritable, with no localising signs or skin lesions. A full septic screen was performed. Cerebrospinal fluid (CSF) showed a neutrophilic pleocytosis and gram-negative coccobacilli. She was treated with intravenous cefotaxime and gentamicin. Within 24 hours both CSF and blood cultures showed growth of gram-negative bacilli. The initial Gram stain, growth on chocolate agar and positive oxidase and catalase tests were suggestive of a Haemophilus species. However, further biochemical tests revealed the organism to be P. multocida. The infant made an excellent clinical recovery, with normal neurological and growth assessments at 6 and 12 months. The family owned two cats but reported no contact between their baby and the pets. A single tonsillar swab performed on each cat by a veterinarian 10 days after the baby’s presentation failed to isolate Pasteurella species. The family elected to keep the pets. Pasteurella meningitis occurs at extremes of age, in the immunocompromised (associated with liver cirrhosis, renal disease and haematological malignancies) and after traumatic head injury.1 Infants aged under 1 year account for almost half the cases of P. multocida meningitis. On review of the literature, we found 37 reported cases of P. multocida infection in infants (Box).1-5 In more than three-quarters of these cases, there was known contact with household animals — in more than half of these contact was non-traumatic (licking or presumed handling of the pet). Molecular studies in one of the cases with no history of traumatic contact confirmed that P. multocida isolates from pet and infected child were indistinguishable.2 This infection is unusual, and, given the popularity of household pets, the risk appears low. However, this case highlights the relative immunocompromise of newborn infants, and is a reminder of the importance of hand hygiene and preventing contact between newborn infants and pets. Details of 38 case reports of invasive Pasteurella multocida infection in infants (including current case)1-5 Mean age (range) 2.6 months (1 day– 11 months) Type of infection Meningitis 30 (79%) Puerperal sepsis, chorioamnionitis 7 (18%) Bacteraemia (postnatal) 1 (3%) Nature of animal contact Traumatic (scratch, bite) 9 (24%) Non-traumatic 22 (58%) Unknown 7 (18%) Type of animal (n = 31) Cat 16 (52%) Dog 11 (35%) Both 4 (13%)

Emma J Best · Monica M Lahra · Pam Palasanthiran

Megan L Counahan,* Ross M Andrews,† Rick Speare‡ * Surveillance Manager, Communicable Diseases Section, Department of Human Services, Level 17/120 Spencer Street, Melbourne, VIC 3000; † Senior Research Fellow, Centre for International Child Health and Clinical Epidemiology and Biostatistics Unit, Murdoch Children’s Research Institute, Melbourne, VIC; ‡ Professor, School of Public Health and Tropical Medicine, James Cook University, Townsville, QLD. megan.counahanATdhs.vic.gov.au To the Editor: For parents to treat head lice (pediculosis) effectively in their children, it is necessary for them first to recognise it is present. We conducted a school-based screening program involving 1838 children from 16 randomly selected primary schools in Victoria between May and October 2001 (participation rate, 55.2%).1 As part of this program, we compared a written report from parents on their child’s pediculosis status against results of our examination (7–10 days later). We examined the scalp and hair of each child for lice (“crawlers”) or viable louse eggs (“active infestation”) and dead or hatched louse eggs (“inactive infestation”) using white hair conditioner, which makes lice and eggs easier to see with the naked eye, and a fine-toothed head lice comb. This is a validated, accurate and sensitive diagnostic technique.2 Parents were unaware of the proposed screening date, and the study team was unaware of the parents’ reports. We compared parental report about pediculosis against results of our screening for 1179 children who could be matched with completed questionnaires. Overall, 149 children (12.6%) had active pediculosis, but parents reported head lice in only 36 children (3.0%) (Box 1 and Box 2). These comprised 24 of the 149 children with confirmed pediculosis (16%), and another 12 children who did not have pediculosis when examined. The positive predictive value (PPV) of parental report was 66.6%, indicating that parental reporting was not a reliable indicator of pediculosis. An implication of the low PPV is that some children may have been unnecessarily treated with insecticide for an infestation they did not have. On the other hand, a substantial proportion of children with head lice had not been identified by their parents and could contribute to ongoing transmission within schools. While it was possible they were infected subsequent to completion of the questionnaire, this seemed unlikely, as 72% were found to have multiple louse eggs, indicating a longer duration of infestation than the 7–10 days since the questionnaire was completed. Our study clearly demonstrates that parental reporting of head lice in their children is unreliable. We suggest several possible reasons: parents did not see the head lice, did not recognise them, or used a diagnostic technique with a lower sensitivity than the method we chose, such as examining dry hair. It is also possible that parents were inhibited from reporting pediculosis by the possible repercussions, such as exclusion of the child from school. Indeed, children whose parents failed to answer the question about pediculosis had a higher prevalence of head lice than those whose parents answered. Nevertheless, parents’ management of pediculosis is likely to improve if a sensitive detection method is used. To improve the sensitivity of parental diagnosis and control of head lice we recommend that parents be instructed to screen their children weekly using hair conditioner and combing. 1 Screening results compared with parental report Pediculosis by parent report Pediculosis on examination Yes No Total Yes 24 12 36 No 99 969 1068 Unsure 26 49 75 Total 149 1030 1179 2 Sensitivity and specificity of parental report versus screening Pediculosis prevalence By parental report 3.0% (36/1179) By screening 12.6% (149/1179) Sensitivity 16.1% (24/149) Specificity* 98.8% (1018/1030) Positive predictive value 66.6% (24/36) Negative predictive value* 89.0% (1018/1143) * Specificity and negative predictive value were calculated after grouping “unsure” and “no” responses.

