Indigenous health

A study design that was simple, relevant and that avoided particular sensitivities in the study population might have helped, as might considerably more guidance from the national funding body The combination of hazardous consumption of alcohol, Aboriginal people, primary care and a randomised controlled trial (RCT) of interventions sets a daunting challenge as a research project. In this issue of the Journal, Sibthorpe et al (page 273) describe, with disarming candour, how they took on this challenge and failed.1 After two false starts, and having recruited only one participant per fortnight (when they had originally aimed to enrol two per working day), the research team felt they had no option but to abandon the project and return the funds to the National Health and Medical Research Council (NHMRC). There is little that is new for clinical practice here, but there are important lessons about the design, execution and funding of research studies. The project was motivated by concerns about the limited external validity of existing evidence about the impact of simple interventions on hazardous drinking in an Indigenous primary care setting. The attempt to conduct a new RCT in such a setting was laudable, but the NHMRC process of reviewing grant applications apparently did not detect that failure was predictable. The inability of the team to conduct the study as conceived should not compound any negative perceptions about Aboriginal Medical Services and Aboriginal patients. Rather, the NHMRC might have served them better by advising the researchers about simplifying recruitment, need for consent and statistical power, as well as taking a more critical view of the underlying rationale for the project. It is not clear whether the original application to the NHMRC was supported by a feasibility study, but, given the challenge faced by the investigators, funding should not have been granted without one. As the project was initially designed, the complexity of the screening and recruitment processes flew in the face of well established principles.2 Simple requirements for enrolment make participation in RCTs easy for both patients and providers of healthcare services. By contrast, the combination of a detailed interview about a taboo subject, extensive paperwork and the need for blood all act as disincentives to participation by members of a community whose standard of education and reading ability are often poor, that sees paperwork as the hallmark of an officialdom that too often has been oppressive, and that attaches special significance to body fluids. All of these should have been identified by the NHMRC's assessors as likely to be prejudicial to success. A requirement to seek informed consent to participation runs contrary to the stated aim of the study to assess "effectiveness" (as opposed to "efficacy"3) of brief advice about drinking in a primary care setting. Alerting potential participants to the existence of a trial of this kind is likely to have a Hawthorne effect, thereby eroding statistical power. It is not clear from the account whether gaining consent was originally proposed by the investigators or imposed by an ethics committee — both would be conscious of the special nature of the target population — but it is another neat example of ethics getting in the way of good science.4 Trials of effectiveness do need ethical oversight, but clear thinking about ethical requirements is required when the control group is to receive "usual care". The counterargument that consent was needed because the study required additional blood tests that did not form part of routine care would not have any bearing when screening and recruitment were simplified. The investigators may have wanted to use γ-glutamyltransferase as an endpoint, but this is "medicalising" a social problem long before it becomes a biochemical one, and, in any case, represents a further departure from a study of "effectiveness". Part of the challenge of working in primary care and Aboriginal health is to devise and apply measures of impact and outcome that are relevant and robust, but also simple and credible. The trial as conceived was almost certainly underpowered statistically through overestimating the likely net effect of a brief intervention. In the study on general practitioner intervention in excessive alcohol consumption by Wallace et al,5 the initial prevalence of imprudent drinking was 35%, and the trial was designed on the assumption that 30% of men drinking excessively would respond to the intervention compared with 20% in the control group, the corresponding figures for women being 40% and 20%. Sibthorpe et al were aiming for an absolute difference in response between intervention and control groups of 20%, a bigger average change. They calculated correctly that 200 participants per group would be required to have a 90% chance of detecting such a difference and declaring it significant at P < 0.01. However, it is easy to overestimate the likely impacts of treatments, and changing personal and social behaviour can be even more difficult. Rather than anticipating that anywhere between 5% and 50% of members of the control group might stop drinking hazardously during the course of the study, a pilot study would have been particularly useful for clarifying the likely absolute prevalences and between-group difference in heavy drinking at follow-up. Finally, the whole concept of this study again throws into sharp focus the tension between high-risk and population-wide approaches to prevention, intervention and control of common health problems so eloquently described by Geoffrey Rose.6 Notwithstanding the fact that the prevalence of drinking alcohol is actually lower in the Aboriginal than in the mainstream population, the damage done by hazardous drinking affects a very great proportion of many Aboriginal communities and social factors play a significant role in the behaviour. Rose has clearly identified the futility of trying to get individuals to change their own health-threatening behaviour in such unsupportive circumstances. In Sibthorpe's project, the principles enunciated by Rose would have dictated that, from the outset, one should simply have attempted to ascertain which of the patients drank alcohol at all; given all of these a simple and unambiguous message about the NHMRC's recommendations about patterns of drinking consistent with best health; told them all about the Aboriginal Sobriety Group; and offered to provide extra help, probably at a separate consultation, to those who then felt that they needed it to achieve change. Eventually, Sibthorpe and colleagues began to stumble down something like this path, but the lesson is a salutary one. Too often, clinicians identify the screening/high-risk/selective medical intervention sequence as a first response to problems that are actually present on a mass scale. There is also an important lesson about both investigators and the NHMRC having available good epidemiological, biostatistical and public health advice at all phases of development and assessment of applications for research funding.

Konrad Jamrozik MB BS, DPhil

To fill a gap in knowledge about the effectiveness of brief intervention for hazardous alcohol use among Indigenous Australians, we attempted to implement a randomised controlled trial in an urban Aboriginal Medical Service (AMS) as a joint AMS–university partnership. Because of low numbers of potential participants being screened, the RCT was abandoned in favour of a two-part "demonstration project". Only 16 clients were recruited for ...

Beverly M Sibthorpe BA(Hons), PhD · Ross S Bailie MD, FAFPHM · Maggie A Brady MA, PhD · Sandra A Ball BCom, GradDip Public Administration · Polly Sumner-Dodd DipManagement · Wayne D Hall BSc, PhD

We are well aware of the excess mortality of Australian Aboriginals and Torres Strait Islanders, their higher hospital admission rates and their longer duration of hospital stay.1,2 However, despite this, relative to their need, Aboriginals and Torres Strait Islanders underutilise specialist healthcare, both as inpatients3 and outside hospitals.4 This situation is exacerbated by demonstrable underfunding of primary care services for Indigenous Australians.4 In this issue of the Journal, Cunningham (page 58)5 reports an analysis of Australian hospital separation data which documents significantly fewer diagnostic and therapeutic procedures performed on patients identified as Indigenous. Cunningham took into account variables possibly affecting use of procedures, including diagnosis, age, sex and place of residence, and acknowledged the problem of incomplete identification of hospital patients as Indigenous. The adjusted data still show fewer recorded procedures in Indigenous compared with non-Indigenous inpatients. These differences are significant within certain disease and diagnostic groups, and of a magnitude which cannot be ignored. Cunningham's study is also consistent with a large body of research from other countries showing disparities according to ethnic group and gender in the use of procedures.6,7 Are the reasons for these disparities in use of procedures related to disease characteristics (including severity), the patient (including preferences and comorbidities), the clinician or the institutional setting? Are they appropriate? And what exactly do these findings indicate? Ideally, decisions regarding medical care are based on evidence, or at least consensus opinion as reflected in a range of standard practices or options. Patient goals and values are then factored in, together with provider and institutional preferences and consideration of available resources. The end-result should be an individualised decision for each patient. Cunningham's findings suggest that, somewhere along this chain within hospitals, different decisions about use of procedures are being made that correlate with, but may not be caused by, ethnic origin. It seems implausible that such significant and Australia-wide differences could implicate large numbers of individual clinicians and result from purely personal biases based on race. The disparities are more likely a result of subtler systemic practices, not ill-intentioned but still discriminatory, and almost invisible within an individual patient–provider encounter. The challenge for clinicians is to further dissect the available information and identify the true cause from the many possible contributory factors. For example, it is likely that in some disease conditions where aetiology is well identified in a population and where the disease is endemic that fewer investigations (and therefore procedures) are needed. Renal biopsy may be performed less frequently to investigate renal disease in Indigenous patients, in whom identified antecedent chronic diseases are endemic. Iron-deficiency anaemia may be treated with anthelmintic drugs rather than first confirming the cause. Alternatively, there may be situations in which a population is genuinely underserviced relative to need (eg, some forms of elective or semi-elective surgery). Possible patient factors should also be identified and dealt with. These include stage of presentation, comorbidities, consent and anticipated postprocedural compliance. All may be reasons why a procedure is not performed, but all these factors can be ultimately overcome, in particular with greater recognition of the importance of primary care. The Royal Australasian College of Physicians has emphasised that adequate primary care is a prerequisite for effective specialist care.8 The uptake of services is more than "patient related" and cannot be separated from the provision of services; societal and institutional factors also structure the doctor–patient encounter within which decisions are made.9 Compliance is likely to improve when a patient's understanding and ownership of his or her disease is matched by a commitment (in the broadest sense) to providing high quality communication and a range of treatment options. The national underdevelopment of key services — Aboriginal Health Workers, Liaison Officers, and particularly interpreter services — shows a lack of appreciation by health institutions of the importance of involvement of Indigenous patients in decision making. Finally, could clinician factors be a major issue in this disparity in the use of procedures? Do we try hard enough and devote sufficient resources to the early diagnosis of serious conditions, to ensuring stabilisation of comorbidities, to obtaining meaningful consent, and to ensuring good postprocedural care and compliance? Do we have preconceived and incorrect perceptions of cultural appropriateness? Are the expectations we factor into our decision making, often derived from our knowledge of group outcomes, appropriate for this individual patient? It is certainly interesting that for trauma and infectious diseases, in which the decision-making process may be less subjective, Cunningham found no difference overall in the likelihood of having a procedure. However, even within these groups, large differences could be seen at an individual "principal diagnosis" level. To improve and structure our medical decision making, we need to continue to develop standardised protocols based on best evidence. Subsequent careful recording of consent processes, together with documentation of the decisions reached and the reasons behind them, will shed further light on the issues raised by Cunningham's data. Cunningham's article shows why clinicians need to contribute to the interpretation of population health information. As presented, these data do not identify the specific clinical procedures possibly denied to Aboriginal and Torres Strait Islander inpatients, and, although the findings have flagged the disparity in procedures, more information is needed for clinicians to take these concerns to the next level of analysis. Specifically, these findings should prompt us to review the decision-making processes determining use of diagnostic and therapeutic procedures in Aboriginal and Torres Strait Islander inpatients. Specialist colleges, societies, hospital units and individual clinicians now have a responsibility to review their own data and establish whether the trend in differential use of procedures applies to their area and, if so, what is driving this difference. The next chapter in this story needs to tease out the connections between healthcare need, use of procedures and health outcomes. If healthcare services are to foster equity rather than further institutionalise inequity, inappropriate reasons for different use of procedures need to be identified and the problems rectified.

Dale A Fisher FRACP, DTM · Tarun S Weeramanthri PhD, FRACP, FAFPHM

Objectives: To determine whether hospital patients identified as Indigenous are less likely than other inpatients to have a principal procedure recorded, and the extent to which any disparity in procedure use can be explained by differences in patient, episode and hospital characteristics. Design: Retrospective analysis of routinely collected administrative data from the National Hospital Morbidity Database (NHMD). Setting: Australian public and private hospitals. Patients: All patients included in the NHMD whose episode type was recorded as acute and whose separation occurred between 1 July 1997 and 30 June 1998. Patients admitted for routine dialysis treatment were excluded. Main outcome measure: Whether a principal procedure was recorded. Results: In public hospitals, patients identified as Indigenous were significantly less likely than other patients to have a principal procedure recorded, even after adjusting for patient, episode and hospital characteristics (adjusted odds ratio [OR], 0.67; 95% CI, 0.66–0.68). This disparity was apparent for most diseases and conditions. In private hospitals, no significant difference was observed (adjusted OR, 0.94; 95% CI, 0.83–1.06). Conclusions: The disparity in procedure use after adjustment for relevant factors indicates that in Australian public hospitals there may be systematic differences in the treatment of patients identified as Indigenous.

Joan Cunningham ScD (Epidemiol)

Indigenous Health Household infrastructure in Aboriginal communities and the implications for health improvement Ross S Bailie and Myfanwy J Runcie MJA 2001; 175: 363-366 Abstract - Methods - Results - Discussion - Competing Interests - Acknowledgements - References - Authors' details - - - More articles on Aboriginal health Abstract Objective: To evaluate housing survey data, describe the state of household infrastructure in Aboriginal communities in the Northern Territory (NT), and to discuss implications for health improvement for people in these communities. Design: Quantitative analysis of survey data and qualitative analysis of the survey process. Setting: All NT houses funded for repairs and maintenance through the Indigenous Housing Authority of the Northern Territory (IHANT). Main outcome measure: Status of infrastructure necessary for four key "healthy living practices" (washing people, washing clothes and bedding, waste removal, and food storage and preparation). Results: 3906 houses (79% of all houses funded by IHANT) were surveyed. Infrastructure components most frequently identified as not functional or not present were those required for the storage and preparation of food (62% not functional). The facilities required for personal hygiene and safe removal of human waste were not functional in 45%-46% of houses. Conclusions: These findings highlight the significance of absent or non-functioning household infrastructure as a potential contributory factor in the poor nutritional status and high rates of respiratory, skin and gastrointestinal infections in Indigenous communities. The environmental health and housing survey in the NT is an important tool for monitoring progress on addressing a key underlying determinant of the health of Indigenous people, and potentially for facilitating research aimed at gaining an improved understanding of the relationship of the household environment to health in Indigenous communities. The most significant improvements in health in industrialised countries over the past two centuries have been attributed to improvements in living and working conditions. Adequate and safe water supply, sanitation, housing, nutritious food, waste disposal, drainage and crowding have all been shown to influence health.1,2 A number of Australian studies have described the inadequacy of housing and the association between the poor living environment and poor health in the Indigenous population.3-6The National Aboriginal Health Strategy, through the establishment of the Health Infrastructure Priorities Projects in 1993 and 1994 and the Environmental Health Program in 1996, provided for large-scale infrastructure development in communities where this would have maximal impact on health. Projects included ensuring adequate water supply, sanitation, housing and drainage, providing internal roads, and dust management.7 The Indigenous Housing Authority of the Northern Territory (IHANT) was established to ensure a coherent housing strategy, with a specific mandate to facilitate planning and allocation of housing programs and to increase Aboriginal consultation, self-determination and self-management. The NT Government Environmental Health Task Group has published Environmental Health Standards for remote communities in the NT that define a minimum set of functional components of household infrastructure for the building and maintenance of houses.8 These standards are based in part on work done in central Australia by the HealthHabitat group in defining a set of "healthy living practices". As the program manager for IHANT, the NT Department of Local Government introduced an annual Environmental Health Survey (EHS) in 1998. Important points in the background to the survey are presented in Box 1. The Menzies School of Health Research was contracted to evaluate the first round of survey data, with a view to advising on improvement in the conduct of the survey and reporting on the current status of housing in the NT.9 We report the findings of this evaluation. Methods The survey methods are described in detail in the survey evaluation report.9Briefly, the survey aimed to cover all houses funded by IHANT, and included all communities in the NT, including remote settlements and communities near or within the boundaries of towns and major centres. Surveys were conducted primarily by environmental health officers of Territory Health Services or community development officers of the Department of Local Government. A number of surveys were also conducted by Aboriginal environmental health workers or other community workers under the direction of the environmental health officers and community development officers, with the intention of ultimately handing over responsibility for the survey to community housing organisations. The survey form included components of infrastructure specified as essential in the Environmental Health Standards,8 with each component scored according to its presence or absence, and, if present, its condition and the level of maintenance required to render it fully functional. The data were entered into a database managed by the Department of Local Government. Evaluation and data analysis The design and conduct of the survey were examined through documentary evidence (held by the Department of Local Government); interviews with the project manager, field officers and database operators; and examination of the database. The data within the database were checked for data entry errors and completeness. Errors were corrected and a subset of the data containing observations for houses with entries in most data fields was downloaded and analysed using SPSS statistical software.10The proportions of houses for which each infrastructure component specified on the survey form was adequately functional (required no or minor repairs only), was not functional (required major repairs or replacement), was not present or for which data on that component were missing were calculated. Of the nine healthy living practices described by Pholeros et al,4 four that are directly dependent on components of household infrastructure examined in this survey were identified. These were washing people, washing clothes and bedding, waste removal, and food storage and preparation. A set of infrastructure components required to allow the effective conduct of each of these four healthy living practices was defined, and the four healthy living practices were expanded to six for the purpose of the analysis, as shown in Box 2. The proportion of houses which had all the infrastructure components required for each practice recorded as functioning was calculated, both overall and for individual communities with 10 or more houses included in the survey. Ethical approval This article is based on data collected primarily for the purposes of housing management and planning rather than for research. No individuals or communities are identified, so there are no issues relating to confidentiality or privacy that require ethical approval for publication. Results Complete data were recorded for 3906 (79%) of a total 4936 houses funded by IHANT. A number of inadequacies in survey conduct and quality control were found. These stemmed primarily from a lack of or inadequate protocols for the conduct of the survey and from inadequate training of surveyors. These inadequacies resulted in inconsistencies in identifying the most appropriate respondent for the survey, and in questioning, inspection and testing of infrastructure components, and may have restricted the survey coverage.9 The components of infrastructure most frequently identified as not functional or not present were the kitchen bench, the stove top and the oven (26%, 41%, and 42%, respectively) (Box 3). The cold water taps and supply to the kitchen sink, shower and laundry were clearly identified as functional in between 76% and 81% of houses. In the bathroom, 30% of houses were identified as having no functioning cold water taps, and 32% as having no functional basin. Hot water taps were functional in the laundry in 68% of houses, and in the shower in 74%. However, the hot water service was functional in only 62% of houses, not functional in 11% of houses and absent altogether in 14%. Electricity supply to switches, power points and lights was functional in different rooms for 72%-79% of houses. Between 63% and 78% of houses had the general structure of the kitchen, laundry, bathroom, bedroom, main toilet, exterior doors and windows and house exterior recorded as functional and not a threat to safety. The general structure was least commonly identified as functional or safe in kitchens. Forty-two per cent of houses were clearly identified as having a functioning refrigerator, 19% had functioning air-conditioning or evaporative cooling and 41% had a functioning washing machine. Thirty-three per cent had a functional fence around the boundary. The proportion of surveyed houses for which the components required to effectively conduct each of the six key "healthy living practices" ranged between 38% and 69%. Those components required for preparing and storing food were least likely to all be in a functional state and those required for removal of rubbish were most likely to be available (Box 2). The proportion of houses that had functioning infrastructure for conducting each of the healthy living practices varied widely between communities. In some communities, and for some healthy living practices, none of the surveyed houses had the required infrastructure functioning, whereas in other communities all of the surveyed houses had the required infrastructure functioning (Box 2). In 13% of all communities where 10 or more houses were surveyed, more than 50% of surveyed houses had the functional amenities to allow all six of the key healthy living practices (Box 4). In 44% of communities 50% of surveyed houses had functional infrastructure components necessary for three or less of the healthy living practices. Discussion Our analysis of the survey data describes for the first time the poor state of household infrastructure in Indigenous communities at a detailed level and across a wide jurisdiction. The findings confirm the poor state of housing previously described at a more localised level.4,5,11 Certain types of infrastructure are commonly in a poor state of repair, most notably the facilities for storage and preparation of food. This is of particular concern in light of the high rates of gastrointestinal infection, undernutrition and obesity in children and obesity in adults,12-14 the associated high rates of "lifestyle"-related disease among people living in these communities, and the now widely accepted evidence of the role of fetal nutrition in the development of chronic disease in adulthood.15 (We recognise that lifestyle is strongly determined by the social, cultural and physical environment.) The poor state of housing and access to adequate facilities for washing have been identified as key underlying factors in the high levels of morbidity and mortality from bacterial respiratory tract infections, and the significant contribution of such infections to the generally poor state of health of many Indigenous Australians.16 Providing sound household infrastructure is clearly important for improving the poor state of health among Indigenous people in Australia. The work of HealthHabitat in central Australia indicates that household infrastructure is used when it is available.4 However, providing a secure and good-quality food supply, and good hygienic and dietary behaviour, is also essential. Although there were concerns about the lack of quality control in the conduct of the survey between different communities and regions, the high level of coverage (it might more correctly be referred to as a census) and the consistency in coding items as not present and missing data across regions9 allay these concerns to some extent. Further, the findings need to be seen as representing the best-case scenario in the NT, as the survey was intended to target permanent dwellings only. An estimated 1000 temporary dwellings (caravans, tin sheds, improvised dwellings) occupied by close to 4000 people17 would not have been included in this survey. This suggests that the level of functional infrastructure reported in this survey overestimates the level for all dwellings in the NT by about 25%. Current infrastructure projects can be expected to contribute to improvements in health for the people they reach. However, projections indicate that, even with these projects, there will be significant unmet need for many years as population growth and aging housing stock tip the balance against the supply of new houses and repairs and maintenance to existing houses.18 Many more resources need to be committed if such projects are to influence health at the wider population level in the near future. The annual environmental health and housing survey introduced in the NT is an important tool for defining areas of greatest need, monitoring progress, and potentially for improving the understanding of the contribution of household infrastructure to a range of health, educational and social outcomes. Competing interests This article was based on an independent evaluation of a survey conducted under contract by the Menzies School of Health Research for the Northern Territory Department of Local Government. There was agreement at the start of the evaluation between the Department of Local Government and the evaluation team that the results of the evaluation could be the subject of articles published in the scientific literature. The authors have no conflict of interest in writing this article, and have not been subject to any undue influence. Opinions expressed are those of the authors and do not necessarily represent those of any employee of the NT Government. Acknowledgements Thanks to the Northern Territory Department of Local Government for its cooperation and funding of the work that led to this report. We acknowledge the decision of the Aboriginal Community Councils to agree to participate in the survey and the contribution of the many people involved in data collection and processing for the survey. We are grateful to a number of people for their cooperation in the survey evaluation, including Sallie Cairnduff, Graham Franklin, Steve Guthridge, Andrew Heath, Barbara Klessa, Esther Pearce, Phillipe Porigneaux, Danni Quickenden, Helen Secretary, Lynette Shields and Nicola Slaven. References Lindheim R, Syme SL. Environments, people and health. Ann Rev Public Health 1983; 4: 335-338. World Bank. World Development Report: Investing in health. New York: Oxford University Press, 1993. Nganampa Health Council Inc, South Australian Health Commission, Aboriginal Health Organisation of South Australia. Report of Uwankara Palyanku Kanyintjaku: an environmental and public health review within the Anangu Pitjantjatjara Lands. Adelaide: Nganampa Health Council, 1987. Pholeros P, Rainow S, Torzillo P. Housing for health: Towards a healthy living environment for Cape York Communities. Newport Beach: HealthHabitat; 1993. Pormpuraaw Community Council, Apunipima Cape York Health Council, Centre for Appropriate Technology, HealthHabitat. Pormpuraaw housing for health project report: Towards a healthy living environment for Cape York Communities. Cairns: Apunipima Cape York Health Council, 1997. Torzillo P, Kerr C. Contemporary issues in Aboriginal public health. In: Trompf P, Reid J, editors. The health of Aboriginal Australians. Sydney: Harcourt Brace & Co, 1997. Guthridge S, Cairnduff S, Gollow P, et al. Structure, function and health: a review of the health impact of infrastructure change in remote Aboriginal communities of the Top End — final draft. Darwin: Territory Health Services, 2000. Northern Territory Government Environmental Health Task Group. Environmental health standards for remote communities in the Northern Territory. Darwin: Northern Territory Government, 1998/1999. Runcie M, Bailie R. Evaluation of environmental health survey data — Indigenous housing. Darwin: Cooperative Research Centre for Aboriginal and Tropical Health, 2000. SPSS [computer program], version 10.0.5. Chicago: SPSS Inc, 1999. Hardy B. Ramingining Manymak Wanga project report. Darwin: Territory Health Services, 1998. Cunningham J, Makerras D. Overweight and obesity: Indigenous Australians. Canberra: Australian Bureau of Statistics, 1994. Ruben A, Walker A. Malnutrition among rural Aboriginal children in the Top End of the Northern Territory. Med J Aust 1995; 162: 400-403. Muller SM, Priestly JR, McComb JR. Malnutrition among rural Aboriginal children in the Top End of the Northern Territory. Med J Aust 1995; 163: 445. Harding JE. The nutritional basis of the fetal origins of adult disease. Int J Epidemiol 2001; 30: 15-23. Mathews JD. Historical, social and biological understanding is needed to improve Aboriginal health. Rec Adv Microbiol 1997; 5: 257-334. Housing and Infrastructure in Aboriginal and Torres Strait Islander communities. Canberra: Australian Bureau of Statistics, 1999. Strategic plan — 1996. Darwin: Indigenous Housing Authority of the Northern Territory, 1996. (Received 18 Apr, accepted 10 Aug, 2001) Authors' details Menzies School of Health Research and Flinders University Northern Territory Clinical School, Darwin, NT. Ross S Bailie, MB ChB, FAFPHM, Associate Professor of Public Health. CSIRO, Sustainable Ecosystems, Canberra, ACT. Myfanwy J Runcie, PhD, Research Scientist. Reprints will not be available from the authors. Correspondence: Professor R S Bailie, Flinders University Northern Territory Clinical School, PO Box 41096, Casuarina, NT 0811 ross.bailieATmenzies.edu.au Make a comment 1: Background to the housing survey The survey is the responsibility of the Indigenous Housing Authority of the Northern Territory (IHANT), the peak body for Indigenous housing issues in the NT. The two elected Zone Commissioners and seven elected Regional Chairs of the Aboriginal and Torres Strait Islander Commission (ATSIC) have a majority on the IHANT Board to ensure appropriate Indigenous representation. The housing survey's purpose is not just to document the condition of housing infrastructure, but to guide and monitor a substantial maintenance and building program. Feedback of information and developing capacity at local and regional levels are key strategies in the program. The survey aims to ensure the most appropriate use of funds and to improve health status. Back to text 2: Percentage of surveyed houses for which the infrastructure components required to effectively conduct each of six "healthy living practices" were functional Healthy living practice Infrastructure components % Functioning in all surveyed houses Median % functioning per community (range)* Wash people Shower hot tap; shower cold tap; shower drainage; bathroom basin; bathroom hot tap; bathroom cold tap 54% 41% (6%-95%) Wash clothes Laundry trough; laundry hot tap; laundry cold tap 68% 69% (14%-100%) Functioning toilet Main toilet pan; main toilet cistern; main toilet water supply; main toilet drainage 55% 58% (7%-95%) Remove waste water Shower drainage; main toilet drainage 61% 61% (9%-100%) Remove waste rubbish Rubbish bin 69% 72% (0-100%) Prepare and store food Kitchen cold tap; stove top; oven; dry place for food storage; kitchen bench 38% 33% (0-100%) *Includes only those communities where at least 10 houses were surveyed. Back to text 4: Funtionality ratings of 86 communities across the Northern Territory with 10 or more houses surveyed Back to text

Ross S Bailie · Myfanwy J Runcie

Indigenous Health Trachoma in Australia Hugh R Taylor Australia is the only developed country in the world where blinding trachoma still exists MJA 2001; 175: 371-372 Trachoma is a disease that has been with us from antiquity. It is discussed in ancient Egyptian texts written on papyrus and in even earlier writings from ancient China. Chronic infection with the trachoma organism, Chlamydia trachomatis, can lead to blindness. The disease came to prominence in Europe during the Napoleonic wars, when tens of thousands of British and French troops returned with trachoma after fighting in Egypt. It spread rapidly through the armies of Europe, where the troops lived in crowded and insanitary barracks. Most of all, trachoma was a disease of the urban slums. In Europe, as people left their relatively healthy rural homes they were crowded into the workhouses and tenements created by the Industrial Revolution. Personal and community hygiene fell to an all-time low and the prevalence of trachoma surged. Trachoma was rampant throughout Europe and North America in the 19th century. In addition to tuberculosis and typhus, trachoma was one of the diseases that would-be immigrants to the United States were examined for — if found to have trachoma, they were sent all the way back to Europe. The early European settlers of Australia brought trachoma with them. Whether the Australian Indigenous people had trachoma before colonisation is unclear, but it seems unlikely, as small groups of nomadic hunter-gatherers can maintain good hygiene. However, with the poor housing conditions of the early settlers, and with the heat, dirt and flies of Australia, trachoma (or "sandy blight" as it was often called) became widespread and well known. It even left its stamp on certain place names (eg, Sandy Blight Junction in the Western Desert and the Ophthalmia Ranges in the Western Australian Pilbara). However, by the beginning of the 20th century, hygiene and living conditions in our larger cities had started to improve. In 1901, one of my predecessors at the Eye and Ear Hospital in Melbourne stated he could no longer find cases of active trachoma from Melbourne to teach his students. Instead he had to find people who lived in the Goulburn or LaTrobe valleys in Victoria. But, even in rural Australia, trachoma was disappearing, and by the late 1930s sandy blight had essentially disappeared as most Australians moved into proper housing with separate beds, running water and adequate sewerage and rubbish removal. The same happened in other developed countries. In England, the trachoma schools and clinics closed before World War II, and the last trachoma hospitals in the United States closed just after the war. In the 1950s, trachoma also disappeared in Italy and the Soviet Union. Despite the disappearance of trachoma from most of the Australian population, it has remained prevalent among certain groups of Indigenous Australians. The late Father Frank Flynn, an Australian-born and London-trained ophthalmologist turned Catholic priest, worked as an Army chaplain in Darwin in 1941. He was the first to recognise the frequent occurrence of trachoma among Indigenous people in the Northern Territory, and their welfare became his life's work. After World War II, Ida Mann, an English ophthalmologist who had worked with Frank Flynn in London before the war, moved to Perth. She subsequently conducted extraordinary trips throughout the outback, examining and treating Indigenous people with trachoma. In the 1960s, Fred Hollows took up his position as Professor of Ophthalmology at the University of New South Wales and became aware of the importance of trachoma in Australia. First working with the Gurindji people at Wave Hill in the Northern Territory and then with the people around Bourke in far western New South Wales, he cajoled the Federal Government and the Royal Australian College of Ophthalmologists into establishing the National Trachoma and Eye Health Program (the "Trachoma Program"). From 1976 to 1978, the Trachoma Program teams visited every Indigenous community in Australia (including some groups in large urban centres), examining over 62 000 Indigenous people and nearly 40 000 others (consisting of whites, Asians, etc, in rural and remote areas). It gave a clear picture of the number of people affected with trachoma and its distribution. They also treated nearly 40 000 people for trachoma and set up clear guidelines and recommendations as to what needed to be done to eliminate trachoma.1 In 1996, I was asked by the Federal Minister for Health to prepare a report on Indigenous eye health.2 It was very satisfying to go back to places like Bourke and Broome and find that trachoma had essentially disappeared over the previous 20 years. Clearly, progress was being made — at least in the towns and larger communities. In other areas, although the amount of trachoma had decreased and fewer children were affected, their elders still had scarred eyelids and blindness from the inturned eyelashes caused by trachoma. However, I was devastated to find that in some other communities, such as Jigalong in the Western Desert, and Amata and Fregon in the Musgrave Ranges, the rates of trachoma in children had not changed one jot over the 20-year period. At a meeting of the World Health Organization (WHO) in Geneva a few years ago, we added up the number of countries where blinding trachoma still occurred. We counted 54 — Australia is the only developed country on that list. WHO has launched a special program for the Global Elimination of blinding Trachoma by the year 2020 ("GET 2020").3-5 Its aim is to eliminate trachoma from the poorest areas of Africa and Asia over the next 20 years. My colleagues from other countries turn to me and ask, "How can you possibly still have trachoma in your country?". Fred Hollows once said that trachoma was a disease of the crèche, the preschool childcare group. Studies I subsequently did, both in the laboratory6,7 and in the field,8,9 identified and confirmed the importance of repeated episodes of reinfection by C. trachomatis. Each episode of infection gives more inflammation that leads to more scarring and a greater likelihood of eventual blindness. Endemic trachoma persists in areas where living standards are inadequate, with poor personal and community hygiene that permit the frequent spreading of infected eye secretions from one child to another. To stop trachoma, one needs to stop the transmission by improving living conditions. After all, this is what happened in mainstream Australia 100 years ago. Nowadays, Australians in both urban and rural areas expect to have the basic facilities that are needed for healthy living, such as a house, electricity, clean running water and sewerage, a made road and a rubbish collection facility. We expect them as a right — just recall the outrage in Sydney when the water supply was contaminated in 1998! Nevertheless, the Aboriginal and Torres Strait Islander Commission (ATSIC) has reported that half of the Indigenous people in the Northern Territory do not have adequate housing,10 and one in six communities do not even have potable water. ATSIC estimated that in 1991 there was a $2 billion deficit in funding for basic infrastructure and housing in Indigenous communities. These are services provided by local and state governments to everyone else in Australia. To eliminate trachoma in Australia we need to upgrade the basic services and housing of Indigenous communities in the outback to the same minimal standard that every other Australian enjoys. This is fundamental and can only occur if the Australian community accepts the need and insists that the problem be rectified. We must direct and empower federal, state and local governments to provide the basic community infrastructure and health hardware. This would be a good example of "practical reconciliation" espoused by the Coalition Government. Using research findings of the past decade or so, we have worked with WHO to devise the so-called "SAFE strategy" to eliminate trachoma.5 The SAFE strategy has four components: "S" for surgery (to correct inturned eyelashes); "A" for antibiotics (to eliminate chlamydial infection); "F" for facial cleanliness (to reduce the spread of infection from one child to another); and "E" for environmental improvement (to upgrade community hygiene and living conditions). Some of the recommendations contained in the review of eye health in Aboriginal and Torres Strait Islander communities2 related to trachoma, and the Federal Government accepted the recommendations that included the implementation of the SAFE strategy in all communities where trachoma still exists. In 1997, when he accepted the report, the Federal Minister for Health, Dr Wooldridge, promised to "do whatever it takes". The Prime Minister also supported this work, and on a visit to Nhulunbuy in 1998 announced the provision of azithromycin to treat trachoma in Indigenous communities. However, since then, disappointingly little has happened. In most places, little has changed, even though the problem has been clearly identified, strategies have been carefully laid out, verbal support has been given by leaders and there has been a lot of discussion with bureaucrats. In areas with severe trachoma, one in five of the older people have inturned lashes, and about half of these are either blind already or will eventually go blind. It is a tragedy to see their children or their grandchildren suffering from trachoma infection, because you know that they are on the same escalator and will certainly suffer the same fate if things do not improve. We can stop this if we as a community care. Trachoma is entirely preventable. Although it disappeared from white Australia 100 years ago, it could take another century to disappear from Indigenous Australia if we do not do something about it. We can not wait that long. All Australians have the right to sight. The time to act is now. Do we have the will? References National Trachoma and Eye Health Program. Sydney: Royal Australian College of Ophthalmologists, 1980. Taylor HR. Eye health in Aboriginal and Torres Strait Islander communities. Report of a review commissioned by the Commonwealth Minister for Health and Family Services, the Hon Dr Michael Wooldridge. Canberra: Commonwealth of Australia, 1997. Dawson C, Schachter J. Can blinding trachoma be eliminated worldwide? Arch Ophthalmol 1999; 117: 974. Taylor HR. Towards the global elimination of trachoma. Nat Med 1999; 5: 492-493. World Health Organization. Future approaches to trachoma control. Report of a global scientific meeting; 1996 June 17-20, Geneva, Switzerland. Geneva: WHO, 1996. (WHO Publication 96.56.) Taylor HR, Prendergast RA, Dawson CR, et al. An animal model of cicatrizing trachoma. Invest Ophthalmol Vis Sci 1981; 21: 422-433. Taylor HR, Maclean IW, Brunham RC, et al. Chlamydial heat shock proteins and trachoma. Infect Immun 1990; 58: 3061-3063. Taylor HR, Millan-Velasco F, Sommer A. The ecology of trachoma: an epidemiological study of trachoma in Southern Mexico. Bull World Health Organ 1985; 63: 559-567. Taylor HR, West SK, Mmbaga BBO, et al. Hygiene factors and increased risk of trachoma in Central Tanzania. Arch Ophthalmol 1989; 107: 1821-1825. Water: a report on the provision of water and sanitation in remote Aboriginal and Torres Strait Islander communities. Canberra: AGPS, 1994. Jones R. The housing needs of indigenous Australians, 1991. Research Monograph No. 8. Canberra: Centre for Aboriginal Economic Policy Research, Australian National University, 1994: 149-151. This is an edited version of a talk presented on the ABC Radio National program Ockham's Razor, 1 July 2001. Authors' details Centre for Eye Research Australia, East Melbourne, VIC. Hugh R Taylor, AC, MD, FRACO, Professor of Ophthalmology. Reprints: Professor H R Taylor, Centre for Eye Research Australia, Locked Bag 8, East Melbourne, VIC 8002. h.taylorATunimelb.edu.au Make a comment

