Volume 185 Issue 7

Australians look forward to dividends from increased funding Despite our relatively small population, Australia has made an impressive global impact in health and medical research (HMR). Our research output is twice the Organisation for Economic Co-operation and Development (OECD) average on a per capita basis,1 with high international visibility by citation,2-4 and Australia boasts five Nobel Prizes in Physiology or Medicine. HMR is a “golden egg”. Its consequences — disease prevention, improved longevity and quality of life — reduce hospital admissions and stays, and contribute to both workforce productivity and wealth creation. Examples of outstanding success in Australian translational HMR include Frazer’s cervical cancer vaccine, Cade’s use of lithium for treating bipolar disorder, Clark’s bionic ear technology, and Marshall and Warren’s unravelling of the role of Helicobacter pylori in peptic ulcer. The Access Economics report commissioned by the Australian Society for Medical Research in 2003 put figures on the value of the golden egg: every dollar invested in health research and development (R&D) yields an average annual return of $5.5 Despite these successes, and the Australian Government’s visionary legislation for a 6-year phased-in doubling of the National Health and Medical Research Council (NHMRC) budget enacted in 1999, Australia has slipped down the OECD ladder in terms of government spending on health R&D (this was 0.12% of gross domestic product [GDP] just a few years ago, compared with the OECD average of 0.2%).1 Many of Australia’s best and brightest health and medical researchers, judged by their peers to be in the top 10% internationally, have been missing out on NHMRC Fellowship support (almost 35% of applicants scoring in the “excellent” category were not funded in 2005). Moreover, without further increased HMR spending, projections indicate that success rates for Fellowships would fall by a further 50% by 2011, with project grant success rates dropping from 21% in 2006 to 8%–9% in 2011. This 5-year scenario, however, was averted in the May federal budget when the government allocated an additional $905 million for HMR. This injection was universally applauded and includes $670 million to be administered by the NHMRC, made up of $500 million over 4 years for research grants, and $170 million for Australian HMR Fellowships which will run over the next 9 years supporting 50–65 outstanding researchers over 5-year terms. The $500 million for grants will be incorporated into NHMRC’s base allocation for research, increasing this from $420 million in 2006 to over $700 million by 2010. The NHMRC will continue to serve as the main administrator of these funds, as it should, for transparency and equitable distribution based on peer review. The remaining $235 million earmarked in the federal budget for HMR will support adult stem-cell research ($22 million) and infrastructure and capital works programs shared among 17 research facilities nationally ($213 million). This is on top of the $200 million in infrastructure provided to institutes last year, builds on Wills’ Strategic review,2 and is the government’s response to the 2004 Grant Investment review.1 The NHMRC has now become a statutory agency. This development strengthens its independence and facilitates clear lines of responsibility for governance and financial accountability. Increased funding coupled with this restructure provides a key opportunity for the NHMRC to improve HMR outcomes through new strategic initiatives, wide-ranging stakeholder consultation, organisational resource-building, and articulating its vision and plan early in its triennium. A recent editorial in the Journal suggested that much of the NHMRC’s success under the new governance structure would be dependent on effective leadership by the new Chief Executive Officer (CEO), who now reports directly to the Health Minister.6 The NHMRC’s new CEO is Warwick Anderson, past Head of the School of Biomedical Sciences at Monash University, and its Chair is Michael Good, Director of the Queensland Institute of Medical Research. In April last year, Anderson described 10 challenges for Australian HMR, which included the capacity to respond rapidly to national and international health needs, improving collaborative links, enhancing our strong record of discovery-based research, and developing a more “wide and deep” workforce.7 Effective change will require a fresh look at policy by the NHMRC and all levels of government, for example, by (i) encouraging increased private sector investment from sources “outside the square” (eg, health and superannuation funds, life insurance companies), possibly through tax incentives; (ii) expanding established schemes (ie, development grants) for increased leverage of non-government monies; (iii) greater recognition of high-performing “David” (rather than “Goliath”) research organisations, that may be embedded in universities and hospitals, with adequate infrastructure support; (iv) restoring faith in career structure for the nation’s best health and medical researchers (eg, narrowing the growing gulf between Career Development Awards and Fellowships; providing local allowances for Fellows just as allowances are provided to C J Martin overseas postdoctoral Fellows depending on location; and encouraging more clinician–scientist researchers into the sector); (v) increased state government support of HMR, building on local strengths in technology and innovation (eg, “Smart State” and “Health Futures” initiatives); (vi) ensuring Australia’s record of groundbreaking fundamental research is not compromised by the “translational (applied research) wave”; and (vii) ensuring health services and population health research continue to develop in capacity and quality, as these will be increasingly relied on as the population ages and socioeconomic differentials widen. The longer term needs to be in our sights, and we should be mindful of sustainability in the post-2010 era, particularly if issues arising from the now complete doubling of the United States National Institutes of Health budget are any guide.8 This is true of the Australian HMR Fellowship scheme, which will attract top scientists (including the most senior NHMRC Fellows, presumably drawing more junior Fellows into the existing scheme), yet the program’s fate is unclear after individual terms. Moreover, even with increased HMR investment, which starts with a modest (around 5%) increase in 2007, the NHMRC has received close to 30% more applications for project grants this year compared with 2005, which may negatively impact on success rates, and mean missed opportunities for knowledge, health and wealth creation unless additional funds can be sourced for 2007. This becomes more of a concern in the current evaluation round, despite commendable intentions of improving efficiency and reducing “reviewer fatigue”, given the absence of external peer review or the opportunity for applicant rebuttal. Mechanisms of perpetually increasing funding for HMR should therefore be explored and debated. This could include indexing the HMR budget to the health budget or the OECD average for government HMR funding. Investment in HMR is vital and should be an ongoing priority for any government in the developed world. Greater funding will help Australian researchers build on previous gains, and turn both curiosity-driven and priority-driven knowledge into new medicines and treatments, with flow-on health, social and economic returns nationally and abroad. We are opening an exciting new chapter in Australian HMR and I can’t wait to turn the pages.

Levon M Khachigian PhD, DSc

Napping at night may benefit both health professionals and their patients Delivering medical care is a 24-hour business that inevitably involves working the night shift. However, night shift requires the health professional to work when the body’s clock (circadian system) demands sleep. Added to this is the problem of “sleep debt”, arising from both prolonged prior wakefulness on the first night shift and cumulative sleep debt after several nights’ work and repeated unsatisfactory daytime sleeps. A further aggravation, particularly for trainee medical staff in teaching hospitals, has been the demand for excessive work hours across the working week. As has been dramatically shown in recent well controlled studies, the net result of this assault on the sleep of health professionals can be impaired patient safety,1 and the health and safety of health professionals themselves.2 The good news is that health organisations and regulators are beginning to treat the matter seriously. In Australia, the United States and Europe, work hours of medical staff have recently been shortened by government regulation, and bodies such as the Australian Medical Association and professional colleges are advising their members on strategies to improve their sleep health and thus work safety. A recent publication prepared by the Royal College of Physicians (London) (RCP), Working the night shift: preparation, survival and recovery. A guide for junior doctors, is an excellent example.3 One proposed countermeasure for excessive sleepiness is the use of strategically placed naps both before and during the night shift. But does napping either before or during the night shift reduce sleepiness and improve performance, and, if so, how practical is it? There are two important, independent mechanisms of sleep and sleepiness that hold the key to these questions.4 Probably the more potent mechanism impairing night-shift alertness is the circadian system. For most individuals, even those working permanent night shift, the circadian system is in sleep mode during the night. This causes slowed reactions, increased feelings of fatigue, impaired concentration, and increased sleep propensity. The second important mechanism affecting night-time alertness is homeostatic sleep drive. This increases in intensity the longer we are awake and, like appetite which is sated by eating, homeostatic sleep drive is reduced by sleeping. If the first night shift starts at midnight following a normal wake time at about 8 am, about 16 hours of wake sleep debt has already been accrued and the rest of the night shift will be performed under intense homeostatic, in addition to circadian, sleep drive. Performance decrements during this night period can be similar to those measured in the daytime with a blood alcohol concentration of 0.05%–0.10%.5 Day sleep in the home environment is likely to be shorter and less effective than night sleep so, even though second and subsequent night shifts may follow fewer wakeful hours (8–10 hours), homeostatic sleep drive is likely to remain elevated during night shifts because of incomplete repayment of the previous sleep debt. To a limited extent, it is possible to “bank” sleep (or pay off residual sleep debt) before the first night shift, potentially reducing subsequent night-time homeostatic sleep drive and improving alertness and work safety. A long (1–2 hours) nap in the afternoon, as recommended in the RCP report, is best. Afternoon sleep is more efficient than early evening sleep as it uses the natural afternoon “dip” in circadian physiology6 and avoids the risk of post-sleep grogginess or sleep inertia impinging on the start of night duty. Between subsequent night shifts, the aim should be to maximise daytime sleep length (at least 7 hours) and efficiency by including the afternoon sleepy period (1–4 pm). What about napping during a night shift to improve alertness and reduce errors and accidents? Brief afternoon naps of 10–30 minutes (so-called power naps) improve alertness and performance. We compared afternoon naps of 5, 10, 20, and 30 minutes of total sleep.7 The 10 minute sleep (about a 15 minute nap opportunity) produced improvements over the 3 hour post-nap period in all eight alertness and performance measures, without any of the post-nap impairment of sleep inertia that followed the 20 and 30 minute naps. Whether these results would be replicated at, say, 3 am in a night-shift environment, with considerably greater homeostatic and circadian sleep drive, is now being tested. Only a few studies have measured the effects of night-shift napping. Long naps of about 2 hours appear as effective at about 3 am as at 3 pm.8 However, 1–2 hour naps were followed by sleep inertia, during which alertness was impaired for up to an hour.9 Longer naps, although beneficial once sleep inertia has been dissipated, may be used reluctantly by medical staff wishing to maintain continuity of patient care.10 Briefer naps (18–26 minutes) have also improved performance in night-shift environments.11 Therefore, the picture emerging from night-shift napping studies is similar to that from the afternoon studies. Very brief naps (10–15 minutes of sleep) may improve alertness immediately without the negative effects of sleep inertia. How long this improvement lasts and what is the optimal nap length on the night shift remains to be determined. In the meantime, as recommended in the recent RCP guide, health professionals who work night shift should, for the sake of their own health and safety and that of their patients, consider the benefits of night-shift napping. Optimal benefit and a higher take-up rate are likely for sleep lengths of 10–15 minutes.