Megan L Counahan · Ross M Andrews · Rick Speare

Fiona M Wood,* Bess V Fowler,† Daniel McAullay,‡ Jocelyn R Jones§ * Plastic Surgeon and Director, † Epidemiologist, Burns Service of Western Australia, Royal Perth Hospital, GPO Box X2213, Perth, WA 6847; ‡ Senior Policy Officer, § Manager, Office of Aboriginal Health, Health Department of Western Australia, Perth, WA. FionawATmccomb.org.au To the Editor: People with major burn injuries (50% total body surface area or more) now have an improved likelihood of survival with the implementation of aggressive treatment regimens, including supportive therapy, nutrition, and advances in the control of sepsis. Technological developments and treatments, particularly expedient wound closure, early surgical debridement, covering of large burn wounds, early skin repair,1 use of cultured epithelial autograft2 and ventilation,3 have also contributed to improved outcomes for people with these injuries. In Australia, there are inequities in access to health services which may particularly affect Aboriginal people.4 We therefore undertook a retrospective, observational study to compare the incidence of major burn injuries, clinical and demographic characteristics of patients with burns, as well as treatment and outcomes between Aboriginal and non-Aboriginal children and adults in Western Australia between 1992 and 2002. Potential cases were identified using data linkage from the Western Australian Department of Health. Raw data came from clinical records. Of the 84 people identified with major burn injuries, nine were Aboriginal (11%) and 75 were non-Aboriginal (89%). The incidence of major burn injury among Aboriginal people is greater than expected, as data from 2001 show that 3.5% of the WA population are Aboriginal. Aboriginal people with major burn injuries were younger than non-Aboriginal people with those injuries (mean, 21 v 35 years). Eight of the nine Aboriginal people (89%) had flame-only burns, compared with 33 of 75 non-Aboriginal people (44%). No statistically significant difference was seen between the groups in the percentage of total body surface area affected, provision of treatment (including number of operative procedures, applications of cultured epithelial autografts, units of blood products used, nasogastric feeds, and antibiotic doses) or length of hospital stay. We found that, although a greater percentage of Aboriginal people sustained major burn injuries, after this group entered the hospital system they experienced comparable levels of service and outcomes to non-Aboriginal people. Further research into burn care is warranted, from culturally and environmentally appropriate prevention through to critical appraisal of outcomes.

Fiona M Wood · Bess V Fowler · Daniel McAullay · Jocelyn R Jones

Huy A Tran Director, Department of Clinical Chemistry, Hunter Area Pathology Service, John Hunter Hospital, Locked Bag No. 1, Hunter Region Mail Centre, New Lambton Heights, NSW 2310. huy.tranAThunter.health.nsw.gov.au To the Editor: I read with interest the recent review of Paget’s disease by Walsh.1 I would recommend that calcium and phosphate levels should be included in the initial biochemical assessment, as both tests are cheap and readily available. As Paget’s disease predominantly afflicts the older population, coexisting vitamin D deficiency is likely. Low (but within the normal range) calcium and phosphate levels may support this diagnosis. Conversely, hypercalcaemia, a rare event in Paget’s disease except in prolonged immobilisation,2 may indicate primary hyperparathyroidism, which is significantly associated with Paget’s disease,3 or, less commonly, metastatic bone disease. Both these conditions have prognoses and management distinctly different from those of Paget’s disease. Serum total alkaline phosphatase levels may not be elevated in 15% of active Paget’s disease.4 While bone-specific alkaline phosphatase level is more useful in these situations, this test is not readily available in some laboratories and, even among those in which it is available, some only provide qualitative results, making it less useful for monitoring Paget’s disease and the response to therapy. A suitable alternative test is urinary deoxypyridinoline/creatinine ratio, which can be done either on a random urine sample or a 24-hour urine collection. In addition, the serum total alkaline phosphatase level can be spuriously low in malnourishment, and specifically in zinc deficiency,5 a frequent occurrence in elderly people. I describe here a case highlighting such a problem. A 72-year-old socially isolated widower of 8 years presented with progressively worsening pain in his right hip in the preceding 3 months. He had poor appetite and had lost 6 kg in weight, but had no symptoms of malignancy. Clinical examination showed a thin man (body mass index, 20 kg/m2), who was otherwise normal with no features of zinc deficiency. A plain x-ray of the pelvis showed bilateral osteosclerosis. His total alkaline phosphatase level was 28 U/L (reference range, 35–110 U/L). Other investigations for metabolic bone disease gave normal results, including one for vitamin D level. Among other nutritional parameters, his zinc level was 5.2 mol/L (reference range, 10.0–18.0 mol/L). A computed tomography scan of the thorax and abdomen showed no evidence of malignancy, and a bone scan was consistent with Paget’s disease. A zinc supplement was prescribed and his diet optimised. At 6-week review, the serum zinc level had improved to 12.5 mol/L, but the serum total alkaline phosphatase level was 250 U/L. This confirmed that the patient’s acquired hypophosphatasia was secondary to zinc deficiency, with zinc being a critical cofactor for alkaline phosphatase activity.4 In light of the “correct” total alkaline phosphatase level, the patient was given intravenous pamidronate, with resulting marked resolution of his symptoms, including a 5-kg weight gain and normalisation of total alkaline phosphatase level. Although this case is unusual, it nevertheless highlights the need to consider occult and coexisting nutritional morbidities in an elderly population.