Hugh R Taylor

Indigenous health Regional variation in the incidence of end-stage renal disease in Indigenous Australians Alan Cass, Joan Cunningham, Zhiqiang Wang and Wendy Hoy MJA 2001; 175: 24-27 Abstract - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Aboriginal health Abstract Objective: To evaluate regional variation in the incidence of end-stage renal disease (ESRD) in Indigenous Australians, and to examine the proximity to ESRD treatment facilities of Indigenous patients. Design: Secondary data review, with collection of primary data regarding patients' place of residence before beginning ESRD treatment. Participants: Indigenous ESRD patients who commenced treatment in Australia during 1993-1998. Methods: We obtained data from the Australian and New Zealand Dialysis and Transplant Registry regarding 719 Indigenous patients who started ESRD treatment between 1 January 1993 and 31 December 1998. We obtained primary data from the treating renal units to determine the place of residence before beginning renal replacement therapy. We calculated the average annual incidence of ESRD for each of the 36 Aboriginal and Torres Strait Islander Commission regions using population estimates based on the 1996 Census, and calculated standardised incidence ratios with 95% confidence intervals for each region. We compared the number of cases with the treatment facilities available in each region. Main outcome measure: Regional standardised ESRD incidence for Indigenous Australians referenced to the total resident population of Australia. Results: Standardised ESRD incidence among Indigenous Australians is highest in remote regions, where it is up to 30 times the national incidence for all Australians. In urban regions the standardised incidence is much lower, but remains significantly higher than the national incidence. Forty-eight per cent of Indigenous ESRD patients come from regions without dialysis or transplant facilities and 16.3% from regions with only satellite dialysis facilities. Conclusions: There is marked regional variation in the incidence of ESRD among Indigenous Australians. Because of the location of treatment centres, there is inequitable access to ESRD treatment services for a significant proportion of Indigenous patients. In Australia, geographical differences in morbidity and mortality have been demonstrated.1-4 In general, people living in rural and remote areas have higher death and hospital separation rates, which have been attributed to differences in socioeconomic status,1,3-5 access to health services,2,6,7 ethnicity4 and racial discrimination.8 Indigenous Australians constitute a disproportionate number of new patients commencing end-stage renal disease (ESRD) treatment:9 in 1997, the incidence rate (adjusted for age and sex) for Indigenous Australians beginning ESRD treatment was nearly nine times that of non-Indigenous Australians.10 Although epidemics of renal disease among Indigenous Australians in defined areas11 have been documented, there have been no systematic reports of the regional patterns of ESRD incidence in Australia. In this study we have attempted to determine these patterns and to examine the accessibility of ESRD treatment facilities for Indigenous people. Methods Databases The Australia and New Zealand Dialysis and Transplant Registry (ANZDATA) maintains a database of patients treated by maintenance dialysis or renal transplantation in Australia. All renal units that provide ESRD treatment in Australia participate in the Registry. Postcode of residence at the start of treatment is collected for all new patients entered into the ANZDATA Registry. ANZDATA maintains a list of hospital renal transplant services, tertiary referral units and satellite dialysis units. Satellite units are defined as dialysis facilities, generally staffed by specialist nurses, that are geographically separate from hospital nephrology services. Data validity Postcode of residence at the start of treatment is an imperfect indicator of the usual place of residence before starting treatment. In remote areas of Australia a single postcode may apply to many communities across a vast area. Furthermore, patients may be required to relocate to a major regional centre to access dialysis services; thus, their postcode at the start of treatment may not reflect their previous usual place of residence. To determine the usefulness of postcode data, we reviewed 104 Indigenous patients who commenced ESRD treatment from 1993 to 1998 at Royal Darwin Hospital, Northern Territory. For these patients the previous usual place of residence was known. Fifty-one patients (49%) had postcodes in the Darwin region, but only nine of these 51 patients previously lived in this region. The other 42 had relocated to Darwin to commence dialysis and were from communities across the "Top End", extending from the Torres Strait in Queensland to Geraldton in Western Australia. As a result of this audit, we decided to collect primary data from each treating renal unit regarding the previous place of usual residence of their Indigenous patients. Indigenous identification was based upon self-identification and discussion with the treating physician. There is often significant concern about the quality of Indigenous identification in morbidity, mortality and demographic data sets. However, we believe that racial identification in the ANZDATA registry is good. A survey form is completed every six months for all patients on maintenance dialysis or with functioning renal transplants. In this survey, question five is about "Racial origin" and includes a prompt regarding Indigenous status. ESRD patients have regular contact with renal services from the time of diagnosis, through intensive maintenance therapy until death. There is heightened awareness of renal disease in Indigenous Australians and multiple opportunities exist to reconfirm data accuracy. Patients From 1 January 1993 to 31 December 1998, 719 Indigenous patients started treatment for ESRD in Australia. We determined the previous place of usual residence for 680 (94.6%). For 38 patients (5.3%) we used the postcode at entry as an indicator of previous place of usual residence. No geographical data were obtainable for one patient. Geography We used the 36 Aboriginal and Torres Strait Islander Commission (ATSIC) regions (Boxes 1 and 2) as our geographic units for analysis. These are legally prescribed administrative areas and the smallest geographical areas for which accurate resident population estimates for the Indigenous population are available.12 We assigned the place of usual residence for Indigenous patients to the appropriate ATSIC regions. We assigned the 38 patients for whom we could not obtain exact information on previous place of residence to ATSIC regions according to their postcode at the time of beginning ESRD treatment. Statistical analysis Using population estimates based on the 1996 Census, we calculated the average annual incidence of ESRD in the 36 ATSIC regions. We used ABS estimates of the Indigenous population, derived using Census information on place of usual residence. These estimates are adjusted for net Census undercount and non-response to the Census question about Indigenous status.13 We used indirect standardisation to calculate an age- and sex-standardised incidence ratio with 95% confidence intervals for each region. Rates for the total Australian resident population were used as the reference (standardised incidence ratio equals incidence in the Indigenous population divided by incidence in the total Australian population, after adjusting for differences in the age and sex composition of both populations). Statistical analysis was performed using Stata.14 Ethical approval We obtained ANZDATA approval to analyse geographic data for Indigenous patients starting treatment for ESRD between 1 January 1993 and 31 December 1998. We also obtained approval for the study from the joint institutional ethics committee of Royal Darwin Hospital and the Menzies School of Health Research. The head of each renal unit gave written consent for us to access potentially identifying patient data in order to determine the previous place of usual residence for Indigenous ESRD patients. Results Mapping reveals significant variation in the incidence of ESRD among Indigenous Australians. The areas of highest incidence (up to 1300 cases per million per year) were the remote regions of Tennant Creek, Aputula and Jabiru in the Northern Territory, Warburton and Kalgoorlie in Western Australia, and Ceduna in South Australia (Box 1). The areas of lowest incidence (less than 100 per million per year) were the regions of Rockhampton and Brisbane in Queensland, Sydney and Queanbeyan in NSW/ACT, Wangaratta (which includes much of eastern Victoria) and Hobart (which encompasses all of Tasmania) (Box 1). The standardised incidence ratio for ESRD (compared with the total national population incidence) ranged from less than two in Rockhampton, Sydney, Queanbeyan and Wangaratta to more than 25 in Aputula, Kalgoorlie and Tennant Creek (Box 2). There were no ESRD patients identified as Indigenous in Tasmania in the six-year period. Tertiary renal services, particularly transplant services, are located within significant population centres such as capital cities. Three hundred and forty-five (48.0%) of the 719 Indigenous ESRD patients lived in ATSIC regions without ESRD treatment facilities (Box 2). A further 117 (16.3%) lived in regions with only satellite dialysis facilities (Box 2). Most Indigenous patients must travel hundreds of kilometres to access transplant services, which are located in Perth, Adelaide, Melbourne, Sydney, Newcastle and Brisbane. Discussion In this study we have demonstrated a large gradient in Indigenous ESRD incidence from urban to remote regions and highlighted inequitable access for remote patients to treatment facilities. However, even in urban regions, the Indigenous ESRD incidence was high after age and sex standardisation. Poor Indigenous health outcomes are not confined to the most disadvantaged or most remote regions, but exist across the Indigenous population. The quality of Indigenous identification is a potential concern in our study. ANZDATA relies upon self-identification and discussion with the treating physician. Self-identification is the method used by the Australian Bureau of Statistics in census collections and is generally used in health-related data collection. We believe that the quality of identification in our study is high owing to the ongoing intensive interaction of ESRD patients with medical and nursing staff, Indigenous status being a prominent question in the six-monthly survey form, and the strong awareness of Indigenous ESRD among nephrologists. The most likely error would be the failure to identify all urban Indigenous ESRD patients. This would result in an underestimate of the true Indigenous ESRD incidence in urban areas and an overestimate of the gradient from urban to remote Indigenous ESRD incidence. Yet, as this gradient is so large, representing an almost 20-fold variation in standardised ESRD incidence, it can not be entirely explained by problems with Indigenous identification. The very high standardised incidence ratios for Indigenous people in remote areas would not change. These results have significant implications for the delivery of services to Indigenous people with ESRD. Satellite facilities opened in the Jabiru region in 1999 and the Katherine region in 2000 (after the patients in this study commenced treatment). Of the 16 regions with the highest Indigenous ESRD incidence, at the beginning of 2001 only Kalgoorlie, Jabiru (Tiwi Islands), Geraldton, Katherine and South Hedland had satellite dialysis units. A satellite unit is scheduled to open soon in Broome and recommendations have been accepted to establish a satellite haemodialysis service in the Torres Strait as part of the recent Queensland Renal Strategy.15 We recognise the significant difficulties related to the establishment and maintenance of renal treatment facilities in remote locations. These include high construction costs, poor reliability of electricity and water supply, variable water quality, difficulties in training and retaining specialised nursing staff, infrequent access to medical staff and provision of housing for patients returning to live in their local community. Despite these difficulties, treatment facilities have been established in some of the most remote communities in Australia. Even with the availability of satellite units, initiation of ESRD treatment usually requires a prolonged stay in a major urban centre. During this stay, vascular or peritoneal access for dialysis is created, the patient starts and is stabilised on treatment and learns skills required for self-care in order to return to a remote satellite dialysis unit. We should develop more innovative methods of patient education, training for self-care and delivery of treatment to allow patients to remain within their communities whenever possible. Improving prevention and treatment services in high-incidence areas should be a priority. Indigenous people living in remote communities demand more equitable access to dialysis services,16 regardless of practical problems related to the establishment of remote treatment facilities. The need to relocate to distant urban areas to access treatment affects the patient, patient's family and community. A recent study of ESRD among Aboriginal people of central Australia concluded: "This level of illness and death [due to ESRD] represents Aboriginal family trauma and loss on a shocking scale, described without exaggeration as sorrows nearly every year [because] the young and the old are dying". 17 Acknowledgements The data reported here have been supplied by the Australia and New Zealand Dialysis and Transplant Registry. The interpretation of these data is the responsibility of the authors and should not be seen as an official policy or interpretation of the Australia and New Zealand Dialysis and Transplant Registry. Dr Alan Cass receives postgraduate research scholarship funding from the Colonial Foundation. Dr Joan Cunningham is supported by a fellowship from the Menzies Foundation. We thank Dr Mark Thomas, Dr Paul Snelling, Dr Meshak Kirubakaran, Dr Tim Furlong, Dr Peter de Jersey and the heads of renal units for providing information regarding the place of usual residence for their patients. References Glover J, Harris K, Tennant S. A social health atlas of Australia. 2nd ed. Adelaide: Public Health Information Development Unit, University of Adelaide, 1999. Sexton PT, Sexton TL. Excess coronary mortality among Australian men and women living outside the capital city statistical divisions. Med J Aust 2000; 172: 370-374 [see comments Med J Aust 2000; 172: 360-361]. National Health Strategy. Enough to make you sick: how income and environment affect health, Research Paper No. 1. Melbourne: National Health Strategy Unit, 1992. Taylor R, Chey T, Bauman A, Webster I. Socio-economic, migrant and geographic differentials in coronary heart disease occurrence in New South Wales. Aust N Z J Public Health 1999; 23: 20-26. Turrell G, Mathers CD. Socioeconomic status and health in Australia. Med J Aust 2000; 172: 434-438. Heller RF. Mortality from cardiovascular disease is too high outside capital cities [editorial]. Med J Aust 2000; 172: 360-361. McLaren B. Renal failure in Arnhem Land: missed opportunities for prevention and treatment. Aust J Rural Health 1996; 4: 61-66. Lowe M, Kerridge IH, Mitchell KR. 'These sorts of people don't do very well': race and allocation of health care resources. J Med Ethics 1995; 21: 356-360. Disney A, Russ G, Walker R, et al, editors. ANZDATA Registry Report 1999. Adelaide: Australia and New Zealand Dialysis and Transplant Registry, 1999. Cass A, McDonald SP, Wang Z. Australians with renal disease: a new national survey [letter]. Med J Aust 1999; 171: 444. Spencer JL, Silva DT, Snelling P, Hoy WE. An epidemic of renal failure among Australian Aboriginals. Med J Aust 1998; 168: 537-541 [see comments Med J Aust 1998; 168: 532-533 and Med J Aust 1999; 170: 191-192]. Australian Bureau of Statistics. Population issues, Indigenous Australians. Canberra: Australian Bureau of Statistics, 1999. Australian Bureau of Statistics. Experimental estimates of the Aboriginal and Torres Strait Islander population. Canberra: Australian Bureau of Statistics, 1998. Stata version 6 [computer software]. College Station, TX: Stata Corporation, 1999. Schmidt B. Northern zone renal services plan 2000-2010, 2000. Devitt J, McMasters A. On the machine: Aboriginal stories about kidney troubles. Alice Springs: IAD Press, 1998. Devitt J, McMasters A. Living on medicine: a cultural study of end-stage renal disease among Aboriginal people. Alice Springs: IAD Press, 1998. (Received 13 Sep 2000, accepted 22 Mar 2001) Authors' details Menzies School of Health Research, Casuarina, NT. Alan Cass, GradDipClinEpi, FRACP, PhD Student and Nephrologist. Joan Cunningham, ScD, Epidemiologist and Menzies Fellow. Zhiqiang Wang, PhD, Biostatistician. Wendy Hoy, MB BS, FRACP, Head of Renal Unit. No reprints will be available from the authors. Correspondence: Dr Alan Cass, Menzies School of Health Research, PO Box 41096, Casuarina, NT, 0811. Make a comment Map numbers refer to Aboriginal and Torres Strait Islander Commission regions as specified in Box 2 Back to text 2: End-stage renal disease among Indigenous Australians from 1993 to 1998 ATSIC region (map references) Treatment facilities† Patients (number) Standardised incidence ratio* (95% CI) Tennant Creek (35) 30 31.05 (20.96 - 44.33) Kalgoorlie (27) S 23 27.75 (17.60 - 41.64) Aputula (33) 58 25.03 (19.01 - 32.36) Warburton (23) 20 22.77 (13.91 - 35.17) Ceduna (18) 10 22.48 (10.78 - 41.34) Jabiru (31) 45 21.87 (15.95 - 29.26) Geraldton (28) S 25 18.20 (11.78 - 26.86) Mount Isa (11) 33 17.74 (12.21 - 24.91) Kununurra (22) 22 16.85 (10.56 - 25.51) Katherine (32) 30 15.64 (10.56 - 22.33) Torres Strait (15) 28 14.99 (9.96 - 21.66) South Hedland (25) S 18 14.75 (8.74 - 23.30) Derby (26) 16 13.40 (7.66 - 21.76) Nhulunbuy (34) 21 11.74 (7.27 - 17.94) Cooktown (12) 21 11.61 (7.19 - 17.75) Broome (21) 11 11.47 (5.73 - 20.53) Port Augusta (19) S 17 10.45 (6.09 - 16.74) Bourke (2) S 21 10.16 (6.29 - 15.53) Townsville (16) T, S 35 9.41 (6.55 - 13.08) Cairns (10) T, S 35 8.71 (6.07 - 12.12) Alice Springs (30) T, S 11 8.55 (4.27 - 15.30) Narrogin (24) S 13 8.20 (4.37 - 14.02) Darwin (36) T, S 17 7.02 (4.09 - 11.24) Perth (20) Tx, T, S 29 6.70 (4.48 - 9.61) Adelaide (17) Tx, T, S 15 4.62 (2.58 - 7.61) Tamworth (5) T, S 12 4.18 (2.16 - 7.30) Roma (14) T, S 8 3.70 (1.60 - 7.28) Coffs Harbour (3) Tx, T, S 24 3.68 (2.36 - 5.47) Ballarat (8) Tx, T, S 10 3.42 (1.64 - 6.28) Wagga Wagga (6) T, S 14 2.98 (1.63 - 5.00) Brisbane (9) Tx, T, S 17 2.51 (1.46 - 4.02) Rockhampton (13) T, S 5 1.78 (0.58 - 4.16) Sydney (4) Tx, T, S 16 1.77 (1.01 - 2.88) Queanbeyan (1) T, S 4 1.75 (0.48 - 4.48) Wangaratta (7) Tx, T, S 4 1.39 (0.38 - 3.55) Hobart (29) T, S 0 0.00 (0.00 - 1.03) * Indirectly standardised to the rates for the total Australian resident population. †Tx = transplant service, T = tertiary renal unit, S = satellite dialysis unit. Geographical data were unobtainable for one patient. Back to text

Alan Cass · Joan Cunningham · Zhiqiang Wang · Wendy Hoy

Editorial Indigenous Australian children: educating for health Education and health outcomes for Indigenous Australians are inextricably linked MJA 2001; 174: 488-489 The conference "Learning lessons — approaching Indigenous health through education", held in Darwin in November 2000 under the auspices of the Australian Medical Association, called for pragmatic approaches to reversing deteriorating educational and health outcomes in Aboriginal children. The conference, and the Australian Medical Association,1 unanimously endorsed the 150 recommendations of the landmark review of Indigenous education in the Northern Territory (the Collins Report),2 but particularly emphasised that links between healthcare services and education be built early and maintained throughout a child's development. All levels of government and key Indigenous Australian health and education agencies must ensure that such links are established at the highest level and in the remote communities. Collins also identified practical strategies that need urgent implementation (Box 1). The conference also reignited the call for full implementation of the 1992 Council of Australian Governments Agreement.3 It decried the partial implementation of the Agreement, which endorsed national principles of equity and access to adequate and culturally appropriate service provision. Although there have been significant advances in our medical treatment of Indigenous Australian children, these have had minimal impact on the many conditions that undermine these children's access to learning and literacy. For example, for at least the past 25 years, four to five hundred Indigenous children from remote communities have been admitted annually to the infectious diseases ward at the Royal Darwin Hospital. Associated comorbidities4 included dehydration (50%), malnutrition (60%), hypokalaemia (70%), iron deficiency (90%), anaemia (25%), pneumonia (24%-32%), chronic suppurative otitis media (37%), urinary tract infection (10%), and scabies (25%), often secondarily infected. All too often, chest disease is associated with chronic suppurative lung disease or bronchiectasis.5 Treatable hearing deficiencies in the context of poor general health are the major health-related contributors to poor literacy among Indigenous children.6 Chronic suppurative otitis media (CSOM) affects children's learning ability through temporary and recurring hearing loss, permanent hearing impairment, and language disorders. The World Health Organization indicates that populations with rates of CSOM of greater than 4% have a health emergency. Rates of CSOM are as high as 50% in some Indigenous communities. The Northern Territory Strategic Results Project showed that 79% of children tested had a hearing disability.2 Equally distressing is the fact that educational outcomes for Indigenous Australian children are actually deteriorating.2 For example, in 1998, in the Northern Territory, 14% of Indigenous students progressed from Year 8 to Year 12, compared with 80% of non-Indigenous students. In 1998, 20% of Indigenous students achieved the national reading benchmark in the Northern Territory, compared with 78% of non-Indigenous students. Low educational attainment is also common to other urban and rural Indigenous communities. Failure to achieve literacy affects further ability to learn and to gain employment, and thus later health (see Box 2). International literature indicates that an additional year of education should reduce infant mortality by 7%-10%.7 Caldwell and Caldwell8 identify the importance of level of education on health in Third World countries, pointing to the relationship between increasing mother's education and decreasing child mortality. It appears that better-educated mothers are more likely to prevent accidents or sickness, prevent minor health problems from becoming major, and interact better with health services in obtaining the best outcomes. However, the particular problems of Indigenous Australians living in impoverished conditions within the First World are poorly understood.9 Trudgen outlines the sense of futility felt by Indigenous people who, after obtaining high school education and skills, find that these skills are inappropriate for the needs of their communities.10 Children with hearing problems are subjected to a dominant school culture that does not meet their cultural and language needs, and promotes a sense of failure and lowers self-esteem. This is the result of loss of control by Indigenous people, poor environmental circumstances, poor education, and a communication crisis between the dominant and Indigenous cultures.10 In order that Indigenous Australians regain control of their lives, their own solutions must be sought, heard, and acted upon as directly articulated, and not misinterpreted by policy and a particular economic agenda. We must bridge wide gaps in mutual understanding and develop partnerships between Indigenous Australians, governments, and health and education professionals.10 The major challenge is for the medical profession to acknowledge that health and education are key strategies in improving health outcomes for Indigenous Australians. Although there have been significant advances in our treatment of acutely sick Indigenous Australian children, we have failed to improve health and education outcomes. We have a responsibility, as do all Australians, to ensure that this iniquitous situation is not exacerbated further by the use of solutions that do not work for Indigenous communities. Only when we sit down and really listen — and hear — will we be able to work together to improve Aboriginal health and education. Paul A Bauert Paediatrician, Royal Darwin Hospital, Darwin, NT Ngiare J Brown Executive Officer Australian Indigenous Doctors Association, Sydney, NSW Bob Collins Consultant to the Northern Territory Government on Indigenous Education Darwin, NT Carmel M Martin Director of Health Services Australian Medical Association, Canberra, ACT Australian Medical Association. Position Statement on the links between health and education for Indigenous Australians. Canberra: AMA, 2001. Collins B. Learning lessons. An independent review of Indigenous education in the Northern Territory. Darwin: Northern Territory Department of Education, 1999. National commitment to improved outcomes in the delivery of programs and services for Aboriginal peoples and Torres Strait Islanders. Perth: Council of Australian Governments, 7 December 1992. Ruben AR, Walker A. Malnutrition among rural Aboriginal children in the Top End of the Northern Territory. Med J Aust 1995; 162: 400-403. Maxwell GM. Chronic chest disease in Australian aboriginal children. Arch Dis Child 1972; 47: 897-901. Leach AJ. Otitis media in Australian Aboriginal children: an overview. Int J Pediatr Otorhinolaryngol 1999; 49 Suppl 1: S173-S178. Acheson D. Independent inquiry into inequalities in health report, 1998. <http://www.official-documents.co.uk/document/doh/ih/part2b.htm> (September 1999). Caldwell JC, Caldwell P. The impact of education on health. Proceedings of the conference "Learning lessons -- approaching Indigenous health through education"; Darwin, November 2000. Darwin: Australian Medical Association, NT Branch, 2000. Gray A, Boughton B. Education and health behaviour of Indigenous Australians: evidence from the 1994 National Aboriginal and Torres Strait Islander Survey (NATSIS). Occasional Paper Series Issue No. 3. Casuarina, NT: Cooperative Research Centre for Aboriginal and Tropical Health, 2001. Trudgen RI. Why warriors lie down and die. Adelaide: Openbook Publishers, 2000. Make a comment 1: Key strategies for improving health through education Providing more maternal, baby and early-childhood care; Teacher education to identify and manage hearing and other health issues in classrooms; Accelerating the training of more Aboriginal health workers and providing them with greater support when trained; Improving access to specialist services and health education programs for Indigenous people; Encouraging community efforts to improve nutritional standards through education and community purchasing and cultivation initiatives; and Improving school-based health education. Back to text 2: Roles of education in influencing inequalities in health7 Educational qualifications are a determinant of an individual's labour market position, which in turn influences income, housing, and other material resources, and ultimately health. Education is a traditional route out of poverty for disadvantaged children. Education prepares children for life by ensuring they have the practical, social, and emotional knowledge and skills to achieve a full and healthy life — not just health-related behaviour, but skills in human relationships, dealing with conflict, and practical skills such as budgeting and cooking. Education prepares children to participate fully in society, aware of their democratic and human rights and responsibilities, able to use services, and work with an understanding of other groups in society. The role of the school as part of the local community is crucial. The education system should protect and promote the current health of children by providing an environment and culture which is safe, healthy, and conducive to learning. Back to text

Ngiare J Brown

Editorial How bright is their future? Post-streptococcal glomerulonephritis in Indigenous communities in Australia Streptococcal skin infection may have a major role in the epidemic of chronic renal disease among Indigenous Australians. MJA 2001; 174: 489-490 In 1836, Richard Bright, from Guy's Hospital, London, described the clinical entity of acute glomerulonephritis, later known as Bright's disease. However, it was not until 1907 that streptococci were suggested as a cause of acute glomerulonephritis. At that time, post-streptococcal glomerulonephritis (PSGN) was rife throughout the world, as it remains today in some developing countries. With increasing living standards, Australia has a very low overall incidence of streptococcal infection, but, in contrast, our Indigenous communities have one of the highest incidences in the world, and corresponding high incidences of PSGN and rheumatic heart disease.1-4In this issue of the Journal, White and colleagues highlight anew the problem of the health of our Indigenous communities and provide some ominous insight into the long-term sequelae of PSGN.5 It has been contentious whether PSGN is a relatively benign disease, as traditionally thought, or whether, as suggested 25 years ago, it may lead to progressive renal disease and eventually end-stage renal failure.6 The reported study of albuminuria and haematuria — the harbingers of progressive renal disease — in a remote Aboriginal community suggests that the latter is correct. The study found that people with a history of PSGN in childhood had a risk of overt albuminuria more than six times that in the control group. In fact, the data show that a quarter of cases of overt albuminuria in this population may be attributable to PSGN in childhood. This is alarming, particularly as the Aboriginal population has an incidence of end-stage renal failure 10 times greater than that of the non-Aboriginal population of Australia.1,7,8 It is even more distressing when we realise that streptococcal disease should theoretically be preventable. Proteinuria is increasingly recognised as the best overall indicator of progressive renal disease, whatever the cause. It would thus be very important to follow the study population, preferably over many more years, to determine whether renal damage does indeed progress and lead to end-stage renal failure. Other aspects of epidemic and endemic post-streptococcal infection could also be explored. It has been suggested that, because of the high rate of nephritis in families, a familial trait may be involved, increasing susceptibility to the disease.9 This may have some relevance to the PSGN epidemics in this population. There is no simple treatment for PSGN, and preventing streptococcal infection remains the most important control strategy.10 Penicillin is beneficial in preventing spread of infection during epidemics.2 No vaccine is as yet available. As concluded by White and colleagues, prevention of streptococcal infection through improved economic and living conditions, and particularly control of skin infections, is possible and should reduce the incidence of renal involvement. However, the real tragedy highlighted by this study is that, despite the passage of up to 20 years since these children were infected with streptococci, nothing much has changed to lower the rates of infection among Aboriginal children. Indeed, a very recent report demonstrated that skin infections still occur in up to 70% of Aboriginal children, with the major pathogens being group A streptococci.4 It is imperative that such important results are heeded. Not until fundamental changes take place in the social, economic and living conditions of our Indigenous communities will this streptococcal disease be eliminated, as it has been in all other areas of Australia. We have a bipartisan Federal Government committed to improving the health of Indigenous Australians and an office for Aboriginal and Torres Strait Islander Health in the Commonwealth Department of Health and Aged Care, which is providing a comprehensive funding strategy for Indigenous health issues. The head of the Northern Territory Peak Aboriginal Health Organisation, Pat Andersen, is on record as describing the Primary Health Care Access Programme, now under way, as the most exciting event in Aboriginal affairs since the 1967 referendum. Furthermore, recent studies have shown that Aboriginal people can participate enthusiastically and effectively in chronic disease management, with improvement in their renal disease.11 Thus, the challenge at this time of reconciliation is to restore social equity and health to Indigenous Australians.12 It is to be hoped that this will eliminate post-streptococcal disease in Aboriginal communities. The future should be bright. Robert C Atkins Professor of Medicine and Director of Nephrology Monash Medical Centre, Melbourne, VIC Gogna NK, Nossor V, Walker AC. Epidemic of acute poststreptococcal glomerulonephritis in Aboriginal communities. Med J Aust 1983; 1: 64-66. Streeton CL, Hanna JN, Messer RD, Merianos A. An epidemic of acute post-streptococcal glomerulonephritis among aboriginal children. J Paediatr Child Health 1995; 31: 245-248. Carapetis JR, Currie BJ. Preventing rheumatic heart disease in Australia. Med J Aust 1998; 168: 428-429. Currie BJ, Carapetis JR. Skin infections and infestations in Aboriginal communities in northern Australia. Australas J Dermatol 2000; 41: 139-143. White AV, Hoy WE, McCredie DA. Childhood poststreptococcal glomerulonephritis as a risk factor for chronic renal disease in later life. Med J Aust 2001; 174: 492-496. Baldwin DS. Poststreptococcal glomerulonephritis. A progressive disease? Am J Med 1977; 62: 1-11. Briganti E, McNeil J, Atkins RC, editors. The epidemiology of diseases of the kidney and urinary tract: an Australian perspective. Adelaide: Australian Kidney Foundation Report, 1999. Available at <www.med.monash.edu.au/Epidemiology/general_info/publications.html> Spencer JL, Silva DT, Snelling P, Hoy WE. An epidemic of renal failure among Australian Aboriginals. Med J Aust 1998; 168: 537-541. Rodriguez-Iturbe B. Epidemic poststreptococcal glomerulonephritis. Kidney Int 1984; 25: 129-136. Chadban SJ, Atkins RC. Post-infectious glomerulonephritis. In: Brady HR, Wilcox CS. Therapy in nephrology and hypertension. Philadelphia: WB Saunders, 1998: 115-124. Hoy WE, Baker PR, Kelly AM, Wang Z. Reducing premature death and renal failure in Australian Aboriginals. A community-based cardiovascular and renal protective program. Med J Aust 2000; 172: 473-478. Eades SJ. Reconciliation, social equity and Indigenous health [editorial]. Med J Aust 2000; 172: 468-469. Make a comment

