Indigenous health

How much should we be spending on health services for Aboriginal and Torres Strait Islander people? By redeploying about 1% of the healthcare budget we could increase spending on indigenous health services by about 50% MJA 1998; 169: 508-509 The health of Australia's indigenous people is much worse than that of other Australians, and worse than that of people in many Third World countries. The life expectancy of Aboriginal and Torres Strait Islander people is about 17 years less than that for other Australians, and their average mortality rate is three times higher. Those living in remote areas have 10-20 times higher death rates from specific diseases, such as diabetes, cervical cancer, and infectious, parasitic and respiratory diseases.1 In attempting to redress this situation, it may be that factors such as housing, sewerage, clean water supplies, education, nutrition, and employment are as important as health services, or perhaps even more important. Nevertheless, improving health services would make a valuable contribution, particularly if the improvements raised the services to a level comparable with those of other Australians. The amount that is spent on health services for indigenous people in Australia has until recently been the subject of much speculation. The newly published Deeble Report on Expenditure on Health Services for Aboriginal and Torres Strait Islander People2 has at last given a more accurate estimate of this figure (Box). Answering the question of what is spent immediately raises the question of what should be spent on health services for indigenous Australians. That question can be answered in a number of ways depending on how one views fairness and equity. One possibility is that health expenditure per capita should be equal for all Australians. This might be fair if everyone had the same health needs, but that is not the case. The elderly, for example, have greater health needs than middle-aged people. The greater health needs of indigenous people mean that equality per capita of health expenditure on indigenous and non-indigenous people -- which is close to what Deeble and his colleagues suggest is currently the case -- is not equitable. How unequal should allocations be to be equitable? In most resource allocation formulas, allocation is on a pro rata basis according to need. However, unless the productivity of healthcare resources is higher for those in greater need, then this may do no more than stop any health gap becoming wider. There is a need to do much more than that. Rather than arguing that all nominally equal health service improvements should have the same value irrespective of who receives them, and allocating resources pro rata with needs, one way to narrow the gap would be to attach a greater weight to health improvements for indigenous people. Thus, a weight of 2, for example, would mean that, in any cost-benefit analysis or evaluation in general, the health benefits to indigenous people would be valued at twice their normal value. This would provide a transparent basis for favouring health services which will benefit indigenous people when allocating health service resources. The precise size of the weighting factor might be determined through consultation with the community, relevant decision makers and stakeholders. In Queensland, a weight of three was formerly proposed for Aboriginality. Apparently this was based solely on the fact that Aboriginal mortality rates were about three times greater than the rates for all Australians.3 In the New South Wales Resource Distribution Formula (RDF) there is now a weighting of 2.5 in an attempt to reflect the "vertical equity" weighting that the State attaches to improvements in Aboriginal health compared with similar gains in the rest of the population.4 It has also been shown that the relevant figure for primary healthcare in the Alice Springs Rural District is in excess of four (and these estimates do not take account of all the factors listed above).5 There is no right level, but there is certainly a case for higher levels of spending for at least the next 10 years. This would be a substantial investment in raising the health status of Australia's indigenous people and would need to take account of the fact that the increase in primary care will lead, in the short term, to even greater demands on hospitals. Beyond that, when the health gains have occurred, then it may be possible to reduce the level of investment again. There also needs to be recognition, as Deeble indicates, of the higher levels of spending needed for delivering services to Aboriginal communities, many of which are in remote locations, and of the need to make the services culturally appropriate. As health status improves in any community there is the prospect that "diminishing returns" will set in. Once the easily achieved gains have been made further health improvements become more difficult. However, providing more resources for those in very poor health may well prove not just equitable but cost-effective, as the improvements in health outcomes per dollar spent on those with poor health status are likely to be higher. From the point of view of the person whose health improves, the lower the starting point, the more the health gain will be valued. The enormous health gap in Australia means that a massive catch-up program is required. Comparisons with New Zealand, Canada and the United States, for example, further emphasise this need. In each of these countries the gap between the health of indigenous and non-indigenous people is much smaller than in Australia.6 Australia is the only First World country that has failed to make real progress in indigenous health (see Ring and Firman)7. Substantially greater investment in research into health services for indigenous people is required. The epidemiology of many areas of indigenous health has been investigated, but there is now a need for a change in research emphasis. We know far too little about the most cost-effective way of delivering culturally appropriate health services to indigenous communities. Certainly, any policy involving a substantial increase in resources should have a major evaluation component built into it. The resource burden on all Australians of investing more in the health of Aboriginal and Torres Strait Islander people is small, simply because they are few in number and there are, by comparison, large numbers of non-indigenous people. Redeploying about 1% of the healthcare budget would increase spending on indigenous health services by about 50%, and could be achieved with very little health sacrifice for non-indigenous Australians (given the low return on the margin of some of the services currently provided). Can such a redeployment not be justified? Put more starkly, the question is: what price a national disgrace? Gavin H Mooney Professor of Health Economics Virginia L Wiseman Health Economist Stephen Jan Health Economist Social and Public Health Economics Research (SPHERe), Department of Public Health and Community Medicine, University of Sydney, NSW Nossal G. We need to spend more on indigenous health. The Sydney Morning Herald 1998; Sep 23: 21. Deeble J, Mathers C, Smith L, et al. Expenditures on health services for Aboriginal and Torres Strait Islander people. Canberra: Commonwealth Department of Health and Family Services, 1998. Queensland Health. Queensland Health Resource Allocation Formula. Brisbane: Policy and Planning Branch, Queensland Health, 1994. NSW Health Department. Implementation of the economic statement for health. Sydney: NSW Health Department Structural and Funding Policy Branch, Policy Development Division, 1996. McDermott R, Beaver C. Horizontal equity in resource allocation in Aboriginal health. Aust N Z J Public Health 1996; 20: 13-15. Kunitz SJ. Disease and social diversity. The European impact on the health of non-Europeans. New York: Oxford University Press, 1994. Ring IT, Firman D. Reducing indigenous mortality in Australia: lessons from other countries. Med J Aust 1998; 169: 528-531. Make a comment Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/>

Gavin H Mooney · Virginia L Wiseman · Stephen Jan

Reducing indigenous mortality in Australia: lessons from other countries Ian T Ring and David Firman Mortality rates from all causes in Maori in New Zealand and Native Americans have fallen substantially since the early 1970s. Comparable mortality rates for Australian Aboriginals and Torres Strait Islanders in 1990-1994 were at or above the rates observed 20 years ago in Maori and Native Americans, being 1.9 times the rate in Maori, 2.4 times the rate in Native Americans, and 3.2 times the rate for all Australians. Circulatory diseases, respiratory diseases, injuries and endocrine diseases (mostly diabetes) are responsible for almost 70% of these excess deaths. Mortality rate trends in indigenous populations in other countries suggest the feasibility of substantial and rapid reductions in mortality rates of Australia's indigenous people. MJA 1998; 169: 528-533 For editorial comment, see Mooney et al Introduction - Methods - Results - Discussion - References - Authors' details - - More articles on Aboriginal health - ©MJA1998 Introduction The poor health of Australian Aboriginals and Torres Strait Islanders is well known. Since the 1970s, indigenous infant mortality rates have been declining, but life expectancy has not changed because of continued high adult mortality rates,1 due largely to high death rates from chronic diseases in middle age.2 This pattern contrasts with that of the indigenous people of Canada, the United States and New Zealand, where marked improvements in health have occurred.3-5 While the health status of Australians as a whole continues to improve, the all-cause death rate for Aboriginal women is unchanged and the rate among men has decreased only slightly.6 As a result, the gap between the death rates for the Aboriginal population and the total Australian population has widened.1,7 Relatively few causes account for most of the mortality rate difference between indigenous Australians and all Australians. We report trends in mortality from these causes of death in indigenous people in Australia, New Zealand (NZ), and the United States (US). Methods Australian data Over the past 10 years, death registration of Aboriginal and Torres Strait Islander people has reached an acceptable level of completeness (90% or more) in two States only -- Western Australia (WA) and the Northern Territory (NT); we have confined our analysis of indigenous death rates to figures from these two States. The accuracy of Aboriginal and Torres Strait Islander censuses has been investigated.8,9 Experimental, adjusted counts have been calculated by the Australian Bureau of Statistics (ABS) for 1986-199110 and for 199411 at the State level. Population counts of indigenous people in the 1996 Census were greater in every State than expected from the 1991 Census and adjusted counts, indicating that more people identified themselves as Aboriginal or Torres Strait Islander than in previous censuses. The 1985-1996 indigenous population counts we used for WA and the NT were based on ABS experimental counts, adjusted for the 1996 Census. In WA, adjusted 1996 population counts were greater than predictions based on experimental counts for earlier years. Consequently, ABS population counts for WA for 1985-1995 were adjusted upwards so that they were compatible with 1996 figures. In the NT, adjusted 1996 counts were consistent with predictions, and ABS experimental counts and predictions were used. Annual total numbers of deaths for all Australia and for WA and the NT, and corresponding populations, were obtained from the ABS for 1979-1996. ICD-9 coding to four digits was used for coding cause of death.12 US and NZ data Numbers of deaths by age, sex and year of registration for Native Americans (including Alaskan natives) living on or near reservations were provided by the United States Indian Health Service for 1972-1992. Population counts were based on US census data, with interpolation between census years. Annual numbers of deaths for Maori for 1974-1994 were obtained from the NZ Health Information Service, and corresponding population estimates were based on census data from Statistics NZ. Excess mortality For a given cause, excess mortality was defined as the difference between the observed number of deaths for 1992-1995 for indigenous people in WA and the NT and the expected number of deaths for that cause calculated