Editorials

Improving glycaemic control in children and adolescents presents unique problems Type 1 diabetes affects one in 500 children and adolescents, and vascular complications remain a major cause of mortality and morbidity in adult life. Blood glucose targets have fallen since confirmation of the unequivocal relationship between glycaemic control and microvascular complications.1,2 In this issue of the Journal (page 235), Craig et al present a population-based, cross-sectional study of 1190 children and adolescents with type 1 diabetes in New South Wales and the Australian Capital Territory.3 Their median HbA1c level of 8.2% probably reflects some selection bias, because 571 (33%) of the population did not participate. However, this level of glycaemic control still represents a considerable improvement over the past 10 years4 and is comparable to levels found in international studies of children with type 1 diabetes.5 This trend accompanies the increasing use of intensive management in children and adolescents, but also the worrying rise in the incidence of severe hypoglycaemia. There are compelling reasons to recommend intensive therapy in adolescents with type 1 diabetes — either multiple daily injections or continuous subcutaneous insulin infusion. The effectiveness of intensive therapy in improving and maintaining good glycaemic control is well established in adolescents under research trial conditions.6 More recent data also indicate that the benefits of intensive therapy and improved glycaemic control persist even when HbA1c levels later rise.7 After completion of the Diabetes Control and Complications Trial (DCCT), adolescents from the former intensive therapy and conventional therapy groups returned to routine care and were advised to use intensive therapy. Despite no difference in their glycaemic control for four years after the end of the DCCT, the benefits of previous better control in the intensive therapy group persisted. Their prevalence of progression to proliferative or severe non-proliferative retinopathy was reduced by 78% during the four years. Suboptimal control during adolescence appears to have a lasting harmful effect, even when better glycaemic control is achieved later. Those caring for children and adolescents with type 1 diabetes may worry about the demands on the family and child of achieving good glycaemic control with intensive therapy. However, good glycaemic control is associated with better quality-of-life scores (QOL) in adolescents and less perceived burden by their parents.8 The intensity of the insulin regimen does not adversely affect QOL. Clearly, the demands of achieving good control are less than the consequences of poor control.8 The limiting factor of achieving ideal glycaemic control remains hypoglycaemia, excluding other problems of adherence or family functioning. Adolescents in the DCCT had higher rates of hypoglycaemia than their adult counterparts, despite having higher HbA1c levels.6 Glucagon secretion, which stimulates hepatic glycogenolysis, is blunted early in the course of type 1 diabetes, increasing the patient's vulnerability to hypoglycaemia. Further, the blood glucose threshold level for catecholamine release in response to hypoglycaemia is lowered in patients with better glycaemic control and this counter-regulatory response is most blunted during sleep.9 Recently available continuous blood glucose monitoring devices have shown that nocturnal hypoglycaemia is frequent in children. However, both new insulin analogues and continuous subcutaneous insulin therapy hold promise of improving control without the attendant increased risk of hypoglycaemia. In Western Australia, children with type 1 diabetes had more hypoglycaemia in association with falling HbA1c levels until 1995;4 since then their control has improved further, but without increased hypoglycaemia. Can the DCCT recommendations that adolescents receive intensive therapy be reproduced in routine care? The Hvidore Study Group has followed more than 2500 children and adolescents over three years in Europe, Canada and Japan.5 Despite more use of intensive therapy, glycaemic control did not necessarily improve with wide differences between paediatric centres. Intensive therapy demands intensive follow-up, education and support, as well as resources that many Australian paediatric diabetes units do not have if most patients are to be supported in this way. Most success in implementing the DCCT recommendations is reported from well-resourced units using diabetes clinical nurse consultants. While it is recommended that adolescents with type 1 diabetes receive intensive therapy, schedules need to be individualised. For example, some schoolchildren need insulin at afternoon tea, most adolescents need longer-acting insulin before bed for night control, and many preschoolers are managed on intermediate-acting insulin in the morning with small doses of insulin analogues to cover hyperglycaemia later in the day. Insulin pumps may provide the best solution for some patients, especially those with frequent hypoglycaemia or hypoglycaemic unawareness, but without government subsidy they are not affordable for most families. None of these options are easy for children and their families and, for some, intensive therapy is not possible. Insulin omission and chronic poor glycaemic control remain problems in adolescence and require ongoing intervention.10 The NSW and ACT study has demonstrated a relatively fast decline in HbA1c levels3 since the DCCT findings. However, glycaemic control (and risk of long term vascular complications) is unlikely to improve further in population studies unless multidisciplinary resources increase. It is especially relevant for more educators to be trained in the unique problems of improving control in this age group, and for their expertise to be available to all children.

Jennifer J Couper MB ChB, MD, FRACP

Publicly available reports of "surgical waiting times" are, at face value, of interest to patients and referring doctors wishing to access surgical care. Such information might be expected to provide a reasonable indication of the absolute time to surgical intervention for an individual patient, and allow reasonable conclusions to be drawn on the relative performance (in terms of waiting times) of surgical services. Definition Healthcare performance indicators: statistics or other units of information which reflect, directly or indirectly, the performance of the healthcare system in maintaining or increasing the well-being of its target population. Surgical waiting times are a specific example of "healthcare performance indicators" (see Definition). In addition to providing information for users, such indicators are likely to inform the opinions of politicians, journalists, hospital managers and state and federal health departments on the adequacy of our healthcare system and relative hospital or regional performances. They may be used to construct "league tables" of the relative performance of surgical units — individual hospitals, surgical units or surgeons may be deemed to have "good" or even "substandard" performance. Public outcries and political pointscoring are likely to ensue. Good indicators should be easy to understand and use by the intended audience. Depending on how these data are collected, processed and presented, reported waiting time data might or might not provide useful information to people seeking guidance on time to treatment. Reports of surgical waiting times that use different definitions of "waiting time", or simply report on past performance, are of limited value. Waiting time data presented as the frequency with which a certain proportion of patients receive treatment within a stated time (eg, 75% treated within 4 weeks) may also fail to adequately inform patients or general practitioners as to likely delays. Few existing systems are capable of adjusting for delays before initial surgical consultation (ie, waiting time to get onto the surgical waiting list), let alone factors such as primary illness severity, comorbidity or health insurance status — all of which influence actual waiting times. In this issue of the Journal (page 253), Cromwell et al report an assessment of the utility of information regarding surgical waiting times available on the World Wide Web.1 Their findings indicate that current Web-derived information has significant shortcomings in data quality. They conclude that waiting time data currently published on the Web are, by and large, unsuitable for informing either clinician referral or patient decision-making.1 This critique should not be misinterpreted as an example of the well-recognised "dot.com" data reliability phenomenon. It is not just Web-based sources of such data that are open to criticism. Analysis of healthcare performance indicator data derived from any existing sources would generate similar critiques, with similar caveats required on interpretation and use.2,3 The appropriate desire to develop performance indicators in healthcare has often seen a race to deliver indicators overwhelm the need for methodological rigour in development and implementation. All too often, too little emphasis is placed on initial identification of who will use the indicator and how and why they will apply the data. The absence of such ab initio clarity of purpose leads to performance indicators that do not meet the needs and expectations of consumers, providers or purchasers of healthcare services.2-5 Surgical waiting times, and many other indicators, generate a natural curiosity to compare or rank relative performance. For comparisons to be made, common indicator definitions must exist and be systematically applied in data generation, with common data collection methodologies and results that are risk-adjusted. As Cromwell et al found, requirements for clear, consistent definitions are frequently not met, rendering comparisons invalid.2-8 It is crucial that people intending to use indicator data for judging comparative performance, or in any potentially punitive fashion, fully understand the strengths and weaknesses of the primary data. Perhaps the greatest error by those who use indicator data is that of assuming the indicator is an objective measure of relative performance based solely upon its apparent face validity. Reported surgical waiting times would then be assumed to be a direct linear measure of access to care. This ignores evidence that clinician decision-making processes and administrative practices have major impacts on reported waiting times. Without adjustment for relative urgency or disease severity (at a minimum), reports of waiting times are of limited utility. Significant progress has been made in developing and refining healthcare performance measurement locally (by the Australian Council on Healthcare Standards among others) and internationally (by groups such as the Joint Commission on Accreditation of Healthcare Organisations and the Health Care Financing Administration in North America). There is, however, still considerable scope for improving the methodological rigour of both indicator development and application in the field. At present, the reliability and utility of indicator data cannot be assumed. Most current indicators of healthcare performance should be viewed as tools that prompt additional inquiry, rather than allowing definitive judgements on quality and safety of care. Over time, robust, credible indicators will increasingly become available to reliably inform consumers and allow accountability to purchasers of healthcare services. Nevertheless, given the complexity of healthcare, the predominant enduring benefit from attempts to measure performance in healthcare is likely to be the use of data generated by providers of care to provoke reflection on existing practice and to plan efforts at improving care.

Neil W Boyce FRACP, PhD, MRACMA

Malaria remains a global crisis that kills at least one to two million people per year, mainly children in sub-Saharan Africa.1 Forty per cent of the world's population is at risk of malaria, and each year more than 300 million people have episodes of acute malaria. In recent times, there has been a breakdown in malaria control programs. This has been caused by failure of health systems in the poorest countries, as well as the emergence of mosquitoes resistant to insecticides and malaria parasites resistant to cheap, widely available drugs. In addition, population movements, large-scale development projects, civil wars and conflicts, as well as environmental changes, have all acted in concert to increase the number of individuals at risk of malaria. In Papua New Guinea, for example, malaria is the commonest cause of outpatient presentation and accounts for an estimated 27% of all attendances at health facilities.2 In some Papua New Guinea provinces, malaria is the reason for more than 40% of health centre attendances, and equals pneumonia as a primary cause of death.2 In recognition of the need for a renewed attack on malaria, a global strategy for malaria control was presented to a World Health Organization Conference of Health Ministers in 1992.3 The strategy, now incorporated into the Roll Back Malaria Campaign, promoted a new philosophy emphasising malaria control (in contrast to eradication), and acknowledging the need for different approaches to disease control in different populations. For example, the approach to malaria control in children and pregnant women in Africa is different to that in adult refugee populations. The strategy emphasised the importance of political commitment, such as that given by the heads of State and governments of African countries in Nigeria in 2000 (the Abuja Declaration).4 All participants resolved to commit to an intensive effort to reduce the burden of malaria by strengthening health systems, implementing action plans, improving local capacity, promoting early recognition and treatment of clinical malaria, and reinforcing efficacious preventive measures such as the use of impregnated bednets and chemoprophylaxis. An important component of the strategy is the development of new antimalarial drugs and vaccines. Vaccines have been shown to be one of medicine's most cost-effective interventions. A malaria vaccine that protects for one to five years with 50% efficacy could substantially reduce all-cause child mortality in endemic areas. The cost of such an intervention compares very well with that of using insecticide-treated bednets, and is likely to have major economic as well as social benefits for the populations currently threatened by malaria. An "experiment of nature" suggests that developing a vaccine should be possible. Although many children die of malaria, the majority survive the life-threatening risk of the first few years of exposure and develop clinical immunity. Provided they continue to be exposed to malaria, this immunity protects them from severe disease for the rest of their lives, except during pregnancy. Unfortunately, the immune response that correlates with protection in these lifelong residents of endemic areas has not been identified, so development of a vaccine that mimics this immunity will be difficult. Moreover, malarial parasites demonstrate extreme antigenic diversity. Recent developments, including better methods for antigen production, improved adjuvants and novel delivery systems, provide optimism that sustained and appropriate long-lived immunity can be achieved. Vaccines could be directed against the sporozoite stage of the malaria parasite to prevent infection, or against the stages in human blood — the asexual stage to prevent clinical disease, or the sexual stage to prevent transmission. The malaria vaccine which has been studied in most detail is designed to induce immunity to the sporozoite and the infected liver cell (ie, to stop sporozoites invading liver cells and to kill sporozoite-infected liver cells). In early studies it was shown to induce protective immunity against experimental challenge.5 Under conditions of natural exposure (in semi-immune adult men in The Gambia),6 the vaccine was shown to be safe and well tolerated, with an estimated efficacy (decrease in malaria infection) of 70% in the first nine weeks of follow-up. However, over the 15 weeks of observation, the efficacy fell to 34%. Further trials will determine whether improved efficacy can be achieved in young children. Australian research efforts have led to a multicomponent recombinant protein vaccine targeting the asexual blood stages. This vaccine was tested recently by the Papua New Guinea Institute of Medical Research and its collaborators. The vaccine caused a 62% reduction in parasite density in children, without any harmful side effects.7 Further development will be necessary to produce a vaccine sufficiently efficacious for routine use. In the past there has been a serious lack of funding for research into malaria, partly because companies engaging in this type of research did not expect it to be profitable. A major change has occurred of late, with increased funding from the Wellcome Trust in the United Kingdom, and from the United States through the National Institutes of Health. A grant from the Bill and Melinda Gates Foundation has funded the Malaria Vaccine Initiative of the Program for Appropriate Technology in Health (PATH) (http://www.malariavaccine.org). This worldwide initiative has the specific goal of enhancing the transition of the many promising candidate vaccines from the laboratory to "proof of principle" research in phase I clinical trials. It has funded Australian projects developing vaccines from asexual stage (merozoite) antigens by researchers at Monash University, La Trobe University and the Queensland Institute for Medical Research, partnered by Biotech Australia (New South Wales), the Cooperative Research Centre for Vaccine Technology (Queensland) and Progen Industries Limited (Queensland).8 There are still many challenges in developing a malaria vaccine, such as the need to cope with diverse antigenic types and the importance of stimulating a lifelong response that is boosted by natural infection. Vaccine-induced sterilising immunity that is not boosted by exposure to malaria could put an individual at increased risk when the vaccine-induced immunity wanes. Most importantly, we need vaccines that can be incorporated into national immunisation programs as part of a coordinated, holistic approach to malaria control. Research to find new methods for vector control and new drugs must also continue, as we know from past antimalarial campaigns that a single technology will not be sufficient to control this devastating disease.