Robert C Atkins

Indigenous Health Research Childhood post-streptococcal glomerulonephritis as a risk factor for chronic renal disease in later life Andrew V White, Wendy E Hoy and David A McCredie MJA 2001; 174: 492-496 For editorial comment, see Atkins Abstract - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Aboriginal health Abstract Objective: To test the hypothesis that post-streptococcal glomerulonephritis (PSGN) in childhood is a risk factor for chronic renal disease in later life. Design: Retrospective cohort study. Setting: A remote Aboriginal community in the "Top End" of the Northern Territory that experienced two epidemics of PSGN in 1980 and 1987, respectively. Participants: 472 people who were aged 2-15 years during either epidemic. They were categorised by clinical features recorded during the epidemics as having clinically defined PSGN (63), "abnormal urine" (haematuria or proteinuria; 86) or controls (323). Outcome measures: Urinary albumin to creatinine ratio (ACR), haematuria (by dipstick urinalysis), blood pressure, serum creatinine level, and calculated glomerular filtration rate (GFR) during community screening in 1992-1998. Results: Overt albuminuria (ACR > 34 mg/mmol) was present at follow-up in 13% of the PSGN group, 8% of the abnormal urine group, and 4% of the control group. The odds ratio (OR) for overt albuminuria in those with a history of PSGN compared with the control group, adjusted for age and sex, was 6.1 (95% CI, 2.2-16.9). Haematuria (> trace) was present in 21% of the PSGN group compared with 7% of the control group (adjusted OR, 3.7; 95% CI, 1.8-8.0). There were no significant differences between the groups in blood pressure, serum creatinine level or calculated GFR. Conclusion: In this population, a history of PSGN in childhood is a risk factor for albuminuria and haematuria in later life. Although unusual in the rest of Australia, post-streptococcal glomerulonephritis (PSGN) is still common in Aboriginal children living in remote communities, where group A streptococcal pyoderma is endemic.1 In these communities, chronic renal disease and end-stage renal failure also occur in adults at alarming rates.2-4PSGN is usually followed by clinical recovery over several days to weeks, and the long-term outlook has generally been regarded as excellent, with no increase in risk of urinary abnormalities or hypertension.5-7 However, some studies have suggested an increase in rates of chronic renal impairment after this illness.8,9 We aimed to test whether a history of PSGN in childhood is a risk factor for later renal dysfunction in Aboriginal Australians living in a remote community. The main outcome measure used, albumin to creatinine ratio, is a sensitive early marker of renal damage. It has been shown to provide a reliable estimate of 24-hour protein excretion and to predict the rate of decline of glomerular filtration rate and progression to end-stage renal failure in diabetic10 and non-diabetic11 nephropathy. Albuminuria has also been shown to mark early chronic renal disease in this population of Aboriginal Australians, and its progression predicts renal failure, as well as cardiovascular disease and mortality.12,13 Methods Study design This was a retrospective cohort study of children from an isolated Aboriginal coastal community in the "Top End" of the Northern Territory of Australia. The community experienced two epidemics of PSGN in 1980 and 1987, respectively, each lasting for three months.14,15 Children were followed up after these epidemics for a mean of 14.6 years (range, 6-18 years). The study was approved by the Joint Institutional Ethics Committee of the Royal Darwin Hospital and the Menzies School of Health Research, as well as a local community health board. Consent was obtained from each individual or guardian at the time of screening. Participants Participants were 472 people who lived in the community and were aged 2-15 years at the time of either epidemic and who participated in health screening examinations between 1992 and 1998. These 472 people represented 98% of the population of the community in the relevant age groups, according to 1996 census estimates.16 Baseline data During the epidemics, children in the community were screened systematically for oedema, hypertension, and urinary abnormalities on dipstick testing; results were recorded in individuals' medical records in the community. We used these data to categorise children by history during the epidemics: The PSGN group had documented oedema (facial swelling or dependent oedema) or hypertension (diastolic pressure ≥ 80 mmHg if aged 2-12 years and ≥ 85 mmHg if over 12, levels corresponding to the 90th percentile for each age range)17 plus haematuria greater than trace or proteinuria greater than trace on dipstick urinalysis. The "abnormal urine" group had haematuria greater than trace or proteinuria greater than trace, but no oedema or hypertension. The control group comprised children who had normal results on clinical examination and urinalysis (trace or less for blood and protein); children with no symptoms suggesting PSGN, but for whom urinalysis was either not performed or not recorded; and children with no entry in the medical record at the time of the epidemics. Children whose ages were in the range 2-15 years during both epidemics were categorised according to their most abnormal findings in either epidemic. Outcome measures Population health screening was undertaken in the community between 1992 and 1999.14 For people screened more than once, results from the latest screening were used. The albumin to creatinine ratio (ACR) was determined in a random urine sample and was categorised as normal (< 1.1 mg/mmol), suspicious (1.1-3.3 mg/mmol), microalbuminuria (3.4-33 mg/mmol), or overt albuminuria (≥ 34 mg/mmol). Glomerular filtration rate (GFR) was calculated using the formula of Cockroft and Gault.18 Dipstick urinalysis was also performed (Multistix 10SG, Bayer Diagnostics), and blood pressure and serum creatinine level were measured. Analysis Baseline characteristics of the groups were compared using Fisher's exact test for categorical variables and, as not all data followed a normal distribution, the non-parametric Kruskal-Wallis test for continuous variables. Logistic regression estimates were used to obtain adjusted proportions of the population with albuminuria. Odds ratios for the outcomes albuminuria and haematuria were obtained from logistic regression models that included the factors age, sex, birth weight and body mass index. Analyses were performed using Stata statistical software.19Results Baseline characteristics Of the 472 people included in the study, 259 were aged 2-15 years during the 1980 epidemic, and 331 during the 1987 epidemic (with 118 in the age group during both epidemics). Overall, 275 (58%) were male. Categorisation of participants Categorisation of participants according to history during the epidemics is shown in Box 1. Of the 63 children with clinically defined PSGN, all had haematuria and proteinuria, 61 (97%) had oedema and 28 (44%) had hypertension. Although evidence of preceding group A streptococcal infection was not required for classification in the PSGN group, serum antideoxyribonuclease B antibody titres were positive (≥ 1:480) in all 36 of the group in whom they were measured, and serum complement levels were consistent with PSGN (low C3 level) in 35 of the 39 in whom they were measured. Of the 86 participants in the abnormal urine group, 84 (98%) had haematuria, and 24 (28%) had proteinuria. Characteristics of participants at follow-up differed significantly between the groups, with the PSGN group being younger, and the abnormal urine group having a lower proportion of males (Box 2). The three control subgroups also differed at follow-up in median age (normal results subgroup, 26.9 years; no urinalysis subgroup, 17.5 years; and not recorded subgroup, 18.4 years; P = 0.001) and body mass index (normal results subgroup, 20.9 kg/m2; no urinalysis subgroup, 19.1 kg/m2; and not recorded subgroup, 19.8 kg/m2; P = 0.007). However, after adjustment for age and sex, there were no significant differences in height or weight. The control subgroups were combined for analysis. Outcomes On follow-up screening, 104 participants (22%) had albuminuria of any degree (micro- or overt; ACR ≥ 3.4 mg/mmol), 27 (6%) had overt albuminuria (ACR ≥ 34 mg/mmol), and 45 (10%) had haematuria (≥ trace), while 64 (14%) had haematuria or overt albuminuria. Albuminuria and haematuria were more prevalent in the groups with a history of clinical PSGN or abnormal urine during the PSGN epidemics than in the control group (Box 3). In the abnormal urine group, outcomes at follow-up were similar whether or not haematuria had occurred alone or in the presence of proteinuria during the epidemics. As the presence of albuminuria is significantly related to age in this community,14 and as albuminuria was more common in females than males (overt albuminuria occurred in 4% of males and 8% of females; P = 0.044), probabilities were adjusted for age and sex (Box 4). The adjusted probability of overt albuminuria at follow-up was 13.6% after PSGN (95% CI, 6.7%-25%), compared with 2.5% in controls (95% CI, 1.1%-4.8%). Odds ratios for albuminuria and haematuria at follow-up according to history during the epidemics are shown in Box 3. After adjustment for age and sex, the odds of overt albuminuria were more than six times greater after PSGN compared with the control group, while the odds of albuminuria of any degree were more than three times greater. The population-attributable fraction, or proportion of overt albuminuria in the study population that can be attributed to PSGN in childhood, was 24% (95% CI, 5%-40%). After adjustment for age and sex, the odds of haematuria were more than three times greater after PSGN compared with the control group, while the odds of either haematuria or overt albuminuria were five times greater. Only three individuals had both haematuria and overt albuminuria, two of whom had a history of PSGN. Birth weight was available for 429 participants (61 with PSGN, 77 with abnormal urine and 291 controls). Adding birth weight to the logistic regression model gave an odds ratio of 7.6 for overt albuminuria in the PSGN group using controls as the reference (95% CI, 2.5-22.5). Adding body mass index to the model did not significantly alter the odds ratios. There were no significant differences in blood pressure, serum creatinine level or calculated glomerular filtration rate between the groups. Discussion This study indicates that a history of PSGN in childhood is a risk factor for albuminuria and haematuria years later, and suggests that about a quarter of cases of overt albuminuria may be attributable to PSGN in childhood. The incidence of renal disease is high in this population of Aboriginal Australians,12 and other risk factors for renal disease are also common, including low birth weight, recurrent infectious diseases, diabetes and features of syndrome X.3,12,20,21 Possibly, it is the combination of insults that leads to high risk for later renal disease. A prospective cohort study would provide the best evidence. Results of other studies on the contribution of PSGN to chronic renal disease have varied, with some studies reporting no link. For example, two large follow-up studies after epidemic PSGN in Trinidad6,22,23 and Venezuela,7,24 respectively, reported low rates of long-term abnormalities, although the Venezuelan study found that 11.2% of participants had proteinuria of > 500 mg/24 h at 11-year follow-up. These studies had high losses to follow-up (31% and 82%, respectively), and neither had a control group nor assessed microalbuminuria. A cohort study after a PSGN epidemic in an American Indian community found no difference at 10-year follow-up between those who had had PSGN and those who had not in blood pressure, serum creatinine level, proteinuria or haematuria. However, urinary abnormalities were common, being present in 17% of the PSGN group and 13% of the control group.5 In contrast, other studies have reported, similarly to ours, clinically important abnormalities at long-term follow-up after PSGN. An uncontrolled study from north India found proteinuria (defined as more than trace levels on qualitative examination) in 13.8% of people two to 10 years after nephritis.25 Protein to creatinine ratios were > 20 mg/mmol in 9% of people recruited from a tertiary London hospital 14-22 years after sporadic childhood PSGN,26 while, in an Italian study, microalbuminuria or greater was present in 46% of 26 patients three to 24 years after PSGN but only 2.5% of 100 control participants.27 Other studies have found significantly lower renal functional reserve in people with a remote history of PSGN compared with control participants.28,29 Our study had the strengths of having a control group and a long follow-up, studying a large proportion of people in a single community and measuring albuminuria in the microalbuminuric range. Its limitations include possible misclassification of participants, as PSGN was diagnosed by clinical criteria. The abnormal urine group may have included people with subclinical PSGN, other renal disease, or isolated haematuria of no significance. However, this is unlikely to have biased results significantly, as the main findings concerned differences between the PSGN and control groups, which had more certain definitions. Nevertheless, some participants classified with PSGN may have had another cause for their renal disease. For example, one child was later diagnosed with mesangiocapillary glomerulonephritis after renal biopsy; she may have been predisposed to PSGN by pre-existing renal disease, may have had consecutive disease processes or may never have had PSGN. Lastly, control participants who were not seen during the epidemics may have had unrecognised PSGN. However, this would have decreased rather than exaggerated differences between the PSGN and control groups. Although some historical data were unavailable, fewer females than males were studied, and follow-up times varied; these factors were unlikely to have affected results. Because albuminuria precedes clinical signs of chronic renal disease, longer follow-up could be expected to show changes in blood pressure, serum creatinine levels and GFR. Other factors may be involved in the observed relationship between PSGN and albuminuria and the postulated relationship with chronic renal disease. Firstly, another underlying renal process may predispose both to PSGN on exposure to a nephritogenic streptococcus and to later albuminuria. Secondly, albuminuria may not have such adverse prognostic significance after PSGN as it does in other circumstances; our follow-up was not long enough to show progression to chronic renal disease. Thirdly, PSGN may increase risk of chronic renal disease only in combination with other insults. Renal disease is extremely common in this community, and, although our findings are likely to apply to similar populations, they may not be universally applicable. In summary, we have presented evidence that, in this community, a remote history of PSGN in childhood is a powerful risk factor for renal damage, as evidenced by increased ACR and haematuria. These findings are important as PSGN is still prevalent in children living in Aboriginal communities in Australia. Prevention of PSGN is possible through improvements to housing, economic and living conditions, along with attention to control and treatment of scabies and skin infections. Preventing PSGN may contribute to reducing the incidence of renal disease and renal failure in the future. Acknowledgements This study was supported by the National Health and Medical Research Council and the Australian Kidney Foundation. We acknowledge the support and participation of the Tiwi community and the staff of the health clinic at Nguiu. Health workers Jerome Kerinauia, Nellie Punguatji, Darren Fernando and Colleen Kantilla and project officers Eric and Elizabeth Tipiloura were key contributors to the field work. We thank Bev Hayhurst, who coordinated much of the screening program, and Zhiqiang Wang, who provided statistical advice. We also acknowledge Kate Walker's work in looking at earlier data. References Streeton CL, Hanna JN, Messer RD, Merianos A. An epidemic of acute post-streptococcal glomerulonephritis among Aboriginal children. J Paediatr Child Health 1995; 31: 245-248. Spencer JL, Silva DT, Snelling P, Hoy WE. An epidemic of renal failure among Australian Aboriginals. Med J Aust 1998; 168: 537-541. 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 [see comments]. Aust N Z J Public Health 1997; 21: 121-126. Cass A, Gillin AG, Horvath JS. End-stage renal disease in Aboriginals in New South Wales: a very different picture to the Northern Territory. Med J Aust 1999; 171: 407-410. Perlman L, Herdman R, Kleinman H, Vernier R. Poststreptococcal glomerulonephritis. A ten year follow up of an epidemic. JAMA 1965; 194: 63-70. Potter E, Lipschultz S, Abidh S, et al. Twelve- to seventeen-year follow up of patients with poststreptococcal acute glomerulonephritis in Trinidad. N Engl J Med 1982; 307: 725-729. Garcia R, Rubio L, Rodriguez-Iturbe B. Long-term prognosis of epidemic poststreptococcal glomerulonephritis in Maracaibo: follow-up studies 11-12 years after the acute episode. Clin Nephrol 1981; 15: 291-298. Baldwin DS, Gluck MC, Schacht RG, Gallo G. The long-term course of poststreptococcal glomerulonephritis. Ann Intern Med 1974; 80: 342-358. Schacht RG, Gallo GR, Gluck MC, et al. Irreversible disease following acute poststreptococcal glomerulonephritis in children. J Chronic Dis 1979; 32: 515-524. Rodby RA, Rohde RD, Sharon Z, et al. The urine protein to creatinine ratio as a predictor of 24-hour urine protein excretion in type 1 diabetic patients with nephropathy. The Collaborative Study Group. Am J Kidney Dis 1995; 26: 904-909. Ruggenenti P, Gaspari F, Perna A, Remuzzi G. Cross sectional longitudinal study of spot morning urine protein:creatinine ratio, 24 hour urine protein excretion rate, glomerular filtration rate, and end stage renal failure in chronic renal disease in patients without diabetes [published erratum appears in BMJ 1998; 317: 1491]. BMJ 1998; 316: 504-509. Hoy WE, Mathews JD, McCredie DA, et al. The multidimensional nature of renal disease: rates and associations of albuminuria in an Australian Aboriginal community. Kidney Int 1998; 54: 1296-1304. McDonald S, Wang Z, Hoy WE. Physical and biochemical predictors of death in an Australian Aboriginal cohort. Clin Exp Pharmacol Physiol 1999; 26: 618-621. Gogna NK, Nossar V, Walker AC. Epidemic of acute poststreptococcal glomerulonephritis in aboriginal communities. Med J Aust 1983; 1: 64-66. Devanesen D, Bernard E, Stokes M, et al. Lessons from an outbreak of glomerulonephritis in an aboriginal community. Annual report 1987-88, Menzies School of Health Research. Darwin: Menzies School of Health Research, 1988. Australian Bureau of Statistics. 1996 census of population and housing: Basic community profile. Canberra: ABS, 1996. (Catalogue no. 2020.0.) Report of the Second Task Force on Blood Pressure Control in Children 1987. Task Force on Blood Pressure Control in Children. National Heart, Lung, and Blood Institute, Bethesda, Maryland. Pediatrics 1987; 79: 1-25. Cockcroft DW, Gault MH. Prediction of creatinine clearance from serum creatinine. Nephron 1976; 16: 31-41. Stata Statistical Software [program]. Release 6.0. College Station, Texas: Stata Corporation, 2000. Hoy WE. Renal disease in Australian aboriginals [editorial]. Med J Aust 1996; 165: 126-127. Hoy WE, Rees M, Kile E, et al. A new dimension to the Barker hypothesis: low birthweight and susceptibility to renal disease. Kidney Int 1999; 56: 1072-1077. Potter E, Abidh S, Sharrett R, et al. Clinical healing two to six years after poststreptococcal glomerulonephritis in Trinidad. N Engl J Med 1978; 298: 767-772. Nissenson A, Mayon-White R, Potter E, et al. Continued absence of clinical renal disease seven to 12 years after poststreptococcal acute nephritis in Trinidad. Am J Med 1979; 67: 255-262. Rodriguez-Iturbe B, Garcia R, Rubio L. Epidemic glomerulonephritis in Maracaibo. Evidence for progression to chronicity. Clin Nephrol 1976; 5: 197-205. Singhal PC, Malik GH, Narayan G, et al. Prognosis of post-streptococcal glomerulonephritis: Chandigarh study. Ann Acad Med Singapore 1982; 11: 36-41. Clark G, White RH, Glasgow EF, et al. Poststreptococcal glomerulonephritis in children: clinicopathological correlations and long-term prognosis. Pediatr Nephrol 1988; 2: 381-388. Buzio C, Allegri L, Mutti A, et al. Significance of albuminuria in the follow-up of acute poststreptococcal glomerulonephritis. Clin Nephrol 1994; 41: 259-264. Rodriguez-Iturbe B, Herrera J, Garcia R. Response to acute protein load in kidney donors and in apparently normal postacute glomerulonephritis patients: evidence for glomerular hyperfiltration. Lancet 1985; 2: 461-464. Cleper R, Davidovitz M, Halevi R, Eisenstein B. Renal functional reserve after acute poststreptococcal glomerulonephritis. Pediatr Nephrol 1997; 11: 473-476. (Received 5 Jul 2000, accepted 7 Dec 2000) Authors' details Menzies School of Health Research, Darwin, NT. Andrew V White, FRACP, Research Student, Menzies School, and Flinders University NT Clinical School, Darwin NT; currently, Paediatrician, Remote Health, Alice Springs, NT. Wendy E Hoy, FRACP, Principal Research Fellow. Royal Children's Hospital, Melbourne, VIC. David A McCredie, MD, FRACP, Nephrologist. Reprints will not be available from the authors. Correspondence: Dr A V White, Remote Health Services, PO Box 721, Alice Springs, NT 0871. Andrew. WhiteATnt.gov.au Make a comment Back to text 2: Characteristics of participants at follow-up, by diagnostic category during post-streptococcal glomerulonephritis (PSGN) epidemics PSGN (n = 63) Abnormal Control (n = 86) Urine (n = 323) P % Male 65% 45% 60% 0.02* Median age in years (range) 18.1 (8-31) 23.4 (13-32) 19.0 (10-33) 0.001† Median BMI (kg/m2) (range) 18.8 (13-45) 20.0 (15-47) 19.8 (13-40) 0.221† BMI = body mass index. * Fisher's exact test. †Kruskal-Wallis test. Back to text 3: Outcomes on follow-up screening, by diagnostic category during post-streptococcal glomerulonephritis (PSGN) epidemics Outcome PSGN (n = 63) Abnormal urine (n = 86) Control (n = 323) ACR ≥ 34 mg/mmol Rate 13% 8% 4% Crude odds ratio (95% CI) 3.8 (1.5-9.8) 2.3 (0.88-6.0) 1 Adjusted* odds ratio (95% CI) 6.1 (2.2-16.9) 1.6 (0.6-4.2) 1 PAF (95% CI) 24% (5%-40%) 8% (-14% to 26%) ACR ≥ 3.4 mg/mmol Rate 32% 30% 18% Crude odds ratio (95% CI) 2.2 (1.2-4.0) 2.0 (1.2-3.4) 1 Adjusted* odds ratio (95% CI) 3.2 (1.7-6.2) 1.4 (0.8-2.6) 1 PAF (95% CI) 11% (4%-18%) 5% (-4% to 14%) Haematuria > trace Rate 21% 9% 7% Crude odds ratio (95% CI) 3.4 (1.6-7.2) 1.4 (0.6-3.1) 1 Adjusted* odds ratio (95% CI) 3.7 (1.8-8.0) 1.1 (0.4-2.6) 1 PAF (95% CI) 20% (5%-33%) 1% (-14% to 14%) Haematuria > trace or ACR ≥ 34 mg/mmol Rate 30% 16% 11% Crude odds ratio (95% CI) 3.6 (1.9-6.8) 1.6 (0.8-3.1) 1 Adjusted* odds ratio (95% CI) 4.6 (2.3-9.0) 1.2 (0.6-2.4) 1 PAF (95% CI) 19% (8%-29%) 3% (-9% to 13%) ACR = albumin to creatinine ratio. PAF = population-attributable fraction. * Adjusted for age and sex. Back to text Back to text

Andrew V White · Wendy E Hoy · David A McCredie

Medicine and the Community The impact of domestic violence on individuals Jill Astbury, Judy Atkinson, Janet E Duke, Patricia L Easteal Susan E Kurrle, Paul R Tait and Jane Turner MJA 2000; 173: 427-431 See Articles 1, 3 and 4 of this series Abstract - Children - Pregnant women - Elderly people - Indigenous people - People of non-English-speaking background - The need for change - References - Authors' details - - More articles on Aboriginal health Abstract There is extensive evidence of the adverse effects of domestic violence across all age groups and cultural backgrounds. The impact of domestic violence may be long-term, affecting emotional adjustment, physical health and subsequent relationships. Health professionals should be aware of the confounding effect of youth, age and cultural diversity on presentation. Shame and isolation militate against disclosure. Specific, sensitive questioning that incorporates awareness of cultural and social issues is essential to detect domestic violence and initiate appropriate assistance. If the idea of "home" implies physical and psychological safety and security as well as shelter, then a child, adult or older person affected by domestic violence experiences a hidden "homelessness".1 Domestic violence occurs across the lifespan2 and across most cultures. Women are at a disproportionately high risk of physical, sexual and psychological violence from an intimate person such as a partner or ex-partner.3 Many children, too, are likely to experience violence from someone they know or be witnesses to violence within their families.4 Domestic violence may be physical, sexual or psychological, but all three can be present. What is subjectively defined and identified as "domestic violence" by victims can be strongly mediated by cultural beliefs, values and previous experience of abuse and may not coincide with standard clinical or research definitions. Domestic violence is always characterised by the use of coercive control and psychological abuse.5,6 Victimisation is associated with alterations in the perception of the perpetrator, especially a belief in his or her omnipotence, and alterations in the victim's perception of self. Feelings of self-blame, shame and loss of self-esteem are extremely common. At the same time, psychological defenses used to cope with violence include denial of its existence and minimisation of its severity.7 Acts of contrition and intermittent kindness by the perpetrator can maintain the relationship and give false hope to the abused person that the violence will end. In addition to the common features of domestic violence, there are important aspects of domestic violence that are characteristic of specific groups in society, such as children, pregnant women, the elderly, Indigenous people, and people of non-English-speaking background. Here we examine some of the specific problems of each of these groups in more detail. Children Children can be at risk of experiencing and witnessing violence within the family or from those known to them.8 The perpetrator is usually in a caring role or a position of trust in relation to the child. Children can be the direct targets of physical violence or can get hurt when they try to protect another family member, often the mother, or try to stop their parents from fighting. It is becoming increasingly apparent that domestic violence results in a similar outcome for many children, whether they are direct victims or only witnesses of the violence. A number of authors have pointed to a clear link between domestic violence and child abuse, with one being a predictor of the other: it has been estimated that children living in domestic violence situations are up to 15 times more likely to be abused or neglected than children from non-violent homes.9-11 Behavioural and psychological consequences of childhood violence include poor school performance, bedwetting, aggression (particularly among males), temper tantrums, oppositional behaviour, self-blame, guilt for the violence between parents, isolation from peers, self-harming behaviour, running away, psychosomatic symptoms, stealing, over-eating, depression, sleep disturbances and excessive anxiety symptoms (see Box 1). Violence by a person in a position of trust impairs the child's ability to trust others and increases the risk of victimisation in later life.12 Recent research has shown that there are significant and possibly persistent neurobiological effects of trauma experienced in early childhood. Work by Perry and others13,14 has demonstrated the importance of critical periods of exposure to secure parenting: exposure to recurring traumatic experiences in early childhood places a child at much greater risk of long-term psychological, emotional and behavioural problems. The type of violence is not the primary factor determining long-term outcome. More important predictors are the duration of violence, its severity and frequency. The cumulative impact of exposure to multiple adverse experiences (eg, violence, psychological or sexual abuse, substance misuse) in childhood is predictive of adverse health outcomes in adult life. In a large US study it was found that exposure to four or more categories of adverse childhood experiences was associated with a 4-12-fold increased risk of alcoholism, drug abuse, depression and attempted suicide.15 Protective factors include a healthy relationship with a primary carer, good social support and positive subsequent life experiences.8,12 Pregnant women The number of unwanted or unplanned pregnancies and terminations is higher among women experiencing domestic violence.16,17 Pregnancy itself is a time of heightened risk and the abdomen is targeted more frequently and more severely in pregnant women.18,19 The Women's Safety Australia survey4 found that, of all the women who reported violence occurring at some time in their lives, 42% were pregnant at the time. Twenty per cent reported that violence occurred for the first time during the pregnancy, although the strongest predictor of violence occurring during pregnancy is a prior history of abuse.12 Furthermore, women abused during pregnancy are at even greater risk of violence in the postpartum period.19 Women experiencing violence during pregnancy often obtain minimal or late antenatal care.20 They are at increased risk of having poor weight gain, anaemia, infections, or preterm labour; of bearing a low birthweight infant; and experiencing postnatal depression.18,21-23 They are also more likely to engage in behaviours harmful to health, such as smoking, drinking excessive amounts of alcohol, and substance misuse.18,21-23 Elderly people Abuse of elderly people is the most recent form of familial violence to come to public attention but it remains a largely hidden problem. Most community-based studies have shown that similar proportions of older men and women are victimised (in contrast to the younger population, in which the number of women experiencing domestic violence is greater than the number of men).24 Close family members (the victim's spouse, adult child or other relative) constitute the majority of abusers and usually live with the victim.25 The reasons for elder abuse are often related to their dependence on others (due to physical or mental impairment, particularly dementia), psychopathology in the abuser, or a long history of family violence26 (see Box 2). Many instances of elder abuse are "victim-victim" situations in which abusers may themselves be worn-out carers. Physical consequences include the actual injuries inflicted (eg, bruising, lacerations, fractures, or burns) as well as the results of neglect, such as malnutrition, decubitus ulceration, and inappropriate use of medication. Older people who are frail may sustain major injuries from an apparently minor cause -- for instance, a shove leading to a fall may result in a fatal subdural haemorrhage. Abuse may also have psychological consequences: feelings commonly experienced are a sense of powerlessness, shame at having to admit that the abuse is occurring at the hands of close family members, fear of retaliation from the abuser, and particularly fear of institutionalisation if the abuse is reported. Such fears increase the victim's reluctance to report abuse,27 often causing a self-imposed isolation. Control by the abuser may be exercised financially through the improper use of an older person's property or finances or misuse of a power of attorney, or may take the form of neglect whereby the necessities of life (adequate food, clothing, medication, or other care) are withheld by a caregiver.28 Indigenous people Domestic violence in Indigenous families and communities in Australia is presently at a level for serious concern.29,30 In 1990, an Aboriginal and Torres Strait Islander Commission briefing document advised the Australian Aboriginal Affairs Council that "the increasing injuries and fatalities as a result of interpersonal violence have risen to levels which not only impair life but also threaten the continued existence of Australian Indigenous peoples".31 Physical assault is commonly associated with psychological abuse, and Indigenous victims of domestic violence (who are mainly women) may view themselves as being of little worth, incompetent, and deserving of abuse.32 The situation becomes more complex when racism and discrimination in social control structures are intertwined with domestic violence32 (see Box 3). Domestic violence in Indigenous communities can only be understood in the context of the historical, political, social and cultural environments in which it occurs.34 Colonisation has had a disastrous impact on the lives of Indigenous people: it has created complex and cumulative forms of traumatic stress that may be articulated as physical, emotional and spiritual distress; misuse of alcohol and other drugs; and violent behaviour arising from a rage that is directed towards the self and other close family members.35 With the breakdown of cultural lore, behaviours that were previously functional in conflict resolution processes have become unstructured and damaging when used under the influence of alcohol or other drugs.36 John Cawte, a psychiatrist and anthropologist, identifies Indigenous communities as suffering from "gross stress", a form of post-traumatic stress disorder in which individuals express their loss and bewilderment as emotional and behavioural disorders.37 Indigenous women are less likely than non-Indigenous women to report an assault, and less likely to seek medical help unless they have severe injuries.38 Historical interactions with police, who were used by the state to forcibly remove Indigenous children under government assimilation policies, and deaths of Indigenous people in custody continue to engender a deep mistrust of law enforcement officials.39 Indigenous women fear for their own safety40 and the safety of other family members if police or social welfare officials become involved. While some Indigenous women may call the police to intervene in violent situations, they are less likely than non-Indigenous women to want to lay charges, and there is a general belief that charging or incarcerating Indigenous men does not reduce male violence. Indigenous women are more likely to ask for other interventions in which their partner also receives help for his drinking and/or violent behaviour.32 People who have been traumatised through violence are more likely to be treated as if they are mentally ill or unstable than to be provided with programs that will meet their needs; however, recent program initiatives in Australia are beginning to respond to the specific and unique needs of Indigenous peoples.29 People of non-English-speaking background The extent of domestic violence experienced in Australia by people of non-English-speaking background has not been extensively studied. However, research suggests that overseas-born males are more likely to commit partner homicide than would be expected from their numbers in the general community.41 This may reflect a higher rate of domestic violence among overseas-born women. Alternatively, these women may be less likely to leave violent situations, and therefore experience escalating violence. For those who are migrants, the strain of migration may compound the problem. However, in most cases in which a couple migrated together, the abuse preceded migration.42 Once in Australia, however, the migrant family may undergo further stresses as traditional gender roles shift. This may encompass unemployment or downward shifts in employment status for men, and paid employment for women. Assimilation of the younger generation into the broader Australian culture may further erode traditional hierarchies based on age and sex. Women who may be at particular risk include Asian women sponsored by non-Asian men,43 and Middle Eastern women brought to Australia for arranged marriages to Middle Eastern men already residing here.42 Such women have not only left behind their family and supports, but have joined partners whose established community networks may not recognise their needs. In some instances, their partner's extended family may collude in the violence, overtly or indirectly, by not offering support.42 Disclosure of domestic violence towards women of non-English-speaking background is inhibited if they have poor command of English (Box 4). For some women, however, the issue is more fundamental -- their concept of sexual assault within marriage may be very different from current Australian values and norms.44 Over 70% of migrant women have minimal knowledge of the legal rights of victims of domestic violence,45 which further inhibits disclosure, and many know little about support services or refuges. Women from Middle Eastern and Latin American cultural backgrounds who experience domestic violence are often reluctant to contact police, in part because they have witnessed oppression or torture at the hands of police in their country of origin.42 Domestic violence often creates a feeling of shame. There may be considerable pressure for a woman to maintain a marriage, and she may fear being deported.46 She may feel the burden of providing financial support for family in her country of origin,47 and consider that their plight outweighs any consideration of personal needs. The erosion of self-esteem accompanying domestic violence is compounded if the woman is isolated by virtue of limited English and lack of family and friends in whom to confide. The adverse health effects are similar to those experienced by abused women in the broader Australian society, although they may be exacerbated by longer delay in disclosure. The need for change Each of the specific groups examined has characteristic issues related to their experience of domestic violence. Nevertheless, the need for change applies equally to all groups. Patients are reluctant to disclose violence if not asked,48 but sensitive questioning can legitimate and encourage disclosure. As the Council on Scientific Affairs of the American Medical Association has observed, knowledge of a history of abuse can provide "the starting point from which to disentangle a confusion of presenting complaints and symptoms".49 Clinical practice and medical education programs in Australia have been slow to respond to the large body of research confirming the harmful health effects of domestic violence. Failure by healthcare providers to detect and treat those affected by domestic violence exacerbates the harm done in several ways. Firstly, the complexity of violence-related negative health outcomes increases if abuse remains undetected. Secondly, the drain on healthcare resources increases as victims present repeatedly to primary and emergency healthcare providers. (Conversely, victims' uptake of preventive healthcare is considerably lower than average, and the role of violence in their "non-compliance" with preventive health behaviours can easily be missed.) Thirdly, non-detection ensures that treatments are necessarily directed at the symptoms rather than the cause.1 A thorough understanding of the multiple adverse health effects and high rate of physical and psychological comorbidity associated with domestic violence must be acquired by all healthcare professionals. Training is required in every aspect of treatment, including initial questioning, counselling and responding to those who do disclose violence, and providing appropriate assistance, including safety plans and advocacy on behalf of patients. A number of our medical colleges have begun this necessary task. In clinical care, the concept of meaningful assistance to patients with health needs associated with domestic violence deserves to be strongly promoted. References Burke T. Housing and poverty. In: Fincher R, Nieuwenhuysen J, editors. Australian poverty. Melbourne: Melbourne University Press, 1998: 165-184. Kleinschmidt KC. Elder abuse: a review. Ann Emerg Med 1997; 30: 463-472. Kessler RC, Sonnega A, Bromet E, et al. Posttraumatic stress disorder in the National Comorbidity Survey. Arch Gen Psychiatry 1995; 52: 1048-1060. Australian Bureau of Statistics. Women's safety, Australia, 1996. Canberra: ABS, 1996. Ratner P. The incidence of wife abuse and mental health status in abused wives in Edmonton, Alberta. Can J Public Health 1993; 84: 246-249. Campbell JC, Lewandowski LA. Mental and physical health effects of intimate partner violence on women and children. Psychiatr Clin North Am 1997; 20: 353-374. Martin J, Anderson J, Romans S, et al. Asking about child sexual abuse: methodological implications of a two-stage survey. Child Abuse Negl 1993; 17: 383-392. Anderson J, Martin J, Mullen P, et al. Prevalence of childhood sexual abuse experiences in a community sample of women. J Am Acad Child Adolesc Psychiatry 1993; 32: 911-919. McKay MM. The link between domestic violence and child abuse: assessment and treatment considerations. Child Welfare 1994; 73: 29-39. Bowker LH, Arbittel M, McFerran J. On the relationship between wife-beating and child abuse. In: Yllo K, Bograd M, editors. Feminist perspectives on wife abuse. Newbury Park, California, Sage Publications, 1988. Stacy W, Sharpe A. The family secret: domestic violence in America. Boston: Beacon Press, 1983. Resnick HS, Acierno R, Kilpatrick DG. Health impact of interpersonal violence. 2: Medical and mental health outcomes. Behav Med 1997; 23: 65-78. Hart S, Brassard M. A major threat to children's mental health: psychological maltreatment. Am Psychol 1987; 42: 160-165. Perry BD. Neurobiological sequelae of childhood trauma: post-traumatic stress disorders in children. In: Murburg M, editor. Catecholamine function in post-traumatic stress disorder: emerging concepts. Washington, DC: American Psychiatric Press, 1994. Felitti VJ, Anda RF, Nordenberg D, et al. Relationship of childhood abuse and household dysfunction to many of the leading causes of death in adults. Am J Prev Med 1998; 14: 245-258. Evins G, Chescheir N. Prevalence of domestic violence among women seeking abortion services. Women's Health Issues 1996; 6: 204-210. Glander SS, Moore ML, Michielutte R, Parsons LH. The prevalence of domestic violence among women seeking abortion. Obstet Gynecol 1998; 91: 1002-1006. Parker B, McFarlane J, Soeken K. Abuse during pregnancy: effects on maternal complications and birth weight in adult and teenage women. Obstet Gynecol 1994; 84: 323-328. Gielen AC, O'Campo P, Faden R, et al. Interpersonal conflict and physical violence during the childbearing year. Soc Sci Med 1994; 39: 781-787. Norton LB, Peipert JF, Zierler PH, et al. Battering in pregnancy: an assessment of two screening methods. Obstet Gynecol 1995; 85: 321-325. Adams-Hillard PJ. Physical abuse in pregnancy. Obstet Gynecol 1985; 66: 185-190. McFarlane J, Parker B, Soeken K, Bullock L. Assessing for abuse during pregnancy: severity and frequency of injuries and associated entry into prenatal care. JAMA 1992; 267: 3176-3178. Berenson AB, Wiemann CM, Wilkinson GS, et al. Perinatal morbidity associated with violence experienced by pregnant women. Am J Obstet Gynecol 1994; 170: 1760-1766. Kleinschmidt KC. Elder abuse: a review. Ann Emerg Med 1997; 30: 463-472. Kurrle S, Sadler P, Lockwood K, Cameron ID. Elder abuse: prevalence, intervention and outcomes in patients referred to four Aged Care Assessment Teams. Med J Aust 1997; 166: 119-122. Kurrle S, Sadler P, Cameron ID. Patterns of elder abuse. Med J Aust 1992; 157: 673-676. Kurrle S. Responding to elder abuse -- a follow-up study of interventions and outcomes. Aust J Ageing 1993; 12: 5-9. Kurrle S, Sadler P. Assessing and managing abuse of older people. Sydney: NSW Office on Ageing, 1994. Report of the Aboriginal and Torres Strait Islander Women's Task Force on Violence. Brisbane: Queensland Government, 1999: 91. Ferrante A, Morgan F, Indermaur D, Harding R. Measuring the extent of domestic violence. Sydney: Hawkins Press, 1996: 28-34. Aboriginal and Torres Strait Islander Women's Task Force on Violence Report Brisbane: Queensland Government, 1999: 3. Aboriginal and Torres Strait Islander Women's Task Force on Violence Report. Brisbane: Queensland Government, 1999: 45-81, 156-200. Lawrence D, editor. Future directions. Proceedings of the Future Directions Queensland Domestic Violence Conference. Yeppoon, Queensland, July 1995. Rockhampton, Central Queensland University, 1995: 235. Mow KE. Tjunpami: family violence in Indigenous Australia. A report and literature review for the Aboriginal and Torres Strait Islander Commission. Canberra: ATSIC, 1992. Aboriginal Coordinating Council. Submission to the Royal Commission into Aboriginal Deaths in Custody. Cairns: ACC, 1991. Atkinson J. Lifting the blankets -- the transgenerational effects of trauma in Indigenous Australia [PhD thesis]. Brisbane: Queensland University of Technology, 2000. Cawte J. Medicine is the law: studies of psychiatric anthropology of Aboriginal tribal societies. Honolulu: University Press of Hawaii, 1974: 193. Bolger A. Aboriginal women and violence. Darwin: Australian National University North Australia Research Unit, 1991. Payne S. Aboriginal women and the law. In: Cunneen C, editor. Aboriginal perspectives on criminal justice. Sydney: Institute of Criminology, University of Sydney Law School, 1992. Kiss J. A matter for regret. Australian Lawyer 1996; 31(2): 14. Easteal P. Killing the beloved: homicide between adult sexual intimates. Canberra: Australian Institute of Criminology, 1993: 47. Easteal P. Shattered dreams -- marital violence among the overseas-born in Australia. Melbourne: Bureau of Immigration and Multicultural Population Research, 1996. Elliott and Shanahan Research. Summary of background research for the development of a campaign against domestic violence, conducted for the Office of the Status of Women, Department of the Prime Minister and Cabinet. Canberra: 1988. Quarter way to equal. A report on barriers to access to legal services for migrant women. Sydney: Law Foundation of New South Wales, 1994. Public violence: a report of violence in Victoria. Melbourne: Victorian Community Council against Violence, 1992. Hansen D, Le Sueur M. Separating mothers and children: Australia's gendered immigration law and policy. Alternative Law Journal 1996; 21: 203-206. Lawton K. Needs of NESB women in women's refuges: a perspective from a remote rural area in the north west of Western Australia. BIR Bulletin 1992; 6: 30-33. Mazza D, Dennerstein L, Ryan V. Physical, sexual and emotional violence against women: a general practice-based prevalence study. Med J Aust 1996; 164: 14-17. American Medical Association, Council on Scientific Affairs. Violence against women: relevance for medical practitioners. JAMA 1992; 267: 3184-3189. Authors' details Key Centre for Women's Health in Society, University of Melbourne, Carlton, VIC. Jill Astbury, MEd, PhD, Associate Professor. Cooperative Research Centre for Rainforest Ecology and Management, Cairns, QLD. Judy Atkinson, PhD, Senior Research Officer, Aboriginal Liaison. Harley Medical Chambers, Fitzroy, VIC. Janet E Duke, FRANZCOG, FRCOG. Faculty of Law, Australian National University, Canberra, ACT. Patricia Easteal, PhD, Visiting Fellow. Rehabilitation and Aged Care Service, Hornsby Ku-ring-gai Hospital, Hornsby, NSW. Susan E Kurrle, MB BS, DipGerMed, Director and Senior Staff Specialist. Child Protection Unit, New Children's Hospital, Westmead, NSW. Paul R Tait, MB BS, FRACP, Head. Department of Psychiatry, Royal Brisbane Hospital, Herston, QLD. Jane Turner, MB BS, FRANZCP, Senior Lecturer. Reprints will not be available from the authors. Correspondence: Associate Professor J Astbury, Key Centre for Women's Health in Society, 720 Swanston Street, Carlton, VIC 3053. j.astburyATkcwh.unimelb.edu.au ©MJA 2000 Make a comment 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/> © 2000 Medical Journal of Australia. We appreciate your comments. 1: Illustrative case of domestic violence involving children Nine-week-old baby "Lee" was taken to the family's general practitioner by her mother, "Anna", who stated that Lee was waking throughout the night and hard to settle. The GP noted some old and new bruising on Lee's head and trunk and asked Anna about these. She stated that Lee had tipped out of a bassinet down some stairs and also tended to bruise easily. Concerned about the possibility of child abuse, the GP referred Lee to the local hospital emergency department and notified the Department of Community Services. Lee was found to have skull and rib fractures and a subdural haematoma. Coagulation studies were normal. Anna was depressed and tearful on presentation. She admitted to the social worker that on several occasions she had "lost it" with Lee and thrown her down into her cot. She said her husband was away for long hours at work and she felt isolated. She later disclosed a long history of verbal, physical and sexual assault by her husband. He was often short-tempered and verbally intimidating towards her and their two-year-old son (who was described as being "very scared" of his father). She had had postnatal depression following the delivery of her first child. It was later learned that Anna had grown up in a family where domestic violence had occurred regularly. Back to text 2: Illustrative case of domestic violence involving an elderly person "Mrs Jones" is an 84-year-old widow with moderate Alzheimer disease. Until recently, she had been living alone, and was managing quite well with assistance from community services and regular visits from her general practitioner. Then her daughter moved in with her, ostensibly to care for her. Her daughter cancelled all services and suggested to the GP that his regular visits were unnecessary. Three months later, one of Mrs Jones' neighbours contacted her GP. He was concerned that Mrs Jones appeared to have lost a lot of weight and was often seen in her backyard crying. The GP visited and was reluctantly admitted to the house by Mrs Jones' daughter. The GP noted that Mrs Jones had indeed lost weight, and she appeared unkempt and had facial bruising. Her mental state had markedly deteriorated. Arrangements were made for Mrs Jones to be admitted to hospital, where she was found to be malnourished, to have an untreated wrist fracture and to have bruising over her trunk and face. Back to text 3: Illustrative case of domestic violence involving Indigenous people "Eva" has been married for nearly 25 years and has been beaten many times and subjected to different forms of abuse by her husband. She has seven children, and prides herself on being a strong Aboriginal woman, a "survivor". She stays in the relationship because "all kids need a father". Calling the police has therefore never been an option when she is being assaulted. Nor would calling the police be of any help. They are already constantly involved in her life, and judge her as being "a bad mother", "a troublemaker" and "emotionally unstable". Her sons are all in trouble with the law for their public behaviour, which is often violent. They are either in jail or in juvenile detention centres, on remand or parole. On release from jail they go back into a family environment that provokes distress and anger. Her eldest son has just served his second jail term for assault, after stabbing a person who said something against his father. He unsuccessfully attempted suicide in jail. He grieves for the loss of relationship with his father and continually attempts to establish some nurturing communication. He says he wants to get married and have a happy life, but all his relationships with young women have ended because of his violence. His mother, whom he has seen bashed many times, is angry at the juvenile justice system, Corrective Services and other state agencies because they just lock her children up without helping them to stop their offending behaviours. She is more involved with her own day-to-day survival than being able to think through how she can help them "break their cycle".33 Back to text 4: Illustrative case of domestic violence involving a woman of non-English-speaking background presenting in general practice "Ruziye" is a Turkish migrant sponsored by her Turkish-Australian husband, to whom she has been married for 18 months. She presents to a general practitioner with a complaint of rectal bleeding and extreme pain. Her husband enters the surgery with her. Background Ruziye's file indicates that she has seen the doctor for vaginal bleeding on several prior occasions. Consultation GP: Mr Amir, I would prefer to see your wife alone. Husband: Her English is not good. I can do translating. GP: That's OK. I have learned to talk to patients from non-English-speaking backgrounds and require that the consultation takes place between Ruziye and myself. [Husband reluctantly leaves the office] GP: When did the bleeding and soreness begin? Ruziye: A few days ago. GP: How did it start? Ruziye: My husband he likes to, you know, that part of me. This is hard to say. Where I come from, we do not talk about these things. GP: I understand that it is not easy for you. To help you though I do need to have an understanding of what has happened. Ruziye: Yes, I see. He does push hard and it hurts. GP: Do you ask him to stop? Ruziye: I tried once but he said it is my duty as his wife. GP: Well, Ruziye, in Australia, it is actually not your duty. In fact, we have laws that say you can say "no" to your husband and if he still does it, he is breaking the law. Ruziye: I did not know this. But in my family, you have to stay married and I have nowhere to go anyway. GP: There is help for you, Ruziye. If you decide that he is hurting you and that you want to leave, I can give you a pamphlet that lists places and people that will help you. Ruziye: Thank you doctor. Ruziye returned to the doctor several times over the next year with similar problems. Each time, the doctor gently talked to her about marital rape and other types of violence. Back to text