R Doug McEvoy MD, FRACP, BMedSc · Leon L Lack BA, PhD

Medicare funding could jeopardise the research needed to establish the benefits and risks of this procedure Recent publications and regulatory decisions about the therapeutic use of vertebroplasty, or injection of bone cement into diseased vertebrae such as osteoporotic fractures, call for a closer look at the evidence. New drug treatments are not considered to have proven efficacy until, at the very least, they have been evaluated in randomised controlled trials. Even then, their safety is not guaranteed, particularly for uncommon adverse effects, or those for which there is a long delay between exposure and clinical manifestation. Adverse effects that have a high prevalence may also be difficult to detect, as exemplified by the much-delayed recognition of the association between myocardial infarction and strokes and rofecoxib.1 In Australia, drugs must also be shown to be cost-effective compared with existing subsidised treatments before they are accepted into the Pharmaceutical Benefits Scheme. The Medical Services Advisory Committee (MSAC) recently recommended vertebroplasty for interim public funding for restricted indications, including painful osteoporotic vertebral compression fractures confirmed by diagnostic imaging and not controlled by conservative medical therapy.2 While technology appraisals of vertebroplasty by health policymakers in a variety of settings, including Australia, have recognised that there is inadequate high-quality evidence on which to base a reimbursement decision, many have subsequently recommended public funding.3 Making these reimbursement decisions in the face of limited evidence raises some concerns. Firstly, while uncontrolled studies have suggested that vertebroplasty may be an efficacious treatment for painful osteoporotic spinal fractures not responsive to conservative management, uncontrolled studies tend to overestimate treatment benefit for a variety of reasons.4 They fail to take into account the natural history of the condition, which is that it improves over time; they make no allowance for the statistical artefact of “regression to the mean”; and they do not adjust for the placebo response, which is likely to be accentuated with an invasive procedure.5 At present, the best available evidence for efficacy of vertebroplasty are data from two controlled before–after studies that compared volunteers who were offered the treatment with those who refused it.6,7 This constitutes level III-2 evidence in the National Health and Medical Research Council (NHMRC) hierarchy of levels of evidence, which ranges from I for the highest level to IV for the lowest level.8 While these studies showed an early benefit of vertebroplasty over conservative treatment, it is likely that they too have overestimated the treatment effect,9 particularly as volunteers who agree to have a new therapy are known to have a better outcome than those who refuse it. Patient self-selection bias in one study meant that, in comparison to those who refused treatment, those who agreed were considerably more disabled at baseline and so had more potential to improve.6 Participants in the other study were treated relatively early after presentation with an acute vertebral fracture, and most of them were admitted as inpatients, so the results may not be relevant to patients who have had pain for longer than a few weeks.7 Of more concern than questionable efficacy is the potential for harm. The risk of subsequent vertebral fracture once a spinal fracture has occurred in patients not exposed to vertebroplasty is very high — the risk within a year of a single vertebral fracture has been estimated to be about 20% in those with untreated osteoporosis and about 10% in those treated with bisphosphonates.10 Several uncontrolled studies have now suggested an increased incidence of vertebral fractures after vertebroplasty, particularly in vertebrae adjacent to treated levels or if cement has leaked into the adjacent disc,11,12 while the two controlled before–after studies have yielded conflicting results in this regard.6,7 Yet, like heart attacks and strokes with rofecoxib, in the absence of rigorous controlled trials that are powered to detect an increased incidence of an already prevalent condition, this may take time to become evident. Furthermore, while the risk of immediate complications (such as cement leakage into the spinal canal, adjacent disc and venous circulation) from the procedure when it is performed by experienced operators, is estimated from published case series to be low, it is likely that the incidence of immediate complications will be higher in routine use, where there is likely to be a learning curve, and there are no restrictions on who can perform the procedure.13 Now that proponents of vertebroplasty have the imprimatur of MSAC approval, promotion of this procedure to the medical community and the public has intensified. For example, a recent “advertorial” in Australian Family Physician claimed that vertebroplasty is a safe, effective, and cost-effective procedure when performed in an appropriate technical environment by adequately trained interventional radiologists.14 Yet, as outlined above, the available evidence is weak and does not justify these strong claims. The way forward is to gather the necessary evidence. To this end, a multicentre, randomised, double-blind, placebo-controlled trial of vertebroplasty for painful osteoporotic spinal fractures has been funded by the NHMRC and is currently underway in Australia. In addition to gathering evidence on short-term efficacy, all trial participants are being followed up for 2 years so that the question of long-term safety and, in particular, risk of future fractures can be assessed. However, public funding of vertebroplasty through Medicare has the potential to seriously undermine the success of this and other trials by not only providing easy access to an unproven treatment, but also by lending implicit support to its use. This may result in a situation where the true effects of this treatment may never be established. At present, the trial has recruited almost a quarter of the required sample and, at the current rate of recruitment, is expected to be complete within 4 years. A second randomised, double-blind, placebo-controlled trial of vertebroplasty for osteoporotic spinal fractures is in progress in the United States. These trials will provide pivotal evidence on the value of vertebroplasty. At present, vertebroplasty, while promising, is of unproven safety, effectiveness and cost-effectiveness. Thus, the promotion and routine use of this procedure outside of the research setting remains unjustified and premature, and the onus remains on the proponents of vertebroplasty to prove their claims. Primum non nocere, or first, do no harm.

Rachelle Buchbinder MB BS(Hons), MSc, FRACP · Richard H Osborne PhD

Rotavirus vaccines are finally available, and introducing them into the routine vaccination schedule will have a significant impact on the health of children After a dramatic false start, oral rotavirus vaccines are now available to prevent severe, dehydrating diarrhoea in small children. Rotavirus infection in children can be as severe as cholera in adults, but affects a group who cannot complain. Since its discovery in Australia in 1973, rotavirus has become accepted as the single most common cause of severe diarrhoea in children worldwide. It still kills over 500 000 young children each year. In Australia, it is estimated that 10 000 children require hospitalisation annually1,2 (more than 4000 actually coded for proven rotavirus3), and as Schultz reports in this issue of the Journal, the impact on Indigenous children is especially severe.4 Oral rehydration has greatly reduced mortality, but the World Health Organization recognises the potential of rotavirus vaccines to further reduce under-5-year mortality rates, Goal 4 of the Millenium Development Goals.5 It is exciting to have two efficacious oral rotavirus vaccines, RotaRix (GlaxoSmithKline [GSK], Boronia, VIC) and RotaTeq (Merck/CSL, Parkville, VIC) licensed this year in Australia. Each has been extensively tested in placebo-controlled trials of more than 60 000 participants. Both vaccines prevented severe disease, and reduced the need for hospitalisation by 85%–94%. There was a reassuring lack of intussusception, a rare (one in 10 000–32 000) event associated with RotaShield, the first licensed rotavirus vaccine, which led to its withdrawal from the United States market in 1999, just 12 months after its introduction.6 Re-analysis of the data suggested that the intussusception risk emerged in infants receiving the first vaccine dose after 3 months of age.7 Thus both GSK and Merck/CSL state that the first dose should be administered before that time. Several issues remain to be resolved with these two new vaccines. Efficacy has not been established in developing countries. Availability will depend on distribution (including the need for a cold chain), the ability to piggyback rotavirus vaccines with other routine vaccinations, and manufacturing capacity. The greatest uncertainty is the cost of the vaccine. Current prices exceed $200 per course in the private market. While tier pricing and subsidisation by international agencies for poorer countries is being considered, it is not clear whether these mechanisms will sustain programs in most parts of the world. Hence, other candidate vaccines linked to developing country manufacture are under early development in China, India, Indonesia and elsewhere. Who should get rotavirus vaccine in Australia? Ideally all children under 3 months of age, as all will eventually be exposed to rotavirus, and one in 25 will be admitted to hospital for rotavirus gastroenteritis during the first 5 years of life. Morbidity across our country is high. Apart from the 10 000 annual hospital admissions, there are 22 000 visits to emergency departments and 115 000 visits to general practitioners.2 Nosocomial infection rates are as high as 14% in children’s hospital wards and may be higher in childcare centres.8,9 Schultz’s report indicates that Indigenous children have 2–4 times the disease burden of non-Indigenous children.4 Gastroenteritis in Indigenous children comes with comorbidities and a significantly increased average length of hospital stay. Add to that the large costs of air transport of patients for hospital admission in northern and western Australia and the disruption to remote families, and the case for rotavirus vaccination of Indigenous infants becomes compelling. The Northern Territory Health Department recognised the importance of rotavirus infection by making it a notifiable disease, and Queensland recently followed suit. Breaking news is that from October 2006, the NT Government will include rotavirus vaccine in the routine vaccination schedule for NT children.10 The only real issue is cost. A 1999 cost–benefit analysis suggested that break-even vaccine cost was $78 per course,11 somewhat less than current prices. However, the community should be prepared to pay something to prevent this wretched disease. For maximum benefit, the first dose should be given before 3 months of age. Infants under 6 months of age accounted for 24% and 9% of rotavirus gastroenteritis cases in studies in the NT and Melbourne, respectively.4,12 In Africa, many infants are infected in the first 2 weeks of life.13 There is enthusiasm for giving the first dose of vaccine within the first month of life, but neither licensed vaccine has been tested at this age. Roll-out of a universal program in Australia has a few caveats. The inevitable concern about intussusception, in spite of the reassuring clinical trial results, probably means that catch-up campaigns, where the first dose is given after 3 months of age, will not happen. Evidence of the spectrum of protection afforded by both vaccines against the full range of human rotavirus serotypes is still lacking. There is a need to continue national strain surveillance to ensure that the current vaccines are appropriately protective against the range of serotypes in Australia, and to monitor the effect of vaccine pressure on the evolution of strains. After three decades, there is real excitement at suddenly having such an effective tool to prevent a common, miserable disease affecting infants and children. Rotavirus vaccination is not only justified on the basis of disease burden, but will be welcomed by all who care for sick children. It will not be hard to measure real improvement for Indigenous children in the NT, given the baseline data presented elsewhere in this issue of the Journal.4 While other candidate vaccines are in development, there is no excuse for waiting any longer for a national program. The improvement in child health will be obvious.