Graham V Brown PhD, FRACP · John C Reeder PhD

Australia does not do well in the early detection of congenital hearing impairment. Only about 25% of infants born with hearing impairment are diagnosed by the age of 12 months, and for many children deafness remains a disability leading to severe and lasting language impairment.1 The technology for newborn hearing screening has now been in regular use in many parts of the world for much of the past decade, and there is at last some persuasive evidence that very early detection helps these children achieve normal language skills.2,3 This evidence is far from perfect: 4 only one randomised controlled trial of detection rates with and without newborn screening has been reported, and no randomised controlled trial has yet examined outcomes of hearing screening. Nonetheless, universal newborn hearing screening has become not only possible but expected in the United States and Canada, the United Kingdom and many European countries. However, it has not yet been widely implemented in Australia. As a result, the excellent diagnostic and rehabilitative services available to all Australian children once the diagnosis of hearing impairment has been made contrasts strongly with our patchy and very incomplete ascertainment of hearing impairment in the first year of life. The Western Australian Newborn Hearing Screening Programme is therefore an important step, as is the recent announcement that a program will commence throughout New South Wales by the end of 2002. In a report of the WA program in this issue of the Journal, Bailey et al (page 180)5 demonstrate that a high-quality, sustainable universal newborn hearing screening program can operate in Australian birthing hospitals. It appears to be a model program, with exceptionally high coverage, high acceptability, low referral rates, and low rates of babies lost to follow-up. It exceeds most benchmarks set in 2000 by the US Joint Committee on Infant Hearing,6 and is in line with the Australian National Consensus Statement on Newborn Hearing Screening.7 Nonetheless, it raises a number of difficult issues. Bailey and colleagues report that the hearing screening program has achieved more than 96% coverage in the five participating metropolitan hospitals. However, together these screened infants represent only about half Western Australia's annual births — unfortunately, the "easy" half. The program operating throughout the US State of Colorado,8 one of the few approaching a true population coverage, has demonstrated that hospitals with fewer than 400 births annually do worse on average than large hospitals in terms of coverage (substantially lower) and referral rates (substantially higher). Australia is characterised by vast distances and a very large number of small hospitals. For instance, the State of Victoria has a similar birthrate to Colorado, but nearly twice as many birthing hospitals (about 110, compared with 60), most of which are small. Statewide or national newborn hearing screening therefore poses considerable logistic and economic obstacles in Australia, and these are not necessarily surmountable. But what are the consequences of limiting ourselves to larger hospitals? Let us assume that 50% of a State's population receives a very high quality hearing screening program which achieves 95% coverage, 90% sensitivity, 95% follow-up, and 80% compliance with early fitting of hearing aids and intervention (as some parents choose neither). This equates to less than a third of that State's hearing-impaired children benefiting from the program. If any one of these parameters is lower, then the number of children potentially benefiting falls even further. Despite individual gain, median age at diagnosis and overall outcomes for the State would improve little. If universal screening is to lead to population benefits, then universal it needs to be — despite the challenges. A poor alternative is to screen only babies with a risk factor for deafness. Asking about the presence of a risk factor becomes the universal "screen", followed by a targeted screening test of hearing itself. At face value, this may seem cheaper, but it is not easier and certainly detects fewer children. While almost all children with hearing loss detected in the Western Australian series so far have had a risk factor, in larger series this applies to only about 50% of babies.8,9 Neonatal intensive care and special care nurseries typically contain about 30%–40% of all infants found to have moderate or greater hearing loss in newborn screening programs9,10 and are relatively easily targeted, as are babies with obvious head and neck abnormalities. Other risk factors, such as family history of early hearing impairment, pose greater problems. Accurate elicitation requires skilled enquiry and mothers may not recall, or even know, that a risk factor is present until after the diagnosis is made, thus reducing sensitivity. The Victorian Infant Hearing Screening Program has recently highlighted the very low positive predictive value of family history and some other risk factors, with close to 200 babies needing to be referred to diagnose one child with hearing loss.11 Low sensitivity combined with poor positive predictive values equates to spending a lot of money to miss many children. Finally, risk-factor screening raises issues of equity, as the many children with hearing impairment, but without a discernible risk factor, would be denied access to hearing screens in such a program. A final issue is that of program sensitivity. At 0.7 per 1000, Western Australia's detection rate for children with bilateral congenital hearing impairment of more than 35 dB HL (hearing level) is lower than the usual rate of 0.9–1.0 per 1000 detected (with hearing impairment of more than 40 dB HL in the better ear).8,9 Most likely, this is a chance finding reflecting the small size of the series — it "just happened" that relatively few babies with hearing impairment were born during this time period. Alternative explanations include equipment problems or program insensitivity. The Western Australian program is unusual in that a baby is not referred until screening has shown three "fail" responses. This lowers the false positive rate and increases program specificity — both of which are desirable. But in screening programs rises in specificity are typically accompanied by falls in sensitivity. It may be that, in this case, the pendulum has swung too far towards specificity at the expense of sensitivity, and that, after years of worrying about excessive referral rates, they are — at last — too low. Currently, we are not serving well the hundreds of children born each year with moderate or greater hearing impairment in Australia. Universal newborn hearing screening seems one way of improving this situation. It is not reasonable to defer implementing a program until the evidence is stronger, since stronger evidence is unlikely to be available soon. Rather than stopping us from implementing programs, this should spur us to acquire such evidence. Because Australia has not yet widely introduced newborn hearing screening, we have an unusual capacity to study these questions prospectively. National benchmarks and a minimum dataset should be established, and we should start carefully and systematically examining outcomes for hearing-impaired babies born now against which to compare gains over the coming years. We should also keep an open mind. In 10 years' time, Australia should be able either to guarantee continuation of an effective program, or to move resources rapidly from a program that, despite best efforts, has proved ineffective.

Melissa A Wake MD, FRACP, MB ChB

In 1997, South Australian women around the age of menopause had one of the highest reported rates of hormone replacement therapy (HRT) use in the world.1 Among women aged 55–64 years, 60% had used HRT and nearly 40% were current users, with a mean length of HRT use of 70 months. HRT is effective at relieving menopausal symptoms, and many women can stop taking HRT within a few years without recurrence of these symptoms. For the women who do experience return of menopausal symptoms after ceasing HRT, there has been the comfort of observational studies that showed that long-term HRT use, although increasing the risk of breast cancer and thromboembolic disease, reduced osteoporosis, bowel cancer, cardiovascular events, Alzheimer's dementia, and possibly stroke.2 Critics of long-term HRT use have argued that selection of relatively healthy women to receive HRT may have influenced its reported long-term effects in unrandomised observational studies.3 Two large randomised trials of postmenopausal long-term HRT use were commenced in the 1990s to determine the benefits and risks. The Women's Health Initiative (WHI) in the United States (see website <http://www.whi.org>) focuses on defining the value of different strategies (eg, low-fat diet, calcium and vitamin D supplementation) that could potentially reduce the incidence of heart disease, breast and colorectal cancer and low-impact fractures in postmenopausal women aged 50–79 years. The Women's International Study of long Duration Oestrogen after the Menopause (WISDOM) (http://www.generalpractice.adelaideuni.org/research_index.htm [No longer available]) is a UK-initiated, placebo-controlled study of women aged 50–69 years taking oestrogen, or oestrogen and progestogen, for 10 years. Endpoints of the study include fracture, cardiac events, cancer, dementia, thromboembolism, quality of life, and death. Some Australian women have been recruited to the WISDOM study. Late in the evening (Australian time) of 9 July 2002, the American Medical Assocation posted a report of a WHI trial and an accompanying editorial on its JAMA website.4,5 The report revealed that this randomised, placebo-controlled, double-blind trial to evaluate combined oestrogen and progestogen therapy in postmenopausal women had been stopped early because there was compelling evidence that health risks exceeded health benefits. Graham Colditz (Professor of Medicine at Harvard School of Public Health and one of the authors of the JAMA editorial), who was visiting Australia at the time, and the Cancer Council, New South Wales, were ready to issue press releases (embargoed until 11.30 pm that evening) highlighting the 26% increased risk of breast cancer in women taking HRT. One of these releases was headed "Women advised to stop combined hormone replacement therapy". By the next morning (10 July), the Australian media were awash with headlines and reports that fuelled considerable alarm among women taking HRT. On the same day, the Australian Therapeutic Goods Administration (TGA) requested that the Australian Drug Evaluation Committee (ADEC) establish an Expert Committee to examine the JAMA article and provide advice on the significance of the study outcomes in the Australian context, the necessary and appropriate action required of the TGA, and the information that should be provided to Australian health professionals and consumers. The rapidly convened ADEC Committee reviewed the JAMA article and editorial and gave the TGA its report, which was released on the TGA website in the late afternoon of 11 July. The report noted that the WHI trial was designed to investigate the efficacy and safety of long-term combined HRT in preventing diseases such as coronary heart disease and hip fracture in postmenopausal women. It was not designed to study the effects of HRT being used to treat menopausal symptoms or established osteoporosis. The mean age of women in the study was 63 years, with two-thirds being over 60. This, and the apparently high frequency of cardiac risk factors in the population (one-third being overweight and one-third obese, 50% being previous or current cigarette smokers, one-third having received treatment for high blood pressure, and over 10% having raised cholesterol requiring medication), may have led to a higher risk of cardiovascular events. However, this must be set against a likely underestimate of the excess risk as a result of treatment dropout and crossover. There was no difference in overall mortality between the HRT and control groups for the duration of the study (mean, 5.2 years). The absolute increase in disease risk for an individual woman shown in the study was small: among 10 000 women in the age group studied and with their characteristics taking combination HRT for a year, there would be seven more cases of coronary heart disease (37 v 30), eight more cases of invasive breast cancer (38 v 30), eight more cases of stroke (29 v 21), and eight more cases of pulmonary embolism (15 v 7), but six fewer bowel cancers (10 v 16) and five fewer hip fractures (10 v 15), than among women not using HRT. Over the five years of the trial, there would be one extra case of an adverse event per 100 women taking the combined HRT continuously. The Expert Committee noted the increase in harm reported was smaller in the first two to three years after starting HRT than it was after three or more years of combined HRT use. Conclusions of the Expert Committee of the Australian Drug Evaluation Committee Combination hormone replacement therapy (HRT) in any form should not be used for long-term disease prevention in postmenopausal women, because the benefits are not sufficient to justify the risks. This conclusion is not necessarily restricted to the particular products used in the trial, but could potentially apply to all oestrogen/progestin combination hormone products. Women can be assured that short-term use of combination HRT and other products to manage symptoms of menopause remains an appropriate treatment option, but women should discuss their particular medical circumstances with their doctors, as individual factors may affect the risks and benefits for them. This is even more so for younger women with a premature menopause, in whom the benefits of HRT would be expected to be greater, and the risks are probably smaller. The continued use of combined HRT for women with established osteoporosis is also an acceptable option for many, but women should discuss the benefits and risks with the treating doctor. In another arm of the Women's Health Initiative study, which has not been discontinued, the use of oestrogen alone for the prevention of disease in postmenopausal women who have had a hysterectomy continues under investigation. It is unsafe for women who have a uterus to use oestrogen without progestin, as use of oestrogen alone increases the risk of uterine cancer. The conclusions of the Expert Committee are presented in the Box. The Committee recommended that the TGA ensure updating of product and consumer information for all products used in combination HRT, undertake a full review of the use of combination HRT in long-term treatment and prevention of osteoporosis, and review all ongoing trials using combination HRT for chronic diseases. The WHI trial report and the abrupt cessation of the combined oestrogen plus progestogen trial have raised concerns among health practitioners, prescribers and consumers of combined HRT products. The previously anticipated health benefits from prolonged combined HRT use — reduced heart disease and strokes — were not borne out in the WHI study. However, the absolute risks associated with HRT are small. Women who are currently taking combined HRT, and their doctors, should not panic, but consider these new findings carefully in the light of their reasons for starting and continuing HRT before deciding whether to continue or stop. In women with osteoporosis, the benefit of a reduced fracture rate with long-term combined HRT must now be balanced against the increased risks of breast cancer, stroke, heart disease and thromboembolism. The relative efficacy and safety of HRT must be considered against that of other interventions, including ensuring adequate calcium intake and vitamin D status, exercise, or taking bisphosphonates or selective oestrogen-receptor modulators.

Martin H N Tattersall MD FRACP

On 8 July 2002, the National Health and Medical Research Council released a discussion paper1 and draft guidelines for xenotransplantation research, with the aim of promoting widespread community debate of the issues involved. In the discussion paper, xenotransplantation is defined as the placement of animal cells, tissues or organs into humans, and includes the exposure of human tissue or cells to animal cells. Examples include the external perfusion of blood through a "bioartificial liver" (ie, an external apparatus containing pig liver cells which are separated from the perfused human blood by a semipermeable membrane), or culture of human skin cells on mouse fibroblasts for later use in treating burns. This definition excludes implantation of inert, sterilised animal tissues, as currently used to create artificial heart valves. The concept of xenotransplantation has arisen because of an ongoing shortage of human donor organs. The discussion paper provides information on this shortfall, and measures pursued in Australia and overseas to try to improve organ donation rates. As there is general acceptance that the demand for donor organs is such that even increased human donation will not overcome the problem, the complex issues attending the shortage of human donors are not pursued further in the discussion paper. So, what are some of the matters requiring community consideration and debate? A key issue is the risk that an infectious agent could cross from an animal to humans, and produce unknown infectious risks for the general community. Cross-species transmission of most known viral and bacterial pathogens is preventable by appropriate breeding, housing and testing of source animals. However, there is serious concern that a virus, such as the endogenous retrovirus present in the pig genome (the pig is currently the preferred source of organs), could "reactivate" in human recipients and, theoretically, later infect close contacts, healthcare workers or the wider community. Although experimental work has demonstrated that isolated human cell lines can be infected with porcine endogenous retrovirus (PERV), retrospective testing of 160 patients exposed to date to pig xenotransplants, such as islet cells or neural cells, or to external perfusion using pig liver cells, has not revealed evidence of PERV infection.2 This risk of infection brings a new ethical dimension to how consent for xenotransplantation research might be given. The discussion paper emphasises that not only will any potential recipient need to be fully informed of any risks, but so too will close contacts of the recipient and members of the healthcare team. An additional ethical issue relates to how a prospective recipient might reasonably choose between risking an experimental therapy or waiting for a human organ transplant. Another issue which requires community debate is the potential use of genetically modified pigs to overcome the intense rejection reaction which, so far, has made xenotransplantation unfeasible. While experimental work to date has involved minimal genetic manipulation, more extensive modification (which could be seen to significantly alter the essential nature of the animal) may not be acceptable ethically or to our community. In all human research, a key ethical principle is that the putative benefits must outweigh the known and theoretical risks. Weighing this balance for any human xenotransplantation research proposal will not be an easy task. The draft guidelines outline multiple conditions which must be met before research can be approved. One such requirement is obtaining convincing data of the efficacy of animal-to-animal experiments (eg, pig-to-baboon xenotransplantation) before pig-to-human trials can be contemplated. A further issue relates to which group of individuals should be empowered to weigh up these benefits and risks and give approval for such human research on the community's behalf. The discussion paper recommends that this should be a task for a national committee, whose membership would include people with relevant scientific, ethical and regulatory expertise, as well as community members. Local human research ethics committees would play a role in monitoring the research, and could reject a proposal, but could not approve a proposal unless it had also received approval from the national committee. The full text of the document, entitled Draft guidelines and discussion paper on xenotransplantation, is available on the National Health and Medical Research Council (NHMRC) website,1 or can be obtained from the NHMRC at PO Box 9848, Canberra, ACT 2601. The document contains advice on how to make a submission by the closing date of 6 September 2002. Submissions will be carefully considered by the working party in making its final recommendations to the Council. The NHMRC regards xenotransplantation research as one of the more important issues for community consideration, and wishes to actively involve medical practitioners in the debate. Medical practitioners are invited to either develop and communicate their own views, or to assist in stimulating debate in the wider community.