Jill Astbury · Judy Atkinson · Janet E Duke · Patricia L Easteal · Susan E Kurrle · Paul R Tait · Jane Turner

Editorial Reconciliation, social equity and Indigenous health A call for symbolic and material change MJA 2000; 172: 468-469 The current state of health of Indigenous Australians is a cause for national shame, and has its roots in the wholesale exclusion of Indigenous people from Australian society since 1788. A comprehensive approach to improving the health of Aboriginals and Torres Strait Islanders involves understanding the close relationships between their social and economic status and their health. At some point in our growth as a nation there must be a commitment by all Australians to social and educational equity and economic prosperity for Indigenous Australians. Only then will there be significant improvements in the health of Indigenous Australians. There is a growing body of knowledge about the social determinants of health,1-3 and evidence that relates disease patterns to the organisation of society and the way society invests in its human capital. Evidence worldwide shows a clear relationship between poverty, deprivation, social exclusion and ill-health. Socioeconomic disadvantage in childhood, inadequate nutrition, poor education, unemployment, and psychosocial factors (such as lack of self-esteem and social support, often associated with addictive behaviours) are causative of ill-health, and this can occur with or without access to good-quality medical care.1-3 Recognition of Indigenous people's prior ownership of the land is central to their achieving social and economic equity in Australia A child raised in an affluent home is likely to succeed educationally, which in turn favours entry to more privileged sectors of the labour market, with financial security in old age. A child from a disadvantaged home is likely to achieve few educational qualifications, leave school at the minimum age, and enter the unskilled labour market, where pay is low, the work often hazardous, and old age means reliance on the welfare system. A number of longitudinal studies confirm these relationships and show that they result in higher morbidity and mortality for the more socially disadvantaged.1,2 There are biologically plausible links between social and economic disadvantage and health. If the biological stress response is activated too often and for too long, there are multiple health effects -- depression, increased susceptibility to infection, glucose intolerance leading to diabetes, and high blood pressure and accumulation of cholesterol in blood vessel walls leading to heart attack and stroke. A life-course perspective views a person's physiological status as a marker of their past social position. Thus, past social experiences become written into the body's physiology and pathology.1-3 The situation for Indigenous Australians is further exacerbated by racism and prejudice, which have marginalised them from various aspects of social and community life, with additional detrimental effects on health. What evidence is there that this relationship between health and social disadvantage has adversely affected Australia's Indigenous people? Life expectancy at birth, which is an overall measure of health status, is 56.9 years for Indigenous men and 61.7 years for Indigenous women, compared with 75.2 years and 81.1 years, respectively, for non-Indigenous men and women.4 In 1997, fewer than 31% of Indigenous students remained in Year 12, compared with over 72% of non-Indigenous students. In the 1996 Census, while Indigenous people made up only 2.1% of the Australian population, they accounted for 19% of the adult prison population,4,5 and 41% of the inmates of juvenile corrective institutions4 (and the proportion of young Indigenous people in detention has increased further since the introduction of the mandatory detention laws in Western Australia and the Northern Territory5). The unemployment rate for all Indigenous Australians is likely to increase from 39% to 47% by the year 2006.6 Indigenous households are more likely to be overcrowded, but, despite this, have a lower median weekly income. Similarly, other measures of social disadvantage also show an over-representation of Indigenous people. Understanding the social determinants of health and these disturbing figures and taking the Indigenous health debate to the next level has always been fraught with misconceptions. A common myth concerns the high levels of spending on Indigenous health, and this has been debunked in a recent report showing that, for all health services, recurrent expenditure on a per-person basis was only 8% higher for Indigenous compared with non-Indigenous people. Furthermore, Indigenous people benefit very little from Medicare and the Pharmaceutical Benefits Scheme, with drawing rates only 27% and 22%, respectively, of non-Indigenous levels.7 Another major myth is that Indigenous people do not want to help themselves. It is true that you cannot help people unless they want to help themselves, but, in relation to education, numerous reviews, inquiries and consultations in recent years have reported that, contrary to popular belief, Indigenous people do place a high priority on education: "They want for themselves and their children no less than is afforded other Australians. They expect that educational processes should lead them to acquire the knowledge and skills necessary to realise their individual potential, lead satisfying lives, and contribute actively to the community."6 The current approach to Indigenous health is exemplified by the Western Australian Indigenous Child Health Survey. This is a population survey of an estimated 3150 children, aged from 0 to 17 years, which aims to improve our understanding of the health and educational needs of Indigenous children. The results will be used to develop a planned approach to the desired improvements in this area. For example, the initial WA Child Health Survey resulted in an improved range of State and national programs. These programs placed an emphasis on early intervention and prevention in child and adolescent mental health services, parenting strategies and programs, school programs for students at educational risk and promotion of mental health in schools. These data are also required for Australia to meet its obligations to the United Nations to report on the health status of Indigenous children. At a national level one of the most significant recent developments has been the establishment of the Office for Aboriginal and Torres Strait Islander Health Services in the Commonwealth Department of Health. Since it was established in 1995, there has been a more comprehensive planning and funding strategy targeting Indigenous health issues, with improved focus on primary healthcare and Aboriginal community involvement in healthcare delivery. While these efforts in health and education are encouraging, they do not address the prevailing attitudes in Australian society which marginalise and disempower Indigenous people. T S Eliot wrote: "We shall not cease from exploration And the end of all our exploring Will be to arrive where we started And know the place for the first time."8 Since arriving in Australia, the non-Indigenous population have wanted to believe that this was a "Terra Nullius", an uninhabited land that they could possess and use to their advantage without recognising the rights of the Indigenous peoples.9 Non-Indigenous Australians might gain a better understanding of Australia when they fully appreciate the inherent truth in Indigenous people's claims to land, justice and livelihood in this nation. Recognition of Indigenous people's prior ownership of the land is central to their achieving social and economic equity in Australia. In March 1999 the United Nations Committee on the Elimination of Racial Discrimination found that the Federal Government's 1998 amendments to the Native Title Act 1993 are in breach of Australia's obligations under the Convention on the Elimination of All Forms of Racial Discrimination. It is argued that these amendments fail to respect the cultural identity of Indigenous people and fail to promote the preservation of their culture, as required by the United Nations.10 The Council for Aboriginal Reconciliation continues working to achieve its vision of "A united Australia which respects this land of ours; values the Aboriginal and Torres Strait Islander heritage; and provides justice and equity for all."11 The cause of reconciliation has been furthered in recent years by improved spending on health services and health programs, particularly by the Commonwealth Government. These efforts need to continue and to become more appropriate and focused. The major challenges of the future centre on the reconciliation process, and the willingness of all Australians to take the actions that bring symbolic and material change. Facing these challenges with integrity and courage will benefit Australia's Indigenous people and the nation as a whole. Sandra J Eades Indigenous Health Research Unit, Population Sciences Division TVW Telethon Institute for Child Health Research Derbarl Yerrigan Health Service; and Department of Paediatrics University of Western Australia, Perth, WA sandyATichr.uwa.edu.au Marmot M, Wilkinson RG, editors. Social determinants of health. New York: Oxford University Press, 1999. Keating DP, Hertzman C, editors. Developmental health and the wealth of nations: social, biological and educational dynamics. New York: The Guildford Press, 1999: 25-35. The relationship between fetal malnutrition and chronic diseases in later life [editorial]. BMJ 1997; 315: 825-826. Australian Bureau of Statistics. Health and welfare of Australia's Aboriginal and Torres Strait Islander peoples. Canberra: ABS, 1999. (Catalogue No. 4704.0.) Human Rights and Equal Opportunity Commission. Mandatory detention laws in Australia. <http://www.hreoc.gov.au/human_rights/child_rights/h5_1_7.htm> (Accessed 19 April 2000). Commonwealth Department of Education, Training and Youth Affairs. Indigenous school to work transitions, 1998. <http://www.detya.gov.au/publications/schooltowork/default.htm> (Accessed 19 April 2000). Commonwealth Department of Health and Family Services. Expenditure on Health Services for Aboriginal and Torres Strait Islander People. Canberra: DHFS, 1998. Four Quartets: Little Gidding: V, lines 26-29. The complete poems and plays of TS Eliot. London: Faber & Faber, 1969: 197. Reynolds H. Why weren't we told? A personal search for the truth about our history. Ringwood: Penguin books, 1999. Human Rights and Equal Opportunity Commission. Submission to the United Nations Committee on the Elimination of Racial Discrimination: Response to the request for information in relation to Decision 1(53) concerning Australia 1998. <http://www.hreoc.gov.au/social_justice/native_title/index.html> (Accessed 19 April 2000). Council for Aboriginal Reconciliation. <http://www.austlii.edu.au/au/orgs/ car/index.htm> (Accessed 19 April 2000). Make a comment