from death rates for the WA and NT (indigenous and non-indigenous) populations for the same period. Excess deaths for a given cause were expressed as a percentage by dividing the number of excess deaths for that cause by the number of excess deaths from all causes. Standardised mortality rates The World Standard Population 196013 was used for directly standardising death rates. We used Poisson regression to fit trend lines to time series of annual mortality rates, and calculated percentage change over time in annual standardised death rates from smoothed, trend-curve estimates rather than observed values. Results All-cause mortality rates Figure 1 shows annual all-cause mortality rates and fitted trend lines for Australian indigenous people, Maori, Native Americans and all Australians. The mortality rate from all causes for indigenous people in WA and the NT fell by 9% between 1985 and 1996. Over the same period, the all-cause rate for all Australians fell by 26%. The indigenous rate was 2.5 times the all-Australian rate in 1985 and three times the rate in 1996. The "hump" in the mortality rates for Australian indigenous people could represent a real increase to the 1990s followed by a decrease, but is more likely to be an artifact due perhaps to changing rates of registration of indigenous deaths. Death rates for NZ and US indigenous people fell relatively rapidly in the 1970s and more slowly thereafter. Between 1974 and 1984 mortality rates in Maori fell 32%, and a further 19% between 1984 and 1994. Mortality rates in Native Americans fell 17% between 1973 and 1982 from levels some 30% lower than those for Maori, and a further 11% between 1982 and 1992. Current mortality rates in Australian indigenous people are comparable with rates in Maori in the early 1970s. By 1990-1994, the average Australian indigenous all-cause mortality rate was 1.9 times the Maori rate, 2.4 times the US indigenous rate and 3.15 times the all-Australian rate. Main causes of excess mortality in Aboriginals and Torres Strait Islanders The ICD-9 coding system groups all causes of death into 17 broad categories. Four groups of conditions accounted for almost 70% of the total excess deaths in the Aboriginal and Torres Strait Islander population of WA and the NT during the five-year period 1992-1996. Circulatory conditions accounted for over a quarter (26%) of all excess deaths, with ischaemic heart disease, cerebrovascular disease and hypertension accounting for most of the circulatory disease excess; the injury and poisoning group, principally transport accidents, homicide and suicide, accounted for 15%, and respiratory conditions, including chronic obstructive airway disease and pneumonia, accounted for 16%; endocrine conditions, largely diabetes, caused a further 10% of excess deaths. International comparisons of mortality trends for the major causes of excess mortality Trends in annual standardised mortality rates for the four main causes of excess deaths in indigenous Australians are presented in Figure 2. (Data shown are for Australian indigenous people [1985-1996], Maori [1974-1994], Native Americans [1974-1992], and all Australians [1979-1996].) Circulatory disease: Current mortality rates for circulatory diseases in Aboriginals and Torres Strait Islanders were 50% higher than corresponding rates for Maori (the next-highest), and 2.5 times the all-Australian rate (Table, below). In the early 1970s, these mortality rates in Maori were above current Australian indigenous rates, but fell rapidly over the ensuing 20 years. Circulatory disease mortality rates in Native Americans have been lower than those in the other groups for the entire period, while the all-Australian mortality rates have held an intermediate course. Mortality rates from ischaemic heart disease in Maori fell in 1974 from above contemporary Australian indigenous rates to a third below by 1990-1994. By 1990-1994, mortality rates from cerebrovascular disease in Maori, after being equivalent in 1974, were down to less than half the corresponding Australian indigenous rates. Respiratory diseases: Mortality trends in respiratory system diseases were generally similar to those of the circulatory system, with Maori rates being initially very high (at the level of current Aboriginal and Torres Strait Islander rates) and then falling rapidly to levels not greatly exceeding current all-Australian levels. The overall reductions in rates of diseases of the respiratory system in Maori have been due largely to reductions in asthma and pneumonia deaths, which accounted for most respiratory system deaths in 1990-1994. In Australian indigenous people, other chronic obstructive pulmonary diseases and pneumonia accounted for a similar proportion of respiratory disease deaths in the same period. Injury and poisoning: The pattern here has been somewhat similar, although the relative positions of Native Americans and Maori are reversed. Death rates in Native Americans and Alaskan Natives were one and a half times the Australian indigenous injury and poisoning death rates in the early 1970s, but US rates have now fallen to below the current Australian level. For Aboriginals and Torres Strait Islanders in WA and the NT, there is little evidence of an overall decline (Figure 2). The decline in mortality rates from injury and poisoning in Native Americans has been driven particularly by changes in transport accidents, but also changes in homicide and suicide rates. For Australian indigenous people in WA and the NT, there appear to have been some relatively small recent falls in homicides and transport accident deaths, but there is some evidence that suicide rates are rising. Endocrine diseases: There has been no substantial improvement in mortality from endocrine diseases (largely diabetes). Death rates from diabetes in Maori fell in the 1970s, but have been rising slowly since the mid 1980s. Diabetes mortality rates in Native Americans have been rising slowly for 20 years. The rate for Australian indigenous people has also risen since the mid 1980s, but much more rapidly. In 1990-1994, the average mortality rate in Australian indigenous people for endocrine diseases was 2.4 times the Maori rate, 3.2 times the Native American rate and eight times the Australian rate (Figure 2). Discussion The health of Aboriginal and Torres Stait Islanders in WA and the NT is relatively poor compared with that of Maori and Native Americans, and has shown little, if any, improvement over the past 20 years. Although Australian mortality data cover only a 12-year period from 1985, there is no reason to believe that rates were much lower in the 10 years before 1985, and may have been somewhat higher. Several factors may influence the validity of comparisons among these three indigenous groups. A fundamental cause of non-random variation in annual mortality rates for indigenous groups is differences in factors influencing identification of a death as an indigenous death, and those determining whether people identify themselves as indigenous at census time. Special efforts to increase completeness in the 1996 Census resulted in a sharp rise in Australian indigenous population counts. However, similar improvements in ethnic identification on death certificates had not occurred by 1996. Indigenous population sizes over the 12 years studied were adjusted upwards to reflect the 1996 Census increase, which means that the Australian indigenous rates are likely to be lower than their true values. For all three indigenous groups, deaths were grouped by year of registration rather than year of death, so that they could be compared on a common basis. The extent of year-to-year variation in the proportion of deaths in a given year that were also registered in that year is unknown for Maori and Native Americans. Such variation would add a component of extra-Poisson variability to annual rate figures, but is unlikely to influence long term trends. The degree of late registration of Australian indigenous deaths is known to be relatively large compared with non-indigenous deaths and to vary from year to year. For this reason, apparent trends in Australian indigenous rates may be influenced to some degree by error in endpoint rate values. Different cause-of-death coding practices may have existed in the three comparison countries over time, leading to different apparent mortality rates for certain diseases. However, comparability of New Zealand and Australian non-indigenous rates suggests that there has been little difference between coding practices in these two countries over time. Furthermore, all-cause rates, not subject to coding variations, display the same patterns and differentials between ethnic groups observed for the separate causes of death. Although the three indigenous groups each have a different heritage and cultures, they share common experiences in their history. They are minority cultures in affluent nations dispossessed of their country and marginalised. However, Maori and Native Americans have made rapid gains in health and life expectancy over the past two decades. This progress is characterised by an initial rapid fall in death rates, followed by a more gradual decline as levels of the non-indigenous population are approached. Australian indigenous mortality shows little or no evidence of this pattern for any of the major causes of excess deaths. For some causes there is evidence of a recent decline, but no significant trend has yet been established. The health problems of Australia's indigenous people, and the circumstances responsible, are not unique. Why, then, has the health of Australia's indigenous people failed to match the improvement seen in other countries? Kunitz14 identified several aspects of Australian postcolonial indigenous experience which he felt contributed to the lack of improvement in health. He argues that Aboriginal affairs have traditionally been first a colonial then a State responsibility; and that there has been constant tension between State interests, particularly relating to land and management of the indigenous population. Furthermore, an official policy of assimilation maintained over many decades discouraged the creation of specialised indigenous health programs. In more recent times, competition for federal health funding by State and non-State bodies has meant that efforts to improve indigenous health have lacked coordination. Another factor, he suggests, is a lack of a sense of a single identity in many present-day indigenous communities, which were created artificially by gathering together people from many different tribal groups. The Treaty of Waitangi has been central to the relationship between Maori and other New Zealanders, and in the United States treaties established some status for Native Americans in their relationships with the "invading" Europeans, although these treaties were often abused. It is therefore difficult to entirely discount the suggestion that the absence of a treaty is a factor in the relative lack of progress in improving Australian indigenous health. Treaties, no matter how loosely worded, have appeared to play a significant and useful role in the development of health services, and in social and economic issues, for the indigenous people of New Zealand, the United States and Canada. Syme15 has hypothesised that the sense of control that people have over their lives and the sense of hope that this creates are important determinants of health status. He links both of these factors to disadvantage. It is arguable that colonial paternalism, an official policy of assimilation, and a lack of formal recognition through treaties have together acted to create and reinforce a sense of powerlessness in Australian indigenous people which is relatively less in other indigenous groups. It may well be that these intangible factors are adversely affecting indigenous health in Australia. The experience of other indigenous people around the world generates considerable confidence that effective action in Australia will produce substantial changes in indigenous health. Progress is needed in five key areas: infrastructure (land, housing, water supply, education, income, etc), self-determination of health services, access to a network of community-controlled primary healthcare services delivering effective health services for priority issues, an adequate level of resources, and a skilled workforce.16 Future success requires much greater progress within each of these five areas than has occurred in the past. A greater sense of control may only come from a wider acceptance and recognition of a valued role for Australian indigenous people in Australian society. References Kunitz SJ, Streatfield R, Santow G. Health of populations in northern Queensland Aboriginal communities: change and continuity. Hum Biol 1994; 66: 917-943. Veroni M, Gracey M, Rouse I. Patterns of mortality in Western Australian Aboriginals, 1983-1989. Int J Epidemiol 1994; 23: 73-81. Hogg RS. Indigenous mortality: placing Australian Aboriginal mortality within a broader context. Soc Sci Med 1992; 35: 335-346. Ring I. The Elkington Oration. Inequalities in health, the challenge for the nineties. Brisbane: Queensland Health, 1993. Runciman C, Ring I. The health of indigenous people in Queensland, some background information. Brisbane: Queensland Health, 1994. Australian Bureau of Statistics/ Australian Institute of Health and Welfare. The health and welfare of Australia's Aboriginal and Torres Strait Islander peoples. Canberra: ABS/AIHW, 1997 (Catalogue No. 4704.0.) Australian Institute of Health and Welfare. Australia's Health 1996. Canberra: AGPS, 1996. Australian Bureau of Statistics. Estimates of the Aboriginal population: review of data sources. Canberra: ABS, 1993. (Demography working paper: 93/2.) Gray A, Tetfaghiorghis H. Aboriginal population prospects. J Aust Popul Assoc 1993; 10: 81-99. Australian Bureau of Statistics. Experimental estimates of Aboriginal and Torres Strait Islander population (June 1986 to June 1991). Canberra: ABS, 1994. (Catalogue No. 3230.) Australian Bureau of Statistics. National Aboriginal and Torres Strait Islander Survey 1994. Detailed findings. Canberra: ABS, 1995. (Catalogue No. 4190.0.) The Australian version of the International Classification of diseases, 9th revision, clinical modification (ICD-9-CM). 