Kerry J Breen, on behalf of the NHMRC Working Party on Xenotransplantation MD, FRACP

Research and practice in grief and loss have been undergoing something of a sea-change in recent years. Past research-based models of grief have attracted much criticism, not only from practitioners but also from researchers in the social sciences. There have been persistent calls for greater sensitivity to the contexts of grief and a more balanced understanding of its positive and cultural influences in our lives. Most of our understanding about grief has been drawn from psychoanalytical sources (eg, the work of Freud or Klein) and later from attachment theory (eg, the work of Bowlby).1 These sources have emphasised the role of the emotions and psychological defences. Research commonly focused on particular populations (such as children, the terminally ill, the mentally ill, or victims of disasters), while the research on community samples examining the loss of spouses, parents or children overidentified grief with bereavement. The conceptual emphasis that emerged from this research stressed issues such as "loss", "disengagement" or "resolution".2 There were debates about whether grief was a "state" or a "process", and later, when the process theories became popular, whether these processes had "phases" or "stages". Many practitioners and popular writers working in bereavement care embraced much of this important early work, which still forms the basis of our understanding of personal control and adaptation in the face of loss. But a concentration on the psychodynamics of attachment and defence inadvertently resulted in overattention to professional interventions and an underemphasis on social relationships, contexts and cross-cultural issues.3 The early work by the psychological professions also led to a concentration on the negative experiences of grief. The traumatic, obsessional and socially destructive aspects of grief were stressed and examined. The concern was to reduce the morbidity and mortality associated with grief, particularly to lessen its role in suicide, substance misuse and other psychiatric conditions, such as severe anxiety or depression. Recent research has attempted to restore greater professional and conceptual balance to these early insights and concerns. There are now increasing numbers of sociologists, anthropologists and historians entering the field, and many of these have been critical of the psychological emphasis on attachment, separation and "letting go".4,5 There has been greater attention to the different ways people grieve according to their own social norms, cultural prescriptions and personal styles.6 There is a growing awareness and theoretical interest in the relationship between bereavement and other kinds of loss, such as the dispossession felt by Indigenous people and refugees, or losses associated with adoption.7 There has been growing international acceptance of a theory of "continuing bonds" — a recognition that people do not necessarily "let go", but transform their former relationships by renewing their meanings about them and continuing the relationship in new ways.8 There has been some recognition of the limits to professional help, reflected by the growing interest, worldwide, in support and self-help groups. The growing input of the social sciences has encouraged a parallel interest in the role of social and cultural differences in the expression of grief and its diverse coping styles. There has been a renewed interest in normal and positive aspects of grieving. There is a growing realisation that the dead may be important role models for the grieving; that they may continue to be "significant others" to the bereaved. People continue to relate to their dead as "active and living memories" at times of personal crisis and success.9 Grief can also create a positive social legacy — in advocacy (influencing policy and education), in political activism (giving rise to groups such as Mothers Against Drink Drivers), in foundations (supporting research or service development) and in careers (heightening the personal achievements and ambitions of survivors).10 Grief also creates "social ghosts" in the form of influential memories, dreams, or visions.11 These can be both comforting and disturbing; motivating and hope-giving as well as upsetting. Furthermore, the general experience of grief can enhance personal empathy and social compassion. These previously under-recognised perspectives present new but complementary challenges for research and practice in the care of people suffering grief. We need to return our attention to the diverse expressions of normal and healthy grieving, while continuing to recognise that grief can cause marked health changes in some individuals. The new insights also highlight the limits to professional care and the need to create supportive environments in our communities for people living with loss. There is a major need for government policy development in this area to reflect a broader public health sensitivity towards our diverse national grief and loss needs. Policy and research priorities might address issues such as the social impact of grief on Indigenous health, on the lives of elderly people, or on the desire for suicide. These research directions will assist us to understand public expressions of creativity or personal experiences of resilience. Our referral options for people suffering grief should include community support, such as pastoral care or the National Association for Loss and Grief, as well as specialist medical and psychological services. These issues are only some of the recent practice and research challenges to emerge in the field of grief and loss, but they point to its constructive and positive revival.

Allan Kellehear

Otitis media — definitions Acute otitis media without perforation: Presence of middle-ear fluid with symptoms or signs of suppurative infection. Bulging of the tympanic membrane is the most reliable sign in Aboriginal children. Acute otitis media with perforation: Acute suppurative infection with recent discharge from the middle ear (within the last 7 days). Otitis media with effusion: Presence of middle-ear fluid without symptoms or signs of suppurative infection. Chronic suppurative otitis media: Persistent discharge from the middle ear through a tympanic membrane perforation for more than 6 weeks. Chronic suppurative otitis media (CSOM) (see Box) is very uncommon in First World countries and is best regarded as a disease of poverty. The World Health Organization has indicated that a prevalence rate of CSOM greater than 4% in a defined population of children is indicative of a massive public health problem requiring urgent attention.1 That CSOM affects up to ten times this proportion of children in many Aboriginal communities is an indictment of the poor living conditions in these communities.2 The associated hearing loss has a life-long impact, as it occurs during speech and language development and the early school years. Why is chronic suppurative otitis media so recalcitrant?Many factors contribute to poor health outcomes. In biological terms, the greatest risk factor for the early onset and persistence of otitis media is nasopharyngeal colonisation by multiple bacterial species and subtypes.3 In Aboriginal communities with overcrowded households, infants are frequently exposed to siblings whose nasopharyngeal carriage rates are almost 100% for each of the major otitis media bacterial pathogens.3 In non-Aboriginal children, the host response to a low-dose infection usually eradicates pathogens, which, in turn, down-regulates inflammation and limits tissue damage. In contrast, we believe that early exposure of very young Aboriginal infants to a large bacterial inoculum (or frequent exposures to immunologically distinct pathogens)4 provides constant stimulation of the inflammatory cascade, which damages mucosal tissue yet fails to eradicate pathogens.5 This begins a vicious cycle that may persist throughout childhood: early exposure, persistent bacterial colonisation, and chronic mucosal disease. Furthermore, such infants themselves become chronic carriers and pose a risk to other, younger infants. This cycle is facilitated by overcrowded and poor living conditions, lack of appropriate washing facilities,6 and limited access to appropriate healthcare services. Bulging of the tympanic membrane is the best diagnostic predictor of perforation.7 Other signs and symptoms of acute otitis media (such as pain, fever, irritability or redness of the tympanic membrane) are frequently absent in this population. The implications of this lack of signs or symptoms are clear — parents do not see their child as unwell and thus children remain untreated. Together, this biological model and clinical pattern help us to understand the intractable nature of otitis media in Aboriginal children. Currently, failure to apply existing knowledge is a more important problem than lack of knowledge. Aboriginal children have poorer access to therapy, hearing aids, special teachers, classroom soundfield systems and other rehabilitative programs.2 Furthermore, there is inequitable distribution of funds from the Commonwealth Hearing Health Services Program, with evidence that the hearing health needs of Aboriginal children are not being met.8 What strategies have worked?A systematic review of existing evidence and primary care guidelines for the management of otitis media in Aboriginal and Torres Strait Islander people2 identified effective primary prevention strategies: improving nutrition and the home environment, increasing breastfeeding, and reducing passive smoking. A small but important role was noted for vaccines (the polysaccharide, polyvalent pneumococcal vaccine and the new pneumococcal conjugate vaccine). Controversies remain regarding the effectiveness of antibiotics in primary prevention and the impact of maternal pneumococcal vaccination on infant disease.2 High doses and prolonged courses of antibiotics are often required for the treatment of acute otitis media and CSOM,7 but the optimal use of topical ear preparations remains uncertain.2 Where appropriate primary healthcare interventions have failed, timely referral to otolaryngologists for assessment and surgical interventions can improve hearing outcomes.2 However, access to such specialist care for children in remote Aboriginal communities is suboptimal. Audiological rehabilitation is critical, requiring the provision of ongoing education about effective communication strategies and appropriate use of devices to assist hearing. These include standard hearing aids and bone conductors, as well as classroom devices such as soundfield amplification systems (which provide a uniform soundfield throughout the classroom and increase the speech-signal : noise ratio), and FM systems (a form of personal amplification whereby an FM signal from a microphone worn by the teacher is picked up by a receiver worn by a child with hearing loss).9 What needs to happen in the future?Greater community control over improvements to education, employment opportunities, housing infrastructure and primary healthcare services is long overdue. To realise these improvements requires substantially increased resources, linked to community responsibility. In the meantime, initiatives that increase access to primary healthcare for the detection and management of ear disease and facilitate access to other services should continue. An example is the Office for Aboriginal and Torres Strait Islanders Health Hearing Health Program.10 Realistic expectations about the benefits and harms of evidence-based healthcare interventions should be incorporated into updates of currently available clinical guidelines, and the information made accessible to families. The Commonwealth needs to reform the provision of rehabilitative services and coordinate approaches to soundfield amplification in schools. The research priority is to determine the best use of preventive strategies and interventions (including educational, medical, surgical and audiological initiatives). Multidisciplinary research in the areas of diagnosis, new antibiotics, the role of biofilm and vaccines is also appropriate. Bacterial biofilm is a community of interacting bacteria attached to a surface and encased in a protective matrix of exopolysaccharide. Formation of biofilm in the middle-ear mucosa of Aboriginal children with CSOM may explain the recrudescence of bacterial otorrhoea after viral upper respiratory tract infections.11 Pneumococcal conjugate and innovative protein-based vaccines are aimed at inducing a mucosal immune response. Several Australian trials are currently examining the impact of pneumococcal conjugate vaccine on nasopharyngeal carriage rates and perforation of the tympanic membrane. Only with urgent attention to improving housing and access to running water, nutrition and quality of care, and giving communities greater control over these improvements, will this massive public health problem be solved so that Aboriginal children can take their rightful place in this, the century of communication.

Harvey L Coates MS, FRACS · Peter S Morris PhD, FRACP · Amanda J Leach PhD · Sophie Couzos FRACGP, FACREM, FAFPHM

It is time to focus on reducing inappropriate test ordering The complexity of modern medicine has promoted an excessive reliance on the results of empirical tests rather than clinical acumen. In Australia, this is reflected in the fact that the rise in the costs of diagnostic testing in pathology and radiology is second only to the rise in cost of pharmaceutical prescriptions, the fastest-growing sector in our healthcare budget. Many reasons have been cited for this increase in clinicians' reliance on pathology and radiology testing. Among community-based practitioners, ordering patterns are most likely to be influenced by medicolegal concerns, time constraints, screening needs, or ingrained practice habits. Among hospital-based clinicians, test-ordering practice may be determined by level of clinical experience, fear of censure for lack of testing, medicolegal concerns, and the desire to provide a "one-stop" service to evaluate all possible physiological parameters.1 In addition, the pressures of shorter consultation times in community practice and diminishing hospital beds have led to the increased use of investigations to fast-track patient throughput. In acute hospital settings, it has been estimated that as many as a third of all tests ordered are inappropriate in terms of their ability to contribute to the diagnosis and treatment of individual patients.2 This overtesting is not without consequences. If a healthy individual is subjected to 10 unnecessary tests, there is a 40% chance of at least one false-positive result.3 As well as exposing the patient to potential harm from unnecessary tests and treatment, this may expose the clinician to an increased, rather than a decreased, medicolegal risk, as patients are exposed to greater risks of complications while they proceed along an unnecessary testing spiral. In a community that is struggling to cope with the financial demands of modern healthcare, the wastage of resources on unnecessary pathology and imaging testing has an adverse effect on the provision of services that are legitimately required. Furthermore, in most settings, it is the relatively cheap, common tests that account for the bulk of testing expenditure. In our own institution, about 80% of the costs of biochemistry and haematology testing are accounted for by full blood counts and testing of electrolytes, urea, creatinine, liver function and cardiac markers. Although more complex investigations, such as gene testing, may individually be more expensive, the sheer volume of common tests drives the overall costs of investigations, and suggests that attempts to reduce inappropriate testing should focus on these tests. In this issue of the Journal, Stuart and colleagues (page 131) report on a comprehensive program of education, audit, feedback and structural change to reduce the number of investigations performed in a public hospital emergency department.4 Although their program focused on reducing inappropriate testing and improving result follow-up in an emergency department, the lessons learned about how to produce sustainable change in clinician practice are equally applicable to the rest of the acute hospital environment, and to the community sector. There has been a plethora of reports on the implementation of educational or other programs aimed at curbing the costs of inappropriate testing. Most describe utilisation of tools such as education programs,5,6 incentives for clinicians,7,8 information about costs of testing, audit of ordering profiles, feedback on ordering patterns, guidelines, decision-support systems, and process changes.9,10 The study by Stuart et al demonstrates the key features required for sustainable improvement in test-ordering behaviour. A multifaceted approach that results in alteration to the core processes of test ordering is more likely to promote lasting improvements than strategies aimed just at increasing awareness or knowledge among individuals. In public hospitals, where the junior medical staff who are responsible for most test-ordering rotate through departments at three-monthly intervals, it is essential that whatever changes are made to improve test-ordering are capable of affecting a mobile workforce. It is unlikely that educational programs alone could cope with the demands of this rostering pattern, unless concomitant process changes are implemented hospital-wide to ensure applicability in all clinical settings. As conceded by Stuart et al, the effects on patient outcomes of attempts to reduce overtesting were not addressed. No data are provided on readmission rates, length of stay, adverse events and rates of missed or incorrect diagnoses. It is possible that attempts to reduce numbers of tests performed could result in harm to patients through underinvestigation of symptoms. Therefore, future studies in this area should include measures of patient outcomes to ensure that an overall improvement in patient care accompanies the reduction in costs of investigation. Computerised systems are widely available in general practice for prescribing, and, in some places, for test ordering, but have yet to be widely implemented in the acute care sector. At present, these systems have focused on facilitating the ordering process rather than ensuring its appropriateness. The future is likely to see implementation of computerised order-entry systems that provide real-time feedback on ordering patterns, guidance on test appropriateness, improved result checking, and information on the costs of tests ordered. Such systems already exist, and are currently being tested in several Australian hospitals. It is hoped that overcoming existing deficiencies in information systems will enable clinicians to order tests and check results more efficiently and more appropriately than they currently do. An academic analysis of current test-ordering practices might suggest that further research is needed into why doctors order tests the way they do, whether there really is such a high rate of unnecessary testing, and what value current ordering patterns add to our highly complex healthcare system. A pragmatic view, however, would suggest that there is enough published evidence that overtesting is a characteristic of healthcare systems in the developed world, and enough information in existing research to guide what should be done to reduce waste and harm resulting from inappropriate testing. It is time that the focus of work in this area shifted to development of practical, sustainable means of improving the appropriateness of testing. Future research may be best directed to understanding the place of sophisticated decision-analysis models, the role of point-of-care guidance and feedback systems, and effective clinical change-management strategies. In the meantime, hospitals around Australia have already embarked upon attempts to change current practice. In Melbourne, the National Institute of Clinical Studies is sponsoring a 12-month project, involving hospitals from four States and Territories, aimed at developing transferable and sustainable changes in test-ordering practices. Similarly, hospitals involved in the Health Roundtable in Sydney have been involved in exchanging information on effective strategies to improve test ordering. The Royal Australasian College of Pathologists is developing undergraduate education programs aimed at improving ordering practices. The lessons learned from these groups should inform national strategies to deal with the problem of inappropriate testing. As in the study by Stuart et al, it is likely that a coordinated, multifaceted, sustained approach to this problem will be required to achieve lasting success.