Graeme L Barnes MD, FRACP · Ruth F Bishop AO, DSc, PhD

Objective: To present data on rotavirus notifications in the Northern Territory to provide knowledge about the local epidemiology of rotavirus gastroenteritis that can be used to inform the use and funding of rotavirus vaccines.Design: Retrospective analysis of data from the Northern Territory Notifiable Diseases Database.Participants and setting: Patients with cases of rotavirus infection notified to the NT Centre for Disease Control from 1 January 1995 to 31 December 2004.Main outcome measures: Patterns of rotavirus notifications over time; infection rates in Indigenous versus non-Indigenous children aged 0–5 years; age groups infected with rotavirus.Results: Numbers of rotavirus notifications over the period 1995–2004 show annual, monthly and regional variability. The rotavirus notification rate for Indigenous children aged 0–5 years was 2.75 per 100 per year, compared with 0.98 for non-Indigenous children, with a relative risk for Indigenous children of 2.17 (95% CI, 1.97–2.39) over the 10 years. Indigenous children infected with rotavirus were younger than non-Indigenous children, with median ages of 11 months and 16 months, respectively. Rotavirus gastroenteritis occurred in outbreaks, transmitted over months throughout the NT.Conclusion: Large numbers of cases of rotavirus gastroenteritis affecting Indigenous and non-Indigenous children in the NT are notified every year. The rate in Indigenous children may be decreasing relative to non-Indigenous children. An effective rotavirus vaccine could prevent significant morbidity.

Rosalie Schultz MB BS, MPH

Objectives: To determine the impact of the Australian provisions for temporary rather than permanent protection for asylum seekers found to be genuine refugees.Design and setting: A comparison of the mental health of Persian-speaking refugees with temporary (n = 49) versus permanent (n = 67) protection visas attending an early intervention program in Sydney, New South Wales, 2002–03.Measures: Standard measures were used to assess past trauma, detention experiences, postmigration stresses, symptoms of post-traumatic stress disorder (PTSD), anxiety, depression and functional impairment.Results: The two groups had experienced similar levels of past trauma and persecution. Nevertheless, holders of temporary protection visas (TPVs) returned higher scores on three psychiatric symptom measures (P < 0.001). Multivariate analyses showed that TPV status was the strongest predictor of anxiety, depression and particularly PTSD. Further analyses suggested that, for TPV holders, experience of past stresses in detention in Australia and ongoing living difficulties after release contributed to adverse psychiatric outcomes.Conclusions: The sequence of postmigration stresses experienced by TPV holders appears to impact adversely on their mental health.

Shakeh Momartin PhD, BA(Hons) · Zachary Steel MPsych(Clinical), BA(Hons) · Marianio Coello MPsych(Clinical) · Jorge Aroche MPsych(Clinical) · Derrick M Silove MD, FRANZCP · Robert Brooks PhD, BA(Hons)

Objective: We aimed to assess the pattern of use of drug-eluting stents (DESs) in patients undergoing percutaneous coronary interventions (PCIs) in Victorian public hospitals.Design, setting and patients: Prospective study comparing the use of one or more DESs versus bare-metal stents (BMSs) only, in consecutive patients undergoing 2428 PCIs with stent implantation from 1 April 2004 to 31 December 2005 at seven Victorian public hospitals.Main outcome measures: Adherence to current Victorian Department of Human Services guidelines which recommend DES use in patients with high-risk features for restenosis (diabetes, small vessels, long lesions, in-stent restenotic lesions, chronic total occlusions and bifurcation lesions).Results: Of the 2428 PCIs performed, at least one DES was implanted in 1101 (45.3%) and BMSs only were implanted in 1327 (54.7%). In 87.7% (966/1101) of PCI with DESs, there was at least one criterion for high risk of restenosis. DESs were more likely to be used in patients with diabetes (risk ratio [RR], 2.45; 95% CI, 2.02–2.97), small vessels (RR, 3.35; 95%CI, 2.35–4.76), long lesions (RR, 3.87; 95% CI, 3.23–4.65), in-stent restenotic lesions (RR, 3.98; 95%CI, 2.67–6.06), chronic total occlusions (RR, 1.30; 95% CI, 0.51–2.88) and bifurcation lesions (RR, 2.23; 95%CI, 1.57–3.17). However, 66.2% (1608/2428) of all PCIs were in patients eligible for DESs according to Victorian guidelines, and in 39.9% (642/1608) of these PCIs, a BMS was used.Conclusion: In Victorian public hospitals, DESs have been largely reserved for patients at high risk of restenosis in accordance with Department of Human Services guidelines. However, many patients with high-risk criteria for restenosis did not receive DESs. Greater use of DESs in these patients may improve outcomes by reducing the need for repeat revascularisation.

on behalf of the Melbourne Interventional Group (MIG) investigators

Objective: To review the evidence for the effectiveness of complementary and self-help treatments for depression in children and adolescents.Data sources: Systematic literature search using PubMed, PsycINFO and the Cochrane Library for 131 treatments up to February 2006.Study selection: There were 13 treatments that had been evaluated in intervention studies.Data extraction: Studies on each treatment were reviewed by one author and checked by a second. A consensus was reached for level of evidence.Data synthesis: Relevant evidence was available for glutamine, S-adenosylmethionine, St John’s wort, vitamin C, omega-3 fatty acids, light therapy, massage, art therapy, bibliotherapy, distraction techniques, exercise, relaxation therapy and sleep deprivation. However, the evidence was limited and generally of poor quality. The only treatment with reasonable supporting evidence was light therapy for winter depression.Conclusions: Given that antidepressant medication is not recommended as a first line treatment for children and adolescents with mild to moderate depression, and that the effects of psychological treatments are modest, there is a pressing need to extend the range of treatments available for this age group.

Anthony F Jorm MPsychol, PhD, DSc · Nicholas B Allen MSc, PhD, MAPS · Colin P O'Donnell MB BCh, BAO, MRCPsych · Ruth A Parslow PhD · Rosemary Purcell PhD · Amy J Morgan BASc, BAppSci(Psychol)(Hons)

Complex societal factors unrelated to evidence of efficacy influence the increasing use of complementary and alternative therapies, which can be viewed as one form of health consumerism. The “therapeutic footprint” is a conceptual model that “plots” medical therapies and complementary and alternative therapies in relationship to one another and to their levels of risk and supporting evidence, acknowledging that medical therapies also entail risks. Philosophies about management of risk and adverse effects differ between complementary and alternative therapies and standard medical care, due to fundamental differences between professionalism within medicine and the demands of health consumerism. In standard medical care, patients’ risks are mediated prior to treatment via the doctor–patient relationship and informed consent. With complementary and alternative therapies, protection mechanisms for consumers come into effect mainly after a problem has occurred. Understanding this difference helps doctors whose patients are using complementary or alternative therapies to define the boundaries between these therapies and professional medicine and provide appropriate disclosure of risks. Discussing complementary and alternative therapies and how they differ from standard medical care can provide opportunities to explore patients’ concerns and improve the therapeutic relationship.

Christine R Sanderson BM BS, MPH, FRACP · Bogda Koczwara BM BS, FRACP, MBioethics · David C Currow BMed, MPH, FRACP

Although viewed with scepticism by the medical and scientific community, complementary and alternative medicine (CAM) is being used by about 50% of Australians. Integrative medicine is a holistic approach to cancer care, with some CAM of proven effectiveness being used as adjuvants to conventional medical treatments. However, there is little evidence of a systematic process of evaluation or dialogue between mainstream cancer medicine and CAM providers in Australia. Collaboration, guidance and support for relevant research in this area are needed. The key elements of a process of furthering integrative medicine include improving knowledge about CAM; addressing uncertainties about CAM efficacy and safety; improving communication about CAM between medical practitioners and patients, and between medical practitioners and CAM practitioners; introducing regulatory frameworks and credentialing of CAM practitioners; and addressing ethical issues.

Monica C Robotin FRACS, MBA · Andrew G Penman MACP, MPH

Alzheimer’s disease (AD) is the most prevalent dementia (accounting for 50%–75% of cases of dementia in people aged over 65 years), followed by frontotemporal dementia (FTD) (10%–20% of cases). AD is characterised histopathologically by Aβ-containing amyloid plaques and tau-containing neurofibrillary tangles, whereas FTD exhibits neurofibrillary tangles alone. Current symptomatic treatments of AD are of limited benefit, as they are not directed at the underlying biological basis of the disease. The development of transgenic animal models has provided insight into disease mechanisms and helped define novel drug targets. More than 50 drugs are currently in clinical trials, and novel and more effective drugs targeting both AD and FTD are expected to become available within 5–10 years.