Huy A Tran

Stephen N Bolsin Director, Division of Perioperative Medicine, Anaesthesia and Pain Management, Geelong Hospital, Ryrie Street, Geelong, VIC 3220. stevebATbarwonhealth.org.au To the Editor: Two recent articles in the Journal highlight the need to re-evaluate the collection of performance data in Australian healthcare, as well as the uses and analysis of these data.1,2 Individual report cards are an extremely good and ethically mandated means of monitoring performance, especially when the information is given to patients as part of an informed-consent process.2 However, it is possible to provide more valuable analyses than simple crude complication or mortality rates. Cusum (cumulative summation) analysis was developed for industrial quality assurance to monitor production processes and detect subtle deviations from a preset, defined level of achievement. It can be applied to clinical practice to identify statistically significant improvements (or decrements) in performance, using agreed definitions of “acceptable” and “unacceptable” performance levels.3,4 It can be risk-adjusted if necessary. Cusum analyses are routinely undertaken by the Geelong Hospital Department of Anaesthesia for monitoring performance of College-accredited trainee anaesthetists, and have been suggested by surgeons as a method for monitoring performance of a series of procedures.5 Although cusum analysis may seem highly threatening to many senior professionals, the support it provides and the cultural change it achieves in trainee anaesthetists have already been well documented in a unique Australian initiative.4 Modern regulatory theory describes three levels of regulation: the individual (micro), organisational (meso), and state or national (macro) levels. The personal professional monitoring program based on personal digital assistants (PDAs) and cusum analysis that was introduced for accredited trainee anaesthetists by Geelong Hospital operates at all these levels. It encourages reflection on individual performance by accredited trainees in a supported environment; organisational review by the supervisor of training within a clinical governance framework; and College supervision, collation and endorsement as part of a national training program. The fact that the reporting structures inherent in this PDA-based model conform to these highest standards of regulatory theory and clinical governance confirms that the required professional change recommended by Irvine1 can be easily achieved through mechanisms already operating in Australian hospitals. The model also achieves cultural change in the trainees and the highest incident reporting rate in modern healthcare (96.7%–100% voluntary reporting of critical incidents occurring in their practice). 6 These two factors should mandate the wider introduction of the PDA-based program in Australian hospitals if the profession and the industry are to be taken seriously on this issue.

Stephen N Bolsin

David G E Caldicott,* Cameron Duff† * Convener, Royal Adelaide Designer Drug Academic Research (RADAR) Unit, Emergency and Trauma Department, Royal Adelaide Hospital, Adelaide, SA; † Director, Centre for Youth Drug Studies, Australian Drug Foundation, Melbourne, VIC. dcaldicoATmail.rah.sa.gov.au To the Editor: Threatened with a surge of Athenian, one-eyed jingoism regarding Australian drug policy that the recent conference report by Ritter et al1 might have elicited, we offer a warning. Australia has achieved much to be proud of with its harm-reduction policies in recent decades. As Ritter et al attest, Australian researchers and practitioners are “leading the way” in generating political and community support for greater harm-reduction efforts. However, the implementation of real harm-reduction measures can hardly be described as “Olympian” under the current administration. Real Australian successes in the area of harm reduction have arguably occurred despite federal and state policy rather than because of it. Individual positions taken by clinicians such as Dr Alex Wodak, in the face of severe opposition and at times intimidation, account for much of this success. The sad reality is that the “Tough on drugs” approach currently pursued in Australia seems doomed to soon fuse with the Americans’ globally denounced “War on drugs”. Real harm reduction can hardly be said to have been given a “fair go” in the past decade, with 85% of the total drugs budget in Australia committed to law enforcement — the paltry remainder split between research and treatment.2 While harm reduction strategies have been widely implemented in response to the problems associated with injecting drug use, such strategies have not been nearly as popular in our responses to other types of drug use. Harm reduction is yet to be embraced as an effective response to the problems associated with the so-called “party drugs”, despite mounting evidence of its efficacy in Europe. Any premature triumphalism on the subject of harm reduction ought to be eschewed. Australia’s recent heritage is quietly being betrayed at a federal level. A little-publicised federal report recently called for a move away from harm minimisation and harm reduction.3 This is despite evidence indicating that functional drug use is emerging as “normal” rather than deviant behaviour among many Australians. 4 Clearly, we must redouble our efforts to ensure that harm reduction becomes a central part of Australia’s public policy stance. In an era in which it often seems easier to succumb to the whims of our larger neighbours than to resist them, it becomes even more important that doctors and health professionals, and particularly the younger generation of researchers, stand firm. We are, after all, standing on the shoulders of giants.

David G E Caldicott · Cameron Duff

Alison J Ritter,* Alex D Wodak,† J Nick Crofts‡ * Head of Research and Deputy Director, Turning Point Alcohol & Drug Centre, 54-62 Gertrude Street, Fitzroy, VIC 3065; † Director, Alcohol & Drug Service, St Vincent’s Hospital, Sydney, NSW; ‡ Deputy Director, and Director, The Centre for Harm Reduction, Macfarlane Burnet Institute for Medical Research and Public Health, Melbourne, VIC. alisonrATturningpoint.org.au In reply: Caldicott and Duff raise a very important question: is the federal government intending to soon terminate Australia’s national drug policy of harm minimisation? This view can be supported by numerous and recent unambiguous speeches by senior government ministers, including the Prime Minister. The government would like Australians to believe that it is implacably opposed to a harm-minimisation approach to illicit drugs. However, a different view appears when federal government funding allocations are examined. For example, the government allocated $215 million to the Illicit Drug Diversion Initiative over 4 years (in addition to a previous allocation of $221 million).1 The intention of this Initiative is to divert selected drug offenders from the criminal justice system to drug treatment. These efforts are, in our view, highly commendable, reducing the use of expensive and largely ineffective custodial punishment and increasing the use of less expensive and more effective drug treatment. They are, however, irreconcilable with a “zero tolerance” or “Tough on drugs” approach to illicit drugs. Another example is AusAID’s recent leadership in the introduction of harm-reduction measures to control HIV epidemics among injecting drug users in Asia. It is also worth noting that the Ministerial Council on Drug Strategy (Australia’s paramount official drug policy-making body since 1985) has repeatedly and recently endorsed a national drug policy of harm minimisation. The present federal government, unlike its predecessor, frequently and stridently attacks emotionally charged symbols of harm reduction, such as the proposed prescription heroin trial or the Medically Supervised Injecting Centre in Sydney. However, as the allocation of substantial funding to the Illicit Drug Diversion Initiative demonstrates, in most respects it is very much a case of business as usual.