Rohan J H Hammett MB BS, FRACP · Roger D Harris MB BS, FACEM

Surgery shows promise for patients with severe, poorly controlled motor fluctuations Parkinson's disease afflicts around 78 000 Australians. Mortality is almost twice that of age-matched controls1 and the mean disease duration is only 13 years.2 No treatment has yet been shown to slow disease progression. Fortunately, motor disability can be markedly improved with levodopa therapy. However, after 3–5 years, the duration for which each dose of levodopa is effective shortens and many patients begin to experience fluctuations in their motor function throughout the day. Involuntary movements appear, in particular painful posturing of the legs or arms, as the beneficial effect of levodopa wears off ("end of dose dystonia") and writhing choreoathetoid movements that accompany part or even all of the period when levodopa is working ("peak dose dyskinesia"). These problems can be ameliorated to some extent by the addition of dopamine agonists or catechol-o-methyltransferase (COMT) inhibitors. Unfortunately, problems that are not reversed by levodopa, such as worsening of balance and speech, cognitive decline and depression, can also supervene. Patients who never experience sustained benefit from levodopa are likely to have a different underlying pathology from idiopathic Parkinson's disease, such as vascular parkinsonism, progressive supranuclear palsy or multiple system atrophy. It is in patients with severe, poorly controlled motor fluctuations that surgical therapy has re-emerged as a treatment option. In this issue of the Journal (page 142), Iansek and colleagues report the results from 14 patients at their centre who underwent bilateral deep brain stimulation of the subthalamic nucleus for the treatment of Parkinson's disease.3 Motor function was improved with subthalamic nucleus stimulation for at least six months when patients were assessed both with and without levodopa treatment. Dyskinesias were also apparently reduced, and mean levodopa dose was reduced by 30% after surgery. The procedure was not without risk (one patient had a disabling intracerebral haemorrhage, another required relocation of the stimulators to the thalamus), but overall this is an exciting and encouraging development. Data were also collected from the first six patients in the reported series as part of an international multicentre trial, which included another Australian centre, St Vincent's Hospital, Sydney.4 Results from 96 patients who underwent bilateral subthalamic nucleus stimulation showed a median reduction of 49% in motor disability without medication using blinded videotape analysis, a mean increase from 27% to 74% of the day spent with good mobility without involuntary movements, a 58% improvement in dyskinesia scores, and a 37% reduction in mean daily levodopa dose. Similar, but less marked, improvement was seen in 38 patients treated with bilateral pallidal stimulation, although the dose of levodopa was not reduced after surgery in these patients. The incidence of intracranial haemorrhage was 2.5%, and infections requiring electrode removal occurred in less than 1%. These are benchmark figures by which the results of Australian centres offering these procedures can be compared. Surgical therapy for Parkinson's disease is not new, but there have been advances in our understanding of why it works. Loss of dopaminergic projections from the substantia nigra to the basal ganglia results in pathological overactivity of the subthalamic nucleus and globus pallidus. Patients undergoing deep brain stimulation have a wire implanted into the brain that is attached to a programmable battery implanted subcutaneously in the chest wall, much like a pacemaker. Deep brain stimulation mimics the effects of stereotactic lesioning, but has the added advantages of being reversible and allowing postoperative programming to optimise the site of stimulation. However, it is expensive and programming is time-consuming, sometimes requiring months before the optimal stimulating parameters can be established. Economic and geographical constraints limit access to therapy for many patients in whom surgery would otherwise be appropriate; such issues need to be addressed by healthcare providers. At present, there are a number of Australian centres performing subthalamic nucleus stimulation and pallidotomy (lesioning of the globus pallidus); experience in pallidal stimulation is as yet limited. The indications and choice of operation are still evolving. Nevertheless, some general guidelines may be suggested. Who should be offered surgery? Surgically fit patients with severe motor fluctuations or dopa-induced dyskinesia, or both, are the main candidates. Surgery does not significantly improve the patient's best response to levodopa (except by reducing dyskinesias). A good or excellent response to levodopa predicts the response to surgery, and is essential.5,6 The procedure, particularly subthalamic nucleus stimulation, may take hours, during which time the patient remains fully conscious, so a degree of stoicism on the part of the patient is required. For the rare patient with disabling parkinsonian tremor that is poorly suppressed by levodopa, without accompanying akinesia, thalamic surgery can be contemplated. Who should not be offered surgery? Patients who have never responded well to levodopa will not benefit from surgery. The presence of cognitive or psychiatric complications of Parkinson's disease (frequent hallucinations, psychosis, parkinsonian dementia, uncontrolled depression) is an absolute contraindication to surgery; significant cerebral atrophy on computed tomography or magnetic resonance imaging is also a contraindication. Levodopa-resistant symptoms such as impairment of balance or speech can worsen after surgery.7 Which procedure? Overall, subthalamic nucleus stimulation appears more promising than pallidal surgery. However, a randomised trial comparing the two has not been performed, and excellent and sustained improvement following both bilateral subthalamic nucleus stimulation and bilateral pallidotomy is seen.8 Physicians should be guided not only by theoretical considerations, but also by local experience and expertise. Objective evaluation of the results of surgery by a neurology team not involved in patient selection or the surgical procedure is an advantage, and this information should be available to patients and their treating neurologists to aid decisions about therapy.9 Where to refer? The process of optimising therapy for advanced Parkinson's disease, differentiating between idiopathic Parkinson's disease and related disorders, and choosing the appropriate operation, is not always straightforward. For this reason, we recommend that patients considering surgical treatment be referred to a unit with specialist expertise in movement disorders, and that surgery be offered in the setting of a multidisciplinary assessment by teams including a neurologist, neurosurgeon, neuropsychologist and Parkinson's disease nurse specialist.

Victor S C Fung PhD, FRACP Director, Movement Disorders Unit · John G L Morris DM, FRACP, FRCP · Malcolm F Pell MB BS, FRACS Visiting Medical Officer

The NCCI is supporting many projects for improvement Many countries place great importance on their strategy for cancer control. The precedent was set by former US President Nixon's "war on cancer", declared in 1971, with the goal of reducing cancer incidence by 50% by the year 2000.1 This optimistic aim occasioned an unprecedented expansion of the US National Cancer Institute, its budget reaching $3.5 billion in 2001.2 More recently, the UK National Health Service embarked on a comprehensive reform of cancer services.3 The high profile of cancer in Western countries relates to its associated high morbidity, the high level of public awareness of the disease and the rapidity of research advances. In 1997, Dr Michael Wooldridge, the then Federal Minister for Health and Family Services, contracted the Australian Cancer Society (now the Cancer Council Australia) to establish the National Cancer Control Initiative (NCCI). The formation of the NCCI was based on a conviction that a better return for expenditure on cancer could be obtained, and that the time had come to introduce new evidence-based cancer-control measures.4 Although an array of cancer-control activities was already in place, it was envisaged that the NCCI could make these processes less capricious by applying a national focus, establishing agreed priorities and forming strategic partnerships across government and non-government sectors.5 The NCCI sees cancer control as comprising "all actions that reduce the burden of cancer in the community [including] every aspect of care, from prevention and early diagnosis to curative treatment and palliative care, all underpinned by the best scientific evidence available".6 The NCCI is concerned with assessing both existing programs and potential new developments for their clinical effectiveness, cost–benefit and equity. Its brief extends to managing strategic projects concerned with translating new findings into public health and clinical practice. The NCCI's activities have mainly revolved around cancer care, early diagnosis, and information needs. To provide good-quality clinical care, we need to know what good care is, what care is currently being provided, what gaps exist, and what opportunities there are for improvement. Defining good-quality care requires evidence-based clinical guidelines. The NCCI has been involved in various projects in this area, including production of guidelines on colorectal cancer for specialists, general practitioners and consumers; production of consumer guidelines on prostate cancer; development of guidelines for psychosocial care of patients with cancer; and development of an evidence-based model of optimum utilisation of radiotherapy. The assessment of current care requires management surveys, ideally involving all relevant specialties and representative groups of patients. One of the NCCI's initiatives has been the funding, through a Commonwealth grant, of a national survey of over 2000 patients with colorectal cancer. Improving clinical care requires a range of information-dissemination and learning strategies, with incentives to apply best care. In financial and practical ways, the NCCI is supporting many projects for improvement, including a consultative project, sponsored by the NCCI in collaboration with the Cancer Council Australia and the Clinical Oncological Society of Australia (COSA), to assess the limitations of cancer care provision; development of a national consumers' cancer organisation to increase the scope and effectiveness of consumer involvement; a review, in conjunction with COSA and state and federal governments, of the infrastructure needs for cooperative group clinical trials; initiatives to achieve earlier diagnosis, such as (i) federally funded pilot studies of colorectal cancer screening;7 (ii) assessment of new screening methods for cervical cancer, ovarian cancer, lung cancer and melanoma; and (iii) a project to improve GPs' expertise in managing prostate cancer and using prostate-specific antigen screening. collaboration with State and Territory cancer registries to improve the documentation of cancer and its outcomes, particularly with regard to staging. (The NCCI has developed a core clinical cancer data set for hospitals,8 which includes information on stage of disease and primary treatment, and is designed to be compatible with data collected by population-based cancer registries.); development of ways to assess the frequency of non-melanoma skin cancer, Australia's commonest cancer, using survey methods similar to those used previously,9 but also considering any new methods that become available. In the future, the NCCI will continue to take a leadership role by consensus through an inclusive, consultative approach in dealing with nationally identified priorities. The organisation's core purpose is to be an expert reference body providing timely advice, identifying appropriate initiatives and making specific recommendations to the federal government and other groups regarding the prevention, detection, treatment and palliation of cancer for all Australians.

J Mark Elwood MD DSc FFPHM · Paul D Ireland PhD

With our high standards of sanitation and healthcare, how important is breastfeeding? Any breastfeeding advocate can rattle off a list of the advantages of breastfeeding to infants, their mothers and society. The list of benefits ranges from better emotional attachment to a lower risk of childhood leukaemia or dental malocclusion. However, claims of benefit have been contentious, with many studies failing to demonstrate a clear advantage and some even showing increased risk of a negative health outcome with breastfeeding. The constituents of human milk suggest that it has evolved to promote infant health and human growth, particularly to protect children from infections and to support the rapid growth of the human brain. Despite advances in science and manufacturing, infant formula will always be a poor copy of human milk. It is improbable that a substitute will ever reproduce the full spectrum of human milk proteins, milk sugars (numbering over 100), live white cells and antibodies programmed by infections in the infant's environment, together with constant variations in milk content to meet the needs of the growing infant. But does this matter in a developed country such as Australia? Is there justification in the argument that women are being pushed too hard to breastfeed, or is there more to infant nutrition than the provision of clean water and biologically safe artificial feeds? Many studies reporting the effects of breastfeeding, both positive and negative, have major methodological flaws. Indeed, robust studies are difficult to carry out. Random allocation of study participants to either a "breastfeeding" or an "artificial feeding" group is unethical, especially if we accept the belief that "the epidemiologic evidence is now overwhelming that, even in developed countries, breastfeeding protects against gastrointestinal and (to a lesser extent) respiratory infection, and that the protective effect is enhanced with greater duration and exclusivity of breastfeeding".1 So evidence for the effects of breastfeeding must rely largely on observational cohort and case–control studies. Blinding to the intervention group is difficult, except at the analysis level. Moreover, mothers who elect to breastfeed differ from those who don't — the former group are generally better-educated women of higher socioeconomic status, who are more likely to have partners and less likely to smoke. All of these factors are likely to be independently associated with positive health outcomes, so failure to adequately adjust for these confounders generally favours positive breastfeeding outcomes. On the other hand, apparently poorer outcomes may result if mothers preferentially breastfeed more vulnerable infants. Difficulties with defining terms such as "breastfeeding" and "exclusively breastfed", and with defining endpoints such as "atopic disease", also make comparisons between studies difficult. So, have the roughly 2000 papers on breastfeeding and human milk listed in Medline since the year 2000 helped answer the question of whether or not it matters if a term infant born in a country like Australia is breastfed? I will confine my comments to the three most common health problems in Australian children: infection, obesity, and asthma. In Australia, there are almost 20 000 hospital admissions a year for acute gastroenteritis in children under five years old. Rotavirus accounts for about half of these episodes and is also one of the most important nosocomial infections in paediatrics. A Belarussian study2 (involving 17 000 healthy mother–infant pairs intending to breastfeed) showed that, in centres randomly assigned to deliver support for breastfeeding (as outlined by the Baby Friendly Hospital Initiative3), there were increases in exclusive and continued breastfeeding and reductions in episodes of gastrointestinal infection. In an Italian study4 of infants aged 1–18 months admitted to an infant ward, fewer breastfed infants contracted rotavirus infection (10.6% v 32.4%), and none of these became symptomatic. It has been shown that human milk lactadherin prevents symptoms in breastfed infants infected with rotavirus by binding to the virus and inhibiting its replication.5 Obesity is the commonest chronic health problem in Australian children. This has health implications both in and beyond childhood, as about half of obese children become obese adults. The effect of breastfeeding on later overweight/obesity remains contentious. A 2001 review of 18 studies6 concluded that most studies examining the effects of breastfeeding on later obesity had found an insignificant effect, although two of the studies actually found a positive association between breastfeeding and later body fatness. Since that review, four large studies7-10 (involving between 2000 and 14 000 children) have shown a lower prevalence of overweight in previously breastfed children, with several showing decreasing risk with longer duration of breastfeeding. The three studies of older children (aged 5–14 years)8-10 also found a negative association between breastfeeding and obesity (with adjusted odds ratios [ORs] ranging from 0.66 to 0.8). Similar results in these three studies, despite differences in method, suggest that the finding may be robust. The second most common chronic health problem in Australian children is asthma. A large Western Australian study showed a substantial reduction in risk of childhood asthma, as assessed at six years of age, if exclusive breastfeeding is continued for at least the first four months of life.11 This was included in a systematic review with meta-analysis of 12 prospective studies,12 which gave a summary OR of 0.70 (95% CI, 0.60–0.81) for asthma among children who had been breastfed, with a greater effect in children from families with a history of atopy (OR, 0.52; 95% CI, 0.35–0.79). The studies were mainly of younger children but included children up to 8.4 years. Another prospective study of more than 330 000 children followed to age 24 months supported these findings: breastfeeding of less than nine months' duration was associated with an increased risk of asthma or wheezing, and a dose–response effect was observed with breastfeeding duration.13 However, a recent report has suggested that atopic children with asthmatic mothers are more likely to develop asthma in later childhood if they have been exclusively breastfed.14 There may be interesting possibilities for intervening to further reduce atopy in at-risk families. Mothers of infants who develop atopic sensitisation have a higher intake of saturated fat,15 and their breast milk is much lower in some long-chain unsaturated fatty acids (which may have antiallergenic properties16). Perhaps improving maternal diets and the use of probiotics17 may reduce the prevalence of atopic disease in their children. I have selected three childhood conditions for which small changes in prevalence or disease severity would have a major impact on the health of the nation. The US Department of Agriculture, Food and Nutrition chose otitis media, gastroenteritis and necrotising enterocolitis, and estimated that the United States would save a minimum of US$3.6 billion dollars a year if breastfeeding rates increased by 10% at initiation and by 20% at the age of six months.18 While we should be careful not to convey to mothers that breastfeeding will make their child a trim, non-atopic, infection-free genius, the balance of the evidence is that breastfeeding is of benefit in many ways. Every healthcare professional in contact with young children and parents should be familiar with their responsibilities under the World Health Organization Code19 to encourage and promote breastfeeding — for the health of the nation.

Patricia McVeagh MB ChB FRACP

A good screening tool seems to offer the best hope, but meanwhile best possible care includes definitive staging and surgery by experienced specialist teams Ovarian cancer is the leading cause of death from gynaecological cancer in Australia, and indeed most Western countries. In the absence of effective primary prevention strategies and screening for early disease, the best possible management of patients with suspected or established ovarian cancer assumes critical importance if inroads are to be made in reducing morbidity and mortality from this disease. In this issue of the Journal (page 11), Grossi et al have reviewed the management of women with ovarian cancer diagnosed in Victoria during the period 1993 to 1995.1 Despite methodological difficulties with research of this type in terms of accurately defining variables such as stage and residual disease, the study is valuable for reflecting what actually happens in everyday clinical life. It shows that more than one in five patients did not undergo a laparotomy, which is required both to make a definitive diagnosis and to adequately stage the disease. Furthermore, a large proportion of patients with this disease are treated by specialists who are not specifically trained in gynaecological oncology, or are treated outside major teaching institutions. This problem is by no means confined to Victoria or indeed Australia. In a recent review of patterns of care of patients with ovarian cancer in the United States, Carney et al found that, of 848 patients with epithelial ovarian cancer, only 333 (39.3%) were seen (not necessarily treated) by a gynaecological oncologist "at some time during their cancer diagnosis and/or treatment".2 The situation in Victoria, as reported by Grossi et al, compares favourably with the US experience. However, both studies clearly demonstrate that significant change is required if women with this kind of gynaecological cancer are to receive the best possible treatment. The Victorian survey suggests that triage of patients to appropriately staffed and equipped gynaecological cancer centres is inadequate. In some measure this may be the result of the relatively low number of patients who had imaging (such as ultrasound) and tumour marker studies (such as carcinoma antigen [CA] 125). These investigations are important in patients who present with a pelvic mass, as, if they suggest a significant risk of malignancy, appropriate referrals can be arranged. This issue is especially important, as Grossi et al have shown that less adequate surgery adversely affects outcomes. Somewhat disturbing is the finding that, even in the hands of trained subspecialist gynaecological oncologists, fewer than half of the patients with apparently early disease had adequate staging performed. For women with early-stage disease the outlook is excellent, and every effort should be made to perform adequate surgery so as to avoid overtreating those whose outcome is not improved by adjuvant chemotherapy and to select those who might benefit from additional therapy. Epithelial ovarian cancers may occur in young women, and in many cases it is possible to both adequately treat the cancer and preserve reproductive function.3 Also revealed by the Victorian survey is the apparent inadequacy of cytoreductive surgery, even when performed by subspecialist gynaecological oncologists. Although residual disease did not appear to be significant in the Victorian survey, other studies have shown that the amount of residual disease at the end of cytoreductive surgery has a major influence on survival,4 and it is accepted that every effort should be made to "debulk" the tumour to the minimum size possible. This can require major resection of bowel or other organs and it can be a formidable undertaking for both the patient and the treating team. Such extensive surgery should only be performed by appropriately trained teams in major centres. Many gynaecological oncology centres both in Australia and overseas report rates of "optimal debulking" of over 70%.5,6 The article by Grossi and colleagues demonstrates that it is a major challenge to ensure that patients with ovarian cancer have timely access to these facilities. What else can be done to improve the outcome for women with ovarian cancer? Ultimately, prevention would be the ideal solution. For women with familial forms of ovarian cancer appropriately timed oophorectomy may offer a high degree of protection. However, for most women, the development of a reliable and acceptable screening method to detect early-stage disease offers the best hope. Currently, there is no acceptable screening method available, but some studies using CA125 and transvaginal ultrasound as screening tools have shown promise.7 A number of large international trials are currently under way to determine if screening will have a significant impact on the mortality of this disease.