Jürgen Götz PhD · Lars M Ittner MD · Nicole Schonrock PhD

We report a fatal case of acute selenium poisoning in a 75-year-old man. After reading on the Internet about a possible role of selenium in prostate cancer, the patient ingested 10 g of sodium selenite. Despite intensive care treatment, he suffered a cardiac arrest and died 6 hours after ingestion. This case illustrates the risks of failing to critically evaluate Internet information and exposes the myth that natural therapies are inherently safe. Clinical recordAfter a single test showing a raised level of prostate-specific antigen, a 75-year-old man became concerned about prostate cancer. Without confirmation of the diagnosis, he researched prostate cancer on the Internet and discovered that selenium may have a role in its prevention and treatment. He purchased sodium selenite powder and tablets from two separate pharmacies for supplementation. He presented to the emergency department with vomiting and diarrhoea at 10:30 am, 3.5 hours after ingesting 10 g of sodium selenite (purity, 96%). He had significant abdominal pain, poor perfusion, and hypotension, with a pulse rate of 76 beats per minute, blood pressure of 75/45 mmHg, and prolonged QT interval. Arterial blood gas examination (breathing 60% O2) showed pH, 7.325 (reference range [RR], 7.35–7.45); PO2, 122 mmHg (RR, 85–100 mmHg); Pco2, 22.4 mmHg (RR, 35–45 mmHg); and HCO3 concentration, 11 mmol/L (RR, 22–28 mmol/L). He also had hypokalaemia (serum potassium concentration, 3.4 mmol/L [RR, 3.5–5.0 mmol/L]). A blood specimen collected at this time later showed a serum selenium level of 68.0 μmol/L (RR, 0.6–2.3 μmol/L). The patient was transferred to the intensive care unit, where fluid resuscitation was continued, and a dobutamine infusion was begun. He remained hypotensive (blood pressure, 85/50 mmHg) but conscious. At 12:10, he developed significant ventricular tachycardia, interspersed with normal complexes with ST depression. Repeat blood gas tests showed worsening acidosis and hypokalaemia. Magnesium (10 mmol) and potassium (25 mmol) were administered intravenously over 40 minutes. Dysrhythmia persisted and worsened. Lignocaine was added with no response. The patient suffered a cardiac arrest, and cardiopulmonary resuscitation was begun. Arterial blood gas analysis performed during the arrest revealed a sudden rise in serum potassium level, to 8.8 mmol/L. Throughout the arrest, rhythms varied, from asystole to broad complex bradycardia to some narrow complexes with an output. Despite cardiopulmonary resuscitation, asystole became permanent and unresponsive. The patient’s pupils became fixed and dilated, and cardiopulmonary resuscitation was ceased. The case was referred to the Coroner who confirmed the cause of death to be acute selenium toxicity. DiscussionThe growth in the use of complementary and alternative medicine in Australia has been well documented.1 Selenium is an essential trace element and an important constituent of the antioxidant glutathione peroxidase.2,3 It is found in many foods, including seafood, grains and eggs,2 and dietary intake is usually 20–300 μg/day.4 An intake below 400 μg/day is considered safe for almost all individuals.5 In Australia, selenium tablets are marketed as a health supplement, while sodium selenite powder is mainly used as a livestock supplement for animals grazing on selenium-deficient soil. Selenium has been discussed in many epidemiological investigations into prevention and treatment of cancer, especially prostate carcinoma.6,7 Excessive doses of selenium result in intoxication, which is characterised by continuous vomiting, garlicky breath, mucosal irritation, abdominal pain, hypersalivation, haemolysis, necrosis of the liver, cerebral and pulmonary oedema, coma and death.3,8 Selenium presents a nutritional conundrum because of its dual status as an essential but highly toxic trace element.9 The exact mechanism of selenium toxicity is as yet unknown.8,10 It has been suggested that the ready substitution of selenium for sulfur in biochemical reactions may inactivate the sulfhydryl enzymes necessary for oxidative reactions in cellular respiration,10 contributing to the acute toxic effect. Cases of selenium poisoning are rare, with Gasmi et al citing only 18 documented cases before 1997, half of them fatal, generally as a result of cardiocirculatory failure and/or pulmonary oedema.11 Although there is no defined point at which selenium becomes toxic, our patient consumed about 10 g of sodium selenite and, 4 hours after ingestion, had a serum level of 68.0 μmol/L (RR, 0.6–2.3 μmol/L), which proved fatal. The ingested quantity of 10 g was about 10 000 times the recommended daily dose of supplemental selenium. It is almost impossible to rapidly reduce a patient’s serum selenium level, as absorbed selenium is mostly contained in erythrocytes or bound to α- or β-globulins. For this reason, haemodialysis is not an established treatment for selenium intoxication, but may reduce serum selenium levels slightly.8 In regard to our patient’s hyperkalaemia, the extracellular potassium level is expected to increase in metabolic acidosis. However, our patient showed a progressively worsening metabolic acidosis with a falling potassium level. The administration of 25 mmoles of potassium over 40 minutes would be expected to raise the serum potassium level, but did not account for the sudden and dramatic rise, from 3.2 mmol/L to 8.8 mmol/L. This sudden hyperkalaemia has not been described in previous cases of selenium toxicity. A brief Internet search revealed 287 000 sites discussing the use of selenium in prevention and treatment of prostate cancer. This provides the public with large amounts of information that is not critically evaluated for validity. After reading Internet information on the possible link between selenium and prevention and treatment of prostate cancer, our patient was able to purchase 200 g of sodium selenite powder without adequate instructions. He selected a dose himself, with catastrophic consequences. This case highlights the risks associated with failure to critically evaluate Internet material and exposes the myth that natural therapies are inherently safe. Internet sites which fail to disclose the potentially fatal effects of advocated treatments are an emerging threat to health. The World Health Organization has devised guidelines to help consumers evaluate medical information on the Internet, which are available online through the Therapeutic Goods Administration.12 Adverse outcomes of complementary and alternative medicines should be better publicised and more stringently reported to the Adverse Drug Reactions Advisory Committee (ADRAC), in tandem with adverse outcomes of conventional medications, to create a database of side effects of all current therapies.

Katharine A See · Peter S Lavercombe FRACP, FJFICM, MBA(Dist) · Jasmine Dillon MB BS, BSci · Riesa Ginsberg FRACEM

. . . a ceaseless flow of students, nurses, doctors, orderlies: fetching and carrying, advising; servants to the patient and their attendant team. Half a dozen medical students have spent the night in the Emergency Department, as the first flight from Bali brings in a dozen or so patients at 2 am. Twenty-six hours earlier, bombs destroyed two nightclubs packed with tourists and local residents at Kuta Beach, Bali.1 Most of the first casualties to arrive are able to walk and, although their injuries are severe, they are soon ministered to in Area 3 (the “walking wounded”) and sent off to the ward. At 5 am, as the first shift of students retires to sleep, the next batch arrives: six 3rd years (of which I am one), Matthias from Switzerland and a couple of 4th years. Didier, Director of Emergency, fills us in on what is happening and tells us to distribute ourselves into the three emergency rooms and two wards: our job is to act as runners, gophers, and extra hands. There is an unseemly wrangling for the best position, but as it turns out we all play our part. In fact, as it turned out, there weren’t enough of us to go round! Word comes that the next flight is due at 6:30 am, so there is time for a bit of a snooze and some nervous chitchat: a seasoned nurse confesses to feeling terrified that she will not be able to cope, that she won’t know what to do. Didier is on the phone constantly; there is a busy flow of information from the airport, from Bali, from interstate hospitals (Box 1). He keeps everyone updated on events as they unfold. Finally, the plane has landed; there are 30 patients, all are severely burnt, one so severely that we can’t tell if it is a man or a woman; six are already earmarked for the Intensive Care Unit. There is a flurry of last-minute instructions and reminders: Didier does his Churchill speech: “. . . great medicine . . . important . . . teamwork . . . faith in you all . . .” It could sound trite, but he means it and he will be proved right. The first ambulance arrives. An ambulance crew wheels in a patient, wrapped in a space blanket, drips and oxygen in a nurse’s hands. An anaesthetist from the airport team reports to Didier: broken forearm, estimated 20%–30% burns to the back and legs, fluids OK, obs stable. An unhurried inspection, a brief conversation with the patient and despatch into the second emergency area: he is not one of the seriously injured patients. The automatic doors at the entrance close on the next stretcher; nobody knows how or if they can be held open — mysteriously, they break and stay open. Ambulances bring patients every 5 minutes, with the same routine: update from the airport doctor, inspection, and triage to the appropriate area (Box 2). The airport team and Didier work in concert to manage the flow: there is always an emergency team waiting to receive each patient, no one is parked in a corridor or left unattended. An ICU patient arrives and is swept upstairs. He’s lucky, a retrieval expert has flown with him from Bali, complete with four bags of emergency equipment. This will mean extra help in ICU for the rest of the day. Emergency Area 1 looks like the inside of an anthill. I have a camera . . . Kerrie, one of the emergency specialists, has asked for some pictures. It’s too early yet for the hospital photographer, so I stand on a table in the resuscitation room, photographing the busy scene below. It looks like madness, but there is a pattern, a disciplined chaos, that resolves into four trolleys — each surrounded by a team of doctors and nurses, standing, quietly busy, playing their parts in a static choreography (Box 3). In between there is a ceaseless flow of students, nurses, doctors, orderlies: fetching and carrying, advising; servants to the patient and their attendant team. A surgeon appears, the first of many, moving from patient to patient, assessing needs and planning the next step in treatment. On my patient, a surgeon is cutting down into the inguinal fold, looking for the femoral artery to plug in a line . . . burns patients leak their body fluids at an alarming rate and we can’t find a vein in his arms or legs to pour liquid into him. Our patient has two bags of fluids up at a time, one with a pressure cuff to squirt it in. I clingwrap a leg which has full thickness burns down one side, while others wrap his arms, back, and buttocks; then we logroll him and see the full extent of the burns on his back. Someone compares the qualities of the different brands of clingwrap — which is the best for burns, which clings and which doesn’t. Jacqui, our team leader, asks the patient if he can remember what happened: “I was sitting at the bar, there was an explosion and I caught fire . . . I rolled on the ground to put it out . . . ” We can tell which side was closest to the bomb — the burns are worse on that side. The nurse asks if he has been in contact with anyone; she brings a mobile phone, so he can phone his mum. The human cost of the bombing strikes home: the burns, shrapnel wounds, infected wounds, blood, urine, moans of pain as we prod and poke. All these make up the professional part of the unfolding drama. We examine and analyse, put up drips, take blood, carefully record the location and extent of burns, peel off bandages, clingwrap body parts. It isn’t hard, it’s not horrific. Not at the time. It’s what we do, the bread and butter of medicine. We fold our professional armour around us with our white gowns. But hearing a young man, twenty-something, good-looking, strong, ask to speak to his mum on the phone — that is the hard part, the side that isn’t protected by a white gown. He’s letting her know he’s alive, that he’s in safe hands (we’ve told him, “you’re in the Royal Darwin Hospital . . . we’ll take care of you”), that he’s going to be all right. But we know he isn’t going to be all right: OK, he will live but, in between our thoughts of what to do next, we know that his future is going to be full of pain and disfigurement and mental trauma, and many of his hopes and dreams were burnt up along with his back and legs. Over on the far trolley, one patient is really seriously ill . . . off to ICU, but not just yet. His arms are burnt all round and the tissue under the burnt skin is swelling, compressing the muscles, slowly killing them, releasing toxins that will inevitably poison him. A surgeon carefully cuts full length down his arm and into his hand, releasing the tight sheath around his muscles, giving them a chance to stay alive. It looks like an anatomy lesson. The surgeon methodically cauterises small arteries, gently holding the patient’s hand as though reading his palm, while the smell of burnt flesh is sucked from the room by the air conditioning. Didier complains about the lack of medical students . . . I think everyone is here; we are all part of the team. Hours pass, and the last patient heads off to the ward: time for a break. There are 10 family-sized pizzas in the tearoom, ordered from the local pizza shop by a wellwisher in Adelaide. I photograph the empty resuscitation room, then snap an emergency nurse beside a neatly made-up trolley, waiting for the next patient — it all looks so normal. Tired people sit and drink tea, eat curry, pizza, sandwiches from downstairs in catering. We go for a walk, up to the ward. Everywhere there are signs of planning and preparation: boxes of fluids, dressings, trolleys, instruments. In the cafeteria are trays of food, cold drinks, desserts . . . the whole hospital plays a part, the “sharp end” functions so well because of those backstage. We hear later of the office staff phoning the families of patients, working as hard as we did to inform, reassure, sympathise; they are at a different sort of sharp end. The next plane lands with 20 more patients and the performance begins again: slick, smooth, fast. After all, we are seasoned now. The first night has been a success, even the students look professional; we are not just runners now. There are tasks to do which are ours: organise bloods; remove dressings; record the history, examination and assessment; clingwrap there, lift here. There are moments of time to watch and appreciate the choreography, the choreographers and the dancers — the emergency teams move with familiar precision and practised teamwork. The ring-ins slowly integrate into their rhythms, so by the end of the day it all seems like some grand ritual. The emergency specialists are like satellites, constantly orbiting each team, assessing, coordinating, advising, helping. By the middle of the afternoon it is pretty much all over for the students. The next plane has just two patients and then there are no more. We walk up to the ward . . . “is there anything we can help with?” We take some blood, struggling to find any sort of vein, finally going for the foot because there is nowhere else. The patient says, “they all find it hard”. One of us has to take blood from a line and doesn’t know how to do it, so I guide her through it: set up a sterile field, glove up, clean the bung, take 10 mL and discard, take the sample, flush the line, flush it again, clean it, clean it . . . it’s precious. It’s time to go home; 12 hours of adrenaline needs dissipating, we need to talk to each other. Someone offers his place, another cooks dinner; we have a beer and begin the debrief, reliving the day. For the next 2 days we are tired. There is a sense of anticlimax. The normal world has gone on around us and it goes on still. Suddenly, the hospital looks no different, except for odd stacks of boxes here and there that have yet to be returned to stores. We have an official debrief and hear the big picture — the confidence that Darwin could handle it, the thoroughness in the planning. We hear the stories from other places, and we praise the work of Denpasar Hospital and the Balinese, and our colleagues there, and on the tarmac at the airports. We feel important and proud to have been part of the grand dance. But someone asks about our patients: where have they gone and how are they and will they be all right; and there is a moment’s quiet, and we each have our own thoughts. 1 “Didier is on the phone constantly” 2 “Ambulances bring patients every 5 minutes” 3 “Trolleys — each surrounded by a team of doctors and nurses”