Alison J Ritter · Alex D Wodak · J Nick Crofts

Barry N J Walters,* Sivanthi Senaratne† * Physician in Obstetric Medicine, University of Western Australia, Subiaco, WA; † Registrar in Obstetric Medicine, Sir Charles Gairdner Hospital, Perth, WA. banjowATiinet.net.au To the Editor: The “Consensus statement on diabetes control in preparation for pregnancy”1 presents a counsel of perfection that is, regrettably, a cry in the wilderness in this most imperfect of all imperfect worlds. None will deny that the glycaemic target specified would represent a wonderful achievement in a woman attending in early pregnancy. Unfortunately, we are far from achieving this goal, for a variety of reasons. Firstly, and most importantly, “preparation for pregnancy” is unusual. At our clinic (King Edward Memorial Hospital, Perth), where we see up to 90 women each year whose diabetes (types 1 and 2) antedated pregnancy, fewer than 15% have been seen for preconceptional counselling, and a similar proportion have an HbA1c level below 7%. Moreover, at the same hospital, the rate of unplanned pregnancy in the general antenatal clinic exceeds 50%. Studies elsewhere have shown that the rate of unplanned pregnancy in women with diabetes is the same or greater,2 and this figure accords with our own observations. Finally, in many women of reproductive age with diabetes, glycaemic targets as recommended by the Diabetes Control and Complications Trial Research Group3 and the recent consensus statement1 are infrequently met. One study of young adults in a type 1 diabetes clinic4 revealed that “. . . only 3.4% . . . achieved an average HbA1c of less than 7% during 11 years of study . . . despite regular specialist physician, specialist diabetes nurse and dietitian input and repeatedly following up failed appointments”. Australian findings are probably not substantially better in this group. Unfortunately, levels espoused by the above authorities are difficult to attain outside the sequestered environment of a clinical trial. Thus, the realisation of the St Vincent declaration,5 which sought to normalise obstetric outcome for women with diabetes, has proven elusive. Statements that recommend ideal levels of glycaemic control before pregnancy, while laudable, are unlikely to improve the high rates of miscarriage, congenital abnormality, preterm birth and perinatal mortality that we observe. What, then, can we do? The most important intervention in the care of fertile women with diabetes is effective contraception, with the aim of preventing pregnancy until adequate control of diabetes has been achieved. Numerous studies have shown that women who plan their pregnancy and attend for preconceptional care demonstrate better periconceptional glycaemic control and, accordingly, lower rates of adverse events in pregnancy.6 Only by raising the matter of family planning repeatedly with all our younger female patients can we hope to avoid the disappointing observation of an unplanned pregnancy, with all its adverse consequences for the woman with diabetes and her baby.

Barry N J Walters · Sivanthi Senaratne

H David McIntyre,* Jeff R Flack† * Director, Endocrinology and Obstetric Medicine, Mater Health Services, South Brisbane, QLD; † Director, Diabetes Centre, Bankstown–Lidcombe Hospital, Bankstown, NSW. David. McIntyreATmater.org.au In reply: Walters and Senaratne raise two important points — that specific preparation for pregnancy is the exception rather than the rule, and that many people with diabetes (including women of childbearing age) demonstrate poor glycaemic control. As a first step to improving this situation, we believe it is reasonable to set a goal. We sought to alert clinicians, especially those with limited experience in this area, to the importance of optimal glycaemic control in preparation for pregnancy. We hope that the consensus statement represents a “signpost” rather than a forlorn “cry in the wilderness”. Many opinions were sought in developing the consensus statement. Some, for reasons similar to those given by Walters and Senaratne, thought the “HbA1c < 7%” goal too strict, while others believed it to be far too lax. In the end, we agreed to include this figure, with the proviso that the level of glycaemia should be the best achievable for each individual patient. We must educate women of childbearing potential with diabetes and their caring health professionals about the need for preconceptional diabetes control as part of their care. In some clinical circumstances, such as assisted reproduction, the timing of conception is actually determined by the treating doctor. In this setting, optimal glycaemic control should be a prerequisite for active treatment. Rather than taking a nihilistic view, clinicians should devote their combined talents and energy to providing optimal pre-pregnancy care to those women with diabetes who do plan their pregnancies, to promoting pre-pregnancy care (including contraception) for those who currently do not, and to assuming an advocacy role in promoting access to and funding for intensive treatment programs for all people with diabetes.

H David McIntyre · Jeff R Flack

Edzard Ernst Director, Department of Complementary Medicine, Peninsula Medical School, Universities of Exeter and Plymouth, 25 Victoria Park Road, Exeter, Devon EX2 4NT, UK. Edzard. ErnstATpms.ac.uk To the Editor: The article by Myers and Cheras1 is a good attempt to evaluate the safety of complementary therapies. However, I have one problem with it, which may be significant. The authors rightly state at the outset that “the critical issue in assessing any therapy is its risk to benefit”. At the end of their article they consider the “wider public safety issues” and point out that the risks of complementary and alternative medicine (CAM) are minimal compared with those of conventional therapies. I think this is not quite logical. Comparing risks of therapies does not make sense, because the “critical issue” is the risk–benefit profile. Comparing the risks and benefits of, for instance, acupuncture for severe pain versus opioids for the same type of pain would, I think, favour the latter over the former, even though the risks of acupuncture are minimal compared with those of opioids. In other words, comparing absolute risks of treatments is tempting, but meaningless.