Anthony M Proietto BSc(Med), MB BS, FRANZCOG, CGO

No one, least of all nursing-home staff, likes to see people in pain Most older people, despite limitations, live happy and active lives. Only a small proportion of them — those with major disabilities and complex medical needs — spend their final days in nursing homes. While these residential facilities may aspire to provide quality care for their residents, there are important gaps. As McClean and Higginbotham point out in this issue of the Journal (page 17),1 one such deficiency is in recognising and managing chronic pain. Disability in older people is still substantial and the trend for compression of morbidity (ie, a reduction in mortality accompanied by a greater reduction in morbidity, resulting in a longer life with more disability-free years) seen in some countries in the past 10 years has, regrettably, been less marked in Australia.2 Chronic pain can be an unfortunate consequence of several degenerative diseases associated with ageing, such as vascular insufficiency, sensory neuropathies, osteoarthritis, osteoporosis, spinal stenosis and vertebral collapse. Such conditions, and the suffering they cause, are major contributors to disability. While older women enjoy greater longevity than men, a disadvantage of their longer lifespan is increased susceptibility to these chronic, disabling, painful diseases. Depression and poor psychological adjustment are also more prevalent in older people who are in pain.3 Moreover, depression appears to heighten the suffering caused by pain.4 Predictably, the prevalence of chronic pain is high among nursing home residents. The Standards and guidelines for residential aged care services manual (Standard 2.8)5 drew specific attention to the need for nursing homes to develop policies and practices to assess and manage chronic pain in nursing home residents. As McClean and Higginbotham show, pain is still underdiagnosed and undertreated, despite these guidelines. Their survey of nursing homes in New South Wales revealed that for many residents who reported being in pain there was no history of pain recorded in their case notes. Furthermore, dialogue with residents about pain was often suboptimal or non-existent, and a substantial number of patients had inadequate pain relief. No one, least of all nursing-home staff, likes to see people in pain. We know that pain prevalence is high in this population, so why are we still failing to discern it? One possible reason is a lack of knowledge about geriatric pain. Undergraduate programs often devote little time teaching about geriatric pain management.6,7 Another probable reason is simply that medical and nursing staff fail to enquire adequately about pain8 or are too busy to spend much time with individual patients. Some staff dismiss pain that does not seem to have an identifiable medical reason and thereby underestimate personal suffering.9 Elderly people themselves often minimise their own pain, putting it down to "getting old",10 and stoically suffer in silence, not wanting to be "a bother". McClean and Higginbotham's study focused on residents' self-report in addition to caregivers' observations, and they rightly point out that deeper probing may have yielded even higher pain prevalence. The authors specifically looked at patients who could communicate about pain, but excluded the 40% of patients who could not. The prevalence of undetected pain is likely to be even higher among people who cannot communicate their pain than in people who can. The prevalence of pain ascertained by McClean and Higginbotham was lower than the rate found in some other studies, but this finding is no excuse for complacency. Although the guidelines may have helped to increase awareness of pain among nursing home residents, it is clear that we are still failing to achieve high-quality pain management. Pain is composed of a sensory component (nociception), a cognitive–affective component that causes the patient to suffer, and a communicative component that expresses the pain to others verbally and/or by pain-related behaviours. Effective pain management needs to assess and manage all these components. Contrary to popular opinion, ageing does not decrease nociception or suffering.11 However, patients with dementia do have less sophisticated ways of communicating pain. While nociception and suffering may be no less in patients with dementia, subjective report is certainly less, and behavioural change may be the main indicator of distress.12 It is essential that anyone working with older people become expert at observing and interpreting visual cues and behavioural indicators of pain.13 Often caregivers put older patients' behavioural changes down to perverseness, personality, or attention-seeking rather than entertain the possibility of pain.5 Frequently, the first-line treatment is antipsychotics or benzodiazepines, drugs that can mask a pain problem or make it worse. As McClean and Higginbotham found, many patients reporting pain had inadequate or irregular analgesia. Had the study included the non-communicating group, it is possible pain treatment in the nursing homes surveyed would have been found even more deficient. Many doctors are reluctant to give analgesics, particularly opioids, to older people. They worry that these powerful drugs may be addictive, produce dangerous side effects, or cause constipation, falls or delirium. Certainly, ageing brain and organ systems are sensitive to opioid analgesics, but withholding them from people in need can have the paradoxical effect of making management even more difficult if patients are behaving in a very uncooperative manner. Most of these drugs are safe if they are sensibly prescribed and the patient is regularly monitored for side effects. Not all patients need strong opioids and many would benefit from milder analgesics. Too many older people have "as required" medication, which is the least effective method to attain adequate blood levels of analgesic. A mild analgesic, such as paracetamol, given regularly in sufficient doses, is safe and effective even in very elderly polymedicated patients.14 Overall, the literature on pain treatments for the elderly is deficient and the area deserves more research attention. Why is it important to address this issue? For the simple reason that chronic pain is unnecessary. Work in palliative care has shown that pain can be correctly identified and effectively managed. The Australian guidelines recommend using pain-assessment tools to ascertain pain.5 While these may be useful, there is no substitute for greater awareness, direct enquiry, clinical intuition, and commitment to alleviate pain whatever its intensity. Evaluating pain in older people may be challenging, but alleviation of another's pain and suffering can be deeply gratifying. Yes, with more focus on the problem, we can improve pain management in our nursing homes.

Pamela S Melding MBChB FFARCS FRANZCP

Improving health outcomes for women with this enigmatic disease Endometriosis remains an enigma despite having been extensively studied. Its aetiology remains unclear, although there is a positive correlation with retrograde menstruation, probably with a background genetic predisposition. Traditionally, the symptoms of endometriosis are said to be pelvic pain and infertility, but, while a causal link between these symptoms and the disease is sometimes clear, the link is not always established. Treatment aimed at eliminating endometriotic deposits is effective in controlling symptoms in a proportion of patients, but recurrence is common. The diagnostic dilemmaEndometriosis is considered difficult to diagnose because the extent of the disease (endometriotic deposits and scar tissue) does not correlate with symptoms. The only accepted diagnostic test is direct visualisation (usually laparoscopically) by an experienced surgeon.1 Arguably, as endometriosis can be diagnosed in up to 40% of menstruating women at laparoscopy,2 it may be detected in all women at some stage of their reproductive lives, only to regress spontaneously in some. In addition, some symptoms associated with endometriosis are common. For instance, dysmenorrhoea occurs in up to 60% of women with regular menses3 and infertility occurs in about 15% of the population (of whom 30% have endometriosis).4 Hence, common conditions (mild endometriosis) may be associated with common symptoms (eg, dysmenorrhoea) by chance, not causally. The enormous variation in symptomatic expression and lack of clear correlation with the extent of endometriosis suggest the need for epidemiological studies of each symptom and of women with either mild or severe disease. This would exclude the possibility that mild endometriosis may be a normal finding in women. Epidemiological studies of women with endometriosis associated with dysmenorrhoea may find a causal link only in women with progressive dysmenorrhoea. In addition, epidemiological studies confined to specific symptoms causally associated with endometriosis (eg, dyspareunia and endometriosis in the uterosacral ligaments, progressive dysmenorrhoea and American Fertility Society stage III and IV endometriosis5) may result in consistent findings of the role of genes in disease development. 6 Management issuesFrom observations that pregnancy resolves symptoms, particularly of dysmenorrhoea, "mimicking pregnancy" became a treatment option. Medications that resulted in amenorrhoea (such as GnRH analogues, danazol and high-dose progestogens) have been used. These work by antagonising the growth-promoting effect of oestrogens or reducing the oestrogenic stimulus for growth, as well as increasing apo-ptosis. Each of these medications has been shown in a recent Cochrane meta-analysis of randomised controlled trials to be equally effective in control of dysmenorrhoea, dyspareunia and pelvic pain, and in decreasing the bulk of endometriotic tissue.7 However, the follow-up period in these trials was usually only three to six months. Annual recurrence rates of endometriosis after treatment are generally accepted to be of the order of 10%.8 Hence, further trials with longer follow-up, and possibly comparisons with the oral contraceptive pill (which has a better side-effect profile than the other drugs), in three-monthly cycles, would be beneficial. That medical therapies are not effective for infertility associated with mild endometriosis has been well established in large-scale, randomised controlled trials.9 Another Cochrane review showed that laparoscopic ablation or excision of the endometriotic tissue is effective in treating endometriosis associated with pelvic pain. However, this conclusion was based on one randomised controlled trial10 and further trials are needed to confirm this finding. Similarly, further evidence to support the effectiveness of laparoscopic surgery for subfertility associated with endometriosis is needed to support the beneficial finding in one randomised controlled trial. This is the aim of a protocol developed by the Cochrane Library.11 While the above conclusions are based on Cochrane reviews of the best available evidence, doubt remains. All trials are subject to a chance of showing a real effect when there is a probability that there is no effect. Continued development of well conducted randomised trials will reduce the probability of an incorrect conclusion. In addition, expert opinion based on the current extensive body of literature, and taking into account the basic mechanisms of the disease process of endometriosis, will help distinguish the causal relationship between each symptom associated with endometriosis. In turn this would lead to improved clinical outcomes for patients with associated dysmenorrhoea, chronic pelvic pain, dyspareunia and infertility. It is argued that current evidence for effective treatment of each of the symptoms associated with endometriosis could be further improved by further randomised controlled trials with clearly defined patient groups (eg, chronic pelvic pain in association with mild endometriosis, in-vitro fertilisation for three to five years of infertility associated with mild endometriosis). In addition, if results of epidemiological studies show no probable causal link between endometriosis and dysmenorrhoea then therapeutic regimens targeted at both symptom relief and monitoring progression of the disease may be more efficacious than excision of endometriotic tissue alone. While many of our current treatment regimens are effective in some patients, continued improvement in long term health outcomes for women with endometriosis requires a mindset open to critical evaluation.

Kevin L Forbes MB BS, FRACOG

The ANU Medical School will have a rural and regional focus, taking advantage of its unique geographic and demographic characteristics After intense public debate and a committee of inquiry lasting eight months, the announcement that the Australian National University (ANU) was to develop Australia's 12th and the world's 896th medical school was made in April 2001 by representatives of the Commonwealth and Australian Capital Territory governments and the Vice Chancellor of the ANU. This event represented the culmination of a process that has evolved over several decades. In the early 1970s the ANU narrowly missed out on a medical school, which went to the University of Newcastle. The 1980s had seen an involvement in the teaching of a small cohort of final-year students from the University of Queensland in Canberra, and in 1993 the University of Sydney began to develop its Canberra Clinical School.1 The Clinical School was successful, especially in its teaching programs, as judged by student satisfaction and assessment scores. This positive experience formed a sound platform on which to develop a fully fledged medical school. But why Canberra? The Commonwealth and some State governments have a track record of supporting the development of medical schools in regional Australia. The medical schools at the University of Tasmania, the University of Newcastle and James Cook University (Qld) are notable examples. Canberra, as well as being the national capital, has grown in recent decades to be an important regional service centre, particularly in the provision of health and education for south-east New South Wales; indeed, the "hole in the doughnut" is a popular colloquial description of the situation, evident on studying a map of the region. In spite of the ACT jurisdictional boundary, Canberra has close links with its surrounding area, which, incidentally, despite appearances to the contrary, includes a number of areas with some of the poorest social indicators in NSW.2 Placing a new medical school in this region, centred on the resource of ANU and building on the already established Canberra Clinical School, will help meet a regional need and will allow the new medical school to meet one aspect of its founding mission: to be rural and community focused. The ANU Medical School (ANUMS) will have links with the ACT Department of Health and Community Care and the Southern Area Health Service of the NSW Health system. Canberra, the "bush capital", is very close to the small population centres of south-eastern NSW. The School intends to take advantage of the diversity of the surrounding area and provide rural experience from very early in the course. For example, we plan a one-day-a-week clinical experience from the first week of the course. We will be able to use close rural locations such as Yass, Queanbeyan, Goulburn and Cooma, all of which are within an hour's travelling distance of Canberra. We plan to give selected students the opportunity to spend one of their clinical years in a rural setting, learning medicine, surgery, obstetrics and gynaecology synchronously while their urban colleagues rotate through traditional blocs. The School will provide a four-year graduate medical program with a thematic structure and a problem-based learning approach. Resources will dictate that our adherence to the problem-based approach will be less during the clinical years than is the case in the University of Sydney's graduate program. However, we intend to push the bounds of certain elements of this type of curriculum further. Taking full advantage of the ANU faculty, the students will have an understanding of international health and the impacts of globalisation, as well as a strong commitment to multiculturalism. At first sight this may seem at odds with a rural and community focus, but the need to develop rural and community medical programs and teaching experiences is indeed global. ANUMS sees itself evolving as a "type A" medical school — one that "prepares its graduates to properly practise in a health system — which it would have contributed to designing — to best serve the priority health needs of society".3 In planning the course in Canberra we intend to avail ourselves of the opportunities afforded by its status as the national capital. Thus, we will approach a number of Commonwealth departments and agencies (eg, the Department of Health and Ageing, Department of Defence, Therapeutic Goods Administration and the Australian Institute of Health and Welfare) to provide input into course planning and teaching. The ANU and the University of Canberra have an understanding to collaborate. This is most likely to occur during the clinical years, when we intend to introduce team training of medical students and other health science students in competency-based clinical skills training. At this stage of the course we intend to introduce combined teaching of medical students from the ANU with other health science students from the University of Canberra. Training together will prepare students for the teamwork of professional life. In this way, the School will have a focus on quality and safety, which are important issues in medicine in Australia in the early 21st century.4 We see this as part of restating the role of medicine as a profession, with a particular emphasis on the obligations that that entails.5 Drawing on the ANU's existing strengths, human rights will become a major focal point of our ethics program. The School faces a challenge in developing a research profile within the ANU, whose medical research organisations (eg, the John Curtin School of Medical Research) are already well established. We will endeavour to complement what already exists and concentrate on community-based and translational research, particularly at the Canberra Hospital. We have agreed from the outset to foster research in our rural clinical school. The long gestation of ANUMS did not lessen the controversy of its birth. We will add 60 places, including 25 rural bonded places, to the medical student population of Australia. ANUMS will be innovative, different and will complement other medical programs, contributing to the rich diversity of medical education that already exists in Australia.6