David E Chapman BA, BM BS

Food allergies in children present with a wide spectrum of clinical manifestations, including anaphylaxis, urticaria, angioedema, atopic dermatitis and gastrointestinal symptoms (such as vomiting, diarrhoea and failure to thrive). Symptoms usually begin in the first 2 years of life, often after the first known exposure to the food. Immediate reactions (occurring between several minutes and 2 hours after ingestion) are likely to be IgE-mediated and can usually be detected by skin prick testing (SPT) or measuring food-specific serum IgE antibody levels. Over 90% of IgE-mediated food allergies in childhood are caused by eight foods: cows milk, hens egg, soy, peanuts, tree nuts (and seeds), wheat, fish and shellfish. Anaphylaxis is a severe and potentially life-threatening form of IgE-mediated food allergy that requires prescription of self-injectable adrenaline. Delayed-onset reactions (occurring within several hours to days after ingestion) are often difficult to diagnose. They are usually SPT negative, and elimination or challenge protocols are required to make a definitive diagnosis. These forms of food allergy are not usually associated with anaphylaxis. The mainstay of diagnosis and management of food allergies is correct identification and avoidance of the offending antigen. Children often develop tolerance to cows milk, egg, soy and wheat by school age, whereas allergies to nuts and shellfish are more likely to be lifelong.

Katrina J Allen MB BS, FRACP, PhD · David J Hill MB BS, FRACP · Ralf G Heine FRACP, MD

Eosinophilic oesophagitis (EO), an isolated eosinophilic inflammation of the oesophagus, is the most common of the eosinophilic gastrointestinal disorders. EO is of increasing clinical significance in many developed countries,1 in parallel with the recent increase in food allergic disorders. A retrospective study of Western Australian children reported a dramatic rise in prevalence of EO (from 0.05 cases per 10 000 children in 1995 to 0.89 cases per 10 000 children in 2004) (Level III-2).2 The estimated prevalence in the US population aged 0–19 years is even higher, at 4.3 cases per 10 000 individuals.3 Clinical features. Patients present with symptoms indistinguishable from those of gastro-oesophageal reflux (GOR); however, unlike people with GOR, they are generally unresponsive to treatment with proton pump inhibitors (Level III-2). Infants often have additional clinical features, including feeding difficulties, feeding refusal and/or poor weight gain. In older children and adults, oesophageal food impaction is the most characteristic symptom (Level III-3), and should alert clinicians to include EO in the differential diagnosis. Typically, patients with EO have associated atopic disorders, including asthma and eczema. Mucosal appearance in EO Cause. The cause of EO is not clear, but the condition is closely associated with atopic disorders, and there is evidence that both IgE- and non-IgE-mediated food allergy are involved in its aetiology. Foods commonly implicated include cows milk, soy, wheat and egg.3 Data from animal experiments and anecdotal clinical observations suggest that inhalant allergens may also contribute. In keeping with murine models, recent gene array studies in people with EO have shown increased gene expression for eotaxin-3, a chemokine that promotes the migration of eosinophils into the oesophagus.1 Diagnosis. The diagnostic hallmark of EO is a dense, eosinophilic infiltrate involving the entire oesophageal mucosa, which is normally free of eosinophils. Key diagnostic criteria are basal layer hyperplasia and the presence of more than 20 eosinophils per high power field (× 400 magnification) in gastroscopic biopsies of the lower and upper oesophagus (Level III-3). Although oesophageal eosinophils are also seen in patients with reflux oesophagitis, mucosal eosinophil counts in such patients are lower (< 5 per high power field), and the eosinophils are limited to the lower oesophagus. There is a typical mucosal appearance in many patients with EO (thickened mucosa, with longitudinal furrowing and superficial white plaques [Box]) — although in about a third of patients the mucosa will look macroscopically normal. Skin prick testing (SPT) and atopy patch testing (APT) (the application of food or food extracts to the skin for 48 hours) are thought to be helpful in identifying potential causative food allergens,3 but prospective studies are needed to evaluate their predictive value. Management. To date, no completed randomised controlled trials evaluating the benefits and adverse effects of medical treatments for EO are available. Infants and young children may respond to dietary allergen restriction or an elemental diet. A diagnostic trial of an amino acid-based formula (AAF) for 6–8 weeks may be useful in determining whether a patient is diet-responsive. The treatment response needs to be assessed by repeat endoscopy, as not all patients will improve. If remission is achieved, food items can be gradually reintroduced into the diet, as tolerated, taking SPT and APT findings into consideration.3 In older children and adults, an elemental diet is often impractical and poorly tolerated due to the taste of AAF. These patients can be treated with swallowed topical corticosteroid aerosols (fluticasone) or, in refractory cases, with systemic corticosteroids.1 Other drugs, including cromoglycate and montelukast, have been used in uncontrolled trials, but their efficacy is poorly documented. Novel monoclonal antibodies against interleukin-5 may also be of benefit in treating EO, but prospective studies are not yet available. Evidence-based practice tip Infants and young children with eosinophilic oesophagitis often respond to an elemental diet, while older children and adults have been successfully treated with swallowed topical corticosteroid aerosols (fluticasone) (Level III-2).* * NHMRC levels of evidence. Prognosis. The long-term prognosis for EO is largely unknown. In some infants and young children with food protein-induced EO, the disease may remit due to development of oral tolerance to the offending food protein. However, EO usually follows a chronic relapsing course. To date, no studies have shown an increased risk of malignancy in patients with EO, but there is evidence that uncontrolled chronic eosinophilic inflammation may cause subepithelial fibrosis and remodelling, which eventually may cause obstructive dysphagia, strictures or persistent oesophageal narrowing.

Alyson Kakakios MB BS, FRACP · Ralf G Heine MD, FRACP

To the Editor: Meningitis is one of the most serious infections in young children. The annual incidence of Haemophilus influenzae type b (Hib) meningitis between 1984 and 1988 was 150 per 100 000 population in Aboriginal children and 27 per 100 000 in non-Aboriginal children younger than 5 years.1 A conjugate Hib vaccination program was introduced in Western Australia in January 1993, before a nationwide program commenced in July 1993. Subsequent marked declines in incidence of Hib meningitis have been reported.2-4 However, there are no recent reports on trends in overall admissions for meningitis. The WA Data Linkage System (WADLS) encompasses statewide population-based record linkage of the statutory birth and death registers, midwives’ notification system, and hospital morbidity database,5 and is one of few such resources worldwide. As part of a larger study to determine the burden of infection in a cohort of births between 1990 and 2000 using the WADLS, we investigated hospitalisation for all-cause meningitis (International classification of diseases, 9th revision, diagnosis codes 003.21, 036.0, 047, 049.0, 054.72, 320-322) in 17 296 Aboriginal and 252 775 non-Aboriginal children younger than 2 years between 1992 and 2000. In Aboriginal infants (< 12 months), the meningitis rate fell by 41% between 1992 and 1993–1994 and by a further 54% in 1995–1996, and has remained stable since (Box). In Aboriginal children aged 12–23 months, rates declined by 44% between 1993–1994 and 1995–1996 and again by 50% in 1997–1998, and no meningitis admissions were reported in 1999–2000. In non-Aboriginal infants, meningitis rates declined by 36%, from 1.8 per 1000 child-years in 1992 to 1.2 per 1000 child-years in 1993–1994, with a further 50% decline in 1997–1998, since when rates have remained stable. Rates declined by 57% between 1992 and 1993–1994 in non-Aboriginal children aged 12–23 months, declined a further 47% in 1995–1996, and have since remained stable at about 0.2 per 1000 child-years. With the decline in meningitis admissions, the disparity between Aboriginal and non-Aboriginal children has narrowed: the relative rate (RR) of Aboriginal to non-Aboriginal meningitis admissions fell from 7.3 in 1992 to 5.0 in 1999–2000 in infants, while in children aged 12–23 months, the RR was > 7.0 in 1993–1996, fell to 3.0 in 1997–1998, and was indefinable in 1999–2000 (Box). In the absence of other relevant interventions, we attribute declines in meningitis admissions to the introduction of Hib vaccine. This is supported by other studies showing a reduction in Hib meningitis following vaccination.2-4 Retrospective data provide an opportunity to assess overall trends in admissions. Future linkages with immunisation and laboratory data will allow us to investigate pathogen-specific admissions and evaluate vaccination programs. Our findings show that substantial improvements can be achieved given government commitment to implement appropriate preventive measures. Adequate funding and continued commitment is needed to ensure these measures are accessible to all WA children. Hospital admission rate for meningitis in Aboriginal and non-Aboriginal children aged (a) < 12 months and (b) 12–23 months in Western Australia, 1992–2000 Relative rate of Aboriginal to non-Aboriginal admissions is shown at the top of each graph.