Edzard Ernst

Stephen P Myers,* Phillip A Cheras† * Director, Australian Centre for Complementary Medicine Education and Research, Southern Cross University, PO Box 157, Lismore, NSW 2480; † Deputy Director, Australian Centre for Complementary Medicine Education and Research, University of Queensland, QLD. smyersATscu.edu.au In reply: We stand by our statement that “the critical issue in assessing any therapy is its risk to benefit”. 1 Ernst appears to miss the point made in the subsequent two sentences — that this assessment is available for conventional medicine, but not yet for complementary and alternative medicine (CAM) therapies and products. In the absence of such data, society must be able to make an assessment of health practices and medicines based on their overall risk. Ernst himself has made significant contributions to this literature, and in fact three of his articles2-4 were cited in our review. The second criterion of the Australian Health Ministers’ Advisory Council Criteria for Assessing the Need for Statutory Regulation of Unregulated Health Occupations asks the question: Do the activities of the occupation pose a significant risk of harm to the health and safety of the public? Answering this question for the currently unregulated CAM professions involves consideration of the “wider public safety issues”. This forms part of the determination about the appropriateness of occupational regulation. The two comments juxtaposed by Ernst to make his point are not mutually exclusive. While awaiting the risk–benefit analysis, society will need to make decisions about the absolute risks.

Stephen P Myers · Phillip A Cheras

Norman Shum Psychologist and Physician, Psychological Medicine, Eastwood, SA. menciusATsenet.com.au To the Editor: Patient arrogance definitely does exist and can complicate the process, described by Ellard, of “diagnosis, prognosis and therapeutics”.1 I believe this state of affairs has arisen for two reasons. Firstly, from the evolution of “informed consent” linked to “patients’ rights” — principles that need no elucidation. Secondly, as a consequence of the explosion of media and technology. Television has given us a surge of medical programs, especially of the so-called “reality” type, and technology has made information easily available on the Internet. Unfortunately, patients become Internet surfers and surfers become patients. When they then present with symptoms, it is often armed with some knowledge — albeit of dubious quality and veracity. If the doctor does not provide a very accepting ear to these proffered “medical data”, the patient often stops listening, becomes intransigent, and tends to prefer the media- or technology-generated opinion, including the suggested treatment for the semi-self-diagnosed disorder or illness. I am reminded of one of Groves’ subtypes of “hateful patients”, namely “entitled demanders”. He wrote, “. . . they use intimidation, devaluation and guilt induction. . . . The patient may try to control the physician. . . . Such patients often exude a repulsive sense of innate deservedness as if they were far superior to the physician.”2 In my own practice, I had one such patient who would arrive and immediately intimidate my secretary by literally throwing his Medicare card on the desk in front of her and ordering her to turn off the radio that was tuned quietly to ABC FM. She has now retired, but, even 2 years later, says she will always remember him! It takes considerable tact and skill to deflect and reduce the hostility of an arrogant patient so that he or she can ultimately benefit from the consultation. Perhaps it is best done by keeping in mind the fundamental principle primum non nocere.

Norman Shum

Zelman Freeman Retired Physician, 1/43 New South Head Road, Vaucluse, Sydney, NSW 2030. zelfreeATbigpond.net.au To the Editor: You recently commented on the closure of public hospital common medical dining rooms in the 1960s and 1970s.1 Traditionally, these common rooms were a place where residents and senior medical staff met. The closure of these facilities had more serious consequences than the loss of “breaking bread”, as you quaintly put it. The daily meeting between residents ending their shifts and those starting work allowed discussion about the sickest patients — after the dining room closure, such discussions became much less effective. Helpful comments and advice from senior staff were no longer available. New medical advances and the strengths and weaknesses of the system were previously subjected to keen analysis, but all this medical “shop talk” was lost. More importantly, the closure of medical dining rooms contributed greatly to the loss of hospital esprit de corps, which included a sense of belonging to a worthwhile institution to which most of the medical staff were sincerely dedicated. Medical dining rooms had a century-old history in the main state hospitals. I suspect that their closure had more to do with a Jacobin ideological mindset in health departments rather than being an “efficiency” move. Medical staff were not allowed to put tables together in the new refectory, as to do so might appear elitist. I remember going into the small staff room of my hospital at that time to have afternoon tea — a service provided to both lay and medical staff — only to be told by the medical administrator that “non-recoupable foodstuffs were no longer to be served to the medical staff”. Meanwhile, the cleaners in their room next door were enjoying their hospital biscuits! This was the beginning of the “doctor-bashing” era that only the older members of the public remember, and it is not unreasonable to claim that many of the public hospital problems in patient management stem from the actions of perverse individuals who undermined the cohesive and dedicated work of the medical staff, just as they did when they abolished the distinctive hospital uniforms and badges of the nurses, who had always taken pride in their own hospital traditions. A bland coloured gown was substituted to remind them that they were “health workers”. No wonder there is difficulty in recruiting new staff and building a sense of dedication to such an amorphous service. Administrators need to be reminded that good traditions should not be abolished without mature reflection on the consequences.

Zelman Freeman

William B Molloy Gynaecologist, Suite 10, Level 7, William Bland Centre, 229-231 Macquarie Street, Sydney, NSW 2000. drmolloyATbigpond.com To the Editor: I congratulate you on your column in the 1 November 2004 issue.1 For years, I have stated that it is a problem, not only in the public hospitals, but now creeping into the private hospitals, that there is no private room available for doctors to talk among themselves. This also includes the theatres, where only one room is available for both nurses and doctors, and I think this is a giant mistake. I remember that when I was a young doctor, consultations were arranged over lunch. Doctors talked to each other and everyone knew about the important cases in the hospital. It was a teaching and learning experience. In addition, in the afternoon, after one had finished work and was relaxing over the newspaper, again there was contact between doctors. At St Margaret’s Hospital, where I was the Medical Superintendent for fourteen-and-a-half years, between 1969 and 1984, I fought until the day I left to maintain these rooms. The dining room was lost, but at least there was a room where doctors could gather after they did their morning ward rounds. There was an enormous amount of work done and many opinions proffered in that room, and to this day many doctors tell me how much they miss that experience in the hospital they now attend. Isn’t there someone who can point out that, although the public health system is a shambles at present, we should not allow the private system to go down the same track? Sadly, it appears to be doing just that.