Paul A Gatenby PhD FRACP FRCPA · Nicholas J Glasgow MD FRNZCGP FRACGP

Ethics and putting the patient first are the primary considerations in deciding what is acceptable advertising of medical services by doctors Type "cosmetic surgery" into your Internet search engine and several hundred thousand sites will appear. All enthuse about the benefits and increasing popularity of their techniques. They identify and detail medical practitioners qualified to work their miracles on the human body. Few negatives are to be found in such promotional material, and much of the hype is not dissimilar to that used to market other lifestyle products. This is but part of the global rise of the entrepreneurial approach to healthcare. Cosmetic surgery is in demand because of the changing culture and attitude of patients. For some in today's world there is a need to satisfy a desire for what, in times gone by, would be unrealistic expectations — changes to their bodies to enhance their appearance — at least in their own eyes. If we take the definition used by the New South Wales Committee of Inquiry into Cosmetic Surgery, "cosmetic surgery" is any cosmetic procedure "performed to reshape normal structures of the body or to adorn part of the body, with the aim of improving the consumer's appearance and self-esteem". It "is initiated by the consumer, not medical need", and "excludes reconstructive surgery".1 This lies outside the traditional boundaries of medicine, which saw the profession dedicated to saving lives, healing and promoting health.2 Cosmetic surgery is not rebatable under Medicare, nor covered by health insurance. There are relatively few referrals. However, it does provide a service for which consumers are prepared to pay. Traditionally, the medical profession has prohibited advertising in its codes of ethics. The traditional view is that doctors should develop a reputation for excellence based on a reputation among their peers, rather than by the advertising of their services directly to the public. This minimises the opportunity for patients to be misled by claims of superiority of a technique or individual. Particularly in Australia and the United Kingdom, general practitioners have long been "gatekeepers" to specialist services. This role has helped maintain quality care for patients and has probably helped to contain overall costs in the healthcare system. But with the demise of paternalism, both in society and in the professions, this way of doing things has attracted increasing criticism. Undoubtedly, this forms part of the rationale for applying trade practice law to the health sector and to advertising by doctors, and to the interpretation of such law by the Australian Competition and Consumer Commission. Under federal law in Australia the Trade Practices Act 1974 (Cwlth) now permits advertising, unless it is likely to mislead or deceive. Direct advertising by doctors to the public is now lawful. The article by Ring in this issue of the Journal (page 597)3 asks if ethical standards are a casualty in the promotion of cosmetic surgery, and shows that this specialty is being seen as part of the beauty industry rather than a procedure for meeting health needs. The promotional strategies used do not sit well within the medical environment. The beauty industry promotes a body image that draws on vanity rather than on health. It creates expectations linked to perpetual youth, which can feed insecurities in people of both sexes, and contributes to a youth culture which treats with contempt the results of the ageing process.2 On the other hand, people who wish to change their image are now being informed that there are treatments available. The World Medical Association Declaration on the Rights of the Patient says that, "The patient has the right to self-determination, to make free decisions regarding himself/herself. The physician will inform the patient of the consequences of his/her decision".4 Should not patient autonomy include the freedom of adults to purchase these treatments, as long as the advertising surrounding them remains within the ethical boundaries of truthfulness? Where should the boundaries lie between medicine as traditionally defined, and lifestyle-modification medicine? The Australian Medical Association (AMA) Code of Ethics encourages doctors to promote the health and well-being of their patients and prohibits doctors from behaving in their own self-interest. It also says that doctors have "a responsibility to their patients to recommend only those diagnostic procedures necessary to assist in the care of patients and only that therapy necessary for their well being".5 Many patients would say that changing their image through cosmetic surgery is for their well-being, as it would improve their quality of life. It is a personal decision based on personal perceptions. If we consider that cosmetic surgery is part of medicine, then the advertising and promotion of such procedures must adhere to the ethical guidelines of the medical profession. The AMA believes that, as a general principle, advertisements must be honest, must not exploit patients' vulnerability or lack of medical knowledge, and should provide only factual information. Any advertisement for a doctor's services should present information that is reasonably necessary for making an informed decision about the appropriateness and availability of the medical services offered.6 In recognition of the need for a middle ground between the traditional ban on advertising and the current deregulated environment, the Medical Practitioners Board of Victoria has produced draft guidelines which will provide clear guidance for doctors who wish to advertise their services. A summary of the guidelines is presented in the Box.7 Summary of the Medical Practitioners Board of Victoria's draft guidelines for medical advertising7* Ban the use of "before and after" photography, which is common in advertisements for cosmetic surgery. Limit advertising to a factual statement of services offered. Warn against the creation of "unwarranted or unrealistic" patient expectations of treatment. Continue the ban on the use of patient testimonials. Prohibit advertising which encourages inappropriate use of medical services and contains information or language which could cause fear or distress or make people believe their health may suffer from not using a medical service. * Reproduced with permission. Whether we agree with changes in contemporary views which have allowed doctors to enter the free market of advertised services, or prefer the traditional culture, the one interwoven thread which must run unbroken through the fabric of medical practice is that of standards of ethical practice and the primacy of the patient.

Trevor J Mudge MB BS, FRACOG · Dorothy A Dashwood BEd, GradDipAdmin

Exposure of the thyroid gland to any irradiation requires lifelong follow-up supervision One of the questions most frequently asked by patients about to receive radioactive iodine as therapy for non-malignant conditions is whether it will result in bodily cancer. This question has been satisfactorily answered in the negative,1,2 so strong reassurance can be given. No such reassurance can be given for the malignant effects of therapeutic external beam irradiation on the thyroid gland. In childhood, the sensitive thyroid gland can be exposed to therapeutic irradiation directly, as in the treatment of localised neck tumours such as lymphoma or sarcoma and in total-body irradiation before bone marrow transplantation. Where the thyroid gland is not directly the target of therapy, it can be affected by scatter irradiation, as occurs during prophylactic cranial irradiation of the central nervous system in haematological malignancies. Thus far, no measures have been found to protect the thyroid gland from external irradiation in these settings. In this issue of the Journal (page 584), Somerville and her colleagues report the first Australian experience in a study encompassing a large number of children recruited to the Late Effects Oncology Clinic of the Children's Hospital at Westmead.3 The period of study covers 10 years. The sample population was divided into a group who received direct irradiation and another, designated as "scatter", in which there was exposure to the upper half of the body as external beam irradiation but no direct irradiation of the thyroid gland. The study was designed to emulate the approach that would commonly be used by a clinician seeking evidence of change in the thyroid gland. Palpation was used to delineate size and other characteristics. The customary thyroid function tests were carried out. These findings were supplemented by high-resolution ultrasound examination of the neck, and, if the findings warranted, fine-needle aspiration biopsy was undertaken. Suspicious findings from any of these evaluations led usually to surgery, but an abnormal ultrasound result was the chief indication for surgery. Some surprising and important revelations have come to light: Palpation of the thyroid gland was unreliable and misleading in a significant proportion of patients, with a preponderance of non-discovery. Ultrasound examination was almost always abnormal when the thyroid gland was palpable, and abnormal in more than 50% of patients in which the gland could not be felt. Thyroid function tests gave little warning of malignancy, and the elevation of thyroid-stimulating hormone in inadequately supplemented patients, although noted, gave no pointer to the status of the thyroid gland as a whole or the underlying presence of malignancy. Fine-needle aspiration biopsy was carried out in a few patients, but did not materially influence their management. The authors advocate total thyroidectomy for multiple nodules on ultrasound examination or where new nodules appear after partial thyroidectomy. Twenty-five patients from the direct-irradiation group had abnormal ultrasound results and underwent surgery, whether or not the thyroid gland was palpable; six of them harboured malignancy. On the other hand, in the scatter group, of 24 patients with similarly abnormal ultrasound results 12 were affected. Not only were localised recurrences frequent, but additional cancers in other areas of the body were noted by the authors, so vigilance in this respect is required. When surgery was carried out, the histological appearance of glands exposed to both types of irradiation indicated widespread damage and evidence of increased endothelial activity ranging from scarring through to nuclear atypia. There are important lessons to be learned. Exposure of the thyroid gland to any irradiation requires lifelong supervision and introspection. This should include high-resolution ultrasound. The extent of thyroid exposure to radiation may be arcane and not recalled when the highlight of the history is focused on areas away from the gland. Most radiation oncology units in Australia have follow-up facilities, but the duration of follow-up is not uniform. Moreover, patients travel and disperse, so their supervision will be most likely carried out by doctors with less experience of such patients. In this regard the American Thyroid Association publishes an excellent information sheet for patients.4 The article concludes with a series of pertinent recommendations which emanate from the study. Although false positive results can occur, the risks demonstrated in this study indicate that the management regimen recommended by Somerville et al far outweighs a sanguine approach to the problem. Implicit in this is the importance of providing patients with information about the potential risks and the need for regular assessment. Somerville et al observe that the Australian experience has disclosed a greater incidence of thyroid abnormality than seen in some other countries. This may derive from differing methods in the extent and depth of the studies, together with the sophistication of the ultrasound. The magnitude of the dose in the reported series did not seem to influence the emergence of malignancy. Only time from the administration of the radiation therapy was important. It will be interesting to learn of the further evolving experience. In this regard, results of fluorodeoxyglucose positron emission tomography, in association with rising thyroglobulin levels, seem to give a clearer delineation of recurrent malignancy than can be obtained by other methods.5 There may come a time when it will be possible to protect patients from scatter irradiation involving the head, neck or upper-body region in the treatment of more generalised cancer such as leukaemia. However, such protection does not appear to be imminent and, even if attained, there will still be a group of potential thyroid cancer subjects as a legacy of the current therapeutic era.

Alex K Cohen AO, MD, FRACP · Agatha A van der Schaaf FRACP

Appropriate use of ambulatory blood pressure monitoring can be cost effective The rationale for the use of ambulatory blood pressure monitoring (ABPM) has been the subject of critical reviews and published guidelines.1-6 Perhaps the most important and challenging finding to emerge from ambulatory blood pressure research has been the detection of "white coat" hypertension (also known as isolated clinic hypertension) in about 20% of subjects with repeatedly elevated casual blood pressure readings taken in the doctor's clinic.7,8 The condition can only be detected by ABPM or self-monitoring, and there are no specific predisposing factors. For people with white coat hypertension and no evidence of cardiovascular disease or comorbidities such as diabetes or renal disease, most experts agree that the best policy is to monitor their clinic blood pressure regularly, with self-monitoring at home, and repeat ABPM at one- to two-yearly intervals. The importance of continued monitoring is borne out by the evidence now emerging that white coat hypertension may not be an entirely innocent phenomenon.5,6 The initial studies that examined the cost savings in the detection of white coat hypertension by ABPM7,8 did not consider the need for long-term surveillance and the conversion of patients with white coat hypertension to established hypertension; this might be as high as 75% over six years of follow-up.9 The development of hypertension on ABPM criteria could not be predicted by changes in clinic blood pressures. The cost-analysis study of ABPM in Australian general practice reported by Ewald and Perkarsky in this issue of the Journal (page 580)10 is important for a number of reasons. The study confirms the high prevalence of white coat hypertension previously reported in the Australian community,11 and reflects current general practice, because GPs decided on the basis of conventional clinic readings that drug treatment was indicated before ordering ABPM. This cost analysis is the first such study based on Australian data, including best estimates of current pharmacological management of hypertension in Australia. It has also factored in a 10% per year conversion rate from white coat hypertension to established hypertension. The sensitivity analysis showed that all monitoring strategies (ABPM at 1-, 2-, or 3-year intervals) were less expensive than no monitoring over a projected seven-year period. The study almost certainly underestimated the average costs of investigations of hypertension, including standard investigations, documentation of target-organ effects and specific investigations in selected subjects to exclude secondary hypertension. The potential costs of adverse drug reactions were not considered. However, both of these would amplify the difference towards greater cost saving with the use of ABPM. Another important attributable cost is that of the perception of unwellness that accompanies inappropriate labelling as "hypertensive", which can lead to loss of productivity, sick leave, anxiety and the development of symptoms. There are other groups of patients in whom ABPM might have cost-saving benefits. Staessen et al12 reported on a study in 419 patients randomised to be treated according to their daytime ambulatory blood pressure or their clinic blood pressure, with the latter group receiving usual care. The mean follow-up was six months, and the two groups had similar mean left ventricular mass at the end of the study. The ambulatory blood pressure group had a 19% decrease in antihypertensive drug use and an 11% fall in doctors' fees. Some treated hypertensive patients exhibit a marked difference between ambulatory blood pressure and clinic blood pressure, and assessment of the effectiveness of antihypertensive therapy using clinic blood pressure readings tends to overestimate responses to drug therapy by including the "placebo" component of the reduction in blood pressure, which is minimal with ABPM. The results of the Syst-Eur study of systolic hypertension show that conventional clinic blood pressure measurements lead to an overestimate of the prevalence of isolated systolic hypertension among elderly patients.13 This suggests the potential for excessive treatment and associated complications in a significant proportion of elderly patients. This white coat effect is reproducible.14 The recognition of white coat hypertension in pregnancy, which may occur in as much as 30% of pregnancies,15 has the potential to reduce anxiety, hospital admissions and drug use, with significant cost savings. Some notes of caution are warranted. A major one is that we still await the results of definitive outcome studies in controlled trials comparing management of hypertension based on clinic blood pressure versus ambulatory blood pressure. The technique of ABPM is specialised, and service providers must use validated monitors and quality control measures. Current provision of ABPM is not regulated in Australia and is not recognised through the Medical Benefits Scheme. Another cautionary note is that all available evidence suggests that hypertension in our community is more undertreated than overtreated. The use of self-monitoring is also increasing, although there are more concerns with self-recording devices. In a recent analysis,16 only five of 23 devices met acceptable criteria. A combination of the two has a lot to offer: ABPM may be better for the initial diagnosis of hypertension and for predicting prognosis, while self-monitoring may be of more value for the long-term follow-up of patients. ABPM is an important diagnostic tool in the management of hypertension. The study by Ewald and Perkarsky indicates that appropriate use can be of cost benefit to the Australian community.