Hannah C Moore · Deborah Lehmann

To the Editor: The current rate of caesarean sections in Australia (29% of all live births) is higher than the rate in other similarly affluent countries.1 In addition, the rate is continuing to increase; for example, it was less than 20% in 1993.1 Some commentators have suggested that this increase is partly a result of caesarean sections undertaken for non-medical reasons, such as patient demand.2,3 We examined trends in the rates of caesarean section for low-risk women using population-based perinatal data for Queensland over 15 years between 1990 and 2004. Our aim was to assess whether caesarean sections were becoming more common among women with no obvious medical indication for the procedure. The increase in caesarean sections among low-risk women was most dramatic in the private health care sector, where the percentage increased from 10% to 19% (Box). This represents an average annual increase of 4.6% (95% CI, 4.3%–5.0%). In the public health care sector, the increase was less — from 6% to 8% — an average annual increase of 2.4% (95% CI, 2.0%–2.7%). The increase in the private sector in Queensland was similar to the increase reported in the United States.4 The appropriate use of caesarean section, as for any medical intervention, should be based on evidence about the benefits and harm, with doctors, women and their families choosing a method of delivery after considering balanced information on potential outcomes of each method. There is continuing debate about the feasibility of randomised trials to clarify the benefits and harm of caesarean deliveries among low-risk women.2 Opposition to such trials is based mainly on ethical concerns about inflicting a surgical procedure on healthy women based only on randomisation. Non-randomised studies have compared outcomes of caesarean section versus vaginal delivery. However, their results are inconclusive because of the difficulty of distinguishing the effects of factors that influence the selection of delivery method from the effects of the delivery method itself (confounding by indication).3,5 In the absence of randomised trials, non-randomised studies that remove this potential bias by restricting the sample to women who remain at low risk throughout the pregnancy and delivery, according to clearly defined criteria, may provide useful information. They would need to assess both short-term and long-term outcomes. Until such better evidence is available, it is impossible to judge whether or not the current increase in caesarean section rates among low-risk women is desirable. Caesarean section rates among low-risk* women in Queensland, 1990–2004 * Low-risk births were defined as singleton, full-term (37–40 weeks’ gestation), vertex delivery with no reported medical risk factors or complications of labour or delivery, based on a list compiled by Declercq and colleagues.4 Women who had a previous caesarean delivery were excluded from the low-risk group.

Trisha C Johnston · Michael D Coory

To the Editor: The incidence of obesity is rising, and physicians are likely to face the problem of obesity-related glomerulopathy (ORG) recently illustrated by Tran.1 But how can the clinician distinguish ORG from primary (idiopathic) focal segmental glomerulosclerosis (FSGS)? Both may present with nephrotic-range proteinuria, but the prognosis and choice of treatment may differ. To date, the largest published study comparing ORG with primary FSGS is one by Kambham et al.2 In an analysis of 6818 renal biopsies, 71 patients with ORG were identified and compared with a control group of 50 patients with classic FSGS. The study showed that ORG less frequently progressed to end-stage kidney failure, with a 5-year renal survival rate of almost 90% (compared with about 50% in primary FSGS).2 While weight loss can reduce hyperfiltration and albuminuria in ORG,3 spontaneous remission is uncommon in primary FSGS.4,5 Does every obese patient with nephrotic-range proteinuria have ORG and an “indolent” course? The degree of weight loss reported in the case described by Tran may not be achievable or sustainable in most obese patients. Do we have the luxury of waiting to assess the impact of weight loss on proteinuria? In about 50% of patients with primary FSGS, the serum creatinine level doubles after an average of 39 months.2 Furthermore, patients with primary FSGS and nephrotic-range proteinuria who do not achieve remission have a 5-year renal survival of only 50%, compared with almost 100% for those who attain remission.4 In addition, patients treated with corticosteroids (with or without cyclosporin or cyclophosphamide) have higher remission rates (30%–63%) than untreated patients (11%–14%).4,5 Therefore, a delay in introduction of specific therapy is not ideal. There are some clinicopathological differences between ORG and primary FSGS that may help distinguish the two entities (Box). However, Kambham et al found that only two parameters were independently significant: serum albumin level and age.2 Although their study was based on a US population, it serves to demonstrate the principle that the major distinguishing feature between ORG and primary FSGS is the presence of full-blown nephrotic syndrome in primary FSGS (as demonstrated by the severity of hypoalbuminaemia). Obese patients have a similar risk of developing primary FSGS to people in the general population, and patients with nephrotic syndrome (particularly older adults) should not be presumed to have ORG and treated with weight loss alone. Certain pathological findings in a renal biopsy are helpful, but not definitive, in distinguishing ORG from primary FSGS. A biopsy would also exclude other treatable causes, such as minimal change disease. In addition to treatment with angiotensin-converting enzyme inhibitors, immunotherapy should be considered for obese, nephrotic patients, after discussing the potential risks and benefits with a nephrologist. Clinicopathological differences between ORG and primary FSGS* Parameter ORG Primary FSGS Mean age at presentation (years)† 42.9 32.6 Ethnicity White (%) 74 52 African American (%) 21 22 Nephrotic syndrome (%) 5.4 54 Mean 24-hour protein excretion (g) 4.1 6.9 Mean serum albumin level (g/L)† 39 29 Mean serum cholesterol level (mmol/L) 5.9 8.6 Presence of pedal oedema (%) 35 68 Mean degree of segmental sclerosis (%) 10 39 Proportion of cases with glomerulomegaly (%) 100 10 Mean arteriosclerosis score (range, 0–3) 1.34 0.98 Mean degree of glomerular podocyte foot process fusion (%) 40 75 ORG = obesity-related glomerulopathy. FSGS = focal segmental glomerulosclerosis. * Adapted from Kambham et al.2 † Independently significant.

Andy K H Lim

To the Editor: Recent articles in the Journal by Kurrle1 and Finn and colleagues2 referred to advance care directives aiding the management of acute illness in elderly residents of aged care facilities. It is our experience that these directives are often unhelpful in elderly patients and, outside certain progressive medical conditions, can result in triage of elderly patients to inappropriate lower levels of care. In chronic medical conditions where the clinical course allows time for patient or family understanding, and the course of organ failure is predictable, then certain supportive but ultimately futile therapies can be avoided by instituting an advance care directive that specifically excludes them. However, these directives are less helpful in acute illnesses. They usually refer to “intensive care”, and “life support”, sometimes specified as mechanical ventilation, dialysis or cardiopulmonary resuscitation. These “general” advance care directives fail, as they assume that prognosis is immediately apparent, and that treatment is “all or nothing”, both of which assumptions are clearly untrue. Determining an accurate prognosis for recovery from a critical illness is difficult and takes time. It involves diagnosing the cause of the illness, quantifying the severity of comorbidities and, most importantly, assessing response to initial treatment. Whether severe sepsis is arising from the urinary tract or abdominal cavity may not be apparent initially. Many elderly patients survive severe septic shock caused by urosepsis with haemodynamic monitoring and short-term high-dose vasopressors. It is also not possible to distinguish which patients with severe respiratory failure will respond to non-invasive ventilation. We followed up critical care patients aged 75 years and over who survived to hospital discharge over a 12-month period and confirmed that acceptance of critical care admission in elderly people is high (unpublished study; details available from the authors). This is the very population that, in our experience, frequently says they do not want to be placed on “life support”, if asked when well. Together with the fact that an accurate prognosis takes time, then a prudent approach should begin with the presumption of aggressive treatment for acutely unwell elderly patients, rather than a presumption of limited therapy or palliation. Advance care directives that refer to therapies need to be specific and to recognise that critical care therapy can be graduated and readily terminated once a more accurate prognosis is known. Furthermore, some critical care therapies, such as non-invasive ventilation and high-concentration oxygen, can significantly improve patient comfort while management plans are formulated. In our experience, patients and their families are often very surprised when they understand the full implications of an advance care directive that refers to generic therapies, such as cardiopulmonary resuscitation and “intensive care”.

Andrew W Holt · Alnis E Vedig

To the Editor: I note with interest Australian medical students’ difficulties in gaining access to patients, as documented by several authors in recent months.1-3 There is an alternative explanation for this paucity of access, and that is the culture in Australian teaching hospitals. I graduated from the University of Otago Dunedin Medical School in New Zealand 9 years ago, and had a somewhat different experience. The hospitals attached to the Dunedin Medical School were the equivalent of one medium-sized acute hospital in Australia, one rehabilitation hospital, and a small peripheral regional hospital. These facilities taught up to 200 clinical medical students — a high student-to-patient ratio. However, we did not face the barriers that Australian students face in gaining access to patients, and so still had a world-class medical education. The system in Otago differed from that in Australia in several ways. If a patient was having an investigation, we accompanied them. Likewise, if they were seeing a staff member, we would often stay. There was a culture where every patient admitted to hospital expected to see a medical student. We approached the patients directly to ask permission to see them, rather than being turned away by nursing staff. Consequently, in non-obstetric patients, I encountered only one refusal to see me in my clinical years, and this was after I had started taking a history and asked about tranquilliser use in too much detail! We also did not wait to see only patients who were ideal teaching cases — patients who speak English, do not have dementia, are not unwell, are not busy, and who have a particularly interesting condition are rare anywhere. If a patient had dementia or was unwell we familiarised ourselves with their history, then saw the patient over the course of several days. If there were visitors, we asked about an appropriate time to come back. We saw all routine cases, as these reflect the real workload of doctors. By comparison, in my years as a resident and registrar in Australia, I have seen very few medical students, and have seen many teaching and learning opportunities pass by. In conclusion, we need to examine the role of medical students closely, and look at ways to facilitate their access to existing patients. There is something to be learned from all patients admitted to hospital. The culture of teaching hospitals and the expectations of students, staff and patients should reflect this fact.