William B Molloy

Peter F Burke Surgeon, PO Box 84, Newborough, VIC 3825. burkeATvic.australis.com.au To the Editor: Somerset Maugham noted, “At a dinner party one should eat wisely but not too well, and talk well but not too wisely”.1 Your recent column lamenting the disappearance of doctors’ dining and common rooms2 precipitated a flood of warm memories of, in my case, St Vincent’s Hospital in Melbourne in the 1960s, 1970s and early 1980s. Now based in the Latrobe Valley, Victoria, I have witnessed first-hand, over almost 20 years, much grievous political and social engineering — the abject failure of the first “privatisation” of a public hospital in Victoria and, in the custom-designed “greenfields” hospital, the near-complete lack of provision of facilities for consultant medical staff, leading to their fleeting meeting in corridors and carparks. It is unlikely that C P Snow had this in mind when he wrote of “corridors of power”.3 Contemporary medical staff are indeed an amorphous lot. The clinical white coat is but a memory, and often the only way to recognise a doctor, usually dressed in a manner that would suggest forthcoming involvement in a “Clean up Australia” gathering, is the fashionably appropriate half-noose stethoscope, which, akin to a saint’s halo, confers immediate status on the bearer. Laennec, who invented the stethoscope in 1819, had surely not foreseen the commercial potential of his epochal invention.

Peter F Burke

Bruce P Waxman Medical Program Director, Surgery Program, Southern Health, PO Box 478, Dandenong, VIC 3125. b.waxmanATsouthernhealth.org.au To the Editor: Your recent experience in a staff cafeteria1 is clearly anecdotal, as are my own. I believe, however, the balance needs to be redressed. There is little point in campaigning for “return of the doctors’ common dining room”, as, at least in the public sector, there are no funds available for this campaign. I have been very impressed with the camaraderie that exists in the staff cafeteria at Dandenong Hospital, Southern Health, because medical care is now a team approach and I have the opportunity to meet with medical students, interns, house medical officers, registrars, nurses and administrators, either over a cup of coffee provided free by the Health Service, or a meal. The staff cafeteria has been a meeting place for the team, engendering a team approach to medical care which, I believe, is appropriate to champion for the future of healthcare delivery in Australia.

Bruce P Waxman

Re: “Doctors in the Pacific”, by Watters D A K and Scott D F in the 6/20 December 2004 issue of the Journal (Med J Aust 2004; 181: 597-601). The photo on page 599 was incorrectly ascribed “courtesy of Carolyn Bennett”. It should have read “courtesy of Carolyn Beckett”. The html and pdf versions of the article published online were corrected on 2 February 2005.

David A K Watters · David F Scott

Bruce Griffiths was born in Ballarat on 13 October 1938 and died on 15 October 2004, only a few weeks after being diagnosed with a brain tumour. A son of the late “W R” Griffiths, obstetrician and gynaecologist and former President of Ballarat Base Hospital, Bruce followed in his father’s footsteps. After graduating from the University of Melbourne in 1963, Bruce spent a year as a Resident Medical Officer at Launceston General Hospital in Tasmania. This, together with being born into a rural medical family, convinced him that eventually his career lay outside the capital cities. He left Australia for 4 years to train in the United Kingdom, and became a Fellow of the Royal College of Surgeons of Edinburgh in 1968. He then returned to Launceston for a year before moving to Ballarat, where he practised for more than 20 years. Bruce was a true generalist, holding appointments as a general surgeon at Ballarat Base Hospital and The Queen Elizabeth Centre, while at the same time practising as a general practitioner in the Ballarat Group Practice. He played a significant role in the Professional Staff Group of the Base Hospital. In particular, he was the Group’s chairman in the late 1980s during the planning of the new ward and operating theatre block. Few staff, patients and visitors who walk through the wonderful building today know that they do so only because of the earlier vision and perseverance of people such as Bruce. Bruce resigned from the Ballarat Base Hospital in 1992, but continued to devote his life to the care of rural Australians. After leaving Ballarat, he practised in Derby (WA) and Maryborough (QLD), before joining an Aboriginal health centre in Kempsey (NSW). He was still working at the centre just 5 weeks before his death. When Bruce left Ballarat, the Director of Medical Services wrote at the time that Bruce was owed a debt for the work he did at the Base Hospital over many years. Perhaps it was in part repayment of the debt that, on learning of his illness, friends travelled from Ballarat to his home in NSW to say farewell. Bruce is remembered as a man of few words, but his opinions were always considered and truly held. He loved music, was devoted to his family, and was a familiar figure walking his labrador dogs around Lake Wendouree. Bruce is survived by his wife Wanda and three sons. Hedley G Peach

Hedley G Peach

The Pope, a former state premier, actors and sportspeople can testify that Parkinson’s disease is no discriminator. Alan Nicholson died on 18 October 2004, following his own courageous battle with the disease. He was born on 8 March 1930 in Melbourne. Alan graduated from the University of Melbourne in 1956. After Resident Medical Officer appointments in Melbourne, he trained as a psychiatrist at the Ballarat Mental Hospital, established to relieve overcrowding at the Kew Asylum in Melbourne. He obtained a Diploma in Psychological Medicine in 1961, and in the same year became a member of the Royal College of Psychiatrists of London and a Fellow of the Australian and New Zealand College of Psychiatrists. Alan’s first appointment as a specialist was to the Larundel Psychiatric Hospital in Melbourne, then in 1967 he was appointed to Ballarat Base Hospital, where he continued to work until illness forced him to retire in 1995. When Alan embarked on his career as a psychiatrist in 1959, the practice of psychiatry was a world apart from the way it is practised today. Alan was fortunate to have entered psychiatry in Victoria during the “Daxian” years. This period saw the advent of the Mental Hygiene Authority, later the Mental Health Authority, chaired by Dr Eric Cunningham Dax, and, with it, major changes to the care of people with mental illness and the education and training of the staff who looked after them. Alan played a significant role in the Professional Staff Group of the Ballarat Base Hospital and was the Group’s chairman in the early 1980s. As chairman, Alan oversaw the introduction of a credentials committee for doctors practising at the Base Hospital. This was a new and major influence on the practice of medicine in Ballarat. The smooth introduction of the committee was due to Alan’s stewardship. An example of his foresight and good judgement was his striving for at least a common liaison member, if not a combined committee, between the Base Hospital and St John of God Hospital in the interest of avoiding duplication and promoting the interrelationship of medical practitioners in the city. Alan also played a significant role in the Australian Medical Association and was Honorary Secretary of its Ballarat subdivision for many years. Apart from his medical work, Alan is remembered as an avid and expert collector, particularly of stamps, old banknotes, antiques and wines. He was an enthusiastic member of the Ballarat Wine and Food Society, serving on its committee and as its President and Cellar Master. Alan had the rare honour of being a member of several international wine and food societies. He was also a member and President of the Board of Sovereign Hill, Ballarat’s renowned reproduction of a goldfields township. Alan is survived by his wife Jane and their five children, two of whom are doctors. Hedley G Peach