Sandra J Eades

Indigenous Health Research Reducing premature death and renal failure in Australian Aboriginals A community-based cardiovascular and renal protective program Wendy E Hoy, Philip R Baker, Angela M Kelly and Zhiqiang Wang MJA 2000; 172: 473-478 Abstract - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Aboriginal health Abstract Objective: To describe results of a systematic treatment program to modify renal and cardiovascular disease in an Aboriginal community whose rates of renal failure and cardiovascular deaths are among the highest in Australia. Design: Longitudinal survey of people during treatment, and comparison of rates of natural death and renal failure with those in a historical control group. Setting: Tiwi Islands (population, about 1800), November 1995 to December 1998. Participants: All adults with blood pressure ≥ 140/90, with diabetes and urinary albumin/creatinine ratio (ACR) ≥ 3.4 g/mol (microalbuminuria threshold), or with progressive overt albuminuria (ACR ≥ 34 g/mol) were eligible for treatment. The historical control group comprised 229 people who satisfied these criteria in the pretreatment period 1992-1995. Interventions: Perindopril, combined with calcium-channel blockers and diuretics if needed to achieve blood pressure goals; attempts to improve control of blood glucose and lipid levels; health education. Main outcome measures: Blood pressure, ACR, serum creatinine level and glomerular filtration rate (GFR) over two years of treatment; rates of renal failure and natural death compared with control group (analysed on intention-to-treat basis). Results: 258 people enrolled in the program, and 118 had complete data for two years of treatment. In these 118, blood pressures fell significantly, while ACR and GFR stabilised. Rates of the combined endpoints of renal failure and natural death per 100 person-years were 2.9 for the treatment group (95% CI, 1.7-4.6) and 4.8 for the control group (95% CI, 3.3-7.0). After adjustment for baseline ACR category, the relative risk of the treatment group versus the control group for these combined endpoints was 0.47 (95% CI, 0.25-0.86; P = 0.013). Treatment benefit was especially marked in people with overt albuminuria or hypertension and in non-diabetic people. The estimates of benefit were supported by a fall in community rates of death and renal failure. Conclusions: Aboriginal people can participate enthusiastically in chronic disease management, with rapid, dramatic improvement in clinical profiles and mortality. Similar programs should be introduced urgently into other Aboriginal communities nationwide. Aboriginal people in the Northern Territory are experiencing an epidemic of cardiovascular disease (CVD) and end-stage renal disease (ESRD). Age-standardised CVD death rates are three times those of non-Aboriginal people,1 while the incidence of treated ESRD in Aboriginal people is approaching 1000 per million, and doubling every four years.2 ESRD treatment costs, at $100 000 per person annually, are becoming a huge burden,3 but premature death is the greater human catastrophe. These problems are especially serious in the communities of the Tiwi Islands, north of Darwin (population, about 1800) (Box 1). The incidence of ESRD among Tiwi people recently reached 2700 per million, and they have one of the highest CVD mortality rates in Australia.2,4In a community-wide screening program starting in the early 1990s, we found a high prevalence of cardiovascular risk factors, including type 2 diabetes and hypertension, and albuminuria (measured by the albumin/creatinine ratio (ACR) of a random urine specimen).5 Albuminuria correlated inversely with glomerular filtration rate (GFR), and its intensity predicted not only renal failure, but also cardiovascular deaths and all-cause natural deaths.6-9 In the early 1990s, use of antihypertensive drugs was increasing gradually in the Tiwi communities, but systematic management of the huge burden of morbidity identified by the screening program was beyond the capacity of the existing health services. In November 1995, we therefore introduced a systematic treatment program to reduce blood pressure and to modify the expression and progression of renal and cardiovascular disease. We describe the results of this program to the end of 1998. Methods The study was a longitudinal survey of people in the Tiwi Islands communities during treatment, and comparison of endpoints with a historical control group. Treatment was offered to eligible people as part of improved standard care. All participants gave informed consent to have their course followed up for the projects The epidemiology and prevention of Aboriginal renal disease, Parts 1 and 2. These projects were approved by the Joint Institutional Ethics Committee of the Menzies School of Health Research and Territory Health Services, Darwin, and its Aboriginal subcommittee, and by the Tiwi Land Council (Part 1) and the Tiwi Health Board (Part 2). Treatment program The program relied considerably on screening and treatment algorithms. Interventions included education about diet, exercise, health behaviours and medical treatment. Medical treatment centred around use of a long-acting angiotensin-converting enzyme inhibitor (ACEi) (perindopril; Coversyl [Servier]), aggressive blood pressure control,10,11 and, where appropriate, oral hypoglycaemic and lipid-lowering drugs. The choice of an ACEi was based on the well recognised antihypertensive and cardiovascular-protective effects of this class of drug12 and several reports, subsequently substantiated, of an additional renal protective effect.13-23 If antihypertensive drugs had been prescribed before entry into the study, they were discontinued or tapered when perindopril was started. Objectives were to achieve a minimum daily dose of 4 mg perindopril and to lower blood pressure, initially to < 130/85, but more recently to < 120/75.10 A stepped approach to achieve these blood pressures included increasing perindopril to 8 mg, with addition of long-acting calcium-channel blockers and/or diuretics if needed. Participants were seen at least monthly while medications were introduced or changed, then at least every three months for the first year, and at least every six months thereafter. Each examination included a minimum of a brief history, medication review, and measurement of weight, blood pressure, urinary ACR and serum creatinine level and, in diabetics, evaluation of blood glucose control. After a start-up period, the day-to-day program was largely conducted by local health workers and community project officers, who were supported by telephone contacts and regular visits by nurse coordinators from Darwin. Doctors, who reviewed eligibility assessments, supported or made treatment decisions and modified the protocols, were less intensively involved. The program has run in parallel with other clinic activities in Nguiu, Bathurst Island, but has been integrated into regular clinic activities at the Melville Island communities of Milikapiti and Pirlangimpi. Participants Treatment group: People eligible for ACEi therapy were those with: hypertension (blood pressure ≥ 140/90 mmHg); diabetes and ACR ≥ 3.4 g/mol (microalbuminuria threshold), regardless of blood pressure; or progressive overt albuminuria (ACR ≥ 34 g/mol on first testing and increasing over time), regardless of blood pressure or diabetes status. All qualifying features needed to be confirmed on at least two occasions. People with past adverse reactions and breastfeeding women were ineligible for ACEi therapy. Fertile women were advised about teratogenic risks and the options of contraception or discontinuation of ACEi medication early in unplanned pregnancy. People with serum creatinine levels over 250 µmol/L were considered ineligible for long-acting ACEi therapy in the first six months of the program, but were later enrolled when treatment proved safe and effective in people with mild and moderate renal insufficiency. To some extent, enrolment was prioritised by disease severity. Thus, most people with overt albuminuria, uncontrolled blood pressure and renal insufficiency were enrolled in the first year of the program. Control group: In the absence of a parallel control group, rates of renal failure and natural death in participants were compared with those of a historical control group from the pre-program period. This control group comprised adults whose results on a single screening examination between July 1992 and September 1995 met the eligibility criteria later used for the treatment program. Selection was blinded to their future course, which was followed to 30 October 1995. Data analyses Analyses were performed using STATA statistical software.24 Clinical profiles in the treatment group were described at baseline, six, 12, and 24 months of treatment, regardless of compliance, and were compared by analysis of variance, using geometric means for ACR and serum creatinine level to normalise their distribution. All endpoint data in the treatment group were analysed on an intention-to-treat basis. Rates of natural death and renal failure were calculated by baseline ACR category for the intention-to-treat and control groups, and the risk ratios for the intention-to-treat group calculated in stratified analysis by ACR category by the Mantel-Haenszel method for cohort studies. Kaplan-Meier survival curves for both groups were derived, and survivals compared by the non-parametric Wilcoxon technique. Results Enrolment By 31 December 1998, 258 people had enrolled in the program (29% of all adults in the island communities) and 227 were still participating. Of these, 39 had completed over three years of treatment, 137 over two years, 168 over one year, and 192 over six months. Of 31 dropouts, nine had died, seven had begun dialysis (two of whom later died), seven had stopped taking the medication because of side effects (cough in four; angioedema, itching and dizziness in one each), four became normotensive without treatment, two chose to quit, one moved, and one entered palliative care with osteomyelitis of the skull. Characteristics of people who enrolled are shown in Box 2: 42% had diabetes, almost two-thirds had hypertension, with a quarter already prescribed enalapril, and almost two-thirds had overt albuminuria. Medications and participation Doses of perindopril prescribed for the 227 people participating at the end of 1998 were 2 mg (5 people; 2%), 4 mg (72; 32%), and 8 mg (150; 66%). Calcium-channel blockers were being taken by 37 people (16%), diuretics by 15 (7%), and both by 13 (6%). Participation was enthusiastic, and compliance increased over time; 65% were taking ≥ 70% of their prescribed dose (assessed by pill counts and interview), 27% were taking medicine occasionally, and 7% were taking little or no medication at the end of 1998. Two-year clinical profiles Of the 137 people who had been treated for at least two years, 118 had largely complete follow-up data and were included in the two-year profile. These 118 were well matched with participants not included in this profile for age, BMI, and blood pressure, but were more likely to have diabetes, overt albuminuria, and to have been taking prior ACEi therapy (Box 2). These differences reflected prioritisation of sicker people for early entry into the program. Two-year clinical profiles for the 118 people are shown in Box 3. Treatment was associated with a swift and sustained fall in blood pressure, as well as stabilisation of ACR and GFR. Results are presented according to participants' clinical categories at baseline in Box 4. The fall in blood pressure was marked in people with hypertension at baseline and less marked but still apparent in those who had been normotensive, as well as in those previously prescribed an ACEi. Good blood pressure responses were seen in people both with and without diabetes, those with micro- and overt albuminuria and those with "normal" and raised levels of serum creatinine. Stabilisation of ACR and GFR was seen in all clinical categories. Indeed, serum creatinine level tended to fall and GFR to rise in all categories. Baseline weight did not change (mean, 74 kg; SD, 16 kg), while mean serum potassium level rose non-significantly from 4.04 mmol/L (SD, 0.46 mmol/L) to 4.14 mmol/L (SD, 0.49 mmol/L). No one developed significant hyperkalaemia. There was no evidence that ACEi therapy accelerated progression to renal insufficiency. Comparisons with control group Two hundred and twenty-nine people qualified as controls from the pre-program period, comprising 123 people who subsequently went onto the treatment program and 106 people who did not. Reasons for not going onto the program included death, dialysis, failure to qualify on subsequent examinations, presence of exclusion criteria (eg, pregnancy, breastfeeding), declining treatment, or moving. Baseline characteristics of the control and intention-to-treat groups are compared in Box 2. The control group was younger at enrolment, had lower BMI, and included fewer people with diabetes or overt albuminuria. The control group was followed up for a total of 564 years (individual mean, 2.5 years; range, 1 month to 3.3 years) and the intention-to-treat group for 560 years (individual mean, 2.2 years; range, 2 weeks to 3.1 years). Endpoints of the two groups are compared in Box 5. The treatment group as a whole had lower rates of dialysis, natural death and the combined endpoint (dialysis or death) than the control group, although the differences were not significant. However, rates of endpoints were strongly correlated with baseline ACR category. Indeed, renal failure necessitating dialysis was confined to people with ACR ≥ 100 g/mol at baseline, and in these people the treatment group had an estimated 57% lower dialysis rate than the control group. In contrast, rates of natural death and of the combined endpoint were lower in the treatment group than in the control group for all categories of baseline overt albuminuria. After adjustment for ACR category, the treatment group had an estimated 45% lower rate of natural death and an estimated 53% lower rate of the combined endpoint. Box 6 shows estimates of the survival advantage in people with various baseline clinical profiles after adjustment for ACR category. Treatment benefit was strong in people with overt albuminuria, non-diabetic people and people with hypertension. It was less marked in diabetic or normotensive people. Survival estimates for people with overt albuminuria at baseline are shown in Box 7. Although the intention-to-treat group showed attrition during the first year (representing ESRD and deaths of seriously ill people prioritised for early entry), a survival advantage over the control group was clear by two years of the treatment program. Discussion This study found that the introduction of a systematic treatment program to the Tiwi Island communities was associated with marked improvements in blood pressure and stabilisation of renal function in people receiving treatment. These changes contrasted sharply with the increase in blood pressure and ACR and fall in GFR noted previously in people matched for ACR category in the pretreatment status quo.10 The treatment program was also associated with a swift and dramatic decrease in rates of renal failure and natural death in the treated group compared with a historical control group, suggesting that the program prevented or at least delayed these outcomes. Further evidence for the existence of this estimated survival benefit was the decrease in community-wide rates of ESRD and natural death -- previously increasing -- after introduction of the program (Box 8). In contrast, ESRD continued to increase among non-Tiwi Aboriginal people in the Top End (Box 9), arguing against a chance background effect. Preliminary estimates of cost effectiveness of the program, based solely on avoidance or delay of dialysis, are already startling.3,25 These results show that Aboriginal people are interested in health issues and receptive to health messages, and will take medications over the long term to protect against future health risk, with excellent response. They also show that a systematic approach, with testing and treatment algorithms and clear goals, is superior to the previous approach of gradually improving medical management. While we cannot apportion relative benefit to individual elements of the treatment program, the observed fall in blood pressures alone would be expected to markedly reduce cardiovascular deaths and progression of renal disease,10,11 compatible with the effects we found. Our intention-to-treat analyses probably underestimate the therapeutic efficacy of treatment, as a third of the intention-to-treat group took the prescribed medications only occasionally or not at all. Use of the historical control group was also a potential source of bias. On the one hand, it may have also led to underestimates of treatment benefit because of the group's potentially better survival prospects, based on its younger mean age, milder disease and the probable inclusion of people with borderline blood pressure or ACR readings, as eligibility for the group was not confirmed by a second examination. On the other hand, the 123 controls who subsequently entered the treatment program might have had superior survival characteristics to the controls who did not enter the program, potentially inflating the apparent benefit of the program. Another source of bias was the prioritisation of the sickest people for early enrolment in the treatment program, many of whom were failing previous management regimens. This predisposes to poor short term outcomes of the program and underestimates of its benefits. Analyses of program results at four and five years, when more people have passed through one to two years of treatment, will dilute the impact of these early events. Longer-term analyses will also be needed to evaluate any survival effect of treatment in people without overt albuminuria, and the extent to which treatment has delayed rather than prevented ESRD and death in people with overt albuminuria. The program could still be improved. Blood pressure control should be better; at two-year follow-up, 31% of people had blood pressures ≥ 140/90, and 50% had blood pressures ≥ 120/75.10 Hypertension, and therefore eligibility for treatment even in the absence of albuminuria, should probably be redefined as blood pressures ≥ 130/80 in this high-risk population.10 Control of blood glucose and lipid levels needs to improve. Finally, we might reassess the notions of the maximally renal-protective dose of ACEi and/or add other renal-protective drugs, such as angiotensin II receptor blocking agents,26,27 for poor responders. Much of the success of this particular program derives from a strong sense of community ownership and control, a non-judgemental, non-authoritarian style, and respect for competing personal and community perspectives and priorities. Individuals appreciate personalisation of their health goals, and many are slowly adopting lifestyle changes. This program is now being integrated into normal clinic activities at Nguiu. Its protocols have also been incorporated into standard care guidelines for Aboriginal adults in the Top End of the NT.28 Extension of its principles to other Aboriginal communities with high burdens of disease nationwide is a matter of urgency.29 Allocation of adequate resources is a challenge, but the clinical benefit and cost-effectiveness mandate the short- and intermediate-term investment. Acknowledgements This study was supported by Servier Australia, the Australian Kidney Foundation, Rio Tinto, the National Health and Medical Research Council, the Stanley Tipiloura Fund, and Territory Health Services. We gratefully acknowledge the support, enthusiasm and participation of the Tiwi community and the staff of the Tiwi Island clinics at Nguiu, Milikapiti and Pirlangimpi. We especially thank the Tiwi Health Board for review of this manuscript, and Treatment Program Coordinators Susan Jacups and Kiernan McKendry, Aboriginal Health Workers Jerome Kerinauia and Nellie Punguatji, and Community Project Officers Eric Tipiloura and Elizabeth Tipiloura for their dedicated work. Finally, we thank Resident Medical Officer, Dr Chris Harrison, for his support and participation. Dr Alan Cass updated the Top End ESRD rates. References Cunningham J, Condon J. Premature mortality in Aboriginal adults in the Northern Territory. Med J Aust 1996; 165: 309-312. Spencer JS, Silva D, Hoy WE. An epidemic of renal failure among Australian Aborigines. Med J Aust 1998; 168: 537-541. You J, Hoy W, Beaver C, Zhao Y. Costs of hemodialysis and hospitalisations for patients with end stage renal disease in the Top End of the Northern Territory. Presented at the 35th Annual Scientific Meeting of the Australian and New Zealand Society of Nephrology; 1999 Mar 3-5; Brisbane (Qld). Jain SK, editor. Trends in mortality by causes of death in Australia, the States and Territories during 1971-1992, and in statistical subdivisions during 1991-1992. Canberra: National Center for Epidemiology and Population Health and Australian Bureau of Statistics, 1994. (ABS catalogue no. 3313.0)Hoy WE, Pugsley DJ, Normal RJ, Hayhurst BG. A brief heath 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. Hoy WE, Mathews JD, Pugsley DJ, et al. The multidimensional nature of renal disease: rates and associations of albuminuria in a high risk Aboriginal community. Kidney Int 1998; 54: 1296-1304. Cockcroft D, Gault MK. Prediction of creatinine clearance from serum creatinine. Nephron 1976; 16: 31-41. Hoy WE, Wang Z, Baker P, et al. The natural history of renal disease in an Australian Aboriginal community. Presented at the 35th Annual Scientific Meeting of the Australian and New Zealand Society of Nephrology; 1999 Mar 3-5; Brisbane (Qld). McDonald S, Wang Z, Hoy WE. Physical and biochemical predictors of death in an Australian Aboriginal cohort. Clin Exp Pharmacol Physiol 1999; 26: 618-621. The Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure (JNC VI). Arch Intern Med 1997; 157: 2413-2446. Collins R, Peto R, MacMahon S. Blood pressure, stroke and coronary artery disease. Part 2. Short term reductions in blood pressure: overview of randomised drug trials in their epidemiological context. Lancet 1990; 335: 827-838. Lonn EM, Yusuf S, Jha P. Emerging role of angiotensin converting enzyme inhibitors in cardiac and vascular protection. Circulation 1994; 90: 2056-2068. Mogensen CE. Angiotensin converting enzyme inhibitors and diabetic nephropathy. BMJ 1992; 304: 327-328. Ravid M, Savin H, Lang R, et al. Proteinuria, renal impairment, metabolic control, and blood pressure in type 2 diabetes mellitus. A 14-year follow up report on 195 patients. Arch Intern Med 1992; 152: 1225-1229. Ravid M, Savin H, Jutrin I, et al. Long term stabilizing effect of angiotensin converting enzyme inhibition on plasma creatinine and on proteinuria in normotensive type 2 diabetic patients. Ann Intern Med 1993; 118: 577-581. Gansevoort RT, de Zeeuw D, de Jong PE. Long term benefits of the antiproteinuric effect of angiotensin converting enzyme inhibition in nondiabetic renal disease. Am J Kidney Dis 1993; 22: 202-206. Lewis EJ, Hunsicker LG, Bain RP, et al. The effect of angiotensin converting enzyme inhibition on diabetic nephropathy. N Engl J Med 1993; 329: 1456-1462. Bedogna V, Valvo E, Casagrande P, et al. Effect of ACE inhibition in normotensive patients with chronic glomerular disease and normal renal function. Kidney Int 1994; 38: 101-107. Cattran DC, Greenwood C, Ritchie S. Long term benefits of angiotensin converting enzyme inhibitor therapy in patients with severe immunoglobulin A nephopathy: a comparison to patients receiving treatment with other antihypertensive agents and patients receiving no therapy. Am J Kidney Dis 1994; 23: 247-254. Mogensen CE, Keane WF, Bennett PH, et al. Prevention of diabetic renal disease with special reference to microalbuminuria. Lancet 1995; 346: 1080-1084. Maschio G, Alberti D, Janin G, et al. Effect of angiotensin converting enzyme inhibitor benazapril on the progression of chronic renal insufficiency. N Engl J Med 1996; 334: 939-945. The GISEN Group (Gruppo Italiano di Studi Epidemiologici in Nefrologia). Randomised placebo-controlled trial of effect of ramipril on decline in glomerular filtration rate and risk of terminal renal failure in proteinuric, nondiabetic nephropathy. Lancet 1997; 349: 1857-1863. Ruggenenti P, Perna A, Gheradi G, et al. Renoprotective properties of ACE inhibition in nondiabetic nonnephrotic proteinuria. Lancet 1999; 354: 359-364. Statcorp. Stata statistical software, release 6.0. College Station (TX): Stata Corporation, 1999. Baker P, Hoy WE, Wang Z, et al. Towards evaluation of the cost-effectiveness of a treatment program for renal disease in Australian Aborigines. Presented at the 35th Annual Scientific Meeting of the Australian and New Zealand Society of Nephrology; 1999 Mar 3-5; Brisbane (Qld). Mackenzie HS, Ziai F, Omer SA, et al. Angiotensin receptor blockers in chronic renal disease: the promise of a bright future. J Amer Soc Nephrol 1999; 10 Suppl 12: S283-S286. Mimran A, Ribstein J. Angiotensin receptor blockers: pharmacology and clinical significance. J Amer Soc Nephrol 1999; 10 Suppl 12: S273-S277. Hoy WE. Screening and treatment for renal disease: the community model. Nephrology 1998; 4 Suppl iii-iv: S90-S95. Minutes of the Inaugural Meeting of the National Aboriginal and Torres Strait Islander Renal Disease Scientific Working Group and its Guidelines Subcommittee. Office of Aboriginal and Torres Strait Islander Health. 1999; Nov 16 Alice Springs (NT). (Received 14 Jul 1999, accepted 6 Apr 2000) Authors' details Menzies School of Health Research, Darwin, NT. Wendy E Hoy, FRACP, Senior Renal Consultant; Philip R Baker, BSc, NHMRC PhD Student, Menzies School of Health Research, and Department of Social and Preventive Medicine, University of Queensland, Brisbane, QLD; Angela M Kelly, RN, BAppSc, Senior Program Coordinator; Zhiqiang Wang, PhD, Epidemiologist and Statistician, and Senior Research Officer. Reprints will not be available from the authors. Correspondence: Dr W E Hoy, Menzies School of Health Research, PO Box 41096, Casuarina, NT, 0811. wendyATmenzies.su.edu.au Make a comment Back to text 2: Baseline characteristics of participants in the treatment program and the historical control group All participantsIncluded in 2-year profiles Historical control group (n=258)Yes (n=118)No* (n=140)(n=229)P?% Men43%47%40%51%0.13Mean age in years (SD)43.4 (11.1)43.5 (10.4)43.4 (11.7)40.8 (12.8)0.02Mean body mass index27.0 (5.7)27.1 (5.7)27.0 (5.8)25.2 (5.4)< 0.001(kg/m2) (SD) Blood pressure (mm Hg) Mean systolic (SD)135 (20)135 (20)135 (21)134 (20)0.58Mean diastolic (SD)82 (14)81 (13)82 (15)85 (15)0.01% With hypertension?65%66%63%65%0.91% With diabetes42%46%37%26%0.001% With ACR ≥34g/mol65%74%58%58%0.02% With raised serum creatinine level§12%13%11%12%0.62Previous ACEi25%33%16%NR ACR=urinary albumin/creatinine ratio. ACEi=angiotensin-converting enzyme inhibitor. NR=no result. *90 had been enrolled less than 2 years, 19 had been enrolled ≥ 2 years but did not have complete data for all visits, and 31 had dropped out. ?For test of significance of difference between all participants (intention-to-treat group) and control group. ?Blood pressure ≥140/90 or taking antihypertensive treatment. §Serum creatinine level > 106µmol/L (women), > 120µmol/L (men). Back to text 3: Clinical profiles over two years of treatment in 118 Tiwi people VariableBaseline6 months12 months24 monthsP*Blood pressure (mm Hg) Mean systolic (SD)135 (20)126 (21)124 (20)122 (22)< 0.001Mean diastolic (SD)81 (13)75 (14)77 (14)74 (14)< 0.001Mean? ACR (g/mol) (95% CI)55 (43-70)50 (39-64)53 (41-69)55 (43-69)0.36Mean? serum creatinine level (µmol/L) (95% CI)89 (85-93)88 (84-92)88 (84-92)84 (79-89)0.44Mean GFR (mL/min/1.73m2) (SD)89 (26)91 (28)89 (26)93 (29)0.54ACR=urinary albumin/creatinine ratio. GFR=glomerular filtration rate. *Test for significance of difference in values among the four intervals by analysis of variance. ?Geometric mean. Back to text 4: Clinical profiles over two years of treatment in 118 Tiwi people, by clinical category at baseline Blood pressure PreviousDiabetes < 140/90 (n=69)≥ 140/90 (n=49)ACEi (n=39)No (n=64)Yes (n=54)BP (mm Hg) Mean systolicBaseline123 (11)152 (17)136 (19)135 (21)136 (19)(SD)24 months117 (20)130 (22)128 (23)122 (15)122 (23)Mean diastolicBaseline75 (9)90 (12)83 (11)81 (15)81 (10)(SD)24 months72 (14)77 (13)78 (14)76 (15)72 (11)Mean ACRBaseline66 (50-87)43 (27-61)62 (40-97)48 (34-68)62 (45-91)(g/mol) (95% CI)24 months75 (57-98)35 (23-54)66 (45-98)50 (36-70)60 (41-87)Mean serumBaseline88 (82-94)90 (85-95)94 (85-103)90 (85-95)87 (81-93)creatinine level (µmol/L) (95% CI)24 months84 (77-92)84 (77-91)93 (82-105)83 (77-89)86 (78-94)Mean GFR (SD)Baseline91 (29)86 (21)91 (31)90 (26)88 (26)(mL/min/1.73m2)24 months95 (32)91 (25)92 (32)96 (28)90 (24) Albuminuria Serum creatinine level Micro-* (n=28)Overt? (n=86)Normal (n=98§)Raised? (n=15§)BP (mm Hg)Mean systolicBaseline 134 (24)135 (18)135 (20)139 (19)(SD)24 months 123 (23)120 (21)123 (22)118 (20)Mean diastolicBaseline 82 (15)81 (12)82 (13)78 (13)(SD)24 months 73 (15)74 (14)75 (14)71 (13)Mean ¶ ACRBaseline 16 (13-19)104 (90-121)49 (38-65)125 (83-187)(g/mol) (95% CI)24 months 19 (15-25)90 (72-112)50 (38-66)88 (45-174)Mean¶ serumBaseline 85 (79-92)90 (85-95)83 (82-88)137 (123-153)creatinine level (µmol/L) (95% CI)24 months 75 (70-81)88 (82-95)78 (75-81)119 (98-144)Mean GFR (SD)Baseline 88 (23)89 (28)95 (23)55 (18)(mL/min/1.73m2)24 months 102 (24)91 (28)99 (24)57 (30) ACEi=angiotensin-converting enzyme inhibitor. BP=blood pressure. ACR=urinary albumin/creatinine ratio. GFR=glomerular filtration rate. *ACR, 3.4-33g/mol. ?ACR >34g/mol. ?Serum creatinine level >106µmol/L (women), >120µmol/L (men). §Data not available for all participants. ¶Geometric mean. Back to text 5: Rates of endpoints in historical control and intention-to-treat groups Historical control group (n=229) BaselineEndpointACR (g/mol)CasesPerson-yearsRate per 100 person-years (95% CI)DialysisAll ≥ 1009 9564 1201.6 (0.8-3.1) 7.5 (3.9-14.4)Natural deathAll < 34 34-99 ≥ 10018 2 9 7555 226 205 1243.2 (1.0-5.1) 0.9 (0.2-3.5) 4.4 (2.2-8.4) 5.6 (2.7-11.2)Combined (dialysis or natural death)All < 34 34-99 100-199 ≥ 20026? 2 9 6 9543 227 205 74 374.8 (3.3-7.0) 0.9 (0.2-3.5) 4.4 (2.3-8.4) 8.1 (3.6-18.0) 24.2 (12.6-46.5) Intention-to-treat group (n=258) Endpoint CasesPerson-yearsRate per 100 person-years (95% CI)Dialysis 7 7548 1971.3 (0.6-2.6) 3.6 (1.7-7.0)Natural death 11 3 3 5560 178 194 1882.0 (1.1-3.4) 1.7 (0.5-5.2) 1.5 (0.4-4.8) 2.7 (1.1-6.4)Combined (dialysis or natural death) 16 3 3 3 7549 178 193 104 732.9 (1.7-4.6) 1.7 (0.5-5.2) 1.6 (0.5-4.8) 2.9 (0.9-8.9) 9.6 (4.6-20.2) Relative risk (RR) (95% CI) Endpoint Crude*Adjusted?P (for adjusted RR)Dialysis 0.77 (0.24-2.33)0.43 (0.17-1.12)0.08Natural death 0.59 (0.25-1.31)0.55 (0.26-1.16)0.11Combined (dialysis or natural death) 0.59 (0.30-1.14)0.47 (0.25-0.86)0.01 ACR=urinary albumin/creatinine ratio. *Overall estimate for treatment group versus control group. ?Relative risk adjusted for baseline ACRcategory. ?People who underwent dialysis and later died were counted only once for the combined endpoint. Back to text 6: Estimated survival advantage for intention-to-treat versus control group, adjusted for ACR category Clinical category at baselineRelative risk (95% CI)?PAll0.47 (0.25-0.86)0.01Overt albuminuria0.36 (0.18-0.72)0.004DiabetesNo0.28 (0.09-0.93)0.02Yes0.65 (0.28-1.51)0.31HypertensionNo0.59 (0.25-1.44)0.24Yes0.38 (0.15-0.98)0.04* ACR=urinary albumin/creatinine ratio. Categories: < 3.4 3.4-33, 34-99, 100-199, ≥ 200 g/mol. ? For combined endpoints of natural death and renal failure, intention-to-treat versus control group. Back to text Back to text Back to text Back to text

Wendy E Hoy · Philip R Baker · Angela M Kelly · Zhiqiang Wang

Indigenous Health Research Increase in prevalence of obesity and diabetes and decrease in plasma cholesterol in a central Australian Aboriginal community Robyn McDermott, Kevin G Rowley, Amanda J Lee, Sabina Knight and Kerin O'Dea MJA 2000; 172: 480-484 Abstract - Subject and Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Aboriginal health Abstract Objective: To document change in prevalence of obesity, diabetes and other cardiovascular diease (CVD) risk factors, and trends in dietary macronutrient intake, over an eight-year period in a rural Aboriginal community in central Australia. Design: Sequential cross-sectional community surveys in 1987, 1991 and 1995. Subjects: All adults (15 years and over) in the community were invited to participate. In 1987, 1991 and 1995, 335 (87% of eligible adults), 331 (76%) and 304 (68%), respectively, were surveyed. Main outcome measures: Body mass index and waist : hip ratio; blood glucose level and glucose tolerance; fasting total and high density lipoprotein (HDL) cholesterol and triglyceride levels; and apparent dietary intake (estimated by the store turnover method). Intervention: A community-based nutrition awareness and healthy lifestyle program, 1988-1990. Results: At the eight-year follow-up, the odds ratios (95% CIs) for CVD risk factors relative to baseline were obesity, 1.84 (1.28-2.66); diabetes, 1.83 (1.11-3.03); hypercholesterolaemia, 0.29 (0.20-0.42); and dyslipidaemia (high triglyceride plus low HDL cholesterol level), 4.54 (2.84-7.29). In younger women (15-24 years), there was a trebling in obesity prevalence and a four- to fivefold increase in diabetes prevalence. Store turnover data suggested a relative reduction in the consumption of refined carbohydrates and saturated fats. Conclusion: Interventions targeting nutritional factors alone are unlikely to greatly alter trends towards increasing prevalences of obesity and diabetes. In communities where healthy food choices are limited, the role of regular physical activity in improving metabolic fitness may also need to be emphasised. The high rates of obesity, diabetes and other cardiovascular disease (CVD) risk factors in Australian Aboriginal communities1-4 lead to high rates of diabetic complications and excess mortality in relatively young people.5-7 With often poor access to appropriate, good quality secondary prevention services,8,9 some communities have sought to emphasise primary prevention of diabetes in community-based health programs aimed at improving individual food choices and the quality of the food supply.10,11In the community described here, a community-based nutrition awareness and healthy lifestyle program was commenced in 1988, after a 1987 survey showed high rates of obesity, diabetes and other CVD risk factors. The program continued for two years and culminated in a risk factor survey and store turnover study in 1991, followed by a series of family-based workshops to provide feedback on the results. A third survey was carried out in 1995. We describe the trends in CVD risk factors (anthropometry, lipid levels, and glucose intolerance) and apparent dietary intake over this eight-year period. Subjects and methods Cross-sectional surveys were carried out in June 1987, May 1991 and April 1995 at a rural Aboriginal community. The surveys were approved by the Alice Springs Institutional Ethics Committee (which, in 1995, had an Aboriginal subcommittee), and by the Deakin University Ethics Committee, after consultation with the community council and health council. All adult members of the community (those 15 years and over) were invited to participate and volunteers gave written informed consent. Pregnant or non-Indigenous community members were excluded. Results were returned to individual participants and summary reports presented to the community council. The resident population at the time of each survey (excluding visitors from other communities) was determined by household census. Blood tests: Twelve millilitres of blood was taken after an overnight fast and a second blood sample collected two hours after a 75 g glucose drink. Blood samples were kept cold until centrifugation and the plasma frozen immediately thereafter until analysis. Levels of glucose, total cholesterol, high density lipoprotein (HDL) cholesterol (after precipitation of other lipoproteins with 15% w/v PEG 6000) and triglycerides were measured by standard enzymatic techniques using commercial kits (Boehringer-Mannheim, Mannheim, Germany). Glucose tolerance was classified according to WHO criteria.12 Hypercholesterolaemia was defined as a plasma cholesterol concentration ≥ 5.5 mmol/L; and Dyslipidaemia was defined as the combination of a low HDL cholesterol level ( ≤ 0.9 mmol/L) plus hypertriglyceridaemia (a fasting plasma triglyceride level ≥ 2.0 mmol/L). Anthropometry: Measurements were made by trained staff using standard techniques.13 Body weight was measured to 0.1 kg, with the subject in light clothing, using digital electronic scales; height was measured to 0.1 cm using a stadiometer; and waist and hip circumferences were measured to 0.1 cm. Obesity was defined as a body mass index (BMI) > 30 kg/m2. Smoking status: Current smoking status was ascertained in 1991 and 1995 using a yes/no questionnaire. Dietary intake: Apparent dietary intake was measured using the store turnover method14 for the three months before each of the surveys. This method estimates general trends in food consumption, as the local store is the main source of food for the community. Expressing data as nutrient density (ie, as a proportion of total energy intake) avoids estimating per capita intake and gives a valid measure of dietary quality for the community.10,14 Intervention: A community-based nutrition awareness and healthy lifestyle program was conducted from 1988 to 1990. The program, which included a resident non-Aboriginal project officer and Aboriginal coworker, concentrated mainly on raising awareness of diabetes in the community, promoting healthy food-buying habits and improving the quality of food purchased by the community store. Some details of the intervention are given in Scrimgeour et al.15 Statistical analyses: Although some community members were screened on more than one occasion (Box 1), analyses were performed assuming purely cross-sectional data. Trends in continuous variables were tested by linear regression using SPSS.16 Separate analyses were performed for men and women. Regression models included year of survey, age group and an interaction term of year of survey with age group. Also included was a dummy variable indicating whether that individual was screened once only or on more than one occasion, the interaction terms of this dummy variable with year of survey and age group, and a three-way interaction term. The latter two variables were excluded from the final model if found to be non-significant. For categorical data, trends in prevalence were tested by a χ2 test for linear association. Confidence intervals for prevalence data were calculated assuming a binomial distribution and adjusted using the finite sampling factor: (N-n)/(N-1), where N is the population size and n is the sample size. Mantel-Haenszel age-weighted odds ratios and exact 95% confidence intervals for risk factors were calculated using EpiInfo software.17 Sensitivity analyses were performed to test for selection bias in the 1991 and 1995 survey samples. Results Response rates Survey participation rates were 87% of the adults normally resident and present at the time of the survey in 1987, 76% in 1991 and 68% in 1995 (Box 1). Participation rates by younger people were progressively lower with each survey. Anthropometry There was no statistically significant change in mean BMI among men (Box 2A; the regression analysis had sufficient statistical power to detect a difference in BMI over time of 0.15 kg/m2). Although mean BMI rose in the two older age groups, this was because men returning for repeat screenings tended to have a higher mean BMI than those screened only once (P = 0.062). Similarly, there was no significant change in waist circumference or waist : hip ratio among men (Box 2). Among women, there was a significant increase in mean BMI, particularly in those aged 15-24 years (Box 2A). The increase in mean BMI (equivalent to about 10 kg in body weight) among women aged 15-24 years was accompanied by an increase in mean waist circumference, but no significant change in waist : hip ratio. Among women 35 years and older, mean BMI remained very high over the eight-year period. For the community as a whole, the prevalence of obesity increased significantly over the survey period: 1987 -- 22.8% (95% CI, 22.2%-23.5%); 1991 -- 32.0% (95% CI, 30.6%-33.3%); 1995 -- 37.0% (95% CI, 35.1%-38.8%); χ2 = 15.5, df = 1, P < 0.001. There was a trebling in prevalence of obesity among women in the age group 15-24 years over the eight-year period (χ2 = 14.4, df = 1, P < 0.001), but no change among men of the same age group (χ2 = 0.2, df = 1, P = 0.636; Box 3). For the older age groups, there was already a high prevalence of obesity among women in 1987, which remained high (Box 3). The prevalence of obesity increased significantly among men aged 25-34 years during the follow-up period (χ2 = 5.2, df = 1, P = 0.022; Box 3). The increase among men aged 35 years and older was not statistically significant (χ2 = 2.0, df = 1, P = 0.155). The statistical power of analyses of prevalence changes in age and sex subgroups was somewhat low because of sparse data and, in some cases, low prevalence. Glucose tolerance For the community as a whole, there was a trend to an increasing prevalence of diabetes:1987 -- 11.6% (95% CI, 11.1%-12.0%); 1991 -- 18.6% (95% CI, 17.4%-19.7%); 1995 -- 20.7% (95% CI, 17.7%-22.2%); χ2= 9.9, df = 1, P = 0.002; with significant increases in prevalence among men aged 25-34 years (χ2 = 4.8, df = 1, P = 0.029) and women aged 35 years and older (χ2 = 3.9, df = 1, P = 0.048; Box 3). However, the prevalence of impaired glucose tolerance (IGT) did not change significantly: 1987 -- 8.4% (95% CI, 8.0%-8.8%); 1991 -- 9.4% (95% CI, 8.6%-10.3%); 1995 -- 7.5% (95% CI, 5.6%-8.5%). χ2= 0.13, df = 1, P = 0.721. Plasma lipids There was a highly significant decrease in mean levels of plasma cholesterol between 1987 and 1991 (Box 2B). This decrease occurred across all ages and in both sexes. This fall in total cholesterol level was partly due to decreases in HDL cholesterol levels, which also occurred in all age- and sex-specific categories, with the largest decrease among women aged 15-24 years (Box 2B). Conversely, among both men and women, there was an increase of similar magnitude in mean fasting plasma triglyceride level in all age groups (Box 2B). After excluding subjects with diabetes from the analysis, these trends to lower total and HDL cholesterol and higher triglyceride levels were still apparent (data not shown). Changes in CVD risk factor profile Box 4 shows the changing prevalence of cardiovascular risk factors as odds ratios compared with baseline. By 1995, community members were more likely to be obese, diabetic and dyslipidaemic (high plasma triglyceride and low plasma HDL cholesterol levels), whereas the risk of hypercholesterolaemia declined. Apparent dietary macronutrient intake Box 5 summarises changes in apparent community intake of sugar, total fat and saturated fat. As a proportion of total energy intake, there was a decline in total and saturated fat and sugar intake. Complex carbohydrate intake was 22%, 21% and 30% of total energy in 1987, 1991 and 1995, respectively. Store turnover data also suggested that, compared with 1987, there were decreases in the approximate per capita daily intake of sugar, fruit and vegetables and increases in flour and bread consumption (data not shown). Representativeness of the survey samples The sensitivity analyses performed assumed that the non-responders in 1991 and 1995 were all non-diabetic and non-obese. With this assumption, the linear trend to an increase in prevalence remained for obesity (χ2 = 5.0, df = 1, P = 0.025) but not for diabetes (χ2 = 1.0, df = 1, P = 0.320). A more realistic, but still conservative, assumption is that the non-responders in the 1991 and 1995 surveys had the same prevalence of obesity and diabetes as in the first survey sample. With this assumption, there were significant increases in estimated prevalences of obesity (23%, 30% and 32% in 1987, 1991 and 1995, respectively; χ2 = 9.4; df = 1; P = 0.002) and diabetes (12%, 17% and 18%; χ2 = 6.1; df = 1; P = 0.014). Among men, regression analysis indicated that those who were screened on more than one occasion had a greater increase in waist : hip ratio with time (P = 0.014) and lower HDL cholesterol levels (P = 0.004) compared with men screened only once. Among women, those who were screened on more than one occasion had higher BMI (P = 0.020) compared with women screened only once. There were no other significant differences apparent between these groups, nor were there any other significant interactions with time. Furthermore, a comparison of baseline data for subjects screened in 1987 and again at either or both of the subsequent surveys with those who were not rescreened revealed no significant differences in mean age, BMI, cholesterol and triglyceride levels or glucose tolerance among either men or women. Together, these observations make it unlikely that the observed trends in obesity, diabetes and plasma lipids are artifacts due to sampling bias. Discussion The community store intervention and education campaign in this central Australian Aboriginal community was associated with a decrease in apparent dietary intake of total and saturated fats and refined carbohydrates and a corresponding increase in complex carbohydrate intake. Associated with the change in dietary fat intake, there were reductions in plasma cholesterol levels in all age groups and both sexes. However, there were increases in the prevalence of obesity (60% increase) and diabetes (80% increase) over the survey period. While the study design does not allow us to ascribe cause-and-effect relationships between the intervention process and the trends in outcomes, the data imply that an attempt to modify diet alone is insufficient to reverse trends to increasing prevalence of obesity and diabetes. Although the biochemical assays at baseline were performed on a different instrument to that used in the two follow-up surveys, the apparent changes in lipid profiles between the first and subsequent surveys are unlikely to be due to methodological differences as the same enzymatic methods were used for all three surveys and the kits purchased from the same source; quality control samples were routinely run and did not vary significantly over the study period; and the changes observed are entirely consistent with the changes in dietary fat intake. Our results are similar to those reported after five years of a non-communicable disease intervention program in Mauritius:18 a major improvement in circulating cholesterol levels, but rapidly increasing prevalence of obesity and diabetes. The increase in prevalence of diabetes that we found approaches the highest recorded.19 The trebling in the prevalence of obesity among women aged 15-24 years was associated with a four- to fivefold increase in prevalence of diabetes. In contrast, there was no change in mean BMI for men in this age range. Thus, weight gain and onset of diabetes in women was apparently accelerated. Anecdotal evidence suggests this sex difference in secular trends in body weight may be due to high participation by young men in vigorous sporting activities such as football, whereas regular exercise by young women is limited in this community. Exercise has been shown to have protective effects against the incidence of diabetes,20 even independently of dietary change. Hence, community-directed interventions aimed at increasing physical activity may improve health outcomes. The prevalence of diabetes in older age groups was extremely high in both men and women. Prior to 1991, diabetes was absent in men under 25 years and relatively uncommon among young women. By 1995, cases of type 2 diabetes were beginning to appear even at this young age. The decreasing age of onset of diabetes in this community has major public health implications with respect to diabetic complications, hyperglycaemia in pregnancy, and the subsequent intergenerational amplification of diabetes risk.21 We have previously reported that body fat distribution, as indicated by waist : hip ratio, among women in this community was unusual for an Aboriginal population, with the central deposition of body fat being less apparent than in other Aboriginal groups.2 Consistent with this, there were no major changes in mean waist : hip ratio for women in the subsequent surveys, even in the young women who had a large increase in waist circumference. Despite these adverse trends in obesity and diabetes, the community has achieved significant improvements in dietary quality, as indicated by the changes in the food supply at the store, and in plasma cholesterol levels. However, a healthy diet consistent with National Health and Medical Research Council (NHMRC) guidelines22 has not been achieved. This problem goes beyond the realm of individual choice and reflects endemic poverty, high prices coupled with low incomes, often poor quality of fruit and vegetables in community stores, household economies which discourage the consumption of fresh foods, lack of domestic refrigeration, and unavailability of many nutritious foods.23 Reversal of obesity is difficult even in the absence of such major environmental and social barriers.24 Hence, early intervention to prevent or delay the onset of excessive weight gain is likely to be more effective in reducing diabetes and cardiovascular risk in such communities.25 In conclusion, our results suggest that a focus on nutrition and dietary habits alone may be insufficient to prevent excessive weight gain and diabetes among adults in Aboriginal communities. Further systematic studies of intervention processes, impacts and associated outcomes are required to address this issue. Acknowledgements This work was supported by grants from the NHMRC (No. 954605) and the Commonwealth Department of Health and Family Services. Special thanks to Fiona McLachlan, Sunil Piers, Nick Williams, Kathy Abbott and the health workers and nursing staff of Territory Health Services in Central Australia. We gratefully acknowledge the expert technical assistance of Connie Karschimkus and Olga Strommer and statistical advice of Elmer Villanueva. References O'Dea K, Guest CS. Diabetes in Aborigines and other Australian populations. Aust J Public Health 1992; 16: 340-349. O'Dea K, Patel M, Kubisch R, et al. Obesity, diabetes and hyperlipidemia in a central Australian Aboriginal community with a long history of acculturation. Diabetes Care 1993; 16: 1004-1010. Gault A, O'Dea K, Rowley KG, et al. Abnormal glucose tolerance and other coronary heart disease risk factors in an isolated Aboriginal community in central Australia. Diabetes Care 1996; 19: 1269-1273. O'Dea K. Westernization and non-insulin-dependent diabetes in Australian Aborigines. Ethnicity Dis 1991; 1: 171-187. Phillips CB, Patel MS, Weeramanthri TS. High mortality from renal disease and infection in Aboriginal central Australians with diabetes. Aust J Public Health 1995; 19: 482-486. Veroni M, Gracey M, Rouse I. Patterns of mortality in Western Australian Aboriginals, 1983-1989. Int J Epidemiol 1994; 23: 73-81. Thomson NJ. Recent trends in Aboriginal mortality. Med J Aust 1991; 154: 235-239. Phillips CB, Patel MS, Carbaron Y. Utilisation of health services by Aboriginal Australians with diabetes. Diab Res Clin Practice 1993; 20: 231-239. Deeble J, Mathers C, Smith L, et al. Expenditure on health services for Aboriginal and Torres Strait Islander People. Canberra: Australian Institute of Health and Welfare, 1998. (Catalogue No. HWE 6.) Lee AJ, Bonson APV, Yarmirr D, et al. Sustainability of a successful health and nutrition program in a remote Aboriginal community. Med J Aust 1995; 162: 633-635. Spinks M, White G. Looma, Western Australia: Diabetes Program. In: Bear-Wingfield R, editor. Sharing good tucker stories. A guide for Aboriginal and Torres Strait Islander communities. Canberra: Commonwealth Department of Health and Family Services, 1996: 63-69. World Health Organization: Diabetes Mellitus: Report of a WHO Study Group. World Health Organ Tech Rep Ser 1985; No. 727. Callaway CW, Chumlea WC, Bouchard C, et al. Circumferences. In: Lohman TG, Roche AF, Masturell R, editors. Anthropometric standardisation reference manual. Champaign, Ill: Human Kinetics Books, 1988: 39-54. Lee AJ, O'Dea K, Mathews JD. Apparent dietary intake in remote Aboriginal communities. Aust J Public Health 1994; 18: 190-197. Scrimgeour D, Rowse T, Knight S. Food purchasing behaviour in an Aboriginal community. 2. Evaluation of an intervention aimed at children. Aust J Public Health 1994; 18: 67-70. SPSS [computer program], version 9.0. Chicago Ill: SPSS Inc, 1998. EpiInfo [computer program], version 6. Atlanta, Ga: Centers for Disease Control and Prevention, 1993. Dowse GK, Gareeboo H, Alberti KGMM, et al, for the Mauritius Non-communicable Disease Study Group. Changes in population cholesterol concentrations and other cardiovascular risk factor levels after five years of the non-communicable disease intervention programme in Mauritius. BMJ 1995; 311: 1255-1259. Dowse GK, Spark RA, Mavo B, et al. Extraordinary prevalence of non-insulin-dependent diabetes mellitus and bimodal plasma glucose distribution in the Wanigela people of Papua New Guinea. Med J Aust 1994; 16: 767-774. Pan X-R, Li G-W, Hu Y-H, et al. Effects of diet and exercise in preventing NIDDM in people with impaired glucose tolerance. The Da Qing IGT and diabetes study. Diabetes Care 1997; 20: 537-544. Pettit DJ, Nelson RG, Saad MF, et al. Diabetes and obesity in the offspring of Pima Indian women with diabetes during pregnancy. Diabetes Care 1993; 16: 310-314. National Health and Medical Research Council. Dietary guidelines for Australians. Canberra: NHMRC/AGPS, 1992. Leonard D, Beilin R, Moran M. Whichway kaikai blo umi? Food and nutrition in the Torres Strait. Aust J Public Health 1995; 19: 589-595. World Health Organization. Obesity: preventing and managing the global epidemic. Geneva: WHO, 1998: 107-158. Macaulay AC, Paradis G, Potvin L, et al. The Kahnawake Schools Diabetes Prevention Project: intervention, evaluation and baseline results of a diabetes primary prevention program with a native community in Canada. Prev Med 1997; 26: 779-790. (Received 11 Oct 1999, accepted 20 Mar 2000) Authors' details Health Surveillance, Queensland Health, Tropical Public Health Unit, Cairns, QLD. Robyn McDermott, MPH, FAFPHM, Director. Monash University, Centre for Population Health and Nutrition, Monash Medical Centre, Melbourne, VIC. Kevin G Rowley, BAppSci, PhD, Research Fellow; currently, Research Fellow, Department of Medicine, St Vincent's Hospital, Melbourne. Kerin O'Dea, BSc, PhD, Head. Menzies School of Health Research, Darwin, NT. Amanda J Lee, GradDipDiet, PhD, Public Health Nutrition Consultant. Territory Health Services, Alice Springs, NT. Sabina Knight, RN, MTH, Staff Development Officer (Remote). Reprints will not be available from the authors. Correspondence: Dr K G Rowley, Department of Medicine, Clinical Sciences Building, St Vincent's Hospital, Fitzroy, VIC 3065. rowleykATmail.medstv.unimelb.edu.au Make a comment 1: Age- and sex-specific response rates for the three cross-sectional surveys in a rural Aboriginal community Men Women 15-24 y25-34 y35 y +15-24 y25-34 y35 y +1987Population, N Sample, n Response rate % Of sample rescreened90 71 79% 56% 54 42 78% 41%58 48 83% 58% 87 81 93% 69%47 45 96% 49% 68 61 90% 56%1991Population, N Sample, n Response rate % Of sample rescreened 87 51 59% 37% 61 35 57% 60%63 54 86% 46% 95 72 76% 46%57 50 88% 54% 72 69 96% 67%1995Population, N Sample, n Response rate % Of sample rescreened81 48 59% 40% 72 38 53% 61%63 43 68% 74% 94 49 52% 33%58 56 97% 73% 81 71 88% 62%Back to text 2: Trends in anthropometric variables and plasma lipid levels, stratified by age and sex 15-24 years25-34 years35 years and overP*P†A: Anthropometric variables Body mass index (BMI), kg/m2Men 1987 1991 199524.5 (23.4-25.6) 24.1 (22.9-25.4) 24.8 (23.3-26.3)26.3 (24.7-28.0) 27.0 (25.0-29.0) 28.7 (27.2-30.2)26.0 (24.7-27.3) 27.8 (26.2-29.5) 28.2 (26.6-29.9) 0.514 0.992 Women 1987 1991 199524.5 (23.2-25.7) 24.6 (23.1-26.1) 29.1 (27.3-31.0)27.8 (26.0-29.7) 28.8 (26.9-30.7) 29.7 (27.7-31.8)30.2 (28.3-32.1) 31.8 (30.0-33.6) 30.4 (28.7-32.1) <0.001 0.004 Waist circumference, cmMen 1987 1991 199586.2 (83.0-89.4) 85.3 (82.0-88.7) 84.8 (81.2-88.4)91.0 (87.3-94.6) 93.9 (89.4-98.4) 95.1 (91.1-99.2)97.9 (93.4-102.5) 99.0 (95.2-102.8) 98.2 (93.1-103.3) 0.834 0.340 Women 1987 1991 199581.5 (78.7-84.4) 82.3 (79.3-85.4) 90.0 (86.7-93.4)92.0 (87.8-96.2) 95.4 (90.5-100.2) 92.2 (88.2-96.3)98.3 (94.1-102.4) 99.9 (96.3-103.5) 94.0 (90.9-97.2) <0.001 <0.001 Waist:hip ratioMen 1987 1991 19950.87 (0.85-0.88) 0.87 (0.86-0.89) 0.88 (0.87-0.90)0.92 (0.90-0.94) 0.94 (0.92-0.96) 0.94 (0.93-0.96)0.97 (0.96-0.98) 0.99 (0.97-1.01) 1.00 (0.98-1.02) 0.293 0.160 Women 1987 1991 1995 0.82 (0.80-0.83) 0.85 (0.82-0.87) 0.85 (0.83-0.88)0.85 (0.83-0.87) 0.89 (0.85-0.92) 0.85 (0.84-0.87)0.85 (0.84-0.87) 0.89 (0.87-0.91) 0.86 (0.84-0.88) 0.134 0.095 Data are means (95% confidence interval). *P-value for change over time. †P-value for interaction of change over time with age group. Back to textB: Plasma lipids Total cholesterol, mmol/LMen 1987 1991 19955.3 (5.0-5.6) 4.5 (4.3-4.8) 4.5 (4.3-4.8)6.0 (5.7-6.3) 4.8 (4.6-5.1) 5.3 (5.0-5.6)6.2 (5.7-6.6) 5.5 (5.1-5.9) 5.5 (5.2-5.8) 0.034 0.571 Women 1987 1991 19955.2 (4.9-5.4) 4.3 (4.1-4.5) 4.5 (4.3-4.8)5.7 (5.3-6.1) 4.8 (4.5-5.0) 4.8 (4.5-5.1)5.5 (5.3-5.8) 5.0 (4.7-5.3) 5.0 (4.8-5.3) 0.001 0.317 HDL cholesterol, mmol/LMen 1987 1991 19951.17 (1.10-1.24) 0.88 (0.82-0.94) 0.83 (0.76-0.90)1.23 (1.10-1.36) 0.84 (0.77-0.91) 0.79 (0.73-0.85)1.05 (0.96-1.14) 0.78 (0.72-0.84) 0.76 (0.70-0.81) <0.001 0.180 Women 1987 1991 19951.45 (1.33-1.57) 0.98 (0.91-1.05) 0.88 (0.81-0.95)1.25 (1.12-1.38) 0.81 (0.75-0.87) 0.86 (0.81-0.92)1.18 (1.10-1.27) 0.84 (0.79-0.89) 0.82 (0.78-0.86) <0.001 0.011 Triglycerides, mmol/LMen 1987 1991 19951.1 (1.0-1.3) 1.6 (1.4-1.9) 1.7 (1.5-1.9)1.6 (1.3-2.0) 2.3 (1.9-2.7) 2.1 (1.8-2.5)2.1 (1.8-2.5) 3.0 (2.5-3.6) 2.9 (2.4-3.6) 0.004 0.419 Women 1987 1991 19951.0 (0.9-1.1) 1.2 (1.1-1.4) 1.6 (1.4-1.8)1.3 (1.2-1.6) 1.8 (1.6-2.1) 1.8 (1.5-2.0)1.6 (1.4-1.8) 2.2 (2.0-2.5) 2.2 (2.0-2.4) <0.001 0.248 Data are means (95% confidence interval), except triglycerides, which are geometric means (95% CI). *P-value for change over time. †P-value for interaction of change over time with age group. Back to text Back to text 4: Risk ratios for cardiovascular risk factors in the follow-up surveys (1991 and 1995) compared with baseline (odds ratios and 95% CIs)* 198719911995Obesity Impaired glucose tolerance (IGT) Diabetes Hypercholesterolaemia Dyslipidaemia Smoking1.00 1.00 1.00 1.00 1.00 - 1.50 (1.03-2.17) 1.04 (0.58-1.87) 1.63 (0.98-2.69) 0.24 (0.17-0.35) 4.73 (3.06-7.61) 1.001.84 (1.28-2.66) 0.76 (0.41-1.41) 1.83 (1.11-3.03) 0.29 (0.20-0.42) 4.54 (2.84-7.29) 0.73 (0.52-1.03) *Compared with 1987 (or 1991 for smoking), Mantel-Haenszel-weighted (for age) odds ratios and exact 95% confidence intervals. Back to text Back to text