Sarah J Abrahamson

To the Editor: The 2005 Cochrane review Home-like versus conventional institutional settings for birth1 has been cited in the public media to claim that birth centres are less safe than labour wards as there was an increased risk of a baby dying during or immediately after childbirth.2 This “headline-grabbing” statement is false. Firstly, this finding from the systematic review did not reach statistical significance.1 Secondly, the outcomes reviewed were related to the allocated place of birth, not the care provided. This fact is critically important, as 48% of women who were booked to have their baby in a birth centre did not give birth there.1 This is a predictable effect of the intention-to-treat principle. However, such high rates of “treatment contamination” negatively affect confidence in the study results.3 Additionally, the vast majority of baby deaths examined in the Cochrane review happened before labour and thus had nothing to do with care during childbirth. One might wonder whether there was a real increased perinatal mortality rate resulting from delayed transfers from birth centres.1 The analysis found 41 deaths in total, but only six that occurred in normally formed babies who reached term (these are the only babies who are eligible to be born in a birth centre). Three of these deaths were associated with birth centre care, and three with standard labour care. The interpretation of this Cochrane review raises questions about the validity of the underlying randomised controlled trials. In this experimental design, researcher control should ensure that people receive the specific treatment that was planned for them (treatment fidelity).4 The Cochrane handbook gives no guidance as to how to evaluate either the quality of the researchers’ definition of the planned treatments, or the fidelity between the treatments provided and the researchers’ plan.3 Most of the trials that formed the basis of the Cochrane review did not adequately define their treatments, nor adequately control the treatments provided to either group. It is not clear how the birth centre trials could sensibly be considered to have been scientifically controlled. The reviewers attempted to deal with this critical point by claiming that they were looking only at the effect of the “setting”, but their question clearly states that they were examining the effect of “care within a setting”.1 We conclude that the Cochrane review of the setting for birth is unreliable because of the weaknesses of the underlying trials. Rather than using questionable research to attack birth centres, it would be more constructive to engage in rigorously designed research that could provide robust evidence on the safety of all forms of maternity care, including standard medical care.

Kathleen M Fahy · Sally Tracy

In reply: Fahy and Tracy highlight the lack of high-level evidence about the relative safety of different models of maternity care. But in criticising the Cochrane review, it is important not to “shoot the messenger”. There is no doubt that the Cochrane review is not ideal but, like it or not, it remains the best evidence we have. The review of 8677 women in six randomised trials found a relative risk (RR) of perinatal death of 1.83 (95% CI, 0.99–3.38) in birth centres versus conventional institutional settings. In the 3332 pregnancies assigned to continuity of care by midwives who did not also work in conventional delivery suites, the RR was 2.38 (95% CI, 1.05–5.41).1 It would be fair to say that such findings should lead to real concerns about lack of safety rather than reassure the unbiased observer. Other published evidence has raised similar concerns. A retrospective review of over 183 000 low-risk births in Stockholm, Sweden, found a statistically significant fourfold increase in intrapartum fetal mortality in women planning birth centre care compared with those planning standard care (three intrapartum deaths in 3256 babies of women planning birth centre care versus 36 deaths in 180 380 babies of those planning standard care).2 The increase in intrapartum mortality was almost sevenfold for primigravidae. These findings led to evidence-based changes in the organisation of the birth centre involved to minimise the identified risks. To paraphrase Fahy and Tracy, rather than criticising the best available evidence reviewing birth centre outcomes, it would be more constructive to engage in rigorously designed research to assess how risk might be minimised in all forms of maternity care.

Andrew F Pesce

To the Editor: I was very concerned to read the letter from Mazza et al1 regarding “positive” family planning and feel I must make a comment. The authors are well known for their work in the area of women’s sexual and reproductive health, but I would like to challenge some of the points they have made. The first point: whether intervention by general practitioners would be appreciated by younger women not yet interested in motherhood. I believe it is part of the role of doctors to inform, even when a person may not be ready for the information. Telling 20-a-day smokers that they are not doing their body any favours doesn’t go down well with some people, but even this brief intervention can change behaviour and save lives. The second point: whether GPs can respect patients’ autonomy. Every day I speak to women who have been offended and upset by doctors who have said something awkwardly, or imposed their own values, or been downright offensive. That won’t change, and recommending that well informed and tactful doctors wait before imparting vital information until the rest of the world lifts its game means we will all be waiting a long time. Part of the art of medicine is judging the audience and knowing the perfect point in a consultation to speak, and how to say it. What can be more appropriate, when seeing a woman in her late 20s who has requested a repeat prescription for the contraceptive pill, than to ask casually (as one is unrolling the sphygmomanometer cloth), “So, do you think there might be any children in your future?” The usual response, as detailed in Cannold’s book,2 is an emphatic “yes”. The next question, “Have you got a time scale when you would be looking at that?”, may give the opportunity to mention such things as rubella vaccination, smoking and folate supplements. And if the woman indicates that pregnancy would be on her to-do list at age 38, then a reasonable and non-harassing response could be, “Could we talk about fertility rates at that age?” The third point: doctors reinforcing the dominant paradigm (of years ago) of the woman as childbearing machine, by asking about a woman’s intentions. This seems to me as misguided as not asking about suicidal ideation in case we make it happen. By all means do research, but don’t ask doctors to be silent about this important issue until the sociologists have spent another 10 years on it. By that time, it will be too late for a lot more women.

Angela M Cooney

Re: “2. Anaphylaxis: diagnosis and management”, by Simon G A Brown, Raymond J Mullins and Michael S Gold, in the 4 September issue of the Journal (Med J Aust 2006; 185: 283-289). In Box 6 on page 287 (“Emergency management of anaphylaxis”), there is an error in the third line. The correct wording should be “Give adrenaline IM (lateral thigh) 0.01 mg/kg (maximum dose 0.5 mg)”. The corrected Box is reproduced in full below. The html and pdf versions of this article have been corrected 6 Emergency management of anaphylaxis IM = intramuscular. IV = intravenous. Adapted with permission from: Brown SGA. Anaphylaxis: clinical concepts and research priorities. Emerg Med Australas 2006; 18: 155-169.17

Simon G A Brown · Raymond J Mullins · Michael S Gold

Re: “The burden of chronic kidney disease in Australian patients with type 2 diabetes (the NEFRON study)”, by Merlin C Thomas, Andrew J Weekes, Olivia J Broadley, Mark E Cooper and Tim H Mathew, in the 7 August issue of the Journal (Med J Aust 2006; 185: 140-144). In Box 2 on page 142, the figures for mean patient age in the first row were reversed. The correct figures are 63.3 years for patients with estimated glomerular filtration rate (GFR) ≥ 60 mL/min/1.73m2 and 73.0 years for those with estimated GFR < 60 mL/min/1.73m2. The html and pdf versions of this article have been corrected.

Merlin C Thomas · Andrew J Weekes · Olivia J Broadley · Mark E Cooper · Tim H Mathew

Re: “Potential for organ donation in Victoria: an audit of hospital deaths”, by Helen I Opdam and William Silvester, in the 4 September issue of the Journal (Med J Aust 2006; 185: 250-254). The acknowledgements section was omitted. It should have read:

Helen I Opdam · William Silvester

SARS. How a global epidemic was stopped. World Health Organization. Geneva: World Health Organization, 2006 (x + 307 pp). ISBN 92 9061 2134. The title of this book suggested to me that it might well be a self-congratulatory review by an organisation trying to claim credit for stopping a brief but frightening epidemic in its tracks. The fact that it was published by the World Health Organization also led me to believe that it might be a dry chronology of events and difficult for the average medical reader to penetrate. So I was pleasantly surprised to find that I enjoyed reading SARS and that facts are presented in a balanced manner. The best feature of this book is that it presents a worldwide phenomenon in easy-to-read prose, with excellent diagrams, pictures and tables, in just over 300 pages. There are detailed accounts, with expert content from each region. In particular, judging from my personal experience, the account from Hong Kong is accurate and concise. The authors start and finish the book by commenting that the lessons learnt from the SARS (severe acute respiratory syndrome) epidemic have not been analysed and promulgated widely enough. This is a view with which I strongly concur. Surveillance and control measures, the process of developing new tests and vaccines, clinical management of unknown viral conditions, and adoption of evidence-based infection control procedures were areas of controversy during the epidemic. The different approaches taken by different groups give important insights and should help guide us in planning for the next epidemic. The reality is that we are still not sure where the SARS epidemic came from, how it spread rapidly sometimes and not others, and why it disappeared completely after only a few months. We do know that many lives were saved by a swift, well coordinated global response, limiting the number of cases and confining the epidemic to just a few regions of the world. This is a great book for anyone interested in the SARS epidemic (or future pandemics) wanting a balanced, well referenced, accessible and concise summary. Peter A Cameron Head, Pre-Hospital and Emergency Trauma Group, Alfred Hospital, Melbourne, VIC

Peter A Cameron

Manual of travel medicine: a pre-travel guide for health care practitioners. 2nd ed. Allen Yung, Tilman Ruff, Joseph Torresi, et al. Melbourne: IP Communications, 2004 (xxiii + 334 pp). ISBN 0 9752374 0 3 As the Asian tsunami disaster has so tragically shown, travel is not always safe or predictable. Making travel as safe as possible is, however, the goal of travel medicine, which has emerged as a specialised discipline as well as an interesting and challenging part of the work of many general practitioners. The popularity of the first edition of this Manual of travel medicine, published by the Victorian Infectious Diseases Service in 1999, demonstrated that doctors and other health professionals providing pre-travel health advice were looking for a desktop reference of high quality information. The fact that the manual comes from a group of very experienced and qualified Australian authors is of substantial value, as it complements the information available in other publications such as the Australian immunisation handbook and the WHO publication, International travel and health. Controversies and differences in opinion, such as whether to recommend hepatitis B vaccination to all or only higher risk subgroups of travellers and the use of bacille Calmette – Guérin (BCG) vaccine in travellers, are discussed, and the recommendations of key authorities, and the authors’ own opinion are provided. The manual focuses on pre-travel health advice and does not cover assessment and treatment of the unwell returned traveller. Although this is a substantial omission, it is not a major drawback for a GP readership who are mainly providing pre-travel health advice. As might be expected with an author list entirely made up of infectious diseases specialists, there is a focus on vaccine preventable diseases plus substantial chapters on malaria prevention, and prevention and management of travellers’ diarrhoea. Non-vaccine preventable diseases including severe acute respiratory syndrome (SARS) are covered, and there are sections on non-infectious problems such as venous thrombosis, altitude sickness and jet lag. Though not as inexpensive as the first, this edition of the Manual of travel medicine is still reasonably priced, and has the advantages of a more professional look and the welcome addition of an index. Nicholas A ZwarProfessor, General Practice Unit, Fairfield Hospital, NSW