Hedley G Peach

In the shadow of “Just wars”. Violence, politics and humanitarian action Fabrice Weissman (editor). London: Hurst, 2004 (xi + 372 pp). ISBN 1 8506 5757 8. Medicins Sans Frontières has a reputation for brave and persistent activity aimed at relieving global human suffering. The group reports here on humanitarian aid efforts in 13 situations of conflict and violence — many in Africa, but also in the Middle East, Kosovo, Chechnya, East Timor and North Korea. Most of its 18 authors are French: some are health workers, the others are journalists, academics, lawyers or anthropologists with formidable credentials and extensive experience in international affairs. Ninety per cent of conflicts in developing countries are internal, between factions or regional groupings within a country, and most continue longer than 5 years, causing complex humanitarian emergencies with cycles of war, civil strife, displacement, food shortages and significant mortality. There have been seven million casualties from these internal wars over the past 15 years, and 75% were civilians. Responses by the Western powers, whether of intervention or abstention, are often justified on the basis of high moral purpose, defending values of liberty, human rights and the rule of law, but can be devastating in their consequences. The relationship between bodies that seek to offer humanitarian aid and the prevailing powers in any situation is equally complex. Thoughtful analyses here show how aid efforts to succour the desperately damaged are always constrained, and sometimes completely negated, by sociopolitical realities, particularly those influencing the major powers. “We must do something” is a common cry when reports are received of terrible cruelty, rape, forced recruitment of child soldiers, casual massacres and genocidal policies. But even the best-prepared and well-supported aid agencies face the risk of tragic failure when they confront unacceptable political imperatives and are forced to compromise their own values or clash openly with authorities. “Helping” resource-poor countries is no easy task; it needs informed and global debate, and here is an excellent start. Ian Maddocks Emeritus Professor of Palliative Care Seacliff, SA

Ian Maddocks

Reading doctors’ writing: race, politics and power in Indigenous health research 1870-1969 David P Thomas. Canberra: Aboriginal Studies, 2004 (xvi + 209 pp). ISBN 0 85575 458 3. This is an apt title for this book. Race, politics and power in Indigenous health research have, not surprisingly, mirrored race, politics and power in Indigenous affairs generally. In order to tackle these subjects, Thomas has provided an interesting history of the development of medical associations and medical journals in Australia. The notion of Aboriginal people as primitive and a dying race who needed to be studied before they became extinct permeated much of the early research — “smoothing the pillow of a dying race”. But it was not simply a matter of Aboriginal people needing to be studied while the opportunity was still there. It was also an issue of the health of Aboriginal people potentially impacting on the health of non-Aboriginal people, and of the potential to learn things of value to the non-Aboriginal population by studying the health of Aboriginal people. This was all caught up with power relationships between Aboriginal people as research subjects and non-Aboriginal people as researchers and administrators. The concept of Aboriginal people being research subjects because they were considered to be more “primitive” was pervasive, and this belief led to a variety of wider paternalistic and repressive policies. In 1961 Sir Paul Hasluck, then Federal Minister for Territories, felt obliged to write that “I myself am not disposed to direct that wards can be sampled like a herd of cattle[.] Personal willingness of native people to assist is essential.” This statement is an interesting reflection on the tenor of the times. The sad part of all of this is that, with few exceptions, little research appears to have been done in that period with the explicit aim of helping to improve the health of Aboriginal and Torres Strait Islanders. Most researchers reflected the prevailing mood, but there were occasional exceptions, continuing the tradition of individual doctors arguing for a wholly different viewpoint against the mainstream, and perhaps with more than a little effect. There is much in this book for those with an interest in doctors’ role over a 100-year period in one of the major unresolved issues in Australian public health. Ian T RingEpidemiologist Health Information Centre Queensland Health, Brisbane, QLD