Barry P McGrath MB BS MD FRACP

Rapid treatment of people believed to be infected, and chemoprophylaxis of all close contacts, are the essentials of both immediate and broader public health management of this disease Although not common, invasive infection with Neisseria meningitidis can be devastating to affected patients and families, and, despite modern treatment, has a case-fatality risk of about 9%.1 In a small proportion of affected patients the disease runs a fulminant course, with death supervening in less than 12 hours. As a result, the disease is a cause of public alarm and receives intense media coverage. In its initial stages the disease may not be recognised, yet an adequate response requires decisive and rapid action from both clinicians and communicable disease control services. To help practitioners meet these demands, in 1996 the National Health and Medical Research Council published guidelines for controlling meningococcal disease.2 These guidelines have recently been superseded by guidelines produced by the Communicable Diseases Network.3,4 While vaccines are available against some serogroups of meningococci (polysaccharide vaccines effective against serogroups A, C, W-135 and Y, and conjugate vaccine against serogroup C), they are not currently recommended for routine use in Australia. As a consequence, and as there is no vaccine against serogroup B, the mainstay of the public health control of invasive meningococcal disease rests on timely and effective treatment of cases and public health interventions to prevent secondary cases (those which follow and are associated with primary cases). Meningococci may be associated with a wide range of clinical syndromes, from asymptomatic nasopharyngeal carriage, through pneumonia, septic arthritis and conjunctivitis to meningitis and septicaemia. Meningococcal septicaemia, with or without meningitis, can be particularly life-threatening and has considerably higher mortality than meningococcal meningitis. Invasive meningococcal disease and meningococcal conjunctivitis may be followed by secondary cases, and both require public health interventions.5 The most characteristic feature of meningococcal septicaemia is a haemorrhagic (ie, petechial or purpuric) rash that does not blanch under pressure. Deaths from meningococcal septicaemia may be prevented by early antibiotic treatment. Patients with suspected meningococcal septicaemia who are given parenteral benzylpenicillin by general practitioners are 2.5 times less likely to die than those not given penicillin.6 The greatest benefit of parenteral penicillin is seen in those who are most ill — those with a haemorrhagic rash. For optimal benefit, benzylpenicillin should be given intravenously. However, if this is not possible, it is quite appropriate to administer benzylpenicillin intramuscularly. All general practitioners should have benzylpenicillin in their surgeries and emergency bags, and should be ready to administer it immediately to a patient with an acute systemic febrile illness and either a petechial or purpuric rash. Box 1 shows dosage guidelines based on United Kingdom recommendations,7 presented in this form here for simplicity in emergency situations. There are other, equally valid guidelines available.8 The use of empirical benzylpenicillin does not necessarily obscure a microbiological diagnosis. While giving penicillin before blood and cerebrospinal fluid specimens are taken does reduce the proportion of positive cultures, it is still possible to isolate meningococci from nasopharyngeal swabs or detect meningococcal DNA by polymerase chain reaction.9 Characterisation of meningococci from these sources may be useful in the public health management of affected patients. Patients presenting to a hospital emergency department with suspected invasive meningococcal disease need to be seen urgently. If a presumptive diagnosis of invasive meningococcal disease is made, they should receive their first dose of antibiotics as soon as possible and no later than 30 minutes after arrival. In some patients other bacterial meningitides may not have been excluded, and empirical therapy with cefotaxime or ceftriaxone plus penicillin or amoxycillin should be used.6 These drugs are intended to cover listeriosis, and pneumococcal and meningococcal meningitis. Antibiotic regimens should then be modified as diagnostic and sensitivity information becomes available. If a general practitioner encounters a patient with a non-specific febrile illness which is not sufficiently distinctive or severe to require referral to hospital, the patient should be kept under frequent review. If a rash develops, or the patient's condition deteriorates in any way, the patient should contact his or her general practitioner urgently or go immediately to a hospital emergency department. Once a presumptive diagnosis is made, the relevant public health unit should be notified immediately so that contacts can be identified and the public health response determined. A public health response is required after diagnosis of either a probable or confirmed case of invasive meningococcal disease, or of conjunctivitis caused by infection with groupable meningococci. Meningococci coincidentally isolated from oropharyngeal, genital or anal swabs are of no public health consequence, and do not require a public health response. Nasopharyngeal carriage of meningococci is common — about 10% of the population carry meningococci at any given time,10 not all of which are virulent strains. In North American and European populations the average duration of meningococcal carriage is about nine months; it is an immunising process, with protective antibodies developing soon after acquisition. Factors associated with an increased risk of carriage include smoking and living in crowded circumstances. Contrary to popular belief, a patient with meningococcal disease is not an efficient transmitter of the meningococcus that is causing the illness. Rather, it is the carrier who transmitted the organism to the patient in the first instance who is much more likely to transmit the meningococcus again, causing further cases.11 The public health response targets people who have been in contact with a patient with meningococcal disease in the seven days before onset of disease. The response comprises providing information to contacts (taking into consideration their cultural and literacy needs), and chemoprophylaxis for each person in the network of close contacts. The rationale for chemoprophylaxis is to eliminate meningococci from any carrier within the network of contacts close to the index case and thereby reduce the risk to other susceptible individuals. This rationale must be explained, and the possible adverse reactions and interactions with other medications need to be discussed. Ideally, chemoprophylaxis should be given as soon as possible (within 24 hours) after the diagnosis of the index case. 1: Doses of parenteral benzylpenicillin for treating suspected cases of meningococcal disease Age group Dose of parenteral penicillin Children aged < 1 year 300 mg Children aged 1–9 years 600 mg Adults or children aged 10 years or over 1200 mg 2: Public health responses in defined settings in which a case of invasive meningococcal disease has occurred Setting Information* and chemoprophylaxis Information* only Household† of an affected person All Not applicable Child-care facilities Children and staff in the same room for 4 or more hours at one time in the 7 days before the onset of illness All other children and staff at the facility Education facilities Very close contacts (essentially those who have been "household-like" contacts) All other students in the same classroom (schools) or tutorial groups (universities) Those who have shared saliva with an affected person (eg, mouth kissing, sharing drink bottles and "bongs") All Even though they may not have shared saliva with a case, other members of any sporting team with an affected member should be given information Those exposed to an affected person after the onset of symptoms Very close household-like contacts; health carers who have either intubated the patient without a face mask or performed mouth-to-mouth resuscitation All others concerned that they may have had contact with the affected person after the onset of symptoms * The disease, including the common signs and symptoms, must be described and the mode of transmission explained. Appropriate action if symptoms suggesting meningococcal infection occur should be described. † "Households" include people in the same dormitory, military barracks or hostel bunkroom in the seven days before the onset of symptoms. This also includes those in seats adjacent to the affected person during long distance travel (8 hours or more). Sexual contacts should be managed as household contacts.

Robert G Hall

Infectious diseases physicians, clinical microbiologists and hospital pharmacists tend to have a love–hate relationship with the antibiotic ceftriaxone and its stablemate cefotaxime. These potent third-generation cephalosporins have an important place in every Australian hospital formulary, and boast numerous entries in the current edition of Therapeutic guidelines: antibiotic (AG).1 Third-generation cephalosporins (3GCs) are the antibiotics of choice for several life-threatening infections including bacterial meningitis. They are convenient to administer and are among the safest antibiotics available. Yet, these drugs have become the bête noire of hospital epidemiologists. So, what's the problem? The problem is the increasing burden of resistant bacteria arising from the constant selective pressure exerted by our extensive use of antibiotics, especially very broad-spectrum agents such as 3GCs. Cefotaxime and ceftriaxone are now known to be associated with the emergence of vancomycin-resistant enterococci, resistant gram-negative bacteria, and Clostridium difficile-associated diarrhoea.2-6 They also likely contribute to the emergence of resistant pneumococcus and the ongoing spread of methicillin-resistant Staphylococcus aureus (MRSA).7,8 Third-generation cephalosporins are active against a wide range of gram-positive and gram-negative bacteria and have the added advantage that they penetrate into cerebrospinal fluid and other normally sterile sites, enabling a number of invasive infections to be treated. However, they have only limited activity against anaerobes and staphylococci and are inactive against MRSA. They are also inactive against Pseudomonas, Listeria, and enterococci — all causes of potentially life-threatening infections in immunocompromised patients. In Australia, we have an antibiotic guidelines handbook that is clear, concise, accurate, extensively peer-reviewed, regularly updated, and, from my own experience, extremely useful! Yet, in this issue of the Journal, Robertson and colleagues (page 524)9 have identified a widespread prescribing problem — and one that probably extends far beyond 3GCs. In a study involving most Victorian hospitals, they found extensive inappropriate use of cefotaxime and ceftriaxone. Three areas of prescribing deserve particular mention. About half of all use of these antibiotics involved empiric treatment of respiratory tract infections, and over three-quarters of these courses were not in concordance with the then current edition of AG. This is despite the fact that simpler regimens are likely to be at least as effective.10 The two other key problem areas found by the authors were inappropriate use for surgical prophylaxis and for treatment of skin and soft tissue infections. As Robertson and colleagues state, improving concordance in surgical prophylaxis should be readily amenable to intervention by withdrawing 3GCs from operating theatres. However, improving concordance in empiric therapy of respiratory and skin and soft tissue infections will require a truly concerted educational effort. A perusal of the current edition of AG1 reveals that 3GCs don't rate a mention in the first-line regimens for empiric treatment of many common infections in non-penicillin-allergic patients. They are not included in any of the first-line regimens for community-acquired or hospital-acquired pneumonia, and not included at all for the treatment of cellulitis or erysipelas or postoperative wound infections. They have virtually no role in surgical wound infection prophylaxis. Clearly, there is discordance between guidelines and practice. After 11 editions of AG in Australia, what more can be done to curb the high rate of inappropriate use of important antibiotics? The United States Centers for Disease Control and Prevention recently highlighted 12 clinicians' "action steps" for preventing antimicrobial resistance in hospitals (Box).11 Improved implementation of clinical guidelines is implicit in these steps. Although the steps highlight inter alia the role of vancomycin in the emergence of antimicrobial resistance, similar recommendations could be applied to 3GCs. Implementation of guidelines must be multifaceted and preferably supported by published evidence.12 In Australia, we must first ensure there is comprehensive and practical access to endorsed guidelines among Australian doctors. No recent surveys of access to AG have been conducted, but they appear to be widely available — almost 20 000 copies of the current edition have been sold to date (Mary Hemming, Chief Executive Officer, Therapeutic Guidelines Limited, personal communication). The Australian medicines handbook13 is also a valuable emerging resource now in its third edition. Given that many of the concordance issues highlighted by Robertson and colleagues also apply to other areas of prescribing, universal access to a range of appropriate prescribing guidelines is an essential and logical complement to the training and continuing education of all doctors in Australia. At the very least, 24-hour paper and electronic access to appropriate guidelines should be available to every public hospital doctor and medical student. Personal digital assistants are also emerging as a major practical platform that should expand access to clinical reference programs.14 Improved and adequate access to clinical guidelines is, however, only the first step to control of inappropriate use of 3GCs. Adherence to guidelines requires the support and endorsement of opinion leaders and medical educators and, in particular, obliges senior clinicians to set an example through sensible prescribing. Pharmacists should be given a greater educational role in both hospital and community practice through academic detailing, surveillance of prescribing patterns, feedback to doctors, participation in clinical decision making, and provision of relevant guidelines to specific clinical groups. Most hospital drug committees attempt to adapt generic guidelines to local conditions, which generally involves imposing restrictions on the prescribing of 3GCs and other broad-spectrum antibiotics. Their efforts are supported by the many studies that attest to reductions in the incidence of resistant bacteria and C. difficile following institution of programs to reduce use of 3GCs.8,15,16 Drug committees also have an important role in monitoring the influence of pharmaceutical industry promotions on local prescribing practice. Recent advances in medical informatics herald exciting new approaches to prescribing in Australia over the forthcoming decade. A range of opportunities is emerging for computerised integration of prescribing guidelines with clinical decision making. Although the main aims are to prevent errors, improve quality of care and reduce costs,17 there is obvious opportunity for benefit at the community level by reducing the burden of resistant bacteria through appropriate prescribing of antibiotics. Many general practitioners in Australia are already using integrated electronic prescribing programs such as Medical Director (Healthcare Portal) and pathology reports have become integrated with prescribing guidelines. The major challenge now is applying computerised prescribing decision-support programs for real-time guideline implementation in hospital wards and emergency departments.18,19 Their application to desktop computers is certainly feasible. Their application to personal digital assistants as a real-time, remote, wide-area data-access and decision-support device is an evolving challenge that will require a major change in the way we approach drug prescribing in hospitals. The report by Robertson and colleagues is not only a timely reminder of the importance of regular evaluation of drug use, but should also inspire us to seek and embrace opportunities to improve antibiotic prescribing in this country. Twelve "action steps" for preventing antimicrobial resistance in hospitals Step 1: Vaccinate — get influenza vaccine; give influenza and Streptococcus pneumoniae vaccine to at-risk patients before discharge. Step 2: Get the catheters out — use catheters only when essential; remove catheters when no longer essential. Step 3: Target the pathogen — grow cultures from the patient; target empiric therapy to likely pathogens; target definitive therapy to known pathogens. Step 4: Consult the experts — consult infectious diseases experts for patients with serious infections. Step 5: Practice antimicrobial control — engage in local antimicrobial control efforts. Step 6: Use local data — know your antibiogram. Step 7: Treat infection, not contamination. Step 8: Treat infection, not colonisation. Step 9: Know when to say "no" to vanco(mycin). Step 10: Stop antimicrobial treatment when the infection is treated or unlikely. Step 11: Isolate the pathogen — use standard infection control precautions; contain infectious body fluids (airborne/droplet/contact precautions); when in doubt, consult infection control experts. Step 12: Break the chain of contagion — stay home when you are sick; keep your hands clean; set an example!

D Ashley R Watson MB BS, MPH, FRACP

In 2000, chronic or unspecified renal failure was listed as a cause of death of 9160 Australians (7.1% of all deaths) (source: Australian Bureau of Statistics, special data request, 2002). Most would have had chronic renal impairment (CRI) for years. Each year, more than 1700 people with end-stage renal disease (ESRD) start dialysis or receive a transplant.1 These figures suggest that the impact of CRI is substantial and that in order to prevent progression to ESRD we need to develop systems for its detection and management. Prevalence and significance of proteinuria. The Australian Diabetes, Obesity and Lifestyle (AusDiab) Study,2 a cross-sectional survey of a sample of over 11 000 Australians aged 25 and over, found proteinuria in 2.5% of the study population and a serum creatinine level above 120 µmol/L (reference range, 50–110 µmol/L [adult women], 60–120 µmol/L [adult men]) in 1.1%. A recent US study estimated that 1.5% of people aged six years and over have proteinuria.3 Extrapolating from these data, it is likely that several hundred thousand Australians have proteinuria, which is associated with a 15-fold increased risk of developing ESRD within 10 years.4 Whose urine should be screened? Current evidence does not support universal screening for proteinuria. The US Multiple Risk Factor Intervention Trial,5 in which more than 300 000 men were screened and followed up for an average of 16 years, showed that older age, smoking, hypertension and diabetes were significant risk factors for ESRD. Familial aggregation of ESRD, in excess of that predicted by clustering of diabetes and hypertension, has also been demonstrated.6 Indigenous Australians, who make up less than 2% of our population, comprise more than 8% of ESRD patients;1 and, in some remote communities where screening has been conducted, almost 25% of adults have been found to have proteinuria.7 Specific groups of people known to be at increased risk of ESRD should therefore be targeted for screening (see Box 1). Dipstick testing is cheap (about $0.50 per test), with immediate results. More than a trace of protein indicates a protein excretion rate greater than 300 mg in 24 hours. In the AusDiab study,2 dipstick testing had about 85% sensitivity and specificity (S Chadban, Nephrologist, AusDiab Steering Committee, personal communication). As about 15% of people without proteinuria have a falsely positive result, people with a positive dipstick result should have their protein excretion rate quantified by further testing. Measurement of 24-hour urinary protein excretion rate has long been the gold standard, but reliable collection is often impractical. Measurement of the albumin–creatinine ratio (ACR) in a morning urine specimen is easier and sufficiently precise.9 An ACR over 34 g/mol indicates a daily protein excretion rate exceeding 300 mg. At the same time as measuring the urinary ACR, a blood sample should be sent for measurement of serum creatinine and electrolyte levels for further assessment of renal function. Most dipsticks also test the urine for substances other than protein. If leukocytes or nitrites are detected, especially with symptoms suggestive of a urinary tract infection, a midstream urine specimen should be cultured. The dipstick test for proteinuria should be repeated after treatment of any infection. Isolated haematuria rarely indicates glomerular pathology associated with progressive renal disease. However, among smokers and people screened on the basis of age, a finding of haematuria should prompt exclusion of urinary tract malignancy. Interpreting the serum creatinine level. Serum creatinine level per se is not an accurate indicator of renal function. The glomerular filtration rate (GFR), which can be estimated from the serum creatinine level, is the most meaningful single measure (see Box 2). In healthy adults, the GFR exceeds 80 mL/min; patients with a GFR between 30 and 80 mL/min have CRI; while a GFR below 30 mL/min indicates severe renal impairment with a high risk of progression to ESRD, warranting prompt referral to a nephrologist. Managing CRI in general practice. General practitioners can substantially reduce the risk of progression of renal impairment. Management guidelines developed by the Australian Kidney Foundation and the Australia and New Zealand Society of Nephrology are accessible at the "Caring for Australians with Renal Impairment" website.11 I discuss here the evidence for the interventions recommended in the guidelines. Further benefit may be obtained by reducing the high risk of cardiovascular events that accompanies renal disease.12 Intensive control of hyperglycaemia and hypertension is beneficial for people with diabetes. (Specific interventions for diabetes are beyond the scope of this article — see the guidelines of the Australian Diabetes Society.8) In all patients with CRI, management aims should be the reduction of proteinuria (to ACR < 100 g/mol) and the maintenance of renal function (ie, stable GFR). These can be achieved through intensive control of hypertension11 (Level I evidence13). Suggested blood-pressure targets are 125/75 mmHg (in people under 50 years) and 135/85 mmHg (in people ≥ 50 years). Multidrug therapy is usually required. Angiotensin-converting enzyme inhibitors and angiotensin-II-receptor antagonists have been shown to be renoprotective (Level I and Level II evidence, respectively).11 Even in the absence of hypertension, they may be effective in people with protein excretion exceeding 1 g/day (ie, an ACR above 100 g/mol). Treatment for this normotensive group should be adjusted according to the level of proteinuria and monitored with three- to six-monthly ACR estimates. Potential risks include hyperkalaemia and, in patients with renal artery stenosis, worsening of renal impairment. In randomised controlled trials of these agents, participant dropout rates due to adverse effects have been low. Because smoking is associated with increased risk of progression of renal impairment (Level III-2 evidence),11 smokers should be assisted to quit smoking. A low-protein diet is not recommended, as the benefit is minimal and malnutrition may ensue. There is little evidence regarding the impact of exercise; however, in view of its cardiorespiratory benefits, regular exercise is advised. There is currently insufficient evidence to warrant lipid-lowering therapy as a means of minimising progression. Who should be referred to a nephrologist? GPs can usually manage patients with CRI, preventing further renal damage and progression to renal failure. Indications for prompt referral to a nephrologist include estimated GFR below 30 mL/min; estimated GFR above 30 mL/min, but declining rapidly; age less than 35; ACR greater than 300 g/mol (nephrotic range for proteinuria); symptoms or signs suggestive of systemic illness (eg, systemic lupus erythematosus); or failure to reach blood pressure or ACR targets within six months of starting antihypertensive drug therapy. 1: Indications for annual dipstick testing for proteinuria Age over 50 Hypertension Smoking Diabetes* Family history of renal disease Aboriginal or Torres Strait Islander descent *People with diabetes also require annual testing for microalbuminuria. (See the Australian Diabetes Society position statement on microalbuminuria in diabetes.8) 2: Calculation of glomerular filtration rate (GFR) by the modified Cockcroft–Gault formula*10 For women Estimated GFR (in mL/min)† = 140 – age (in years)] x weight (in kg) serum creatinine level (in µmol/L) For men Calculate estimated GFR as for women, then multiply by 1.23. * The modification is an arithmetic simplification of the original formula. The GFR estimate obtained will be 4% lower for women, and unchanged for men, compared with an estimate obtained using the original formula. † A number of computerised clinical record systems include a calculator for this formula.