2nd edition. Sydney: National Coding Centre (NCC), 1996. Waterhouse J, Muir C, Correa P, Powell J, editors. Cancer incidence in five continents. Vol III. Lyon: International Agency for Research on Cancer, 1976. (IARC Scientific Publications No. 15) Kunitz SJ. Disease and social diversity: the European impact on the health of non-Europeans. New York: Oxford University Press, 1994. Syme SL. Individual vs. community interventions in public health practice: Some thoughts about a new approach. Health Promotion Matters (Vic Health) July 1997; (2): 2-12. Ring I. An open letter to the President of the Public Health Association. Aust J Public Health 1995: 19: 228-230. (Received 8 Apr, accepted 22 Sep 1998) Authors' details School of Public Health and Tropical Medicine, James Cook University, Townsville, QLD. Ian T Ring, MB BS, MPH, MSc, Professor; and Head. Health Information Centre, Queensland Health, Brisbane, QLD. David Firman, MMath, Statistician. Reprints: Professor T Ring, School of Public Health and Tropical Medicine, James Cook University, Townsville, QLD 4811. E-mail: ian.ringATjcu.edu.au - Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/>

Ian T Ring · David Firman

Synopsis With increasing implementation of casemix-based funding for hospitals, quantitative data were needed to confirm the clinical impression that treating Aboriginal (compared with non-Aboriginal) inpatients consumes significantly more resources. Utilisation data, collected over a three-month period in 10 hospitals, were used to determine a cost per inpatient episode, which was grouped according to AN-DRG-3 to give a cost per AN-DRG for Aboriginal and Torres Strait Islander (ATSI) patients and non-ATSI patients. ATSI patients had consistently longer average length of stay and significant variation in relative frequency of admissions, compared with non-ATSI patients, with higher prevalences of infectious diseases. Degenerative and neoplastic conditions were more common in non-ATSI patients. There were significant differences in casemix-adjusted costs per patient episode (ATSI, $1856; non-ATSI, $1558; P < 0.001). Our study has quantified differential resource consumption between two Australian populations, and highlights the need for recognition of some hospitals' atypical populations and special funding requirements. Introduction There is substantial evidence in the medical literature of poor health outcomes for Aboriginal and Torres Strait Islander (ATSI) people despite high hospital utilisation rates.1 Among the reforms designed to improve health outcomes, casemix classification (Australian national diagnosis-related groups, AN-DRGs) for hospital inpatients could, on the contrary, have deleterious effects if its limitations were not appreciated. The principle underpinning casemix systems -- that clinically similar patients consuming similar resources can be grouped into a DRG which will have an equal spread of patients consuming more and less resources -- means that a hospital with an atypical population will be inappropriately funded. Health service providers who treat patients from remote Aboriginal communities believe that treating Aboriginal patients is considerably more expensive for a range of reasons (severity of disease at presentation, comorbidities, and social factors relating to culture, education and remote location), but there are few data quantifying their resource consumption during inpatient care. With increasing implementation of casemix, quantitative data were urgently needed, so that hospitals caring for such populations would receive appropriate funding. The first study attempting to quantify differential resource consumption of Aboriginal and non-Aboriginal patients2 had considerable methodological problems, resulting in the data being of limited use. In 1993 the Australian Casemix Clinical Committee recommended to the (then) Commonwealth Department of Human Services and Health that a multicentre study be conducted to quantify differences in resource consumption patterns between ATSI and non-ATSI inpatients in rural and remote settings. Methods In view of the complexity of the project, a representative steering committee was established to define the scope and provide clinical oversight for the proposed research. After an analysis of Australia-wide hospital morbidity data, including utilisation rates by ATSI patients, a sampling framework was developed. Ten hospitals of more than 30 beds from Western Australia (Kalgoorlie), Northern Territory (Royal Darwin, Katherine and Alice Springs), South Australia (Port Augusta) and Queensland (Cairns, Mount Isa, Cunnamulla, St George and Innisfail) agreed to participate as study sites. External consultants (Brewerton and Associates, Adelaide) were appointed to facilitate data collection and analysis within the guidelines established by the steering committee. Collection and review of data, and consultation Data were collected from each site over a three-month period. Six sites commenced collection on 1 July 1995. The remaining four sites began one month later. For each patient in the study, a range of detailed utilisation data was obtained. Specific proformas were developed to collect details on nursing time, medical time, diagnostic services (pathology and imaging) and therapeutic services (theatre, pharmaceuticals, allied health). Additional information on diagnosis, procedures and morbidity was obtained from the hospitals' information systems. The utilisation data were used to determine a cost per inpatient episode. The costed patient data were grouped according to AN-DRG-3 to produce a cost per AN-DRG for the two populations. Traditional costing studies, which use cost information extracted from the hospital's general ledger and allocated to DRG classes, would not have provided costing information to the required level. Therefore, we used national unit prices to complete the cost allocation process (Box 1). This also overcame the lack of sophistication of many of the hospitals' cost reporting, and avoided the need to make accrual adjustments to hospitals' general ledgers for the three-month period. The national unit prices were based on national and State labour force data, and recently completed national casemix costing and service weight studies and analyses undertaken to generate AN-DRG-3 cost weights.3 This approach also removed idiosyncratic local cost variations and enhanced the reliability of the results. Thus, for the purposes of our study, costs such as those for a unit of nursing time, and individual radiology and pathology tests, were the same for all hospitals. Patients were classified according to AN-DRG-3. To ensure satisfactory coding standards, a random audit of medical records was undertaken in each hospital before the commencement of data collection. Interim results were compiled and presented at a workshop in Alice Springs in April 1996. Attendees included health service providers from the study hospitals and State Health Departments, as well as representatives from consumer groups, such as the National Aboriginal Community Controlled Health Organisation (NAACHO) and the Office of Aboriginal and Torres Strait Islanders (OATSI). As a result of this meeting the data were further refined, allowing for more clinically accurate and culturally appropriate interpretation. A final report was presented to the Commonwealth Department of Health and Family Services in April 1997.4 Ethical approval Participating hospitals were required to consider the ethical implications of the research project, and, in particular, issues of confidentiality. The hospital data and the study report were not to include any information identifying individual patients or communities. At the conclusion of the study, hospitals were provided with their own data in addition to that of the total cohort. No hospital had access to another hospital's data unless by private arrangement. Statistical analysis Collation of data was facilitated by a specially designed application using dBase as the programming tool. SPSS (SPSS Inc, Chicago, Illinois, USA) and standard spreadsheet packages were used for the analyses, which were based on t tests, as comparisons were between two populations with large sample sizes. For both populations, only those AN-DRGs with a sample size exceeding 20 separations were analysed. Results The study collected clinical and demographic data on 31 222 inpatient episodes and utilisation data relating to 128 813 occupied bed-days. These data were trimmed to remove incomplete episodes during the study period. A total of 27 768 separations were analysed in detail (Box 2). It was not possible to standardise the data by sex and age for the total study population, as population data for the hospitals' catchment areas were not available. Standardised data for the Northern Territory (not presented here) revealed higher admission rates for male and female ATSI patients compared with non-ATSI patients in all age groups. While ATSI separations represented 33.9% of the total cohort they represented 66% (115/174) of patients and 67.6% (3157/4673) of separations of those assigned AN-DRG 572, Admit for renal dialysis. Because of the impact this caseload would have had on cost analysis (eg, one population would have a disproportionate number of "day-only" admissions), data relating to dialysis were excluded from relevant sections of the analysis. The average length of stay in the ATSI population was two days shorter when AN-DRG 572 was included in the analysis, but in the non-ATSI cohort it was only 0.3 days shorter. Differences in DRGs The ATSI population was distributed across 426 of a possible 667 (64%) DRGs. In contrast, the non-ATSI population was distributed across 547 DRGs (82%). Box 3 highlights the consistently longer average length of stay of ATSI patients, as well as a significant variation in relative frequency of admissions. For example, DRGs for gastroenteritis and respiratory infections contain more ATSI patients, despite there being twice as many non-ATSI patients in the cohort. In contrast, DRGs for gastroscopy and colonoscopy have a higher proportion of non-ATSI patients. Dental extractions and restorations recorded low separation rates in ATSI patients. The following DRGs were not encountered in ATSI patients during the data collection period: Other major joint and limb reattachment procedures without comorbidities and complications; Major shoulder or elbow procedures, age < 60; and Hip and femur procedures except major joint, age > 54 without comorbidities and complications. Boxes 4 and 5 show the top 20 DRGs by volume for ATSI and non-ATSI patients, respectively. Of note is the prevalence of infectious diseases in the ATSI population compared with the non-ATSI