Robyn McDermott · Kevin G Rowley · Amanda J Lee · Sabina Knight · Kerin O'Dea

Editorial Mortality from cardiovascular disease is too high outside capital cities Do we accept this situation or look for ways of changing it? MJA 2000; 172: 360-361 The report by Sexton and Sexton1 in this issue of the Journal updates our knowledge about geographic differences in death rates from cardiovascular disease (CVD) in Australia. Their major finding is that deaths from coronary heart disease (CHD) in 1996 were 30% higher for men and 21% higher for women who live outside our capital cities than for those who live in capital cities. The gap widened over the period of study -- in 1986 the CHD mortality difference (in both men and women) was 13%. The gratifying decline in deaths from CVD over the last number of years has been greater for those who live in capital cities, and this has led to a widening of the geographic gradient in CVD deaths. Of particular concern in the report is that the excess mortality outside capital cities is greater among younger age groups. The demonstration of social and geographic gradients in death rates is not new.2,3 The findings of Sexton and Sexton are disturbing -- what could be the explanation? What can we do about them? There are two reasons for excess CHD deaths -- risk factors among the population and inadequacies in the level of medical care provided. A combination of changes in these factors has been found to be the explanation for the recent decline in CHD deaths seen in Australia.4Sexton and Sexton allude to differences in socioeconomic status between urban and rural areas, which together with higher levels of unemployment outside capital cities may be part of the "explanation" of the higher CHD mortality. Their report does not examine separately death rates in Aboriginal people, and, while these are likely to contribute to the overall picture, Indigenous people constitute too small a proportion of the total population for this to be the whole explanation. Data on risk factor levels are scarce outside capital cities, but some limited data discussed in the report suggest that differences in risk factor levels mirror the excess rural mortality. The strength of the article by Sexton and Sexton is the demonstration of a widening of the mortality gap over time. There have been major changes in the provision of medical care for patients with heart disease between 1986 and 1996, and it seems most appropriate to focus here on the level of healthcare provided in and outside capital cities. The data from Sexton and Sexton do not allow us to distinguish between disease incidence and case fatality, but other data indicate that there are differences in case fatality and in medical care for acute myocardial infarction (AMI) between metropolitan and non-metropolitan hospitals.5,6 There are differences in the types of hospital in and outside capital cities and in the distribution of specialist cardiologists. There is ample evidence that hospital type and size and the speciality of the treating physician are related to the outcome and the practice of evidence-based care for patients with CHD.7-10 A recent report in this Journal found that the evidence-based use of drugs after AMI was lower among doctors in smaller non-metropolitan hospitals in New South Wales.7 It is not beyond credibility to suggest that at least part of the reason for the widening geographic gradient in CHD deaths in Australia is differential levels of care for those with the disease. Rural areas have smaller hospitals and fewer cardiologists (who prefer to have access to investigative facilities, which have become such an important part of their speciality). We must find solutions to the need to practise evidence-based care and prevention throughout the Australian healthcare system, irrespective of access to specialist services and tertiary care facilities. Guidelines and clinical pathways have been promulgated as a response to the demonstration of variations in medical care, and may have an impact on changing patterns of care.11,12 However, the solution to the structural inequalities in the provision of care is likely to be much more complex than the use of these clinical decision aids, especially given the relatively small impact they might be expected to have.12 Do we just accept that people who live outside capital cities in a large country where the population is thinly spread will inevitably have less access to high quality medical care (as they have less access to many other resources such as the arts and retail outlets)? These are fundamental questions about societal expectations. Where is the consumer pressure for change? What is the responsibility of the health professions for the health of the whole of the population, and how is this expressed? A number of these questions were discussed at the recent Federal Government Regional Australia Summit, at which, despite the comment that "There are no easy solutions facing regional Australia", a number of key priorities and proposed strategies were identified.13 For example, two of the key priorities under the health theme are: "Regional, rural and remote communities require improved and expanded access to healthcare services . . ." and "Resource allocation for regional, rural and remote communities must be equitable in terms of health need relative to the urban population." One of the proposed strategies to achieve this latter priority is "A health services plan will be established to set optimal levels of services for communities of different sizes. The Commonwealth Health Department will act as broker for funding to any community which wishes to invoke those benchmarks." Maybe the demonstration of a reduced geographic gradient for CVD deaths could be a future marker of the success of this and other interventions. Richard F Heller Professor of Community Medicine and Clinical Epidemiology Centre for Clinical Epidemiology and Biostatistics Faculty of Medicine and Health Sciences The University of Newcastle, Newcastle, NSW Sexton PT, Sexton T-L H. Excess coronary mortality among Australian men and women living outside the capital city statistical divisions. Med J Aust 2000; 172: 370-374. Taylor R, Chey T, Bauman A, Webster I. Socio-economic, migrant and geographic differentials in coronary heart disease occurrence in New South Wales, Australia. Aust N Z J Public Health 1999; 23: 20-26. Marmot M, Ryff CD, Bumpass LL, et al. Social inequalities in health: next questions and converging evidence. Soc Sci Med 1997; 44: 901-910. Dobson AJ, McElduff P, Heller R, et al. Changing patterns of coronary heart disease in the Hunter Region of New South Wales, Australia. J Clin Epidemiol 1999; 52: 761-771. Huy Dinh Vu, Heller RF, Lim LLY, et al. Hospital mortality after acute myocardial infarction is lower in metropolitan than non-metropolitan regions. J Epidemiol Commun Health. In press. Lim L, O'Connell R, Heller R. Differences in management of heart attack patients between metropolitan and regional hospitals in the Hunter Region of Australia. Aust N Z J Public Health 1999; 23: 61-66. Lim LLY, Heller RF, O'Connell R, D'Este C. Stated and actual management of acute myocardial infarction among different specialties. Med J Aust 2000; 172: 208-212. Chen J, Radford MJ, Wang Y, et al. Do "America's best hospitals" perform better for acute myocardial infarction? N Engl J Med 1999; 340: 286-292. Jollis JG, Delong ER, Peterson ED, et al. Outcome of acute myocardial infarction according to the speciality of the admitting physician. N Engl J Med 1996; 335: 1880-1887. Weitzman S, Cooper L, Chambless L, et al. Gender, racial, and geographic differences in the performance of cardiac diagnostic and therapeutic procedures for hospitalised acute myocardial infarction in four states. Am J Cardiol 1997; 79: 722-726. Kitchiner DJ, Bundred PE. Clinical pathways [editorial]. Med J Aust 1999; 170: 54-55. Gupta L, Ward JE, Hayward RS. Clinical practice guidelines in general practice: a national survey of recall, attitudes and impact. Med J Aust 1997; 166: 69-72. Regional Australia Summit communiquŽ. Presentation of the summit recommendations. <http://www.dotrs.gov.au/regional/summit/communique.htm> (Accessed 23 March 2000). Make a comment

Richard F Heller

Abstract Objective: To describe the epidemiological pattern of newly diagnosed HIV infection and AIDS among Indigenous Australians. Design and setting: National surveillance for newly diagnosed HIV infection and AIDS in Australia. Information on Indigenous status was sought at HIV/AIDS notification in all State/Territory health jurisdictions, except the Australian Capital Territory, and Victoria before June 1998. Main outcome measures: Number of people with newly diagnosed HIV per year and population rate of HIV diagnosis; demographic characteristics of people with HIV and AIDS diagnoses by Indigenous status. Results: From 1992 to 1998, 127 Indigenous Australians were newly diagnosed with HIV infection and 55 were diagnosed with AIDS. The population rate of HIV diagnosis among Indigenous Australians (5.23/100 000 per year) was similar to that among non-Indigenous Australians (5.51/100 000 per year). The annual number of HIV diagnoses among Indigenous people was relatively stable, but among non-Indigenous people it declined steadily over time. A higher proportion of Indigenous people diagnosed with HIV were women (26.8% v 8.9%; P < 0.001). Although male homosexual contact was the predominant source of exposure for both Indigenous (46.7%) and non-Indigenous (75.0%) people with HIV infection, exposure by heterosexual contact (36.7% v 15.3%; P < 0.001) was reported more frequently among Indigenous people. Conclusion: Although HIV incidence was similar among Indigenous and non-Indigenous Australians, the lack of a recent decline in incidence and the higher proportion of Indigenous people exposed to HIV by heterosexual contact indicate the need to intensify interventions to prevent HIV transmission among Indigenous people. Introduction The epidemic of HIV transmission peaked in Australia in the mid 1980s, and there was a subsequent peak in AIDS incidence of nearly 1000 cases in 1994.1 The estimated number of people diagnosed with HIV infection in Australia to the end of 1998 was 16 714, with an estimated 11 800 living with HIV infection. Although the peaks of both the HIV and AIDS epidemics in Australia have passed, HIV infection continues to be transmitted, predominantly through male homosexual contact, at an estimated level of 450 cases per year.1 Despite evidence of a relatively well-controlled HIV epidemic in Australia, evaluation of the Third National HIV/AIDS Strategy noted an increase in the reported number of Indigenous Australians diagnosed with HIV infection in the early 1990s.1 Furthermore, high rates of other sexually transmissible infections in some Indigenous communities indicate the potential for HIV transmission.1 To define the pattern of HIV infection among Indigenous Australians, and to assess time trends in new diagnoses of HIV infection and AIDS, we examined national HIV and AIDS notification data by Indigenous status for the years 1992-1998. National Health and Medical Research Council guidelines on ethical matters in Aboriginal and Torres Strait Islander health research were followed.2 Methods National surveillance procedures Surveillance procedures for newly diagnosed HIV infection and AIDS have been described previously.3,4 Briefly, newly diagnosed HIV infection and AIDS are notifiable conditions in each State or Territory health jurisdiction in Australia. Information sought at national notification of newly diagnosed HIV infection includes the State or Territory of diagnosis, postcode of residence, namecode (based on the first two letters of the family name and the first two letters of the first given name), sex, date of birth, Indigenous status, date of HIV diagnosis, CD4 cell count at HIV diagnosis, evidence of newly acquired HIV infection, and patient-reported source of exposure to HIV. Information sought at AIDS notifications also includes the date of AIDS diagnosis, AIDS-defining illnesses, and use of antiretroviral therapy before AIDS diagnosis. People with newly diagnosed HIV infection with evidence of newly acquired HIV infection (ie, a negative or indeterminate HIV antibody test result or a diagnosis of HIV seroconversion illness within 12 months of HIV diagnosis) were defined as having "newly acquired HIV infection". People with AIDS were classified as having "late HIV diagnosis" if HIV infection was newly diagnosed within three months of AIDS diagnosis. Indigenous status From 1985, information on Indigenous status, obtained through self-identification as Aboriginal or Torres Strait Islander, was routinely sought at notification of HIV infection and AIDS for people newly diagnosed in the Northern Territory, Queensland, South Australia, Tasmania and Western Australia. In New South Wales, Indigenous status has been sought for newly diagnosed cases of HIV infection and AIDS since 1992. Indigenous status was not available for people with HIV infection or AIDS diagnosed in the Australian Capital Territory, or from Victoria before June 1998. Information on Indigenous status has been sought nationally from 1995; available information on Indigenous status for cases diagnosed before 1995 was obtained retrospectively through State or Territory health authorities. Exposure category HIV exposure was classified as male homosexual contact, male homosexual contact plus injecting drug use, injecting drug use, heterosexual contact only, haemophilia/coagulation disorder, receipt of blood or tissue, mother with or at risk for HIV infection, and other or undetermined exposure. Statistical analysis A χ2 or Fisher's exact test and odds ratios were used to test for differences between Indigenous and non-Indigenous cases with respect to demographic characteristics (sex, residence), newly acquired HIV 1infection, late HIV diagnosis, HIV exposure category, and individual AIDS-defining illnesses. Residence was divided into "metropolitan" and "non-metropolitan" on the basis of postcode. "Metropolitan" was defined as capital city (including Canberra), and "non-metropolitan" was defined as other than capital city. In the analyses, cases without information on Indigenous status were grouped with non-Indigenous cases. The population-based rate of HIV diagnosis was calculated by Indigenous status and year (for States and Territories other than Victoria and the ACT) using Australian Bureau of Statistics (ABS) census data for 1996.5 Results Information on Indigenous status was available for 91% of people with newly diagnosed HIV infection. For the period 1992-1998, 5313 cases of newly diagnosed HIV infection were notified to the national HIV surveillance centre, of which 127 (2.4%) were Indigenous cases. For the same period, 3638 AIDS cases were notified, of which 55 (1.5%) were Indigenous cases. The annual number of HIV diagnoses among Indigenous people was relatively stable over this period (Box 1). In contrast, the annual number of HIV diagnoses among non-Indigenous people gradually declined over the years 1992-1998. During this period, the annual HIV diagnosis rate per 100 000 population among Indigenous people (diagnosed in States and Territories other than Victoria and the ACT) (5.23) was similar to that among non-Indigenous people (5.51) (Box 1). A higher proportion of Indigenous people with HIV were female (26.8% v 8.9%; P < 0.001) (Box 2). The median age at HIV diagnosis (30 years v 33 years; P < 0.001) and AIDS diagnosis (32 v 37 years; P < 0.001) was lower among Indigenous cases. The pattern of exposure to HIV reported by Indigenous people was different from that reported by non-Indigenous people both for newly diagnosed HIV infection and AIDS (Box 2). Although male homosexual contact was the predominant source of exposure to HIV for both Indigenous (46.7%) and non-Indigenous (75.0%) people, a history of heterosexual contact only was reported more frequently by Indigenous people (36.7% v 15.3%; P < 0.001). The proportion of Indigenous and non-Indigenous people with AIDS with "late HIV diagnosis" was similar (23.6% and 18.3%; P = 0.42), as was the proportion reporting antiretroviral therapy before AIDS diagnosis (56.4% and 62.2%; P = 0.5). No difference between Indigenous and non-Indigenous cases was observed in the median CD4 cell count at diagnosis of HIV and of AIDS. The spectrum of AIDS-defining illnesses for Indigenous and non-Indigenous people with AIDS is shown in Box 3. Cryptococcal disease (odds ratio [OR], 3.3; 95% CI, 1.4-7.6; P = 0.004), oesophageal candidiasis (OR, 1.8; 95% CI, 0.95-3.38; P = 0.05), and atypical mycobacterium (OR 8.3; 95% CI, 2.4- 25.42; P = 0.002) were more frequent among Indigenous AIDS cases, whereas Kaposi's sarcoma was less frequent (OR, 0.12; 95% CI, 0.01-0.80; P = 0.01). Among people with HIV, there were more Indigenous than non-Indigenous cases in non-metropolitan locations (36% v 16%) (P < 0.01). Similarly, among people with AIDS, there were more Indigenous than non-Indigenous cases in non-metropolitan locations (37% v 19%) (P = 0.002). Discussion The HIV epidemic among Indigenous Australians has been relatively limited to date, with an overall rate of HIV diagnosis comparable with that for non-Indigenous Australians over the years 1992-1998. However, there have been contrasting trends in these rates, with a declining rate of HIV diagnosis among the non-Indigenous population, but a relatively stable rate among Indigenous people. Features that distinguish the Indigenous from the non-Indigenous HIV epidemic are a higher proportion of women affected, a higher proportion with heterosexual exposure to HIV, a younger age at HIV and AIDS diagnosis, and a higher proportion of people with HIV in rural areas. The low proportion of people with "late HIV diagnosis" among both Indigenous and non-Indigenous AIDS cases would suggest that a large pool of undiagnosed HIV infection is not present in Australia. The very low HIV prevalence among prison entrants in all States and Territories, including those where Indigenous Australians constitute a large proportion of prison inmates, is further confirmation that HIV prevalence among Indigenous Australians remains low.6 Our findings also extend those of an earlier study that showed comparable rates of HIV infection in both the Indigenous and the non-Indigenous population in Queensland.7 In interpreting our findings, several limitations to the study methods need to be considered. Firstly, the lack of a uniform reporting system for Indigenous status in all States and Territories may result in under-reporting in some jurisdictions. However, there is evidence that in recent years Indigenous status has been more completely reported, with 91% of HIV notifications in those States/Territories other than the ACT and Victoria currently reporting Indigenous status.1 Secondly, reporting of Indigenous status was based on "self-identification", which may either not be reported correctly by the patient, or not requested by the clinician. If identifying as Indigenous is more likely in a census setting than in clinical practice, our rates of Indigenous HIV diagnosis may be underestimates. Thirdly, reported rates of HIV and AIDS diagnoses are dependent on the level and extent of HIV testing. Poor access to and uptake of confidential testing by some Indigenous people, and fear of possible stigmatisation arising from positive test results, may influence the extent of HIV testing among Indigenous people. The explanation for the apparently limited HIV epidemic among Indigenous Australians is almost certainly multifaceted. The drop in HIV transmission from the mid 1980s has meant that the extent of the Australian HIV epidemic has been limited compared with many other countries.1 Behaviour change among homosexual men was largely responsible for the initial reduction in HIV transmission from the mid 1980s,1 with other measures such as the widespread introduction of harm minimisation programs for injecting drug users,8 and high condom use and low rates of sexually transmissible infections among most sex workers9 contributing to the ongoing relatively low level of HIV transmission. The absence of substantial levels of HIV infection among injecting drug users and female sex workers1 may have limited the spread of HIV into the heterosexual population. Despite the fact that the proportion of HIV diagnoses attributed to heterosexual contact has increased in recent years, homosexual contact remains the exposure category for about 85% of new HIV diagnoses.1 Australia's Indigenous people are not a homogeneous group. There are many hundreds of language groups and a wide diversity of cultural, social, economic and geographical settings within and between Indigenous Australian communities. Most Indigenous Australians suffer a higher burden of illness and die at a younger age than non-Indigenous Australians for almost every type of disease or condition for which information is available.10 Indigenous Australians are more likely to have lower annual incomes, are less likely to have qualifications beyond secondary school,11 and are 15 times more likely to be imprisoned than non-Indigenous Australians.11 These factors, combined with the remote locations in which many Indigenous Australians live and the resulting poor access to health services, contribute to their vulnerability to sexually transmissible infections.12 Associations in other industrialised countries between socioeconomic disadvantage and HIV transmission from heterosexual exposure and injecting drug use13 highlight the need to provide HIV prevention services which reach all sectors of society. The higher proportion of Indigenous people with HIV in rural areas should alert policymakers to the need for access to culturally appropriate health services in these locations. Likewise, the higher proportion of Indigenous people with HIV infection who are women, who report heterosexual exposure only and who inject drugs shows a need for broadly focused HIV prevention programs. This demographic pattern, the relatively stable level of HIV diagnoses in Indigenous people, and the continuing high rates of other sexually transmissible infections among some Indigenous communities,1 highlight the need to strengthen both sexual health and harm-minimisation strategies for Indigenous Australians. Following the recommendations of the Evaluation of the Third National HIV/AIDS Strategy, several measures have been implemented in an attempt to reduce the higher rates of sexually transmissible infections among Indigenous Australians and the associated risk of HIV infection. These include the establishment of an Indigenous Australians' Sexual Health Working Party and the subsequent implementation of the National Indigenous Australians' Sexual Health Strategy 1996-97 to 1998-99, which proposed a comprehensive approach to HIV prevention through a range of strategies considering treatment and care, partnership agreements and a properly resourced workforce.14 In particular, the Strategy emphasises the need for access to primary care services for communities without adequate facilities for diagnosing and treating sexually transmissible infections and the provision of information on reducing the risk of acquisition. Strategies aimed at the underlying causes of low socioeconomic status, low levels of education and low levels of employment must also be employed in order to reduce the risk of transmission of HIV and other sexually transmissible infections in Indigenous Australians. Acknowledgements The National Centre in HIV Epidemiology and Clinical Research (NCHECR) is funded by the Commonwealth Department of Health and Aged Care. We would like to acknowledge the valuable input and feedback received from the National Australian Indigenous Sexual Health Working Party during the drafting of this article. We also thank Ms Yueming Li for statistical analyses, Ms Patty Correll (NCHECR) for her assistance in extracting data, and Ms Suzanne Blogg (National Centre for Epidemiology and Population Health [NCEPH]) for her guidance and assistance. We thank the doctors who reported cases of newly diagnosed HIV infection and AIDS under national surveillance procedures, and the National HIV Surveillance Committee for their collaboration. The National HIV Surveillance Committee comprises Ms Irene Passaris (ACT), Mr Robert Menzies (NSW), Dr Jan Savage (NT), Dr Hugo Ree (QLD), Ms Therese Davey (SA), Mr Neil Cremasco (TAS), Ms Cathy Keenan (VIC), Dr Gary Dowse (WA), Professor John Kaldor (NCHECR), and Ms Ann McDonald (NCHECR). References Commonwealth Department of Human Services and Health. Valuing the past -- investing in the future. Evaluation of the National HIV/AIDS Strategy 1993-94 to 1995-96. Canberra: AIDS/Communicable Diseases Branch, CDHSH, 1995. National Health and medical Research Council. Guidelines on ethical matters in Aboriginal and Torres Strait Islander health research. Canberra: NHMRC, 1991. McDonald AM, Crofts N, Blumer CE, et al. The pattern of diagnosed HIV infection in Australia, 1984-1992. AIDS 1994; 8: 513-519. Kaldor J, McDonald AM, Blumer CE, et al. The acquired immunodeficiency syndrome in Australia: incidence 1982-1992. Med J Aust 1993; 158: 10-17. Australian Bureau of Statistics. Population distribution, Indigenous Australians. Canberra: ABS 1997. (Catalogue No. 4705.0.) McDonald AM, Ryan J, Brown PR, et al. HIV prevalence at reception into Australian prisons, 1991-1997. Med J Aust 1999; 171: 18-21. Neilson G, Hill PS. Human immunodeficiency virus notifications for Aborigines and Torres Strait Islanders in Queensland. Med J Aust 1993; 158: 155-157. MacDonald M, Wodak A, Ali R, et al. HIV prevalence and risk behaviour in needle exchange attenders: a national study. Med J Aust 1997; 166: 237-240. O'Connor CC, Berry G, Rohrsheim R, et al. Sexual health and use of condoms among local and international sex workers in Sydney. Genitourin Med 1996; 72(1): 4-51. Australian Bureau of Statistics. The health and welfare of Australia's Aboriginal and Torres Strait Islander peoples, 1997. Canberra: ABS, 1997. (Catalogue No. 4704.0.) Office of the Aboriginal and Torres Strait Islander Social Justice Commissioner. Indigenous deaths in custody 1989 to 1996. Sydney: Human Rights and Equal Opportunity Commission, October 1996. Fairley CK, Bowden FJ, Gay NJ, et al. Sexually transmitted diseases in disadvantaged Australian communities. JAMA 1997; 278: 117-118. Centers for Disease Control and Prevention. HIV/AIDS Surveillance Report 1998; 10 (No. 2): 1-43. ANCARD Working Party on Indigenous Australians' Sexual Health, Commonwealth Department of Health and Family Services. The National Indigenous Australians' Sexual Health Strategy, 1996-1997 to 1998-1999. Canberra: CDHFS, 1997. Authors' details National Centre in HIV Epidemiology and Clinical Research, Sydney, NSW. Jillian A Guthrie, BA, MAE (Indigenous Health) also at National Centre for Epidemiology and Population Health, Australian National University, Canberra, ACT. Gregory J Dore, FRACP, MPH, Lecturer. Ann M McDonald, MPH, Coordinator, National HIV/AIDS Surveillance. John M Kaldor, PhD, Professor; and Head, Epidemiology Unit. Reprints will not be available from the authors. Correspondence: Professor J M Kaldor, National Centre in HIV Epidemiology and Clinical Research, Level 2, 376 Victoria Street, Darlinghurst, NSW 2010. jkaldorATnchecr.unsw.edu.au 2: Newly diagnosed HIV infection and AIDS, 1992-1998, by Indigenous status and selected characteristicsHIV diagnoses IndigenousNon-IndigenousP Odds ratio (95% CI)Total casesn=127n=5186Males93 (73.2%)4726 (91.1%)<0.0010.27 (0.17-0.41)Median age (years)3033Median CD4 cell count4844000.10Newly acquired HIV*24 (18.9%) 930 (17.9%)0.79Late HIV diagnosis?---HIV exposure categoryn=120?n=4507?Male homosexual contact56 (46.7%)3382 (75.0%) <0.0010.29 (0.20-0.43)Male homosexual contact and injecting drug use 12 (10.0%)191 (4.2%)0.0022.51 (1.29-4.78)Injecting drug use6 (5.0%)176 (3.9%)0.3Heterosexual contact only44 (36.7%)689 (15.3%)<0.0013.21 (2.16-4.77)Receipt of blood/tissue0 (0.0)34 (0.8%)0.4Mother-to-child transmission2 (1.7%)35 (0.8%)0.2Other/Undetermined7679 AIDS diagnoses IndigenousNon-IndigenousPOdds ratio (95% CI)Total casesn=55n=3583Males43 (78.2%)3411 (95.2%)<0.0010.18 (0.09-0.37)Median age (years)3237<0.001Median CD4 cell count90600.71Newly acquired HIV*---Late HIV diagnosis?13 (23.6%)675 (18.8%)0.42HIV exposure catergoryn=52?n=3405?Male homosexual contact26 (50.0%)2783 (81.7%)<0.0010.22 (0.12-0.38)Male homosexual contact and injecting drug use7 (13.5%)167 (4.9%)0.0162.95 (1.20-6.93)Injecting drug use1 (1.9%)127 (3.7%)0.4Heterosexual contact only17 (32.7%)238 (7.0%)<0.0016.28 (3.33-11.75)Receipt of blood/tissues0 (0.0)76 (2.2)0.3Mother-to-child transmission1 (1.9%)15 (0.4%)0.2Other/Undetermined3178 *A negative or indeterminate HIV antibody test result or a diagnosis of HIV seroconversion illness within 12 months of HIV diagnosis. ?HIV infection newly diagnosed within three months of AIDS diagnosis. ?The "other/undetermined" category was excluded from the calculation of the percentage of cases attributed to each HIV exposure category.