Ian T Ring

Children of parents with mental illness. Personal and clinical perspectives. Vicki Cowling (editor). Melbourne: ACER Press, 2004 (xix + 242 pp). ISBN 0 86431 473 6. It is difficult to believe that only a short time ago parents were routinely vilified when their children developed psychiatric illness. Obvious examples are “the schizophrenogenic mother” and the lack of maternal communication skills that were blamed for the development of autism. Since we have come to understand the biological basis of psychiatric disorders, such blaming concepts appear foolish. On the other hand, people who are or who will become parents may suffer from mental illness. The children of these parents may be affected through genetic inheritance, quality of parenting, family relationships, and psychosocial adversity. The editor, a social worker and psychologist, has estimated that, in 1995, 27 000 Australian children were affected by maternal psychosis alone. Many ill parents parent well, and not all children are affected, but up to two-thirds probably experience negative consequences. Amazingly, the needs of these children have been largely ignored. Cowling has brought together 20 contributors from various disciplines to produce a highly instructive book addressing “coalface” issues for children of mentally ill parents. Four of the contributors had experienced parents suffering from schizophrenia, depression, bipolar disorder and Huntington’s disease. These personal accounts are extraordinarily revealing and I regret that there were not more of them included. The first part of the book provides some vital background information on the genetics, behavioural and psychosocial effects of major psychiatric illnesses. An excellent chapter outlines the possible impact of different illnesses and their symptoms on infants and children of different ages. Different treatments for disorders, as well as preventive interventions, are also outlined. The role of the partner of the mentally ill parent and wider family ramifications are also considered. There is a chapter with advice on how to talk to children and another that examines the impact on adolescents. In a welcome departure from the political correctness of cognitive behaviour therapy, a chapter relates anecdotes from the psychoanalysis of an 11-year-old boy who had been adopted away from his mentally ill mother at the age of 2½. There are other chapters on placing children in out-of-home care and adoption. A highlight of the book is its description of peer-support activities — various ways of organising group therapy for children of parents with mental illness. Group peer support combats isolation, shame and despondency and the benefits of group therapy can be enormous, but are frequently underestimated. In summary, this is a book that provides irreplaceable insights about children whose parents have mental illness. I found most of the book easy to read, highly instructive and often deeply moving. Medical students and doctors should set aside some reading time for this wonderful book. Nicholas A KeksPsychiatrist Box Hill, VIC

Nicholas A Keks

Heavy metal — Indian style US researchers have warned that users of some Ayurvedic (traditional Indian) herbal medicine products may be at risk for heavy metal toxicity. They found that 14 of 70 (ie, 1 in 5) of such products manufactured in South Asia intended for oral use and available for sale in the Boston area — including several recommended for paediatric use — contained potentially harmful levels of lead, mercury and/or arsenic. The researchers said that, in the US, imported Ayurvedic herbal medicine products have not required proof of efficacy or safety, as they are marketed as dietary supplements. They called for mandatory testing of these products for toxic heavy metals, and also suggested that doctors consider intake of Ayurvedic herbal medicine products in the differential diagnosis of unexplained heavy metal toxicity. JAMA 2004; 292: 2868-2873 Keyhole prostatectomy Minimally invasive laparoscopic radical prostatectomy can be safe and effective for treating prostate cancer, according to a report from New Zealand. A single surgeon, experienced in laparoscopic surgery, has undertaken this procedure successfully in an initial series of 30 patients. With increasing experience, the operating time required fell from about 7 hours to about 4 hours. No conversions to open surgery or reoperations were required. Advantages over open surgery included less blood loss, less pain, a shorter hospital stay and an earlier return to normal activity. At 6-month follow-up, continence rates were 83%. A laparoscopic nerve-sparing procedure was not offered, so all patients in this series were either impotent preoperatively or uninterested in maintaining potency.1 The Australian author of an accompanying commentary said that telerobotic prostatectomy could dramatically reduce the (much-vaunted) learning curve for this procedure.2 1. Aust N Z J Surg 2004; 74: 1065-1068 2. Aust N Z J Surg 2004; 74: 1038 Works like a charm Wearing a magnetic wrist bracelet could help to reduce osteoarthritis-related pain in joints elsewhere in the body, say UK researchers. They conducted a randomised, placebo-controlled trial in five rural general practices, involving 194 men and women with osteoarthritis of the hip or knee. The researchers wanted to compare the effect of standard-strength magnetic bracelets (mean strength of 186 mTesla) with "weak" magnetic bracelets (which turned out to be of variable strengths due to a manufacturing error) and non-magnetic, dummy bracelets. Pain from osteoarthritis of the hip and knee decreased when wearing the magnetic bracelets, but it is uncertain whether this is a specific or non-specific, placebo effect. BMJ 2004; 329: 1450-1454 Birth risk: what’s your view? A large, multicentre US study of more than 33 000 women with singleton pregnancies and a prior caesarean delivery has found that, compared with an elective repeated caesarean delivery, a trial of labour carries a slightly higher perinatal risk.1 However, an estimated 588 caesarean deliveries would be needed to prevent a severe adverse perinatal outcome.2 Of note, women with clear indications for a caesarean delivery were excluded from the study. 1. N Engl J Med 2004; 351: 2581-2589 2. N Engl J Med 2004; 351: 2647-2649 Armed ovary Autotransplantation of an ovary to a patient’s upper arm could help cervical cancer patients sidestep the premature ovarian failure and infertility that can follow postoperative radiotherapy. Dutch doctors have now successfully completed this procedure in a 29-year-old woman from Suriname, South America, after anastomosing the ovarian artery and vein to the brachial artery and basilic vein, respectively. Although the patient declined postoperative radiotherapy because of severe homesickness and subsequently experienced local recurrences of malignant disease, the transplanted ovary demonstrated adequate function over more than one year of follow-up. The patient experienced cyclic swellings of the upper arm without major discomfort, and ultrasound monitoring showed follicular activity at different stages. Cancer 2004; Nov 8 (Epub) Acu-moxi in Bell’s palsy Acupuncture and moxibustion — acu-moxi — may be beneficial in treating facial palsy, according to Chinese researchers. They conducted a multicentre, randomised, single-blind trial in 480 patients with unilateral Bell’s palsy, comparing the effects of acu-moxi with a program of prednisone, vitamin B1 and B12, and oral dibazole, administered with or without acu-moxi. The researchers found that acu-moxi treatment alone led to the best improvement in scores of facial paralysis and disability. Further, treatment was more effective in cases of mild and acute (less than 8 days since onset) facial paralysis than in severe and non-acute (from 8 to 90 days) cases. Severe side effects, such as fainting during acupuncture and scalding during moxibustion, were not encountered in this trial. (Moxibustion involves the burning of a herb, in this case applied indirectly.) Chin Med J (Engl) 2004; 117: 1502-1506 Dr Ann Gregory, MJA

Ann Gregory