population, whereas the non-ATSI population has a high prevalence of degenerative diseases and DRGs related to neoplastic conditions. Cost differences The unadjusted average cost of an ATSI inpatient episode was $1627 compared with $1545 for non-ATSI inpatient episodes (this difference was not significant). The casemix-adjusted costs, however, showed significant differences (P < 0.001) per episode at $1856 and $1558 for ATSI and non-ATSI patients, respectively (Box 6). Box 7 shows the breakdown of total and average costs and confirms that the cost differential is a result of increased utilisation of most services. Theatre and pathology services are the only areas where costs are higher for non-ATSI patients. Further analysis of the data showed that operating room expenses were higher for ATSI patients. However, the average cost is lower because a significantly smaller number of ATSI patients had operations. The data also confirm that ATSI patients have longer lengths of stay and higher costs in most Major Diagnostic Categories (MDCs) (Box 8). An unexpected observation was the shorter length of stay and cost for this population in MDC 19 (Mental Diseases and Disorders), and MDC 20 (Alcohol/Drug Use and Alcohol/Drug Induced Organic Mental Disorders). Discussion The study confirmed the clinical perception that caring for ATSI inpatients consumed greater resources for the same DRG than caring for non-ATSI inpatients, and demonstrated a 39% overall differential cost. For some DRGs (eg, those including paediatric infectious diseases) the increase in resource consumption was considerable in ATSI patients. In MDCs 19 and 20, non-ATSI patients used slightly more resources. The greater costs in ATSI patients are believed to be related to disease severity on admission as well as comorbidities and complicating factors. Data obtained during the project support this. Other studies have also found that resource utilisation for ATSI patients is lower for mental disorders.5 Easier reintegration of ATSI patients into their community may facilitate shorter lengths of stay. Social networks and supports may also favour outpatient psychiatric care. The same may be true for DRGs associated with alcohol abuse, although given the known prevalence and impact of substance abuse in ATSI patients, we may also be identifying a need for further review of the models of healthcare delivery to ATSI patients. Actual needs were not addressed by our study. We only measured the current state of healthcare provision, which is largely a result of historical funding arrangements. However, many clinicians would argue that current health services for underprivileged groups are inadequate. This is the first study to quantify differential resource consumption between two Australian populations. It highlights the need to recognise potentially confounding factors when a casemix classification funding system is implemented. The Northern Territory, South Australia and New South Wales have recognised the disparity and incorporated funding adjustments for ATSI patients. As with ATSI patients in remote and rural hospitals, other socially disadvantaged groups including Aboriginals in urban settings and immigrant subpopulations may also have a cost and utilisation profile different from the "typical" Australian population. Hospitals caring for a significant proportion of such patients may equally need recognition for their "atypical" population. Appropriate funding of such hospitals can be either through funding adjustments or by an improved classification system. Future versions of AN-DRGs are likely to make greater use of complicating clinical factors (CCFs), which could include indicators of social disadvantage. Notwithstanding these efforts, hospitals caring for atypical populations remain vulnerable because their relatively small number of patients lack statistical importance when national figures are reviewed. One of the great challenges of casemix implementation is to provide the basis by which hospitals can be funded appropriately for appropriate care. If this challenge is not met it is the sickest patients from the most disadvantaged subpopulations who will suffer. The Aboriginal and Torres Strait Islander Casemix Study has demonstrated a genuine risk in this regard. 1: Standard unit of cost Unit cost per minute by nursing level Obtained from:Market Basket Database: CDHS&H Applied to:Patient attributable time by nurse per patient Unit cost per minute by allied health professional level Obtained from:Market Basket Database: CDHS&H Applied to:Patient attributable time by allied health professional by patient Unit cost by banded time range for medical officer Obtained from:Banded ranges and standard cost as specified in the MBS schedule and adopted by the South Australian Health Commission Applied to:Frequency of consultations by time range by medical officer Unit cost per operating minute by procedure Obtained from:National Operating Room Service Weight Study: CDHS&H Applied to:Time spent in theatre and recovery rooms Unit cost per day in intensive care/critical care/neonatal intensive care Obtained from:National Intensive Care Service Weight Study: CDHS&H Applied to:Time spent in intensive care/critical care/neonatal intensive care Unit cost per pathology test by type Obtained from:National Pathology Service Weight Study: CDHS&H Applied to:Each pathology test ordered and undertaken per patient Unit cost per diagnostic imaging service by type Obtained from:National Diagnostic Imaging Service Weight Study: CDHS&H Applied to:Each diagnostic imaging procedure performed per patientUnit cost per pharmaceutical by type Obtained from:Average unit price based upon data provided from the participating sites Applied to:Drug type administered per patient by dosage and frequency Unit cost per prosthesis by type Obtained from:Standard List National Operating Room Service Weight Study: CDHS&H Applied to:Prostheses consumed in theatre Unit overhead rate Obtained from:Development of AN-DRG-3 Cost Weights: CDHS&H Applied to:Each day of stay, covering overhead costs plus each day of stay for a boarder CDHS&H = Commonwealth Department of Human Services and Health (now, Commonwealth Department of Health and Family Services). MBS = Medical Benefits Schedule. 8: Average cost by major diagnostic category (MDC) (including AN-DRG 572) MDC DescriptionATSINon-ATSI SepsALOSAverage cost ($)SepsALOSAverage cost ($) 0 Pre MDC3058.23826.9138710.04229.00 1 Diseases and Disorders of the Nervous System2828.42946.617416.62291.44 2 Diseases and Disorders of the Eye873.21482.152162.21093.66 3 Diseases and Disorders of the Ear, Nose, Mouth and Throat3003.31460.268392.11056.30 4 Diseases and Disorders of the Respiratory System7585.81902.799775.71905.76 5 Diseases and Disorders of the Circulatory System2507.92757.718705.82558.46 6 Diseases and Disorders of the Digestive System4646.42185.7418912.91284.93 7 Diseases and Disorders of the Hepatobiliary System and Pancreas877.62039.80535.32141.82 8 Diseases and Disorders of the Musculoskeletal System and Connective Tissue4137.12964.0616015.42225.52 9 Diseases and Disorders of the Skin, Subcutaneous Tissue and Breast3576.52103.137973.61413.75 10 Endocrine, Nutritional and Metabolic Diseases and Disorders17611.53136.521606.52034.64 11 Diseases and Disorders of the Kidney and Urinary Tract34161.6484.1118821.6514.51 12 Diseases and Disorders of the Male Reproductive System592.71360.241862.41179.23 13 Diseases and Disorders of the Female Reproductive System2004.21753.858192.41250.05 14 Pregnancy, Childbirth and the Puerperium6755.11609.2121153.11104.41 15 Newborns and Other Neonates5296.23310.7110804.52901.82 16 Diseases and Disorders of the Blood and Blood Forming Organs585.72019.621412.8959.71 17 Myeloproliferative Diseases and Poorly Differentiated Neoplasms255.21286.682991.9591.75 18 Infectious and Parasitic Diseases8910.43257.201835.61949.19 19 Mental Diseases and Disorders838.52086.4342210.62542.97 20 Alcohol/Drug Use and Alcohol/Drug Induced Organic Mental Disorders473.7852.04854.51291.02 21 Injury, Poisoning and Toxic Effects of Drugs2254.61714.035863.41487.49 22 Burns7012.95454.901938.93297.14 23 Factors Influencing Health Status and Other Contacts with Health Service4625.81551.5716282.4677.04 Total94174.61627.27183513.91545.65 ATSI = Aboriginal and Torres Strait Islander. Seps = Separations. ALOS = Average length of stay (days). AN-DRG 572 = Admit for renal dialysis. 3: Top 20 DRGs by volume - total study population AN-DRG and descriptionTotalATSINon-ATSI SepsALOSSepsALOSSepsALOS 572 Admit for renal dialysis46731.0131571.0215161.00 943 Other factors influencing health status18402.363955.4914411.49 727 Neonate, admission weight <2499g without significant operating room procedure, without problems9943.702684.257263.50 674 Vaginal delivery without complicating diagnoses8053.451633.846423.35 952 Ungroupable6147.932887.063268.70 683 Abortion with D&C, aspiration curettage or hysterectomy5151.15701.464451.10 332 Other gastroscopy for non-major digestive disease without comorbidities and complications3801.41252.323551.34 686 Other antenatal admission with moderate or no complicating diagnoses3572.44883.572692.07 172 Respiratory infections/inflammation, age <55 without comorbidities and complications3514.782455.241063.72 350 Gastroenteritis age <103385.771888.881501.85 187 Bronchitis and asthma age <50 without comorbidities and complications2662.69563.252102.54 659 Conisation, vagina, cervix and vulva procedures2591.57352.692241.39 780 Chemotherapy2561.23152.602411.14 885 Injuries age <652542.301032.971511.84 491 Cellulitis age <60 without comorbidities and complications2224.14915.371313.29 484 Other skin, subcutaneous tissue and breast procedure2131.98324.501811.53 335 Other colonoscopy without comorbidities and complications2111.6793.442021.59 128 Dental extractions and restorations2081.26321.591761.20 349 Oesophagitis/gastroenteritis/other digestive disease age 10-742082.26482.981602.05 660 Endoscopic procedures, female reproductive system2061.34421.901641.20 ATSI = Aboriginal and Torres Strait Islander. Seps = Separations. ALOS = Average length of stay (days) Acknowledgements This study was funded by the Commonwealth Department of Health and Family Services and sponsored by the Australian Casemix Clinical Committee and received constant support from all members and the then Chair, Professor John Hickie. We would like to acknowledge the cooperation of staff at the study hospitals and State and Territory Health Departments and the assistance of the University of Adelaide Statistics Department. Countless individuals were also major contributors to the study, including Art Huston and Jenni Bowen (Brewerton and Associates) and Alan Browne and Josie Lanza (Commonwealth Department of Health and Family Services). The study also owes its success to the other members of the Steering Committee, Dr Mark Salmon, Mr Peter Woodley, Ms Marian Kickett, Mr Garnett Brady and Dr Chris Wagner. References Plant AJ, Condon JR, Durling G. Northern Territory health outcomes, morbidity and mortality 1979-1991. Darwin: Northern Territory Department of Health and Community Services, 1995. Harkin K. Incremental resource consumption by Aboriginal inpatients: a research project conducted at Alice Springs Hospital from 1 October to 31 May,1992. Report to the Department of Human Services and Health. Darwin: NT Dept of Health and Community Services, 1994. Casemix Development Program. Report on the development of AN-DRG Version 3 Cost weights. Canberra: Commonwealth Department of Human Services and Health, 1995. Commonwealth Department of Health and Family Services. Report on National Aboriginal and Torres Strait Islander Casemix Study. Adelaide: Brewerton and Associates Pty Ltd, April 1997. Jablensky A. The epidemiology of schizophrenia. Curr Opin Psych 1993; 6: 43-52. Authors' details Royal Darwin Hospital, Darwin, NT. Dale A Fisher,* FRACP, DTM&H, Physician and Senior Lecturer. Classification and Payments Branch, Department of Health and Family Services, Canberra, ACT. Jo M Murray,* BSc(Med), Acting Assistant Secretary. Princess Alexandra Hospital, Brisbane, QLD. Michael I Cleary,* FACEM, MHA, Executive Director of Medical Services. Brewerton and Associates, Adelaide, SA. Rita E Brewerton, BSc(MaSc)Hons, Director. Reprints will not be available from the authors. Correspondence: Dr D A Fisher, Royal Darwin Hospital, PO Box 41326, Casuarina, NT 0811. E-mail: dale.fisherATnt.gov.au *Steering Committee members (other members are listed in the Acknowledgements above).