Jillian A Guthrie · Gregory J Dore · Ann M McDonald · John M Kaldor

Editorial Hepatitis A, liver transplants and Indigenous communities Vaccination plus improved living conditions and healthcare are needed to combat hepatitis A in remote Indigenous communities MJA 2000; 172: 6-7 In this issue of the Journal, Hanna et al highlight the serious problem of acute hepatitis A in Indigenous children in far north Queensland communities.1 This should come as no surprise, as these communities are plagued by poverty, educational disadvantage and poor living conditions -- the very circumstances in which this infection occurs. Indeed, Indigenous children in rural and remote Australia generally have an extraordinarily high burden of infectious disease, with attack rates for conditions such as invasive pneumococcal disease as high as any in the world.2 The incidence of hepatitis A virus (HAV) infection in north Queensland in 1996-1997 was up to six times higher among Aboriginal and Torres Strait Islander people than among non-Indigenous people.3 Indigenous people accounted for 29% of all HAV infections but only 8.1% of the population, and contracted HAV infection at a mean age of 12 years compared with 30 years for the general population. The most common risk factor for HAV infection was living in or visiting a rural Aboriginal or Torres Islander community. An effective hepatitis A control program requires effective vaccines as well as generic programs for improving Indigenous health. An effective vaccine for HAV infection exists,4 but it has been suggested that HAV vaccination is not necessary in Aboriginal and Torres Strait Islander communities, as HAV infection is endemic (eg, a 1994 study found that 98.5% of people over the age of 10 years had had HAV infection5). However, young children (aged three to five years) are both very vulnerable to severe infection and significant transmitters of infection, and could be targeted by community-wide HAV vaccination programs.3 The patients reported by Hanna et al highlight a severe complication of HAV infection -- fulminant hepatic failure. As the case fatality rate for HAV infection in Australia is thought to be 0.2%,6 cases of fulminant hepatic failure are not unexpected in communities with a high prevalence of HAV infection. Generally, outcomes of fulminant hepatic failure are better if it is secondary to HAV infection than to other causes, such as drugs, hepatitis B or hepatitis "X" (caused by unidentified viruses).7 However, children aged under 10 years and adults aged over 40 years do worse, irrespective of cause.7 The children reported by Hanna et al were all under 10 years, had severe hepatitis and were transferred to tertiary care centres relatively late in the course of their illness. All three died of cerebral oedema, raising the important issue of fluid management in patients with fulminant hepatic failure: aggressive fluid replacement is not part of the management of acute liver failure and may even be detrimental by precipitating cerebral oedema. In the children reported by Hanna et al, delayed diagnosis and late referral were probably contributing factors to cerebral oedema. Early indicators of fulminant hepatitis include a serum bilirubin level of > 300 µmol/L, prolongation of clotting time and hypoglycaemia.7 These cases also raise the issue of organ transplantation in Aboriginal and Torres Strait Islander populations. Aboriginal people from remote regions have worse outcomes than non-Aboriginal people after renal transplantation, probably because of their higher rates of comorbidity, especially "syndrome X" disorders (insulin resistance, associated obesity and hyperlipidaemia).8 Obviously, this would be much less of a problem for liver transplantation in Aboriginal children with fulminant hepatic failure.8 There is no reason that Aboriginal and Torres Strait Islander people would have inherently poorer outcomes after liver transplantation than other people, although issues related to primary health care and long term follow-up must be addressed. Indeed, the high prevalence of hepatitis B in the adult Aboriginal community makes the issue of liver transplantation even more relevant. Liver transplantation should clearly be considered a therapeutic option for severe liver disease in the Aboriginal population. The Australian National Liver Transplant Unit has performed liver transplants on two Aboriginal adults with good medium-term outcomes. However, none of the above issues can be addressed in isolation from general issues of Aboriginal health. Prevention and detection of disease and treatment of severe infection are possible only if the basic requirements for improving Aboriginal health are in place. These include improved environmental and living conditions and comprehensive and competent primary healthcare delivery systems. There is now considerable evidence that poor living conditions in Aboriginal communities can be improved by focusing on delivery and maintenance of "health hardware" (such as waste removal and supply of cold and hot water and the means to clean living areas).9 Furthermore, effective vaccination programs and appropriate primary care management of sick children can occur only in the setting of sustainable, primary healthcare systems. This requires a range of initiatives, in particular supply of a competent rural health workforce. Appropriate protocols for referring sick children are also needed, as well as access to rapid and appropriate evacuation to large regional hospitals. We believe that the recommendations of Hanna et al on when to refer are far too conservative. Surely, any young child with clinical or biochemical hepatitis needs to be referred at least to a large base hospital, where immediate investigation and assessment is possible. The patients reported by Hanna et al raise many issues about healthcare in Aboriginal and Torres Strait Islander communities, including the need to: provide and maintain functioning "health hardware"; establish sustainable primary healthcare systems; deliver effective vaccines for common infectious diseases; develop protocols for patient referral; provide rapid access and evacuation to large regional hospitals; and demystify organ transplantation as an effective therapeutic procedure for fulminant hepatic failure. These are all achievable! Geoffrey W McCaughan A W Morrow Professor of Gastroenterology and Hepatology A W Morrow Gastroenterology and Liver Centre Australian National Liver Transplant Unit Royal Prince Alfred Hospital and University of Sydney, Sydney, NSW Paul J Torzillo Medical Director, Nganampa Health Council, Umuwa, SA Clinical Associate Professor of Medicine Department of Respiratory Medicine Royal Prince Alfred Hospital and University of Sydney, Sydney, NSW Hanna JN, Warnock TH, Shepherd RW, Selvey LA. Fulminant hepatitis A in Indigenous children in north Queensland. Med J Aust 2000; 172: 19-21. Torzillo PJ, Hanna JN, Morey F, et al. Invasive pneumococcal disease in central Australia. Med J Aust 1995; 162: 182-186. Merritt A, Symons A, Griffiths M. The epidemiology of acute hepatitis A in North Queensland 1996-1997. Commun Dis Intell 1999; 23: 120-124. Bader TF. Hepatitis A vaccine. Am J Gastroenterol 1996; 91: 217-222. Bowden SJ, Currie BJ, Miller NC, et al. Should Aboriginals in the "Top End" of the Northern Territory be vaccinated against hepatitis A. Med J Aust 1994; 161: 372-373. Amin J, Heath T, Morrell S. Hepatitis A in Australia in the 1990s: future directions in surveillance and control. Commun Dis Intell 1999; 23: 113-120. O'Grady JG, Alexander GHM, Haylor KM, Williams R. Early indications of prognosis in fulminant hepatic failure. Gastroenterology 1989; 97: 439-445. Spencer JL, Silva DT, Snelling P, Hoy WE. An epidemic of renal failure amongst Aboriginal Australians. Med J Aust 1998; 168: 537-541. Pholeros P, Rainow S, Torzillo PJ. Housing for health -- towards a healthier living environment for Aborigines. Sydney: Healthabitat, 1994. Make a comment

Geoffrey W McCaughan · Paul J Torzillo

Notable Cases Fulminant hepatitis A in Indigenous children in north Queensland Jeffrey N Hanna, Tim H Warnock, Ross W Shepherd and Linda A Selvey Since 1993, three Indigenous children in north Queensland have died of fulminant hepatitis A. Even if the children had been able to undergo liver transplantation, prolonged immunosuppressant therapy and the likelihood of opportunistic infections would inevitably have jeopardised any chance of long-term survival. As hepatitis A has become a leading infectious cause of death in young Indigenous children in north Queensland, hepatitis A vaccine has recently been introduced into the vaccination schedule for these children. MJA 2000; 172: 19-21 For editorial comment, see McCaughan & Torzillo Introduction - Clinical record 1 - Clinical record 2 - Clinical record 3 - Discussion - Acknowledgement - References - Authors' details - - More articles on Aboriginal health Introduction Fulminant hepatitis A is rare in children, and most recent reports have been from developing countries.1-4 Occasional cases in children from industrialised countries tend to be in those who have recently travelled to hepatitis A endemic areas5,6 or who live in conditions of considerable socioeconomic disadvantage.7We describe three cases of fulminant hepatitis A in Indigenous children in north Queensland, all of whom died. This uncommon but serious manifestation of a relatively common infection in Indigenous children presents major difficulties in clinical management,8 illustrating the importance of preventive public health measures. Clinical record 1 A 4.5-year-old Torres Strait Islander boy, who had previously been in good health, presented to a local health centre in early 1993 with anorexia, dark urine and jaundice of several days' duration. Vomiting and irritability persisted for five days, and he was evacuated to Thursday Island Hospital. Two days later, he had a generalised seizure and became semi-comatose after an episode of haematemesis, and was evacuated to Cairns Base Hospital. On admission in Cairns, the boy was deeply jaundiced, with hepatic fetor and moderate hepatomegaly. He did not respond to painful stimuli, and was generally hypertonic with upgoing plantar reflexes. He had raised serum bilirubin and liver enzyme levels, markedly elevated serum ammonia level, hypoglycaemia and a bleeding diathesis (see Box). He was positive for hepatitis A IgM, confirming acute hepatitis A; subsequent serological tests were negative for hepatitis B and C, cytomegalovirus (CMV) and herpes simplex virus (HSV) infection. The boy was stabilised, placed on ventilator support and transferred the next day to the Royal Children's Hospital in Brisbane for consideration of liver transplantation. However, on arrival in Brisbane, he had fixed, dilated pupils, and urgent computed tomography showed gross cerebral oedema. Despite intensive treatment, his condition deteriorated, and he died the next day, nine days after initial presentation. Postmortem examination showed massive hepatic necrosis and diffuse hypoxic ischaemic brain injury, secondary to cerebral oedema and raised intracranial pressure. Clinical record 2 A 4.5-year-old Aboriginal girl was admitted to a community hospital near Townsville in late 1997 with fever, lethargy, dark urine and jaundice of uncertain duration. Apart from a persistent tinea capitis infection, she had been in reasonably good health. Four months before the current illness, she had been treated with a four-week course of ketoconazole, and results of liver function tests were normal at that time. On admission, she had raised serum bilirubin and liver enzyme levels (Box). Serological tests confirmed acute hepatitis A; subsequent tests were negative for hepatitis B and C, CMV, HSV and Epstein-Barr virus infection. Four days after her admission, the girl's family took her from the hospital, and on her return the next day she was delirious. She was transferred to Townsville General Hospital. On admission in Townsville, she was deeply jaundiced and irritable, with a depressed level of consciousness and moderate hepatomegaly. Peripheral reflexes were brisk, with up-going plantar reflexes and bilateral ankle clonus. Her serum bilirubin level had risen further (Box), she was hypoglycaemic, had a bleeding diathesis, and soon became hypokalaemic (serum potassium level, 2.7 mmol/L [RR, 3.5-4.5 mmol/L]). Several hours after admission, she had an episode of profound hypotension (systolic pressure, 50 mmHg) after aspiration of a large volume of bloodstained fluid from the nasogastric tube. She was transferred the next day to the Royal Children's Hospital in Brisbane for consideration of liver transplantation. On arrival in Brisbane, her serum ammonia and sodium levels were both markedly elevated (ammonia, 158 µmol/L; sodium, 151 mmol/L [RR, 133-143 mmol/L]). Computed tomography showed cerebral oedema with a possible ischaemic lesion in the right cerebral hemisphere. She was listed for urgent liver transplantation pending a suitable donor, but the next day developed signs of raised intracranial pressure which did not respond to medical management. She died eight days after initial presentation. Clinical record 3 A 2.5-year-old Aboriginal girl, who had previously been in good health, presented to a health centre in a Cape York community in September 1998 with malaise and jaundice of one day's duration. She was reviewed the next day by the visiting Royal Flying Doctor Service; a clinical diagnosis of acute hepatitis was made, but, because she did not appear particularly unwell, no specific treatment was requested. Liver function tests on that day (Day 2) showed her serum concentrations of bilirubin, AST and ALT were raised (Box). Serological testing confirmed acute hepatitis A, and tests for hepatitis B and C were negative. The girl was reviewed two days later by health centre staff. She reportedly had stopped eating and appeared lethargic, although she responded appropriately to voices and other stimuli. When seen the next morning, she had deteriorated markedly, no longer responded to her environment and was obtunded and dehydrated, with grunting respirations. She was evacuated urgently to Cairns Base Hospital. On admission in Cairns she was deeply jaundiced, with hepatic fetor and mild hepatomegaly. She was semi-comatose, had brisk symmetrical reflexes and upgoing plantar reflexes. Her serum ammonia level was markedly raised and she had a bleeding diathesis (Box). Urgent transfer to Brisbane was arranged, but she deteriorated nine hours after admission with extensor posturing and diminished respiratory effort; her limbs subsequently became flaccid and areflexic. She died several hours later, five days after initial presentation. Discussion All three of the reported children were critically ill with fulminant liver failure and grade III hepatic encephalopathy9 when referred to specialist services in Cairns or Townsville. Mortality rates in fulminant hepatitis approach 70% in children,8 with death usually occurring within 8-10 days. Youth and severity of hepatic encephalopathy are both strong predictors of poor outcome;10 the main cause of death is cerebral oedema.10Liver transplantation is the only option for children with fulminant hepatitis A and advanced stages of encephalopathy who are considered unlikely to survive with medical supportive therapy alone.6,8-10 Published criteria for transplantation include either PT > 100 s or any three of the following: PT > 50 s, age < 10 years or > 40 years, jaundice for > 7 days before onset of encephalopathy, or serum bilirubin > 300 µmol/L.11 However, in practice, the availability of a suitable donor organ may be the critical issue, and therefore most transplant centres list patients as soon as transplantation is considered, and make a final decision if and when a donor organ becomes available.8 Two of the children (Patients 1 and 2) clearly met the above criteria and were listed for urgent transplantation on arrival in Brisbane, but it soon became apparent that irreversible brain damage had occurred. However, even if they had received a successful liver transplant, the difficulties of monitoring prolonged immunosuppressant therapy and the likelihood of opportunistic infections in their home communities would have inevitably jeopardised any chance of long-term survival. Hepatitis A has been the most frequent infectious cause of death in preschool-aged Indigenous children in north Queensland since 1993 (excluding neonatal deaths and pneumococcal infections, for which data are incomplete) (J Hanna, unpublished data). Two deaths resulted from the "standard" vaccine-preventable diseases (measles and Haemophilus influenzae type b infection), and one from meningococcal infection. Over the same period, no non-Indigenous children died of hepatitis A in north Queensland. We can only speculate that "host factors", as well as the quantity of viral inoculum,6 may determine why some Indigenous children develop fulminant hepatitis A. The notification rates of hepatitis A in children under five years of age in north Queensland in 1996-1997 were 264 and 10 per 100 000 in Indigenous and non-Indigenous children, respectively.12 About 25% of notified cases of hepatitis A in Indigenous people in north Queensland occur in children under five years of age,12 indicating considerable circulation of the hepatitis A virus among these young children. However, nearly half the notified cases in Indigenous people in north Queensland occur in children aged 5-14 years,12 indicating that many Indigenous primary school-aged children are susceptible to the infection. Very few notifications are in Indigenous adults over 30 years of age. Because hepatitis A is common in Indigenous children in north Queensland, and because of the demonstrated unsatisfactory outcome in those few children who develop fulminant liver failure, the emphasis must be on preventing infection. Hepatitis A virus is readily transmitted in environments with inadequate sanitation and water supply, suboptimal hygiene and overcrowding.13 The current status of housing and environmental health infrastructure throughout Indigenous Australia has recently been detailed elsewhere, and others have described some of the health consequences of these circumstances.14,15 Despite considerable recent improvements in provision of adequate housing and sanitation infrastructure in several Indigenous communities in north Queensland, many communities still have unresolved problems of overcrowding, water supply and waste disposal.16 Some communities continue to experience environmental contamination by raw sewage during wet season floods, and several Torres Strait Island communities experience severe water shortages in the dry season.17 Some of these problems are likely to persist for the foreseeable future. Paradoxically, as environmental circumstances improve, the age of reported patients will likely shift upwards, and the "visibility" of hepatitis A -- and public health concern -- will increase.13 Indigenous communities in North America have experienced cyclical outbreaks of hepatitis A every 5-10 years for many years,18 a pattern that may become more obvious in Indigenous Australian communities. Inactivated vaccines with proven effectiveness in preventing hepatitis A in children19,20 have recently become available in Australia. These vaccines have also been shown to interrupt transmission in "closed" communities prone to recurrent outbreaks,21,22 leading to the recommendation of routine hepatitis A vaccination for Indigenous children in North America.18 An inactivated hepatitis A vaccine has been offered to Indigenous children in north Queensland since early 1999. Two doses six months apart have been recommended, integrated as far as possible into the standard vaccination schedule, with the first dose at 18 months of age and the second at 24 months, necessitating only one "extra" visit to a vaccination service. Current resources allow for catch-up hepatitis A vaccination up to the sixth birthday; about 5500 Indigenous children aged 2-5 years live in north Queensland. Young children play a particularly important role in maintaining transmission of hepatitis A virus to older susceptible individuals during community-wide outbreaks,24 because of their lack of bowel control and attention to hygiene, and need for adult supervision of their toileting needs. Therefore, vaccination of preschool-aged Indigenous children provides a means not only to prevent further cases of fulminant hepatitis A in Indigenous Australian children, but also to reduce the extent of future outbreaks in their communities. A particular challenge will be to ensure that Indigenous children in rural towns and urban settings gain access to the vaccine.25 Acknowledgement We wish to thank the families of the three children for allowing us to describe their children's final illness. References Zacarias J, Brinck P, Cordero J, Velasco M. Etiologies of fulminant hepatitis in pediatric patients in Santiago, Chile. Pediatr Infect Dis J 1987; 6: 686-687. Ozsoylu S, Kocak N. Acute hepatic failure related to hepatitis A [letter]. Lancet 1989; 313: 901. Ciocca M, Ramonet M, Cuarterolo M, et al. Fulminant hepatic failure for viral hepatitis in children. IX Triennial International Symposium on Viral Hepatitis and Liver Disease; Rome; 1996 21-25 Apr. Abstract no. A 316. Arora NK, Nanda SK, Gulati S, et al. Acute viral hepatitis types E, A and B singly and in combination in acute liver failure in children in north India. J Med Virol 1996; 48: 215-221. Masada CT, Shaw BW, Zetterman RK, et al. Fulminant hepatic failure with massive necrosis as a result of hepatitis A infection. J Clin Gastroenterol 1993; 17: 158-162. Debray D, Cullufi P, Devictor D, et al. Liver failure in children with hepatitis A. Hepatology 1997; 26: 1018-1022. Friedland IR, Zuckerman M, Kala UK, Parbhoo KB. Fulminant hepatitis in children: report of 12 cases. Ann Trop Paediatr 1991; 11: 207-211. Shepherd RW. The treatment of end-stage liver disease in childhood. Aust Paediatr J 1988; 24: 213-216. Suchy FJ. Fulminant hepatic failure. In: Behrman RE, Kliegman RM, Arvin AM, Nelson WE, editors. Nelson textbook of pediatrics. 15th ed. Philadelphia: WB Saunders, 1996: 1150-1152. Hoofnagle JH, Carithers RL, Shapiro C, Ascher N. Fulminant hepatic failure: summary of a workshop. Hepatology 1995; 21: 240-252. O'Grady J. Management of acute and fulminant hepatitis A. Vaccine 1992; 10 Suppl 1: S21-S23. Merritt T, Symons D, Griffiths M. The epidemiology of acute hepatitis A in north Queensland, 1996-1997. Commun Dis Intell 1999; 23: 120-124. Gust ID. Epidemiological patterns of hepatitis A in different parts of the world. Vaccine 1992; 10 Suppl 1: S56-S58. McLennan W, Madden R. The health and welfare of Australia's Aboriginal and Torres Strait Islander peoples. Canberra: AGPS, 1997: 11-19. (ABS Catalogue no. 4704.0.) Mathews JD. Historical, social and biological understanding is needed to improve Aboriginal health. Recent Adv Microbiol 1997; 5: 257-334. Legislative Assembly of Queensland: Public Works Committee. The provision of infrastructure in Cape York. Report no. 38, June 1997. Henderson G, McKenna P, Kingsley A, et al. Hepatitis A and water supply in the Torres Strait Area. Aboriginal Torres Strait Islander Health Inform Bull 1995; 21: 48-58. Welty TK, Darling K, Dye S, et al. Guidelines for prevention and control of hepatitis A in American Indian and Alaska Native communities. S D J Med 1996; 49: 317-322. Werzberger A, Mensch B, Kuter B, et al. A controlled trial of formalin-inactivated hepatitis A vaccine in healthy children. N Engl J Med 1992; 327: 453-457. Innis BL, Snitbhan R, Kunasol P, et al. Protection against hepatitis A by an inactivated vaccine. JAMA 1994; 271: 1328-1334. Werzberger A, Kuter B, Nalin D. Six years' follow-up after hepatitis A vaccination [letter]. N Engl J Med 1998; 338: 1160. McMahon BJ, Beller M, Williams J, et al. A program to control an outbreak of hepatitis A in Alaska by using an inactivated hepatitis A vaccine. Arch Pediatr Adolesc Med 1996; 150: 733-739. Australian Bureau of Statistics. 1996 Census of population and housing. Smith PF, Grabau JC, Werzberger A, et al. The role of young children in a community-wide outbreak of hepatitis A. Epidemiol Infect 1997; 118: 243-252. Hanna JN, Malcolm RL, Vlack SA, Andrews DE. The vaccination status of Aboriginal and Torres Strait island children in Far North Queensland. Aust N Z J Public Health 1998; 22: 664-668. (Received 6 Apr, accepted 24 Aug, 1999) Authors' details Queensland Health, Cairns, QLD. Jeffrey N Hanna, MPH, FAFPHM, Public Health Physician, Tropical Public Health Unit; Tim H Warnock, FRACP, Paediatrician, Cairns Base Hospital. Department of Gastroenterology and Hepatology, Royal Children's Hospital, Brisbane, QLD. Ross W Shepherd, MD, FRACP, Director. Communicable Diseases Unit, Queensland Health, Brisbane, QLD. Linda A Selvey, PhD, FAFPHM, Manager. Reprints will not be available from the authors. Correspondence: Dr J N Hanna, Tropical Public Health Unit, Queensland Health, PO Box 1103, Cairns, QLD 4870. md1AThealth.qld.gov.au Results of investigations of three Indigenous children with fulminant hepatitis AReferencePatient 2Patient 3TestrangePatient 1On admissionDay 5Day 2Day 5Serum bilirubin level (µmol/L)<20389166269225202Aspartate aminotransferase level (U/L)10-6016016785137853672279Alanine aminotransferase level (U/L)<4017502690187322851352Blood glucose level (mmol/L)3.5-6.01.7ND1.9ND3.2Prothrombin time (s)10-15>180ND147ND84Activated partial thromboplastin time (s)23-37135ND107ND65Serum ammonia level (µmol/L)10-35416NDNDND205ND = not done

Jeffrey N Hanna · Tim H Warnock · Ross W Shepherd · Linda A Selvey

Research End-stage renal disease in Aboriginals in New South Wales: a very different picture to the Northern Territory Alan Cass, Adrian G Gillin and John S Horvath MJA 1999; 171: 407-410 Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Aboriginal health Abstract Objectives: To compare the incidence of end-stage renal disease (ESRD) among Aboriginals in New South Wales with the incidence among Aboriginals in the Northern Territory, and to compare the patterns of ESRD among Aboriginals and non-Aboriginals in NSW. Design: Secondary data analysis of information from unpublished and published Australia and New Zealand Dialysis and Transplant Registry reports. Main outcome measures: Average annual incidence of ESRD (persons per million); form of renal replacement therapy; mortality at 31 March 1998; patient and graft survival one and five years after transplant. Results: Each year in NSW, 5-17 new Aboriginal patients are treated for ESRD. There was no increase in the average annual incidence of ESRD among NSW Aboriginals (118 per million in 1988-1989 and 111 per million in 1996-1997), whereas incidence in the NT increased from 255 per million to 800 per million. In NSW, ESRD was attributed to diabetes in 32% of Aboriginal patients, compared with 13% of non-Aboriginal patients (P < 0.001). In NSW, Aboriginal patients were younger and more likely to be female, a pattern similar to that in the NT. The outcome of ESRD treatment is not significantly different between Aboriginals and non-Aboriginals in NSW. Conclusion: There is a different pattern of incidence of ESRD and of outcomes with treatment among Aboriginals in NSW compared with those in the NT. A possible explanation is that the lower incidence in NSW reflects less profound socioeconomic disadvantage and better access to primary and specialist care. Introduction Indigenous Australians experience high morbidity and mortality due to end-stage renal disease (ESRD). In the Northern Territory, the average annual incidence of ESRD for Aboriginals in 1988-1993 was 17.4 times that for non-Aboriginals,1 a disparity made more apparent by age adjustment.2 The number of dialysis treatments in the NT is doubling every two years.3The 30 June 1996 estimate of the Indigenous population (386 049) represented 2.1% of the total Australian population,4 but Aboriginals constitute 5% of the Australian members of the Australia and New Zealand Dialysis and Transplant Registry (ANZDATA).5 Whether the increasing incidence and prevalence of renal disease is occurring in NSW as well as nationally and in the NT has not been well documented. The aims of our study were to document the number of new Aboriginal patients with ESRD in NSW during 1987 to 1998 and compare recent trends in incidence with national and NT data, and to compare for Aboriginal and non-Aboriginal patients in NSW: the patterns of aetiology of ESRD; the demographic characteristics at the time of being entered into ANZDATA; the outcomes for individuals who were notified to the Registry during the period 1987 to 1998; and patient and graft survival for those who received transplants during the period 1987 to 1998. Methods Information was obtained from ANZDATA Annual Reports (12 and 18-21)6-10 and unpublished data from ANZDATA. All nephrology units in Australia and New Zealand that provide dialysis or transplant services submit detailed six-monthly reports to ANZDATA. The reports give information regarding new patients accepted onto treatment programs, deaths that have occurred, and any alteration in treatment for current patients, including changing the mode of dialysis or receiving a transplant. For NSW, the NT and across Australia, we analysed: the number of Aboriginal patients entered into ANZDATA from 1987 to 1998 in NSW, the NT and across Australia; and the average annual incidence of ESRD. For NSW only, we analysed: primary renal disease diagnostic category; mean age; outcome data at 31 March 1998 for people who had been entered into ANZDATA since 1 January 1987. Outcomes were categorised as death, functioning transplant, haemodialysis, continuous ambulatory peritoneal dialysis (CAPD), and loss to follow-up or having moved interstate; causes of death, categorised into cardiac, vascular, infection, social, malignancy and other; patient survival and graft survival for transplants performed between 1 January 1987 to 31 March 1998. The average annual incidence of ESRD was calculated using Australian Bureau of Statistics (ABS) estimates and projections of the Aboriginal and Torres Strait Islander population for the years between actual Census counts. These estimates are based upon current trends in fertility and mortality and take into account an increasing propensity for people to identify themselves as being of Indigenous origin. The definition of "Aboriginality" from both data sources (ANZDATA and ABS) relies upon self-identification. Annual incidence was calculated as an average for each two-year period, as there is marked variability in the number of new patients per year, and small absolute numbers. Statistical analysis of demographic and outcome data was performed using STATA 5.0.11 A t test of means and χ2 test or Fisher's exact test of proportions were performed. Survival analysis was performed at the ANZDATA Registry. Data were provided as actuarial life-table estimates and the log rank test was performed. The data were entered into STATA 5.0 and graphed. Results Incidence Each year in NSW, 5-17 new Aboriginal patients are treated for ESRD (Table 1). The average annual incidence of ESRD among Aboriginals in NSW for the two years 1988-1989 was 118 per million. This remained substantially unchanged at 111 per million in 1996-1997. During the same period the average annual incidence of ESRD in Aboriginals across Australia increased significantly (Table 1); in the NT, the rise in incidence was more marked. The crude incidence for non-Aboriginals in NSW was 78 per million for 1993-1997, a slight rise from the 1980s due to increased acceptance for dialysis of patients over the age of 65 years. Diagnostic categories Diabetes, glomerulonephritis and hypertension are the most common primary renal diseases among Aboriginals with ESRD in NSW (Table 2). Diabetes is listed as the primary renal disease in 32% of Aboriginals, compared with 13% of non-Aboriginals (P < 0.001). Analgesic nephropathy affects a significantly greater proportion of the non-Aboriginal population, mainly among females: 28% in non-Aboriginal females, compared with 10% in Aboriginal females. No definite diagnosis was recorded for 11% of Aboriginals, compared with 5% of non-Aboriginals (P = 0.004). Demographics Significantly more Aboriginal females than males entered the ESRD program in NSW (Table 3), the reverse pattern to non-Aboriginals (P = 0.03). The Aboriginal population was younger at entry to the program and there were significantly fewer people over the age of 65 years (P < 0.001). Outcome, or patient status at 31 March 1998, was not significantly different between the groups (P = 0.59). However, no attempt at age or sex standardisation has been made in this analysis. Causes of death The differences between Aboriginals and non-Aboriginals in NSW in causes of death approach statistical significance (P = 0.07). A significantly larger proportion of Aboriginals died from cardiovascular diseases (P = 0.01). A significantly smaller proportion of deaths were due to social reasons (P = 0.02). Patient and graft survival after transplant Aboriginal patients receiving transplants in NSW during the study period were younger (Figure 1), but experienced lower patient survival and graft survival rates (Figures 2a and 2b), although these differences were not significant (Table 4). Discussion Our data show no evidence of an epidemic of renal failure among Aboriginals in NSW, although the incidence remains higher than among the non-Aboriginal population. Aboriginal patients in NSW with ESRD are on average 10 years younger than non-Aboriginal patients, more likely to be female, and more likely to have diabetes and to die of cardiovascular disease. These features are similar to those reported in the NT.2 However, in NSW, there is no significant difference in outcome between Aboriginal and non-Aboriginal patients who have been entered into the Registry since January 1987, whereas, in the NT, survival is significantly worse in Aboriginal than in non-Aboriginal patients.2 The persistently high rate of withdrawal up to 1997 of NT Aboriginal people from ESRD treatment, about 25%,3 is not present in NSW. Our results show that diabetes, glomerulonephritis and hypertension are the prominent primary causes of ESRD among NSW Aboriginals. The rise in renal failure attributed to diabetes follows a similar pattern to that noted in Aboriginals across Australia.10 The pattern of primary causes of renal disease is consistent between Aboriginal populations in different States.10 Impediments to effective and culturally appropriate service delivery to Aboriginal patients have been postulated as reasons for poor survival and high withdrawal rates from treatment.12 Therapeutic programs have typically removed people from their cultural and social support networks by requiring patients to leave their land, families and communities.13 Unlike in the NT, South Australia and Western Australia, there are few remote, non-urbanised communities in NSW; Aboriginals in NSW reside predominantly in cities and rural towns. The higher proportion of Aboriginal patients with uncertain aetiology of their ESRD is consistent with a lower renal biopsy rate, which may relate to late referral and lack of access to renal specialist services. In NSW, specialist renal services are increasingly being provided where Aboriginals live. The Statistical Local Areas with the highest proportion of Indigenous people are Brewarrina (53.1%), Central Darling (25.3%), Bourke (24.5%) and Walgett (20.4%).14 CAPD training is now occurring in some larger rural centres, and haemodialysis facilities are provided in Bourke and Brewarrina. These initiatives, which significantly reduce the dislocation of patients from their community and remove impediments to the delivery of appropriate ESRD services, may facilitate improved survival. There is a tendency towards lower patient survival and graft survival among NSW Aboriginals compared with non-Aboriginals, despite the Aboriginal graft recipients' being younger. In the NT, graft and patient survival among Aboriginals are significantly worse at one and five years than among non-Aboriginals.2 A significant difference in survival is not evident in the NSW data. The larger 95% confidence intervals in the NSW Aboriginal group are a consequence of fewer transplants being performed: 36 among Aboriginal patients, compared with 1755 among non-Aboriginal patients. These numbers do not provide sufficient power to detect a significant difference between the groups. The pattern of rapidly increasing incidence of ESRD among Aboriginals across Australia, especially in the NT, is not seen in NSW. Spencer et al argue that the increase in the NT is real, not due to ageing of the Aboriginal population or improved ascertainment.2 The reason for this difference in incidence is not clear. It may be due to differences between the populations in apparent predisposition to renal disease or to differences in the prevalence of primary causes and promoters of chronic renal disease. The epidemic of disease in the NT is not only due to an increased prevalence of diabetes. Community screening studies show a prevalence of significant proteinuria in marked excess of the prevalence of diabetes or impaired glucose tolerance.2,15 In the NT, from 1988 to 1993, the average annual incidence of ESRD not attributable to diabetes was 350 per million per year among Aboriginals.1 Lower incidence of ESRD in NSW Aboriginals may reflect less profound socioeconomic disadvantage and readier access to effective primary and specialist care. However, there may be poor ascertainment, particularly in rural areas of NSW. Further study is indicated to analyse this question. Acknowledgements The data reported here have been supplied by the Australia and New Zealand Dialysis and Transplant Registry. The interpretation of these data is the responsibility of the authors and in no way should be seen as an official policy or interpretation of the Australia and New Zealand Dialysis and Transplant Registry. Dr Alan Cass is the recipient of a postgraduate research scholarship from the Centre for Kidney Research, New Children's Hospital, Sydney. We thank Dr Wendy Hoy, who critically reviewed the manuscript, and Dr Zhiqiang Wang, who provided statistical advice. 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, McFarlane R, Pugsley DJ, et al. Markers for cardiovascular and renal morbidity: expectations for an intervention programme in an Australian aboriginal community. Clin Exp Pharmacol Physiol 1996; 23: S33-S37. Spencer JL, Silva DT, Snelling P, Hoy WE. An epidemic of renal failure among Australian Aboriginals. Med J Aust 1998; 168: 537-541. Australian Bureau of Statistics. Experimental estimates of the Aboriginal and Torres Strait Islander population. Canberra: ABS, 1998. (Catalogue No. 3230.0.) Disney AP. Demography and survival of patients receiving treatment for chronic renal failure in Australia and New Zealand: report on dialysis and renal transplantation treatment from the Australia and New Zealand Dialysis and Transplant Registry. Am J Kidney Dis 1995; 25: 165-175. Disney APS, Collins J, Russ GR, et al. ANZDATA Registry Report 1989. Adelaide: Australia and New Zealand Dialysis and Transplant Registry, 1989. Disney APS, Collins J, Russ GR, et al. ANZDATA Registry Report 1995. Adelaide: Australia and New Zealand Dialysis and Transplant Registry, 1995. Disney APS, Collins J, Russ GR, et al. ANZDATA Registry Report 1996. Adelaide: Australia and New Zealand Dialysis and Transplant Registry, 1996. Disney APS, Collins J, Russ GR, et al. ANZDATA Registry Report 1997. Adelaide: Australia and New Zealand Dialysis and Transplant Registry, 1997. Disney APS, Collins J, Russ GR, et al. ANZDATA Registry Report 1998. Adelaide: Australia and New Zealand Dialysis and Transplant Registry, 1998. STATA statistical software [computer program]. Version 5.0. College Station, Texas: Stata Corporation, 1997. Bennett E, Manderson L, Kelly B, Hardie I. Cultural factors in dialysis and renal transplantation among aborigines and Torres Strait Islanders in north Queensland. Aust J Public Health 1995; 19: 610-615. Willis J. Fatal attraction: do high technology treatments for end-stage renal disease benefit aboriginal patients in central Australia? Aust J Public Health 1995; 19: 603-609. Australian Bureau of Statistics. Census of population and housing -- selected social and housing characteristics for statistical local areas, New South Wales and Jervis Bay. Canberra: ABS, 1996. (Catalogue no. 2015.1.) Van Buynder PG. The epidemiology of renal disease in Aboriginal Australians [Master of Public Health thesis]. Sydney: University of Sydney, 1991. (Received 12 Feb, accepted 19 Jul, 1999) Authors' details Menzies School of Health Research, Darwin, NT. Alan Cass, MB BS, FRACP, PhD student. Department of Renal Medicine, Royal Prince Alfred Hospital, Sydney, NSW. Adrian G Gillin, FRACP, PhD, Staff Specialist; John S Horvath, MB BS, FRACP, Professor. Reprints will not be available from the authors. Correspondence: Dr A Cass, Menzies School of Health Research, PO Box 41096, Casuarina, NT 0811. alancassATmenzies.edu.au Back to textBack to textBack to textBack to textBack to textBack to text