Nicholas A Zwar

Tolkien II — a needs-based, costed stepped-care model for mental health services. Gavin Andrews and the Tolkien II Team, University of New South Wales at St Vincent’s Hospital. Sydney: World Health Organization Collaborating Centre for Classification in Mental Health, 2006 (vi + 376 pp). ISBN 0 9578073 4 1 Rarely does a book grab you by the shirt front and shake you in the way that this one does. It is an in-your-face call for reform in the way mental health services are configured and delivered, claiming “a plan in which a 30% increase in budget could treat 50% more people and produce a 90% increase in health gain”. Mental illness is one of the key contributors to burden of disease. Burden of disease studies, though, don’t give any indication of marginal benefits that would accrue from additional investment and so do not per se provide useful information for an investment strategy. This book does. It starts with an analysis of the cost-effectiveness of the contemporary allocation of resources for the various classes of mental illness, suggesting, for example, that the cost-effectiveness ratio for affective disorders is $20 for each year of disability averted, compared with schizophrenia at $196 for each year of disability averted. It proposes a new configuration of investments, with greater reliance on community-based accommodation, for instance, and estimates that its proposals would lead to improved cost-effectiveness across all of the major illness subgroups. In format, it has a very brief introduction followed by proposed treatment recommendations or intervention models for each of the main classes of psychiatric illness. The “stepped-care model” in the title is reflected throughout the book in investments in front-end primary care and community interventions, designed to filter patients so that the use of the high-cost inpatient end of the treatment continuum is minimised. These plans are designed from a societal point of view, with implementation impacting on both Commonwealth and state responsibilities. I am not a psychiatrist, so I cannot make any assessment of the validity of the proposed treatment plans, but an impressive range of expert consultants has been used in the development of the plans. The weakness of an expert-panel approach is acknowledged, and the lack of approaches based on higher levels of evidence is claimed to be because of the lack of such evidence. There are nine people in Australia who, without a doubt, must read this book, or at least the first few pages: the Directors-General/Secretaries of the state, territory and Commonwealth Health Departments. They should then request their Directors of Mental Health to evaluate the book and the recommendations therein, and to advise on why this should not be the approach adopted for future investments in mental health funding. Stephen J DuckettExecutive Director, Reform and Development Division, Queensland Health, Brisbane, QLD

Stephen J Duckett

New thinking about mental health and employment. Bob Grove, Jenny Secker, Patience Seebohm (editors). Oxford: Radcliffe Publishing, 2005 (xxii + 162 pp). ISBN 1 85775 769 6. Sigmund Freud stated that the pillars of psychological wellbeing are love and work. Unfortunately, it is work that is most sensitive to the impact of mental illness. Return to work has always been a key aim of psychiatric rehabilitation. At times, the illness proves a turning point in life, motivating positive change and greater achievement of life goals. The majority of patients get back to work, but for a minority, work outcomes are bleak. The impact of treatment has even, at times, been negative (for instance, conventional neuroleptics causing the “zombie-like” state of drug-induced Parkinsonism). The response of the community and employers has been an even greater handicap. Discrimination is still rife. Given that 49% of the population will develop a mental illness in their lifetime, the impact of the new dismissal laws may create enormous social upheaval in Australia. Very little has been written about employment and mental health, and I keenly looked forward to reading New thinking about mental health and employment, only to be seriously disappointed by contributions from the editors. The book opens with the statement, “Most people who suffer from periods of mental ill health would like to work and yet less than 20% are in employment”. This statistic applies to sufferers of chronic schizophrenia, not mental illness in general. While it is totally legitimate for the editors to concentrate on people with chronic psychoses, they should say they are doing so. After all, the editors indicate that they advise government authorities on employment for the mentally ill. Yet only one is identified professionally as a professor of nursing, and the other two, for reasons I cannot discern, omit their professional backgrounds. The editors argue that the “all-pervasive medical model” has created a system that actually excludes people from employment. This is a tired old argument. There is much in public psychiatry that deserves profound censure, but doctors’ alleged lack of concern about employment is not one of them (the capacity to do much about it may be another story). It is absolutely undeniable that effective medical treatment will improve the capacity of patients to return to work, and hence will facilitate any assistance given by employment services. Much more justifiably, the editors tackle therapeutic nihilism in schizophrenia, again with anecdotes of doctors telling patients they will never work again, where this was manifestly wrong and damaging. The issue is difficult as people with schizophrenia often do have a poor outcome, but I also see patients who continue to work at the highest professional levels despite suffering chronic illness. Rather than pointing to the heterogeneity of schizophrenia, and how differently patients may be affected, the editors run the old argument that schizophrenia does not actually have a poor prognosis if only clinicians developed better attitudes. A new paradigm “of intervening to halt and reverse the journey to exclusion” is the way to go. Who could disagree? What saves the book is that most of its content comes from contributors other than the editors. There is a great deal of useful information. The biographical accounts, feedback on services, and perspectives of the users are both articulate and enormously instructive, although recounted treatment experiences are often tragic. Chapters such as “What do service users want?” and “What’s kept me working?” are invaluable. The evidence of “what works” is well presented but the conclusions fall down by attempting to generalise where there are enormous differences in individual needs. Accounts of actual services and how to develop interventions are useful. On balance, this book is worth reading because it contains information that will assist clinicians to help patients with chronic psychoses get back to work. Nicholas A KeksProfessor of Psychiatry, Monash University, Melbourne, VIC

Nicholas A Keks

Not for the hip? Results of an Australasian randomised, placebo-controlled trial have challenged the recommendation that all patients undergoing total hip replacement should take a short course of postoperative NSAIDs to prevent residual symptoms by preventing ectopic bone formation in the soft tissues around the operated hip. The trial involved 902 patients undergoing elective primary or revision total hip replacement surgery who were randomly assigned to receive 14 days’ treatment with either ibuprofen (1200 mg daily) or placebo, starting within 24 hours of surgery. While postoperative ibuprofen reduced ectopic bone formation after the surgery, this does not translate into less pain or disability 6 to 12 months after surgery. There was also an increased risk of major bleeding complications in the ibuprofen group during admission. The researchers said that their findings provided evidence that clinical care guidelines should be based on clinically important outcomes rather than unproven surrogate outcomes, like radiographic ectopic bone formation. BMJ 2006; 333: 519-523 GP defibrillators Equipping GPs with defibrillators could be a useful strategy for reducing deaths from sudden cardiac arrest, according to UK research. Since 1985, the British Health Foundation, a major national charity, has funded the purchase of defibrillators for UK GPs on condition that GPs are capable of responding rapidly to calls for help and that they agree to return a report form after each resuscitation attempt. An analysis of the 555 report forms received from 1986 to early January 2004 found that 149 resuscitated patients (27%) survived to leave hospital. Survival was much more likely when the initial rhythm was shockable (VF or pulseless VT), with 144 of 351 such patients (41%) surviving, and also when heart disease was responsible for the arrest, with 148 of 436 such patients (34%) surviving. While about half of the cardiac arrests occurred in the patient’s home, about one in five occurred at or near the doctor’s surgery. Resuscitation 2006; 70: 229-237 18 holes to healthier living In the fight against overweight and obesity, walking 10 000 steps each day has been promoted as a part of a general physical activity plan. Now, GPs can be reassured by Mayo Clinic research which has determined that playing an 18-hole round of golf is likely to meet this recommendation, whatever the patient-player’s golf handicap. Adult volunteers (12 men; 30 women) walked each of three municipal 18-hole golf courses while wearing an electronic pedometer. The golfers carried their clubs or used a push or pull cart or an electric golf caddy. Each golfer took an average of about 12 000 steps per round. Mayo Clin Proc 2006; 81: 1041-1043 Oils ain’t oils Virgin olive oils may be more beneficial in modifying cardiovascular risk factors than refined olive oils, according to European research. The Effect of Olive Oil on Oxidative Damage in European Populations (EUROLIVE) Study Group compared the effects of three different types of olive oil on plasma lipid levels in 200 healthy male volunteers. Although each of the olive oils had a similar monounsaturated fatty acid content, they differed in phenolic content — high (virgin olive oil, 366 mg/kg), low (refined olive oil, 2.7 mg/kg) and medium (mixed oils, 164 mg/kg). Volunteers took 25 mL daily of one of the oils for 3 weeks, preceded by a fortnight’s washout period, and then did the same for each of the other two oils. As phenolic content of an olive oil increased, so did HDL cholesterol, whereas the total cholesterol to HDL cholesterol ratio and triglyceride levels decreased. A higher phenolic content was also associated with a decrease in serum biomarkers of oxidative damage. Ann Intern Med 2006; 145: 333-341 Serotherapy for bird ‘flu? A modern-day meta-analysis of eight studies conducted during the Spanish influenza epidemic in the early 20th century has determined that serotherapy may be useful in combating an avian influenza (H5N1) epidemic. The data, although from studies of poor design by today’s standards, suggest that early transfusion of influenza-convalescent human blood products reduced mortality as well as clinical signs and symptoms in patients with influenza complicated by pneumonia. The biological hypothesis is that the virus was neutralised by anti-influenza antibodies in the blood products. A US expert, commenting on the meta-analysis, called for more coordinated clinical research among institutions in countries currently experiencing cases of avian influenza, including proving the concept of serotherapy for treatment of severe H5N1 infections. Ann Intern Med Online, 29 August 2006 Dr Ann Gregory, MJA

Ann Gregory