Kidney disease in Australian Aboriginals: time for decisive action Can governments and healthcare services in northern and central Australia afford not to get organised? MJA 1998; 168: 532-533 The continued alarming rise in incidence of renal failure in Australian Aboriginals living in the Top End of the Northern Territory (NT) is documented in this issue of the Journal by Spencer and coworkers1 from the Royal Darwin Hospital and the Menzies Institute of Health Research. Are their findings an isolated observation, why is it happening, and what should be done to address the problem? The numbers are real. The Darwin incidence and prevalence figures for endstage renal disease (ESRD) in Aboriginals are entirely consistent with figures from other Aboriginal community surveys of the Kimberley, Pilbara and Goldfields regions of Western Australia (WA). The WA Health Services Research Linked Database shows that in the past 8 years there has been a yearly rise in (age-standardised) incidence of dialysis from 67 to 819 per million in Aboriginal men, and from 130 to 758 per million in Aboriginal women. The current rates are, respectively, 12-fold and 20-fold more than the non-Aboriginal rates (Ms K Brameld, Research Officer, Department of Public Health, University of Western Australia, personal communication). Whole-of-Australia incidence data recorded by the Australian and New Zealand Dialysis and Transplant Registry (ANZDATA Registry) also support these findings (Box), with a marked disparity increasing over time between rates for Aboriginals and non-Aboriginals, particularly in the north of Australia. The difference in ESRD rates between Aboriginal and non-Aboriginal populations, described by Spencer et al, increases after age-standardisation and is further accentuated by the non-Aboriginal population in Darwin having a lower ESRD rate (37-47 per million) than the non-Aboriginal population of the rest of Australia (62 per million in the same time period). This lower rate probably reflects the "healthy migrant worker" phenomenon, seen in other isolated cities such as Perth, with relatively low rates of chronic diseases. The increasing number of new cases over time represents a combination of better ascertainment, with the development of the Aboriginal Medical Services, greater acceptance of ESRD therapy by the Aboriginal community, as well as a probable true increase in incidence of renal disease. The trends predate the appointment of a full-time nephrologist in Darwin in 1996. Why is it happening? The problem has multiple causes. An unfortunate mix of racial predisposition is aggravated by multiple adverse environmental and metabolic factors.3 Aboriginal kidney biopsy and autopsy data from the University of Melbourne have shown a range of pathological states (diabetic, hypertensive, and proliferative), underpinned by a remarkable increase in glomerular size of up to threefold normal.4 Whether this unusual glomerular change is entirely genetic or is exacerbated by intrauterine malnutrition followed by subsequent dietary excess has yet to be resolved. The infective insults present in Aboriginal communities have been amply documented,5 with repeated bacterial infections of ears, nose, chest, skin, gut and genitourinary systems, as well as endemic intestinal parasites. Even in the absence of recognised nephritogenic organisms, systemic infection will activate glomerular proliferation, affecting mesangial cells in particular.6 It is probably the development of widespread obesity and "Syndrome X" (raised body mass index, blood pressure, blood glucose, and triglyceride levels; and insulin resistance, and disordered uric acid metabolism) that most closely parallels the renal disease epidemic.7 The background social and legal factors involved are well described:8 loss of employment after voting rights and equal-pay legislation were enacted, access to alcohol, increased welfare benefits, and availability of a high-fat, high-carbohydrate diet. It is ironic that the outstanding success in correcting malnutrition and infective disease in Aboriginal children over the past 30 years should have contributed to creating a cohort of obese adults with hypertension and diabetes.9 Alcohol has several indirect but definite adverse renal effects. Each 10 g of alcohol consumed causes a rise in blood pressure in both white10 and Aboriginal11 populations. The carbohydrate load causes obesity, increasing the risk of diabetes and subsequent diabetic nephropathy. Alcohol both stimulates intestinal production and reduces hepatic clearance of IgA, increasing the risk of IgA nephropathy. (Although this is the commonest form of chronic glomerulonephritis in the non-Aboriginal population, it accounts for only a minority of cases of renal disease in Aboriginals.) Smoking is also recognised in epidemiological surveys as an independent risk factor for renal disease.12 Both these behaviours are very common in Aboriginal communities.13 What can be done about this renal disease epidemic? Remote-area dialysis works. Although renal transplantation usually gives the best rehabilitation at the lowest cost, its application is limited by scarcity of donors (cadaveric or fit live-related), disparate tissue typing between Aboriginal and white populations, and unsuitability of some recipients because of infections or poor medication compliance. The next-best option is self-care dialysis. There is a natural and understandable cultural imperative for patients in kidney failure to wish to return to their families and homes. How to deliver dialysis in remote areas is a challenge that has been successfully met by a number of nephrology units around Australia. In Townsville, Queensland, with a semi-urbanised and relatively sophisticated Aboriginal population, a chronic ambulatory peritoneal dialysis program has been in place for over a decade (Dr P de Jersey, Nephrologist, Townsville Base Hospital, personal communication). In Western Australia, since 1989, both CAPD and self-care haemodialysis have been delivered in areas up to 3500 km away from the parent nephrology unit. This has required some innovative technical approaches (such as inline water coolers, and repressurisation pumps) and training of staff to ensure cultural sensitivity (eg, using photographic rather than written instructions, and showing respect for name avoidance after family deaths).14 These nephrology units have shown that the challenge can be met with complication rates and dialysis survival that approach and occasionally better those observed in metropolitan dialysis units treating white populations.15 While about 25% more expensive than metropolitan self-care dialysis, remote-area dialysis is still half the cost of maintaining dependent, depressed and non-compliant patients against their will in the city. However, there remain patients and areas where self-care dialysis is not practicable. Hospital dialysis units can benefit from the use of Aboriginal liaison officers to improve cultural awareness, and to limit the sense of alienation for patients. Reorganisation of renal referral patterns around geographical proximity rather than along State borders (eg, referring patients from East Kimberley to Darwin, rather than to Perth) would also reduce the extent of dislocation. Screening and intervention programs are a priority. Most of the necessary components of such programs are in place and merely require coordination for maximum efficiency and effectiveness. Chronic disease screening (diabetes, hypertension, obesity) easily lends itself to the incorporation of urinalysis for protein, which, if positive, can be followed by serum creatinine estimation. Given the high rate of medical clinic attendance in Aboriginal communities, such screening can be opportunistic, reserving targeted case finding for a select identified few.16 The prime target remains improved environmental conditions.17 Availability of healthier food choices can reduce renal injury.18 Improvements in lifestyle and medication compliance have been achieved in a sizeable proportion of communities with active programs, particularly where there is Aboriginal "ownership" of the service. Reducing the blood pressure level below 140/90 mmHg (with a target of 125/85 mmHg) can slow the rate of progression of renal disease by up to 50%.19 Further, there is a particular role for angiotensin-converting enzyme inhibitors in proteinuric renal diseases, with or without diabetes.20 The cost-benefit equation is obvious. Every year of dialysis deferred for a single patient could pay the salary of another Aboriginal health worker. Can northern and central Australia healthcare services and governments afford not to get organised? Mark A B Thomas Head, Department of Nephrology Royal Perth Hospital, WA Acknowledgements: The data reported here were supplied by the Australia and New Zealand Dialysis and Transplant Registry. The interpretation and reporting of these data are the responsibility of the author and in no way should be seen as an official policy or interpretation of the Australia and New Zealand Dialysis and Transplant Registry. Spencer J, Silva D, Snelling P, Hoy WE. An epidemic of renal failure among Australian Aboriginals. Med J Aust 1998; 168: 537-541. Disney APS, Russ GR, Walker R, Sheil AGR, editors. Twentieth report of the Australian and New Zealand Dialysis and Transplant Registry 1997. Adelaide: Queen Elizabeth Hospital, 1997. Hoy WE, Mathews JD, McCredie DA, et al. The multidimensional nature of renal disease: findings in a high risk Australian Aboriginal community. Kidney Int 1998. In press. Bertram JF, Young RJ, Seymour AE, et al. Glomerulomegaly in Australian Aborigines. Nephrology 1998. In press. Gracey M, Spargo RM, Smith P, et al. Risk factors for ill-health in a remote desert-dwelling Aboriginal community in Western Australia. Aust N Z J Med 1996; 26: 171-179. Lovett DH, Bursten SL, Gemsa D, et al. Activation of glomerular mesangial cells by gram-negative bacterial cell wall components. Am J Pathol 1988; 133: 472-484. Hoy WE. Markers for cardiovascular and renal morbidity: expectations for an intervention program in an Australian Aboriginal community. Clin Exp Pharmacol Physiol 1996; 23(Suppl 1): S33-S37. Reid J, Trompf P, editors. The health of Aboriginal Australia. Sydney: Harcourt Brace Jovanovich, 1991. O'Dea K, Trainedes K, Hopper JL, Larkins RG. Impaired glucose tolerance, hyperinsulinaemia, and hypertriglyceridaemia in Australian Aborigines from the desert. Diabetes Care 