Alan Cass MB BS, FRACP, GradDipClinEpid

The immediate health effects of bushfire smoke are well known to Australia's volunteer firefighters, who willingly fight bushfires each summer with no remuneration and at considerable personal risk. However, the population health impacts of pollution associated with large bushfires or "backburning" operations (prescribed burning to reduce the fuel load and the intensity of future bushfires) are less well defined, but are a matter of concern for emergency, environmental and public health agencies. A study from Darwin, published in this issue of the Journal by Johnston et al (page 535),1 is a welcome addition to this area of research. Johnston and colleagues1 analysed emergency department presentations for asthma in the Darwin region during the "dry" season, April – October (2000), when bushfire activity is high. The authors found that asthma presentations increased significantly (by nearly 2.4 times) on days when PM10 levels (ie, the concentration of respirable particulate matter with an aerodynamic diameter of 10 microns or less) were above 40 µg/m3, compared with days when PM10 levels were less than 10 µg/m3. The Australian National Environment Protection Council's target for maximum mean PM10 concentration is set at 50 µg/m3 in a 24-hour period.2 This level was exceeded on six days, with the maximum being 70 µg/m3. In fact, this value is relatively low in the international context. The Indonesian forest fires in 19973 produced maximum daily PM10 averages of over 1500 µg/m3. During Sydney's Christmas 2001 bushfires, PM10 levels above 150 µg/m3 were sustained for 10 days. In Sydney's 1994 bushfires,4 the peak PM10 was 210 µg/m3, compared with background levels of about 30 µg/m3. Previous Australian studies examined the effects of pollution in Sydney from backburning in May 19915 and bushfires in January 1994.6 Both studies analysed daily numbers of asthma presentations at several metropolitan hospitals for up to a month. The first study provided weak support for a link between particulate air pollution and asthma attendances, but the second found no difference in asthma presentations in the periods before, during and after the high-pollution event. There have been two more detailed studies of the health impacts of the 1994 Sydney bushfires. The first7 extended the period of analysis to six to seven weeks and compared asthma attendances with those in the same period the previous year. The researchers used a more complex analysis strategy, incorporating lag periods of one and two days for independent variables. They found that bushfire-generated particulate air pollution did not result in an increase in asthma presentations to emergency departments in western Sydney. The second study4 measured changes in evening peak expiratory flow rates (PEFR) during the bushfire period in children with wheeze, and used a direct measure of PM10, including pollen and alternaria counts, and meteorological factors (temperature and humidity). Thirty-two children were recruited to the study over a period of one week. Peaks in PM10 levels occurred three days before recruitment and on Days 3 and 8 (PM10 levels of about 70 µg/m3, 150 µg/m3 and 210 µg/m3, respectively, were recorded). Overall, there was no association found between mean PM10 and PEFR. Subgroup analysis of 20 of the children without bronchial hyperreactivity recorded significant falls in PEFR with rising PM10 levels. The remaining 12 children with bronchial hyperreactivity showed no significant association between PM10 and PEFR. The relative timing of exposure and recruitment may have caused changes in respiratory function before the study period, thereby biasing the results. All but one of the previous studies5-7 used indirect measures of particulate pollution, did not account adequately for confounders and did not use appropriate time-series methods. Notwithstanding these shortcomings, the potential for bias is probably low, as most important confounders do not vary on a daily basis. Johnston and colleagues' study1 has the advantage of running for a longer time period, with the episodes of pollution occurring during the study. The findings of the Darwin study should stimulate further research on the health effects of bushfire smoke. Current public health approaches to bushfire or other pollution episodes are to invoke a tiered system of warnings, moving from advice for susceptible subgroups (people with asthma, other chronic respiratory disease, or cardiovascular disease) to whole-population warnings as pollution increases. Applying "backburning" as a fire control measure, in itself an effective public health tool, may be restricted, partly because of the perceived impact of the resultant particulate pollution on urban populations. Better information about these effects will result in more appropriate risk management.

Peter R Lewis DipObsRACOG, MPH, FAFPHM · Stephen J Corbett MPH, MRCGP, FAFPHM

"of insects . . . only the ants were troublesome . . . one green as a leaf and living upon trees where he built his nest . . . by bending the leaves together and glueing them . . . their stings were by some esteemd not much less painfull than those of a bee . . ." Joseph Banks, August 17701 Indigenous Australians co-existed with native ants for thousands of years, using them as food (honey ants) and in medicinal decoctions (green tree ants).2 It was the green tree ant (Oecophylla spp.) that first attacked the white invaders from the Endeavour, and a number of native ant species, in particular the jumper or hopper ant (Myrmecia pilosula), still cause significant morbidity. But a foreign ant has now assumed the role of invader. In this issue of the Journal, Solley et al3 (page 521) describe the first Australian patient with anaphylaxis caused by the venom of the Red Imported Fire Ant (RIFA), Solenopsis invicta, and outline the appropriate diagnostic and management strategies, including successful desensitisation. Where did the RIFAs come from? Why are they a threat to our economy as well as our health? Can they be eradicated? February 22, 2001, was a dark day for Australia with the identification of S. invicta at two sites across Brisbane. This ant has the potential to be one of Australia's biggest ecological disasters, with the ability to have an impact on the economy, the environment and society. The ant itself appears innocuous. It is a small (2–6 mm), reddish-brown ant that is hard to distinguish from many other common ants. Its behaviour sets it apart as one of the world's great invaders. The ants will literally boil out of the nest ready to attack in huge numbers. The sting is painful, which accounts for the name "fire ant". Multiple stings are the rule rather than the exception and can be excruciating. The nest is dome-shaped and the colonies consist of up to half a million ants. S. invicta originated in South America, spread to Alabama in the 1930s and now infests 12 US States. Fire ants are thought to have entered Australia via shipping containers. There are two RIFA epicentres, one on the east of Brisbane around the port area, the other in Brisbane's western suburbs and part of Ipswich. The eastern infestation has been identified by DNA testing and chemical analysis of its venom as being from the United States or northern South America. The western infestation may have originated from Argentina (Dr Robert K Vander Meer, Research Chemist, United States Department of Agriculture/University of Florida, Center for Medical, Agricultural, and Veterinary Entomology, unpublished data, personal communication). Despite this multiple encroachment, the pest seems confined to Brisbane. Ecological modelling shows that the ants are capable of surviving in most parts of Australia, while spread modelling suggests that, if uncontrolled, the ants could spread up to 2 million square kilometres (ie, about a quarter of the area of Australia) over the next 30 years.4 A study of the environmental impact of fire ants5 shows that areas infested with the ant have fewer native ant species, lower total biodiversity and an absence of scincoid lizards. The ants can decimate ground-nesting birds, turtles and frogs, and can damage farm, irrigation and electrical equipment.6 The Australian Bureau of Agriculture and Resource Economics7 estimates that the cost of fire ants over 30 years, if uncontrolled, would be $8.9 billion. Australia's response to this invader is a $123 million, five-year National Fire Ant Eradication Program funded by the Commonwealth and the State governments. What about the medical aspects? It is appropriate to compare the RIFA with our most dangerous native ant, the jumper ant: Jumper ants are distributed throughout Australia; RIFAs have only been identified in the Brisbane area. Both jumper ants and RIFAs grasp the skin with the mandibles and sting repeatedly using a retractile stinger on the end of the abdomen. Stings from jumper ants usually cause a local weal-and-flare, while RIFA stings, because of the high alkaloid content of their venom, invariably result in sterile pustules. These pustules should not be broken. Venom proteins from both ants can result in immediate sensitivity. Two proteins have been cloned and sequenced from jumper ants (Myr p 1–2) and four from RIFAs (Sol i 1–4). There is no cross-reactivity between the main proteins of the two ants. Both jumper ants and RIFAs can cause large local allergic reactions that may need to be treated with oral corticosteroids. Up to 3% of Australians describe systemic allergic reactions to jumper ant stings,8 with most allergic sting reactions reported from Tasmania, Victoria and South Australia. In comparison, 30%–60% of people living in areas infested by RIFAs in the United States are stung, with 0.6%–16% of those stung developing anaphylaxis.6 Patients with anaphylaxis should be referred to an allergist/immunologist, and must carry self-injectable adrenalin. The best device, although expensive and still not subsidised by the Pharmaceutical Benefits Scheme, is the EpiPen Autoinjector (CSL, Melbourne). There is no commercial extract for desensitising patients with anaphylaxis to jumper ant venom. A clinical trial of a jumper ant extract has just been completed in Tasmania (Dr Simon G A Brown, Director, Department of Emergency Medicine, Royal Hobart Hospital, personal communication), but commercial production will not occur without financial help from government or private sector sources. At least three commercial desensitising extracts for RIFA venom are available from the United States. Deaths from anaphylaxis to jumper ant stings9 and RIFA stings6 have been documented. Perhaps, with luck and hard work and lots of money, we might eradicate RIFAs from Australia, but no State in the United States has been successful in such a program once the ant has invaded. In some parts of the southeastern United States, stings by fire ants are the commonest cause of anaphylaxis. Let's hope that that is not the case in Australia in 2030. The cost to our health and ecology would be enormous. Interested readers may wish to refer to two excellent web sites: <http://www.dpi.qld.gov.au/fireants/> (Queensland) and <http://fireant.tamu.edu/> (Texas).

Keith I McCubbin · John M Weiner

A more coordinated, national approach to parasite control would have substantial benefits In January 2000 the World Health Organization launched a program aimed at global elimination by 2020 of the lymphatic filarial parasites Wuchereria bancrofti and Brugia malayi. These parasites together infect in excess of 120 million people, and cause significant morbidity through elephantiasis. A major stimulus to the implementation of this and other programs, such as those aimed at the elimination of leprosy and Chagas' disease, was the successful global elimination of smallpox in 1977, and major advances in programs to control polio, measles, dracunculiasis (guinea worm) and onchocerciasis (river blindness). So, what of Australian parasite control programs? In Australia, endemic malaria and lymphatic filariasis have been eradicated, and leprosy, a once feared and politically significant disease, is in decline through sustained control programs conducted by dedicated public health agencies over long periods using effective drugs. However, the same cannot be said for other common parasitic diseases which are still endemic in Australia, including scabies, giardiasis, cryptosporidiosis, hookworm, strongyloidiasis and trichuriasis. These parasite infections have remained highly prevalent among Indigenous Australians living in the tropical north of the country in areas where infrastructure development has lagged, and improvements in living standards have not matched those seen elsewhere.1-3 Rather than being of trivial importance, such parasite infections cause substantial preventable morbidity. Secondary infection of scabies lesions with group A streptococci contributes to the exceptionally high rates of rheumatic fever and renal disease seen in Indigenous people, while enteric parasites cause a range of adverse health effects, including anaemia from hookworm, septicaemia from strongyloidiasis, and malabsorption and diarrhoea in children from giardiasis and cryptosporidiosis. Further, the merit of control programs for geohelminth infection is supported by studies suggesting benefits in educational outcomes among children treated for these infections.4 Despite the progress made in hookworm control during the course of the Australian Hookworm Control Program in the early part of last century, this infection has remained endemic in many Indigenous communities across our tropical north, and contributes to iron deficiency and anaemia in women and children. The limited success of attempts to control hookworm in one remote northern Australian Indigenous community of about 350 people has been published in the Journal (with rates of hookworm infection documented in 1992 of up to 93% in children 5–14 years of age).2 Recently, our group has published the successful outcome of a 78-month hookworm infection control program in the same community.5,6 This program's success was due to close liaison with the community, the setting of clear goals, and a commitment to improve environmental infrastructure and local health education, as well as regular targeted, population-based chemotherapy over a sustained period. The change of anthelmintic from pyrantel (to which parasite resistance had been demonstrated7) to single-dose albendazole was an additional significant factor in the success of the program. Parasite control programs based on community-wide distribution of albendazole among school-age children have also been implemented in the Northern Territory, and a similar community treatment strategy using permethrin therapy for scabies has recently been shown to reduce the prevalence of scabies in one community from 35% to 3%.3 Such successful programs are useful models for further community programs and national initiatives. Could and should parasitic disease in northern Australia be controlled more effectively? While the determinants of parasitic disease in northern Indigenous communities are complex, there are common themes. Contributing factors include poverty, lack of health knowledge, poor environmental infrastructure and housing, remoteness from health services, family mobility across health regions, and haphazard opportunistic treatment of parasites as they are encountered in clinical practice. To be successful, parasite control programs must be consistent, coordinated and sustained, and accompanied by local health education and improvements in health infrastructure. At present, regional and State parasite control programs lack a consistent approach across primary and secondary sectors and across State borders, and in some regions are ignored or left largely to enthusiasts. A more coordinated, national approach to parasite control would have substantial benefits: It would allow Aboriginal health organisations to fully participate and "own" the program from the national planning level through to the local community, thus facilitating rational debate on this emotive issue; Funding would be made available for nationally agreed strategies and continuing infrastructure improvements in affected communities; The use of standard surveillance techniques, reporting and targets would enable monitoring of progress; The reduction of parasite burden would be achieved through coordinated, programmed use of proven, safe drugs, including albendazole, ivermectin, tinidazole, and permethrin, at a community level; and Programs would be monitored for the development of drug resistance (a problem already present in veterinary practice where related drugs are used8). Two critical factors for the success of such a program are political will, and a will on the part of the communities themselves, together with local healthcare providers, and government and Indigenous health organisations. While the cost of the drugs is not the major barrier to the implementation of such programs, the positive publicity gained by two pharmaceutical companies from their leadership in donating ivermectin and albendazole to the WHO-sponsored filariasis program could have some local lessons. Leadership in Australian parasite elimination programs should come from both the Indigenous and medical communities through an alliance of Indigenous people and public health, infectious diseases and paediatric practitioners.

James S McCarthy · Stuart C Garrow