1988; 11: 23-29. Puddey IB, Beilin LJ, Vandongen R, et al. Evidence for a direct effect of alcohol consumption on blood pressure in normotensive men. A randomised controlled trial. Hypertension 1985; 7: 707-713. Smith RM, Spargo RM, King RA, et al. Risk factors for hypertension in Kimberley Aborigines. Med J Aust 1992; 156: 562-566. Orth SR, Ritz E, Schrier RW. The renal risks of smoking. Kidney Int 1997; 51: 1669-1677. Hoy WE, Norman RJ, Hayhurst BG, Pugsley DJ. A health profile of adults in a Northern Territory Aboriginal community, with an emphasis on preventable morbidities. Aust N Z J Public Health 1997; 21: 121-126. Lim C, Matthews M, Whishaw J. Self-care dialysis training for Aboriginal patients. Dial Transplantation 1994; 23: 137-139. Feutrill J, Thomas L, Lazberger J, et al. Determinants of CAPD peritonitis rates in Aboriginal and non-Aboriginal patients. Kidney Int 1996; 50: 1411. Couzos S, Murray RB. Chronic renal failure. In: Aboriginal primary health care -- an evidence-based approach. Melbourne: Oxford University Press, 1999. In press. Gracey M, Williams P, Houston S. Environmental health conditions in remote and rural Aboriginal communities in Western Australia. Aust N Z J Public Health 1997; 21: 511-518. Nath KA, Grande J, Croatt A, et al. Redox regulation of renal DNA synthesis, transforming growth factor-b1 and collagen expression. Kidney Int 1998; 53: 367-381. Zucchelli P, Zuccala A, Borghi M, et al. Long-term comparison between captopril and nifedipine in the progression of renal insufficiency. Kidney Int 1992; 42: 452-458. Ruggenenti P, Remuzzi G. Angiotensin-converting enzyme inhibitor therapy for non-diabetic progressive renal disease. Curr Opin Nephrol Hypertens 1997; 6: 489-495. - Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/>

Abstract Objective: To define recent trends (1993-1996) in incidence of endstage renal disease (ESRD) among Australian Aboriginal people in the Top End of the Northern Territory (NT). Design: Analysis of hospital and clinical records of the Darwin-based ESRD treatment program from 1993 to 1996 and comparison with data accumulated since 1978. Participants: All people entering the ESRD treatment program from 1978 to 1996. Main outcome measures: Number of patients treated for ESRD; their ethnicity, age and sex; comorbidities in Aboriginal patients; treatment methods and outcomes. Results: More Aboriginal people presented with ESRD between 1993 and 1996 (87) than in the previous 15 years of the program (68). The incidence of ESRD in Aboriginals reached 838 per million in 1996, and is doubling every 4 years. Aboriginal people presenting with ESRD are younger than non-Aboriginal people with ESRD, and, in contrast to non-Aboriginals, ESRD rates are higher in women than men. The numbers and proportions of Aboriginal ESRD patients who have hypertension, type 2 diabetes and cardiac disease are rising. Haemodialysis remains the most common form of treatment, and the number of dialysis treatments is doubling every 2.5 years. Only 9% of Aboriginal patients entering the program in 1993-1996 were treated with chronic ambulatory peritoneal dialysis and only 3% received transplants. Despite their younger age, survival of Aboriginal people on dialysis is low (median 3.3 years v. 6.5 years in non-Aboriginals), and graft survival after transplant is poor (37% at 5 years v. 88% in non-Aboriginals). Survival has not improved in the past 4 years, with fewer deaths from infection offset by more deaths from cardiovascular disease. Conclusions: The predicted doubling of ESRD incidence among Aboriginal people by the year 2000 will add an enormous burden to limited resources. Risk factors for renal disease underlie all the excess morbidity and mortality in NT Aboriginal adults, and arise out of accelerated lifestyle changes and socioeconomic disadvantage. Better living conditions and education, robust and integrated primary healthcare programs, and systematic screening for early renal disease and treatment of those with established disease are all matters of urgency. Introduction The high rate of endstage renal disease (ESRD) in Australian Aboriginal people is attracting increased attention.1-4 The Northern Territory (NT) faces particular challenges in dealing with this problem. It has the lowest population (179 000 people) and tax base of any Australian State, and the highest proportion of Aboriginal people (22% of the population, compared with 5%-6% for Queensland and Western Australia -- the States with the next-highest proportion). It has an area of 1 346 200 km2, and only two dialysis centres, 1500 km apart (one in Darwin and one in Alice Springs), which can scarcely accommodate the increasing numbers of Aboriginal people needing treatment. In a previous article,1 we reported the rising rates of ESRD among Aboriginal people in the Top End of the NT (Figure 1), with an average annual incidence of 440 per million from 1988 to 1993. Aboriginal patients were younger than their non-Aboriginal counterparts and, in contrast to the non-Aboriginal population, more women than men were affected. There was little use of chronic ambulatory peritoneal dialysis (CAPD), and the few transplants gave poor results. Comorbidities were high and there was a shorter survival time on treatment than in non-Aboriginal people. Tiwi people living on Bathurst and Melville islands had especially high rates of ESRD, but for other communities there were too few cases to allow calculation of population-adjusted rates. We present data for ESRD treatment in the Top End of the NT for the period 1993-1996, thus extending the period of analysed data to 19 years. The expanded data allow calculation of regional population-specific rates, and illuminate trends in diagnoses, comorbidities, treatment methods and survival. Methods Study population The total study population comprised all people entering the Top End ESRD treatment program from January 1978 to December 1996 inclusive. Our data sources were dialysis unit records and hospital files. We used Australian Bureau of Statistics aggregate and regional data from the 1987, 1991 and 1995 population censuses for the denominators for calculating ESRD rates for the 4-year intervals 1985-1988, 1989-1992, and 1993-1996.5The 1991 Aboriginal community census was used to calculate individual community rates for the three 4-year intervals. People moving to the NT from other countries or other States and becoming residents are potentially included in the census and thus the denominators. Statistical analysis We calculated age-standardised rates of ESRD with Epi-Info6 using aggregate Australian non-Aboriginal data from the 1996 Australian and New Zealand Dialysis and Transplant Registry (ANZDATA) as the reference population.7χ2 tests with Yates' correction were used to examine differences between groups. Kaplan-Meier survival analyses were performed by SPSS for Windows,8 and the log-rank test was used to compare the differences between the groups. Results In the period 1993-1996, 104 people entered the ESRD treatment program, making a total of 214 for the period 1978-1996. Of the total, 155 (72%) were Aboriginal, and 59 (28%) were non-Aboriginal. Incidence of treated ESRD Figure 2a shows the dramatic increase in incidence of ESRD in Aboriginal people over the three 4-year periods, with an average doubling time of about 4 years. More Aboriginal people (87) presented for treatment in the 4 years 1993-1996 than in the previous 15 years of the program (68). Within this most recent 4-year period, rates have continued to rise at an average of 22% per year, peaking at 838 per million9 in 1996 (compared with 39 per million in non-Aboriginal people in the NT). With age adjustment, the 1993-1996 average annual rate represents a 15-fold increase and the 1996 rate a 21-fold increase over ESRD rates in non-Aboriginal Australians nationwide. NT rates for non-Aboriginals, which did not change over this time period, are lower than Australian aggregate rates (62 per million from 1993-1996) because the NT has a younger population. All regions of the Top End are experiencing the same phenomenon, although current rates vary. Figure 2b shows the changes in incidence in Aboriginal people in the five regions with the highest current rates. The number of Aboriginal people receiving ESRD treatment (the prevalence), including those with functioning transplants, peaked at 2871 per million in 1996 versus 377 per million for non-Aboriginals. Finally, the number of dialysis procedures (which accrue most of the costs) is rising by 28% per year, or doubling every 2.5 years.9 Sex and age distribution of ESRD patients Ninety-three (60%) of the 155 Aboriginals with ESRD were women and 62 (40%) were men, compared with 23 (39%) women and 36 (61%) men among the 59 non-Aboriginal patients. Figure 2c shows the higher ESRD rates in Aboriginal women than men at each time period, resulting, in 1993-1996, in an age-adjusted relative risk of 31 in women versus 16 in men. On average, Aboriginal people were 5 years younger than non-Aboriginal people on entering the program (44 v. 49 years). However, the age distributions were quite different, with Aboriginal people most commonly presenting between the ages of 30 and 49 years, and non-Aboriginals between 50 and 69 years. Figure 3 shows that ESRD rates in Aboriginal people rose in most age groups over the life of the program, so that the average age and age distribution did not change appreciably. The age-specific incidence of ESRD in Aboriginal people peaked at age 50-59 years, and in non-Aboriginals at over 70 years. Renal failure causes and comorbidities in Aboriginals The Table compares the distribution of "causes" of ESRD in the two most recent 4-year intervals in those patients with documented causes. The proportion of ESRD in Aboriginal people attributed to (but not always solely due to) diabetes has almost doubled, that classified as glomerulonephritis has fallen by more than half, and the proportion in the "unknown" category has increased markedly. Aboriginal people with ESRD are more likely than non-Aboriginal people to have type 2 diabetes (48% v. 24%; P = 0.002) and hypertension (52% v. 32%; P = 0.01). Furthermore, these proportions have increased recently: for diabetes from 37% pre-1993 to 60% in 1993-1996 (P < 0.005); and for hypertension from 43% to 57% (P = 0.1); and for people with both diabetes and hypertension from 19% to 38% (P = 0.011). Treatment for ESRD Fifty-one per cent (30) of non-Aboriginal people, but only 17% (26) of Aboriginal people, have received transplants since 1978, and only 3% in the period 1993-1996. Potential reasons for this discrepancy include medical ineligibility, discouraging earlier results, distance to the transplant centre (in Adelaide), underservicing and difficulties in supervision of care in remote areas, lack of living related donors, and difficulties in HLA matching with donor organs. In 1996, only 11% of Aboriginal people with ESRD had functioning transplants versus 65% for non-Aboriginal people. Chronic ambulatory peritoneal dialysis (CAPD) rates in Aboriginal patients remain low, with only 5% of incident cases pre-1993 and 9% in 1993-1996 treated in this manner. Patient and graft survival Despite the younger age of Aboriginal patients with ESRD, their "integrated" survival (with all forms of treatment, ie, dialysis and transplantation) was significantly worse than that of non-Aboriginal people, with median survival times of 3.6 versus 12.3 years (P = 0.0025). This difference was reflected in those with and without diabetes. While survival on dialysis (CAPD and haemodialysis), as shown in Figure 4, tended to be lower in Aboriginal people (median 3.3 v. 6.5 years; P = 0.34), both graft and patient survival after transplantation were clearly worse (Figures 5 and 6). Patient survival at 1 and 5 years after transplantation was 92% and 60% for Aboriginals, compared with 97% and 93% for non-Aboriginals (P < 0.001), and graft survival at 1 and 5 years was 73% and 37% for Aboriginal people, compared with 97% and 88% for non-Aboriginal people (P < 0.001). There has been no improvement in integrated survival, or in dialysis or transplant survival separately, in the period 1993-1996. Causes of death The causes of death in Aboriginal people have changed for the period 1993-1996. Deaths due to cardiac disease have increased from 33% before 1993 to 51% after 1993. Deaths due to voluntary withdrawal from treatment are unchanged (24% and 25%, respectively). In contrast, only one non-Aboriginal patient has ever withdrawn from treatment, and none in the past decade. Discussion These data for 1993-1996 confirm and further define the rise in incidence of renal failure among Aboriginal people in the Top End of the Northern Territory. No community is spared, and this pattern is repeated in Central Australian Aboriginals, who have even higher rates (1400 per million in 1996).4 Current incidence rates are now comparable with those of Afro-Americans and Native Americans (800 and 744 per million, respectively, in 1995); however, age-adjusted rates are much higher in Australian Aboriginals (due to their very youthful population) and are increasing much faster, with a doubling time less than 4 years versus 10 years for the US minority groups.10 These alarming figures are nonetheless underestimates, because some Aboriginal people, especially older people and those from very remote communities, decline treatment for ESRD or are medically unsuited. Most of the increase is real. It is not due to ageing of the Aboriginal population, as it is reflected across every age group; and it is not due to improved ascertainment, at least in the major communities, as awareness has been high since the mid 1980s. The disability and the personal, family and community disruption are great, and the resource requirement will be truly formidable if current rates of increase, which project up to 500 new cases between 1997 and 2004 (exponential progression), are sustained. The data confirm the younger age and female predominance of Aboriginal people with ESRD. The latter might be due, in part, to lower birthweights and the relatively higher adult body weights in women, with more marked insulin resistance and earlier onset of type 2 diabetes.11,12 Both occur also in Central Australia.4 Some of the change in attributed cause of ESRD over the most recent 8-year period reflects subjectivity in assignment criteria, but much reflects reassignment of the common finding of bland glomerulomegaly with absent or minimal inflammation13-15 from the "glomerulonephritis" category to the "unknown" category. The rise in renal failure attributed to diabetes is compatible with the dramatic increase in rates of diabetes and its complications in all Aboriginal communities,16 but clinical and biopsy data show that diabetes is more often a facilitating factor for disease expression and progression rather than the prime or sole cause of the underlying nephropathy.11,14 The increased incidence in all communities of Syndrome X (obesity, hypertension, dyslipidaemia, dysglycaemia and predisposition to cardiovascular disease), which is attributed to insulin resistance, likewise explains the increasing proportions of Aboriginal people presenting for ESRD treatment with diabetes and hypertension as comorbidities.11,16-18 These conditions are already generating more heart attacks, strokes, coronary angioplasties, coronary artery bypass graft procedures and cardiovascular deaths among Aboriginal ESRD patients. As the epidemic grows and the Aboriginal population ages, these complications will become more common, and further increase costs, complicate treatment and compromise survival. The persistently high rate of withdrawal of Aboriginal people from ESRD treatment reflects difficulties with chronic disability, the complex treatment regimen, and loss of social and family support and "land identity" associated with relocation from their community to Darwin for treatment.19,20 Initiatives to move treatment closer to home include attempts to promote CAPD, which has low rates of technical failure and peritonitis, but major problems with exit-site infections;20 a renewed focus on transplant (seven Aboriginal people received transplants in 1997); construction of the first community-based dialysis unit with seven stations on the Tiwi islands; and the possibility of placing haemodialysis stations in clinics in high risk remote areas. However, deliberations about efficient and equitable delivery of ESRD treatment must no longer be allowed to dominate the dialogue. Dialysis in the Top End currently costs $496 per treatment, which is about $75 000 per patient per year. This cost does not include medicines, relocation and housing, transportation and hospitalisations.9 The allocation of resources of this magnitude to people with a median life expectancy of 3.3 years must be balanced by serious and sustained community-based initiatives to prevent and ameliorate the underlying problem. Most renal disease in Aboriginal communities is marked by albuminuria, and all renal failure arises in people with a history of progressive overt albuminuria.11Risk factors for renal failure include low birthweight and infant malnutrition, infections (scabies, poststreptococcal glomerulonephritis), increasing adult weight, high blood pressure, increasing glucose levels, insulin resistance, dyslipidaemia, and heavy drinking.11 Several risk factors can operate simultaneously, progressively compounding the decline in renal function that accompanies increasing age. The current epidemic is probably explained by the confluence of many risk factors over a short time period, associated with dramatic lifestyle changes and serious socioeconomic disadvantage. Ironically, the great fall in infant mortality between the late 1950s and late 1970s, a consequence of better hospital management of sick babies, means that those low birthweight babies now surviving to adult life are at high risk for renal and other chronic diseases.11,21 This multifactorial perspective on renal disease necessitates a rethinking of renal disease classifications.11 There is a need for a stronger focus on community and individual risk factor profiles and on pathophysiological interactions, and some de-emphasis of categorical definitions. It justifies a general preventive health services model, which will also reduce the diabetes, hypertension, cardiovascular disease, chronic lung disease and infections that contribute to the excess mortality in NT Aboriginal adults.17 In addition, screening programs to recognise early and established renal disease, and treatment (including angiotensin-converting enzyme inhibitors) to arrest disease progression, must be incorporated into regular adult healthcare in every Aboriginal community as a matter of urgency.22,23 Acknowledgements This study was supported by the National Health and Medical Research Council of Australia, and the Australian Kidney Foundation. We thank Dr David Pugsley, who led the way with renal services in the Northern Territory, and established the basis of these observations, and Dr Diane Howard and Dr Sid Selva-Nayagam, who have had the longest tenure of care of renal patients. We thank the staff of the Nightcliff Dialysis Unit and the Renal Unit at Royal Darwin Hospital for their excellent care and cooperation. Dr Zhiqiang Wang assisted with statistical analyses, and Ms Susan Jacups with clerical and graphic support. References Hoy WE, Mathews JD, Pugsley DJ. Treatment of end-stage renal disease in the Top End of the Northern Territory: 1978-93. Nephrology 1995; 1: 307-313. Hoy WE, Silva D. NT Top End Aboriginal end stage renal disease data and projections. Darwin, NT: Renal Strategy Committee, Territory Health Services, February 1997. Hoy WE. Renal disease in Aboriginal Australians. Med J Aust 1996; 165: 126-127. Renal disease in Central Australia -- challenges and opportunities for better health. Health Strategies, Deakin. Melbourne: Deakin University, September, 1997. Australian Bureau of Statistics. 1996 Census of population and housing. Aboriginal community profiles, small area data. Canberra: ABS, 1996. (Catalogue No. 2020.0.) Dean AG, Dean JA, Coulombier D, et al. Epi-Info, version 6: a word processing, database and statistics program for epidemiology on microcomputers. Atlanta, Ga: Centers for Disease Control and Prevention, 1994. Disney APS, editor. ANZDATA Report 1996. Nineteenth report of the Australian and New Zealand Dialysis and Transplant Registry. Adelaide: Queen Elizabeth Hospital, 1996. SPSS -- Statistical Package for the Social Sciences [computer program], release 6.1, standard version. Chicago: SPSS Inc, 1988. Margetts C, Morris E. Cabinet submission to the NT Legislature for renal services funding. Darwin: Royal Darwin Hospital, February 1998. United States Renal Data System (USRDS). Annual Data Report. Bethesda, MD: The National Institutes of Health, NIDDK, April 1997. Hoy WE, Mathews JD, McCredie DA, et al. The multidimensional nature of renal disease: findings in a high risk Australian Aboriginal community. Kidney Int 1998. In press. Hoy WE, Norman RJ, Hayhurst B, G Pugsley DJ. A health profile of adults in a Northern Territory Aboriginal community, with an emphasis on preventable morbidities. Aust N Z J Public Health 1997; 21: 121-126. Lloyd ML, Moore L, Pugsley DJ, Seymour AM. Renal disease in an Australian Aboriginal population: a pathologic study. Nephrology 1996; 2: 315-322. Howard DM, Davis J, Pugsley DJ, et al. Morphologic correlates of renal disease in a high risk Aboriginal community. Proceedings of the 31st Annual Scientific Meeting, Australian and New Zealand Society of Nephrology; Perth, WA; March 5-8, 1996. Sydney: Australian and New Zealand Society of Nephrology, 1996. Bertram JH, Young RJ, Seymour AE, et al. Glomerulomegaly in Australian Aborigines. Nephrology 1998. In press. Markey P, Weeramanthri T, Guthridge S. Diabetes in the Northern Territory. Darwin: Diabetes Australia (Northern Territory), 1996. Cunningham J, Condon J. Premature mortality in Aboriginal adults in the Northern Territory, 1979-1991. Med J Aust 1996; 165: 309-312. Reaven GM. Insulin resistance and compensatory hyperinsulinemia: role in hypertension, dyslipidemia, and coronary artery disease. Am Heart J 1991; 121: 1283-1288. Willis J. Fatal attraction: do high technology treatments for end stage renal disease benefit Aboriginal people in Central Australia? Aust J Public Health 1995; 19: 603-609. . Snelling P. I hit beautiful serves -- but my partner keeps putting the ball in the net: renal transplantation in Aboriginal patients. Proceedings of the 10th Dialysis and Transplant Workshop of the Australian Kidney Foundation and the Australian and New Zealand Society of Nephrology; Launceston, Tasmania; October 1997. Sydney: Australian and New Zealand Society of Nephrology, 1997: 62-63 Barker DJP. Mothers and babies and disease in later life. London: BMJ Publishing Group, 1994. Hoy WE. Markers for cardiovascular and renal morbidity: expectations for an intervention program in an Australian Aboriginal community. Clin Exp Pharmacol Physiol 1996; 23 (Suppl 1), S33-S37. Hoy WE. Guidelines for screening and treatment of renal disease in Aboriginal communities. Nephrology 1998. In press. (Received 5 Jan, accepted 10 Mar, 1998) Authors' details Menzies School of Health Research, Darwin, NT. Janine L Spencer, FRACP, DTM&H(Lond), Paediatrician, Australian Kidney Foundation Research Fellow. Wendy E Hoy, BScMed, FRACP, NHMRC Senior Research Fellow, Director of Renal Program; and Renal Community Services Specialist, Territory Health Service. TVW Telethon Institute for Child Health Research, Perth, WA. Desiree T Silva, FRACP, MPH, Paediatrician. Royal Darwin Hospital, Darwin, NT. Paul Snelling, FRACP, Nephrologist, Royal Darwin Hospital, and Territory Health Service. Reprints will not be available from the authors. Correspondence: Dr W E Hoy, Menzies School of Health Research, PO Box 41096, Casuarina, NT 0811. E-mail: wendyATmenzies.su.edu.au Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia ".

Janine L Spencer · Desiree T Silva · Paul Snelling · Wendy E Hoy

At the end of the 20th century, the good news about rheumatic fever is that it has become so rare in most of Australia that many medical practitioners will never see a case. This is a dramatic change from the first half of the century; in Melbourne during the 1930s, more than 50% of paediatric hospital medical beds were occupied by children with acute rheumatic fever or acute poststreptococcal glomerulonephritis, with rheumatic fever patients outnumbering those with glomerulonephritis (Dr Howard E Williams, previously In-Patient Physician, Royal Children's Hospital, Melbourne, personal communication). The decline of rheumatic fever in affluent populations occurred largely as a result of economic development and improved living conditions, with perhaps a small contribution from antibiotics and the possibly altered virulence of circulating group A streptococcal strains.1 The bad news is that socially and economically disadvantaged populations worldwide, including some indigenous and minority populations living in affluent countries, continue to have high rates of rheumatic fever and rheumatic heart disease. The highest published incidence of acute rheumatic fever in the world is in Aboriginal people living in the "Top End" of the Northern Territory.2 In this population the annual incidence of acute rheumatic fever (1989-1993) is between two and seven cases for every 1000 children aged 5 to 14 years, while up to three per cent of all people in some of the remote Aboriginal communities have established rheumatic heart disease. In contrast, the prevalence of rheumatic heart disease in the non-Aboriginal population is 0.014 per cent, and no non-Aboriginal children had acute rheumatic fever over this five-year period.2 While rheumatic fever appears to occur in only a subset of any given population, there are no data to support any major predisposition based on ethnicity. Similar high rates were documented in non-Aboriginal people in Melbourne during the 1930s and 1940s.3 The current high rates of rheumatic fever in the Aboriginal population are not related to ethnicity, but are likely to reflect high levels of exposure to group A streptococci, which, in turn, are related to overcrowding and continuing poor living conditions.4,5 The World Health Organization has promoted the use of rheumatic fever registers in developing countries,6 with the major aims of coordinating individual patient management and improving adherence to secondary prophylaxis to prevent recurrent rheumatic fever and the associated cumul ative valve damage. Registers are useful not only for developing countries: a register-based program in New Zealand, with acute rheumatic fever as a notifiable disease, helped reduce from 22% to 6% the proportion of hospitalised cases of rheumatic fever which were recurrences.7 The Commonwealth Department of Health and Family Services, together with the Australian Institute of Health and Welfare, has taken the commendable step of funding a register-based control program in the Top End of the Northern Territory (Dr Vicki Krause, Director, Centre for Disease Control, Territory Health Services, Darwin, personal communication). This program will also involve new health promotion strategies in Aboriginal communities -- directed at both health and education staff and at people with rheumatic fever and rheumatic heart disease and their families. Videos, booklets and treatment charts have been developed by indigenous educators and researchers.8 The program will attempt to create a partnership for change, involving indigenous and non-indigenous health professionals and government and non-government health services. Secondary prophylaxis will reduce the number of people developing rheumatic heart disease or requiring intervention for worsening valvular damage, but it will not stop initial episodes of acute rheumatic fever. This is where rheumatic fever control becomes difficult. While efforts to address social and economic inequities, particularly living conditions and overcrowding in Aboriginal communities, cannot be overemphasised,4,5 in some remote communities substantial change in these areas has not been evident over the past two decades and, in the current economic climate, is unlikely, we believe, to occur for some time. Conventionally, primary prevention relies on the accurate diagnosis and timely treatment with penicillin of group A streptococcal pharyngitis. However, most developing countries do not have the finances, skilled staff or laboratory facilities to do this well. Furthermore, more than two-thirds of cases of acute rheumatic fever may not follow symptomatic pharyngitis,9 so concentrating only on sore throats probably will not prevent most cases of rheumatic fever. Important progress is being made towards the development of a group A streptococcal vaccine, including current Australian initiatives,10 but in the shorter term other approaches are needed. In one such approach, a program of regular throat swabbing and treatment of streptococcal carriers in one Aboriginal community appeared to coincide with fewer cases of rheumatic fever,11 although the program was not sustained over the long term.12 This program appears to be the sole published effort to improve primary prevention of acute rheumatic fever in an Aboriginal community. While an association between streptococcal skin sores and acute rheumatic fever remains speculative, clues to further primary prevention strategies may come from understanding the epidemiology of group A streptococcal diseases in Aboriginal communities -- where the prevalence of streptococcal pyoderma (skin sores) may be up to 70% in children, but throat carriage rates of group A streptococci are often low.13 The ongoing epidemic of scabies in Aboriginal communities must underlie much of the streptococcal skin disease. More research is needed to better understand the epidemiology and best management of sore throats, streptococcal pharyngitis and skin sores in Aboriginal communities, as well as the relationship between streptococcal throat and skin infections and rheumatic fever. In the meantime, primary prevention strategies should include measures to reduce the reservoir of circulating streptococci found in skin sores; coordinated programs to control skin sores and underlying scabies can be effective in Aboriginal communities.13 Successful primary prevention strategies developed in Australia could have global implications for rheumatic fever control. Rheumatic heart disease in Aboriginal communities can be controlled in the short term through the use of comprehensive strategies to improve adherence to secondary prophylaxis regimens and to reduce exposure to group A streptococci, and possibly, in the longer term, with a vaccine. However, the ultimate aim must be improved living conditions for Aboriginal people, including emphasis on water supply, taps and showers, the disposal of sewage and solid waste, and resources to support better hygiene.

Jonathan R Carapetis · Bart J Currie

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Estrella Munoz BAppSc, RN, FRCNA · Jennifer R Powers BSc · John D Mathews BSc, MD BS, PhD, FRACP, CPA

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Susan M Sayers FRACP, DCH, AmBdNeonatPerinat · Jennifer R Powers BSc, AssocDipAppSc(Comp)