Alan Cass · Adrian G Gillin · John S Horvath

Editorial The health of Australia's mothers and babies Improvements in the collection of perinatal statistics are needed to fill the gaps MJA 1996; 164: 198-199 Childbirth in Australia is relatively safe, as measured by the traditional outcomes of maternal and perinatal mortality. About 1 in 8000 mothers die from all direct, indirect and incidental causes associated with pregnancy and childbirth.1 The perinatal death rate, which includes fetal deaths and neonatal deaths up to 28 days of infants weighing at least 500 g, declined to 8.2 per 1000 births in 1993,2 the lowest level yet achieved. During the last two decades, all States and Territories have developed perinatal data systems that provide valuable information on maternal risk factors and complications and the outcomes of mothers and infants. This information, collected by midwives and medical practitioners, is increasingly being used for research and policy development and discussion about issues relating to pregnancy and childbirth. The 1992 report on Australian mothers and babies drew attention to births to teenage mothers, mothers born overseas and Australian Aboriginals and Torres Strait Islanders, and to factors associated with caesarean births.3 Teenage births. Births to teenage mothers in Australia, of just over 20 per 1000 in the early 1990s, were well below the peak of 55.5 per 1000 in 1971.4 However, these figures give an incomplete picture of teenage pregnancy because only South Australia and the Northern Territory have population-based data about induced abortions. Analysing trends in birthrates fails to indicate the total extent of teenage pregnancy. In 1992, 14 396 teenage mothers gave birth in Australia: 4115 were aged under 18 years (2503 were aged 17; 1133 were aged 16; 357 were aged 15; and 122 were under 15 years). The South Australian data showed that for every 100 births to teenage mothers, there were 82 induced abortions.5 Extrapolating from these data, the estimate of teenage pregnancies nationally in 1992 was in excess of 26 000. Based on these annual figures, about one in five teenagers will become pregnant at some stage between the ages of 15 and 19 years, and one in 10 will give birth. Women born overseas. Of all the women who gave birth in Australia in 1992, more than one in five (22.7%) were born overseas, and 6.3% of all mothers were born in Asia. Of those born in Asia, 3605 women (1.4% of all births) were from Vietnam, 2660 (1%) from the Philippines, 1881 (0.7%) from China, 1365 (0.5%) from Malaysia, 1164 (0.5%) from India and 1046 (0.4%) from Hong Kong. Perinatal outcome did not seem to differ greatly from that of infants of Australian-born mothers,6 but further research is needed to determine the effects of maternal risk factors on outcomes such as birthweight and perinatal mortality. The recent substantial increase in births to Asian-born mothers, notably Vietnamese and Chinese women, places extra demands on health services to ensure that their special needs are met, particularly in Sydney and Melbourne, where disproportionate numbers of people from non-English-speaking backgrounds live. These women often have vastly different cultural beliefs and practices associated with pregnancy and childbirth. Bicultural health workers are increasingly being recognised as having an important role in establishing support networks for these women, familiarising them with the Australian health system, and assisting them in overcoming language and attitudinal barriers. Australian Aboriginals and Torres Strait Islanders. Many aspects of caring for overseas-born women are also pertinent to health services for Australian Aboriginals and Torres Strait Islanders. In 1991, 7027 Aboriginal and Torres Strait Islander women gave birth, and 7257 did so in 1992, accounting for 2.9% of all mothers in both years. Many of these women travel long distances from remote communities to hospitals in larger centres, and thus frequently give birth in an unfamiliar environment. In 1992, one in four births in this group were to teenage mothers and almost one in three of these teenagers had had at least one other child. The average birthweight (3150 g) of babies born to Aboriginal Australians and Torres Strait Islanders was 206 g less than that of all Australian babies, and the proportion of babies that were of low birthweight (< 2500 g) was 12.9%, more than double the rate of 6.3% for all births. Caesarean births. The seemingly inexorable rise in deliveries by caesarean section in Australia continues unabated, with a peak at 18.3% of total deliveries in 1992. South Australia (22.1%) and Queensland (20.9%) consistently have the highest caesarean rates and Tasmania (16.1%) usually the lowest. The caesarean rate of 22.4% for women with private health insurance was more than 40% higher than the rate of 15.8% for women without insurance (partly attributable to more older women in the insured group). Caesarean rates for women with insurance having their first baby increased with maternal age, from 21.9% at 25-29 years to 28.1% at 30-34 years, 37.4% at 35-39 years, and 47.4% at 40-44 years. High caesarean rates were also associated with multiple births (39.2% for twins and 85.3% for triplets, compared with 18% for singleton births), with breech presentation in singleton births (73.8%), and with very low birthweight babies (53.8% for singleton babies weighing 1000-1499 g). Relatively simple measures, such as more detailed recording of the indications for caesarean section and obtaining an opinion from another obstetrician about whether operative intervention is indicated, have proved effective in reducing caesarean rates.7The Royal Australian College of Obstetricians and Gynaecologists should address the issue of high caesarean rates in Australia by requiring regular audits of hospitals and medical practitioners. The quality and usefulness of information about perinatal health can be enhanced in several ways. Firstly, it should be recognised that analysis of trends in teenage pregnancy and the formulation of preventive strategies require data about induced abortions as well as data about births. Secondly, by linking registrations of perinatal and infant deaths to information for all births from the perinatal data systems in every State and Territory, the association between maternal risk factors and outcomes can be better evaluated.8,9 Thirdly, while the patterns of risk factors, type of care and outcomes are remarkably consistent from year to year, shortening the interval between the year of birth and the publication of State and national reports is an important goal. Paul A L Lancaster Director, Australian Institute of Health and Welfare National Perinatal Statistics Unit, University of Sydney, NSW National Health and Medical Research Council. Report on maternal deaths in Australia 1988-90. Canberra: AGPS, 1993. Australian Bureau of Statistics. Perinatal deaths, Australia 1993. Canberra: ABS, 1994. (Catalogue No. 3304.0.) Lancaster P, Huang J, Pedisich E. Australia's mothers and babies 1992. Sydney: AIHW National Perinatal Statistics Unit, 1995. Australian Bureau of Statistics. Births, Australia 1993. Canberra: ABS, 1994. (Catalogue No. 3301.0.) Chan A, Scott J, McCaul K, Keane R. Pregnancy outcome in South Australia 1992. Adelaide: South Australian Health Commission, 1993. Guevara V, Taylor L. The health of mothers born in non-English-speaking countries and their babies, NSW 1990-1993. New South Wales Public Health Bull 1995; 6 Suppl S2: 1-52. Myers SA, Gleicher N. A successful program to lower cesarean section rates. N Engl J Med 1988; 319: 1511-1516. Perinatal Data Collection Unit. The Consultative Council on Obstetric and Paediatric Mortality and Morbidity. Births in Victoria 1983-1992. Melbourne: Department of Health and Community Services, 1994. Gee V. Perinatal statistics in Western Australia. Tenth annual report of the Western Australian Midwives Notification System, 1992. Perth: Health Department of Western Australia, 1993.

Editorial The human element of adverse events Is a certain level of error inevitable in healthcare? MJA 1999; 170: 404-405 The Quality in Australian Health Care Study (QAHCS),1 together with the Harvard study on which it was based,2 were groundbreaking studies that for the first time systematically revealed the nature and scale of iatrogenic injury in healthcare. Morbidity due to healthcare appears to be a major public health problem, and it is very unlikely that this problem is confined to Australia and the United States. The QAHCS revealed particularly high levels of adverse events (AEs), in part because it took a broader, quality-of-care approach rather than one focused on negligence and compensation. In this issue of the Journal, review and content analysis of textual summaries of the AEs by Wilson et al, the QAHCS team, have now yielded a deeper understanding of these events.3 The major categories of human error, accounting for over 70% of AEs, were: Failures in technical performance; Failure to decide and/or act on available information; Failure to investigate or consult; and A lack of care or failure to attend. Do the failures identified by the QAHCS team imply carelessness and/or incompetence on the part of healthcare staff? On occasions this may be so, but research on human error paints a more complex picture.4 Tempting though it may be to simply blame the doctors and nurses, identifying a failure in the process of care is usually just the first step in understanding the causes of AEs. This is especially so when the failure occurs not in some routine procedure, but in complex diagnostic or technical tasks, in which the term "error" may be a misleading oversimplification.5 Should we therefore accept that a certain level of error is inevitable in healthcare? We certainly should not accept such high levels of iatrogenic injury, much of which is preventable. In one sense, though, it is necessary to accept error. Before there can be any serious hope of reducing AEs there must first be a recognition of the frequency of error and of imperfect decision-making in healthcare, as is the case in other human activities.6 The next step, as the QAHCS team argues, is to look beyond the immediate failures to their deeper causes.3 Analyses of accidents in medicine and elsewhere have led to a much broader understanding of the causes of AEs, with less focus on individuals and more on pre-existing organisational factors. The conditions which give rise to failures in the process of care can be considered in a broad framework of individual, task, team, work environment and organisational factors.7 A failure to consult, for instance, may be due to overconfidence in a junior member of staff, inexperience, inadequate knowledge, delay in obtaining test results, or the unavailability of senior members of staff. Each of these problems may be specific to that occasion or may reflect more general problems: the attitudes of individual members of staff, the training policies of the hospital, poor supervisory practices, inadequate and haphazard systems of communication or interpersonal problems within a team. The National Taskforce on Quality in Australian Health Care produced a comprehensive, multifaceted plan of action to reduce healthcare injuries and deaths.8 The Taskforce was surely correct to see both the problem and the solution as multidimensional, as the systems approach implies. Safety programs in industries, involving sociotechnical systems with many similarities to medicine, target the tasks, teams and conditions of work, as well as ensuring that staff are highly skilled.4 Safety needs to be addressed both at the level of the particular clinical process and at the interpersonal and organisational levels. Where tasks can be clearly specified, then greater standardisation, clear guidelines and less reliance on the vagaries of human memory and vigilance are essential. Team and communication failures have been strongly implicated in many accident analyses and remedial measures can be straightforward. Systems have also been developed in industry to monitor the conditions of work, as well as the associated organisational factors and decisions that give rise to these conditions. The Taskforce recommendations have been widely supported9 and a number of working groups have been established by Australian health departments. In 1997, a National Expert Advisory Group on Safety and Quality in Australian Health Care was established, and their recommendations will be considered by the Health Ministers later this year. In the 1998 Australian Health Care Agreements, $658 million was allocated for quality improvements within the public health system over five years, and a further $253 million for, among other objectives, improving the integration of public hospital and community services. Welcome though these initiatives are, the pace of change nevertheless seems slow given the stark message of the original QAHCS study four years ago. The findings from QAHCS suggested that each year 50 000 Australians suffer permanent disability and 18 000 die at least in part as a result of their healthcare. Further evidence emerged in 1997 with the publication of AE rates in Victorian hospitals.10 Since then, thousands more Australians have presumably been injured or died through deficiencies in the healthcare system. Furthermore, the QAHCS found that AEs lost Australia over three million bed-days per annum. In its interim report, the National Expert Advisory Group pointed out that the extrapolated potential saving from preventable AEs in 1995-96 would be $4.17 billion.11 AEs also lead to increased disability benefits and time lost off work, which all impact on the Australian economy. Achieving change on the required scale will require a specific commitment from all healthcare providers, administrators and consumers, as well as unequivocal, sustained government support. It is hoped that 1999 will see the necessary consensus for urgent action from all the parties involved and the implementation of specific, carefully evaluated safety initiatives. It would be tragic if the "lack of care and failure to attend" and "failure to decide and act", revealed as causes of AEs, ultimately also applied to those professional and government bodies responsible for programs of prevention. Charles A Vincent Reader in Psychology, Clinical Risk Unit, Department of Psychology University College London, UK Wilson RM, Runciman WB, Gibberd RW, et al. The Quality in Australian Health Care Study. Med J Aust 1995; 163: 458-471. Brennan TA, Leape LL, Laird NM, et al. Incidence of adverse events and negligence in hospitalized patients. N Engl J Med 1991; 324: 370-376. Wilson RMcL, Harrison BT, Gibberd RW, Hamilton JD. An analysis of the causes of adverse events from the Quality in Australian Health Care Study. Med J Aust 1999; 170: 411-415. Reason JT. Understanding adverse events: human factors. In: Vincent CA, editor. Clinical risk management. London: BMJ Publications, 1995. Cook RI, Woods DD, Miller C. A tale of two stories: contrasting views of patient safety. Report of the National Patient Safety Foundation. Chicago: American Medical Association, 1998. Leape LL. Error in medicine. JAMA 1994; 272: 851-857. Vincent CA, Taylor-Adams S, Stanhope N. A framework for the analysis of risk and safety in medicine. BMJ 1998; 316: 1154-1157. The Final Report of the Taskforce on Quality in Australian Health Care. Canberra: AGPS, June 1996. Wilson RM, Harrison BT. Are we committed to improving the safety of health care. Med J Aust 1997; 166: 452-453. O'Hara D, Carson NJ. Reporting of adverse events in hospitals in Victoria 1994-1995. Med J Aust 1997; 166: 460-463. National Expert Advisory Group on Safety and Quality in Australian Health Care. Interim report - Commitment to quality enhancement. July 1998. <http://www.health.gov.au/about/cmo/neag.htm> 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/> We appreciate your comments.

Charles A Vincent

Research An analysis of the causes of adverse events from the Quality in Australian Health Care Study Ross McL Wilson, Bernadette T Harrison, Robert W Gibberd and John D Hamilton MJA 1999; 170: 411-415 For editorial comment, see Vincent Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Administration and health services The Quality in Australian Health Care Study (QAHCS), published in the Journal in 1995,1 reported that 16.6% of hospital admissions were associated with an iatrogenic patient injury, termed an adverse event (AE) (see Box 1). This compares with the rate of 3.7% for AEs in the Harvard Medical Practice Study (HMPS),2 and a rate of 17% in a more recent study with an alternative observational method of determining AEs.3 Fifty per cent of the AEs in the QAHCS were judged to have a high preventability score (4 or more on a scale of 1-6 of increasing likelihood of preventability).1 The disability caused by these adverse events ranged from temporary disability (fully resolved in one month) in 46.6% of AEs, to death in 4.9% of AEs. Although recording AEs emphasises only the "complications" of rather than the benefits derived from healthcare, AEs are of great significance to individual patients as well as to the whole healthcare system. Abstract Objective: To examine the causes of adverse events (AEs) resulting from healthcare to assist in developing strategies to minimise preventable patient injury. Design: Descriptions of the 2353 AEs previously reported by the Quality in Australian Health Care Study (QAHCS) were reviewed. A qualitative approach was used to develop categories for human error and for prevention strategies to minimise these errors. These categories were then used to classify the AEs identified in the QAHCS, and the results were analysed with previously reported preventability and outcome data. Results: 34.6% of the causes of AEs were categorised as "a complication of, or the failure in, the technical performance of an indicated procedure or operation", 15.8% as "the failure to synthesise, decide and/or act on available information", 11.8% as "the failure to request or arrange an investigation, procedure or consultation", and 10.9% as "a lack of care and attention or failure to attend the patient". AEs in which the cause was cognitive failure were associated with higher preventability scores than those involving technical performance. The main prevention strategies identified were "new, better, or better implemented policies or protocols" (23.7% of strategies), "more or better formal quality monitoring or assurance processes" (21.2%), "better education and training" (19.2%), and "more consultation with other specialists or peers" (10.2%). Conclusion: The causes of AEs or errors leading to AEs can be characterised, and human error is a prominent cause. Our study emphasises the need for designing safer systems for care which protect the patient from the inevitability of human error. These systems should provide new policies and protocols and technological support to aid the cognitive activities of clinicians. Introduction An additional analysis of data from the Quality in Australian Health Care Study (QAHCS)1 was undertaken in order to understand more fully the causes of the adverse events (AEs) identified and to assist in developing prevention strategies. Here, we describe the error or errors in the delivery of healthcare which led to the AEs. This contrasts with our previous report,1 which focused on the patient characteristics associated with AEs and the nature and consequences of the AEs. Methods The method of determining AEs in the QAHCS has been described previously.1 The AEs were re-examined with the specific goals of determining the causes for, or the underlying errors leading to, each AE. In addition, strategies that were judged to have the potential to prevent AEs were recorded. To obtain this information the first and subsequent review forms (RF1 and RF2 forms1) collected during the QAHCS were re-examined. The source material for these forms had been the hospital medical records, but neither the hospitals nor the medical records were revisited in this analysis. Categories for the causes of the AEs were devised by an iterative process during a three-day workshop. For this, we sought additional expertise in clinical epidemiology and qualitative research methods. Using these categories, the AEs recorded on the review forms were assessed by three of the senior medical specialists who had originally reviewed the medical records in the QAHCS. All the material from each AE was reviewed by only one reviewer, as the agreement between the medical reviewers in determining the presence or absence of an AE during the QAHCS was 80% (kappa, 0.55). A proforma was completed which asked the reviewer to identify the error and then classify it by human cause and preventive strategy. All AEs were also categorised into some of the processes of clinical care. Results for the "delay", "treatment" and "investigation" categories are presented. The categories were not mutually exclusive. These data were then entered into a database, merged with the original data from the QAHCS for each case and analysed. Two of the original total of 2353 AEs were missed in this review; thus, results are given for 2351 AEs. Our analysis provides the frequency of occurrence of each of the categories of causes of AEs, together with the proportion in each category resulting in permanent disability (including death) and the proportion with high preventability. Results Human error categories Box 2 shows the frequency of occurrence of each of the human error categories, and the proportion of the AEs in each category judged to have permanent disability and high preventability. Of the 2351 AEs, 1922 (81.8%) were associated with one or more human error categories. As the error categories were not mutually exclusive, the 1922 AEs were associated with 2940 causes. "Complication of, or failure in, the technical performance of an indicated procedure/operation" was the most frequent cause of AEs; examples of this category are shown in Box 3A. Human errors associated with categories of failure of cognitive function were the next most frequent cause of AEs (Box 2). These included "Failure to synthesise, decide and/or act on available information", "Failure to request or arrange investigation, procedure or consultation", and "Misapplication of, or failure to apply, a rule; or use of a bad or inadequate rule". The most frequent error category, "complication of, or failure in, the technical performance of an indicated procedure/operation", had a lower proportion of AEs with permanent disability (14.2%). The next five most frequent human error categories all had a high proportion of AEs with permanent disability (25% or more) (Box 2). This pattern was also seen in the proportions of AEs with death as the outcome: 2.2% in the first category, and 8% or more in each of the next five categories. Of the 1201 AEs having high preventability, 9 (0.7%) were not associated with a human error category; for the remaining 1192 AEs, 2051 causes were identified (Box 2). Delay categories The importance of timeliness to the quality of healthcare led to further analysis of all AEs to ascertain the nature and role of delay in their causation (Box 4A). Delays contributed to 20.0% of AEs: of these, delays in diagnosis accounted for 56.8% and treatment delays for 40.6%. Diagnostic delay was usually the failure to make, or attempt to make, a diagnosis of a patient's condition rather than just providing symptomatic or even no treatment. Treatment delay was when the diagnosis had been made but there was a delay in initiating specific therapy. Examples of AEs in the delay category are included in Box 3B. The AEs with delay categories were judged to have very high preventability (86%-90%) compared with the average (51.2%) for all AEs (Box 4A). Treatment categories AEs categorised as caused by a treatment error were also analysed (Box 4B). In 19.6% of all AEs, treatment error contributed to the cause. The majority of AEs in this group fell into the categories of "no or inadequate treatment" (51.5%), or "wrong or inappropriate treatment" (27.4%). As with AEs caused by delay, these AEs were judged to have much higher preventability than the average for all AEs. Examples of AEs involving treatment errors are shown in Box 3C. Investigation categories Analysis of the AEs caused by patient investigation issues is shown in Box 4C, and examples are given in Box 3D. There was a problem with clinical investigation in 10.7% of AEs. Paralleling the results in the treatment category, most (78.6%) of these AEs were in this category because an investigation was not done, rather than the investigation being inappropriate (3.6%), or not acted upon (15.5%). Consistent with other AEs that are attributed to cognitive failure, there was a very high percentage of these AEs rated as high preventability. Strategies for preventing AEs When describing AEs, preventability refers to the identification of an avoidable error that led to the adverse event. This is not to say that the error could be avoided on every occasion, and that the adverse event would not occur. Rather, it implies that, with the current state of knowledge and technology, it is possible to identify and avoid that particular error, and hence reduce the probability of an AE. The reviewers were making a judgement, having identified the error, on the particular strategy for a change in the healthcare system that could have prevented the AE. The outcomes of these judgements are given in Box 5. Nineteen (1.6%) of the 1201 high preventability AEs did not have a prevention strategy category. Of the 2613 prevention strategies identified in the 1182 AEs with high preventability, 24.7% (646) were for "better education and training", 20.9% (545) were for "new or better implemented policies or protocols" and 18.6% (486) were for "more or better formal quality monitoring or assurance processes". Discussion AEs are important to patients, healthcare providers and to the custodians and funders of health services. One estimate of the national cost to the Australian healthcare system of just the additional hospital bed-days (as a result of the AEs identified in 19921) is in excess of $800 million dollars per year.4 This estimate ignores any subsequent hospital admissions and out-of-hospital healthcare expenses, loss of productivity of the patients involved, and long term community costs of permanent disability from AEs. It also ignores the benefits received from healthcare. Providing insights into how AEs occur can help in developing prevention strategies to reduce the frequency and severity of patient injuries during healthcare. Our review and analysis of the AE data from the QAHCS have shown that the causes of AEs or errors leading to AEs can be characterised, and that human error is a prominent cause. It is important to recognise that human error is inevitable for even the best-trained and best-qualified healthcare providers. Weed has recently pointed out that the unaided human mind is incapable of performing consistently at the necessary level to provide optimal healthcare.5 However, other studies6 have noted that the label "human error" is prejudicial and non-specific; it may retard rather than advance our understanding of how complex systems fail. It is postulated that within complex systems error is a symptom of organisational problems, and this is likely to apply to healthcare. Therefore, we need a healthcare-system response to error that moves the system towards being as "failsafe" as possible rather than one that blames the clinician who may have erred. Examples from the more frequently studied area of adverse drug events7 would be decision-support technology for antibiotic prescribing,8 with its demonstrated benefits, and electronic prescribing to reduce prescribing and transcription errors in hospital.9 Our analysis identified broad functional categories that are linked to the processes that make up the system of healthcare delivery and hence cut across specialties, diagnosis-related groups (DRGs) and particular patient groups. The sample size is large enough to provide useful information even when several AEs could not be classified into the categories chosen, or insufficient information was available to indicate cause. On the other hand, several factors bias the information available for assessing AEs because of an emphasis on procedures and short term outcomes and possible under-reporting of the contribution of the supporting systems to the cause of the AEs. Firstly, because the original data source was the hospital medical record, the information available about AEs is biased towards the patient involved and away from other potentially important contextual events at the time. Further, the medical record often focuses more on the actions of clinicians involved in direct or procedural patient intervention, and less on the actions of other staff or systems with a more supportive role. These and other factors will lead to an emphasis on procedures and short term outcomes, and a possible under-reporting of the contribution of supporting systems in causing AEs. Finally, information about subsequent or prior hospitalisations is usually only available if the patient attended the same hospital on all occasions. Having acknowledged these potential limitations, cognitive failure (Box 2) appears to have a role in 57% of all the causes of AEs, and most of the AEs involved were judged to be of high preventability and to have caused significant disability. These AEs were largely associated with errors of omission rather than commission. Does this represent a minimum "obligatory" error rate resulting from a combination of human error and our healthcare system, and hence which cannot be improved? Our data are not able to answer this question unequivocally, but we believe they show sufficient opportunities for moving the system towards a failsafe mode to suggest that the answer is no. Until recently there has been an under-recognition of the role and responsibilities of the healthcare system and its custodians in providing a "safe environment" using systems-improvement tools.10 One response to these data should be to look at the factors in healthcare delivery that may interfere with the cognitive or technical performance of healthcare providers. Insufficient use of information technology to assemble the necessary information at the time of decision-making may increase error. Another important factor is fatigue, which has already been shown to increase error in doctors.11 Sleep deprivation may have a much more significant role in human error in healthcare than the current work-load patterns pay heed to, but more research is needed. Other factors that may be important include the level of supervision provided to junior staff, and the pervasive effect of the culture of medical practice, which can unhelpfully portray error as individual failure or deviation from perfection.12 Our study method does not provide direct information about the role of these factors. The high proportion of causes of AEs involving cognitive failure must represent a manifestation of human error occurring in a system that is not patient protective, if one accepts that these practitioners are appropriately trained and competent by international standards. Our study provides clear guidance on methods for improvement, with "new, better, or better implemented policies or protocols" accounting for 24% of prevention strategies identified for the AEs, "quality monitoring and assurance processes" accounting for 21%, and "better education and training" for a further 19%. In summary, improvement is needed in the agreed processes of care, supported by information systems that allow general dissemination of current knowledge of diseases or treatments, and information on outcomes of care for each patient, through appropriate quality processes. Simple examples are the availability of practice guidelines and protocols at the point-of-care, and the use of automated reminders for patients and practitioners when a particular test or follow-up is required. In addition, having adequate patient "outcome" information in a form that can be benchmarked is a powerful tool in identifying unacceptable variation. Acknowledgements We acknowledge the contributions of Professor B Armstrong, Professor W R Runciman, Professor R Holland, Dr T Robertson and Dr A Hobbes. References Wilson RMcL, Runciman WB, Gibberd RW, et al. The Quality in Australian Health Care Study. Med J Aust 1995; 163: 458-471. <eMJA pdf> Brennan TA, Leape LL, Laird N, et al. Incidence of adverse events and negligence in hospitalised patients: results of the Harvard Medical Practice Study I. N Engl J Med 1991; 324: 377-384. Andrews LB, Stocking C, Krizek T, et al. An alternative strategy for studying adverse events in medical care. Lancet 1997; 349: 309-313. The Final Report of the Taskforce on Quality in Australian Health Care. Appendix 7. Canberra: AGPS, June 1996. <http://www.health.gov.au/pubs/hlthcare/toc.htm> Weed LL. New connections between medical knowledge and patient care. BMJ 1997; 315: 231-235. Cook RI, Woods DD. Operating at the sharp end: the complexity of human error. Human performance in anaesthesia: a corpus of cases. Report to the Anaesthesia Patient Safety Foundation, 1991. Columbus, Ohio: The Ohio State University: 255-307. Classen DC, Pestonick SL, Evans RS, et al. Adverse drug events in hospitalised patients: excess length of stay, extra costs and attributable mortality. JAMA 1997; 227: 301-306. Evans RS, Pestonick SL, Classen DC, et al. A computer-assisted management program for antibiotics and other anti-infective agents. N Engl J Med 1997; 338: 231-238. Bates DW, Boyle DL, Vander Vliet MB, et al. Relationship between medication errors and adverse drug events. J Gen Intern Med 1995; 10: 199-205. Leape LL. A systems analysis approach to medical error. J Eval Clin Pract 1997; 3: 213-222. Nocera A, Khursandi DS. Doctors' working hours: can the profession afford to let the courts decide what is reasonable. Med J Aust 1998; 168: 616-618. Leape LL. Error in medicine. JAMA 1994; 272: 1851-1857. (Received 4 May 1998, accepted 20 Jan 1999) Authors' details Royal North Shore Hospital, Sydney, NSW 2065. Ross McL Wilson, MB BS, FRACP, Senior Specialist in Intensive Care; Director of QARNS (Quality Assurance Royal North Shore); Bernadette T Harrison, RN RM, Manager QARNS. University of Newcastle, Newcastle, NSW 2308. Robert W Gibberd, PhD, Associate Professor, Department of Statistics; and Director of Health Services Research Group. John D Hamilton, MB BS, FRCP, Professor of Medicine, Faculty of Medicine and Health Sciences. Reprints: Dr R McL Wilson, Director of QARNS, Royal North Shore Hospital, Pacific Highway, St Leonards, NSW 2065. Email: rwilsonATdoh.health.nsw.gov.au 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/> 1: Terms and definitions Adverse event (AE): An AE was defined as an injury or complication which resulted in disability or prolongation of hospital stay and was caused by the healthcare received rather than by the disease from which the patient suffered. The AE either occurred during the hospital admission, or during an earlier contact with healthcare services, and was responsible for all or part of the hospital admission. Error: An act of commission or omission that caused, or contributed to the cause of, the unintended injury. for errors of commission this will usually be the immediate morbid consequences of the error for errors of omission this will usually be the continuation of, and consequences of, an existing morbid state that could have been cut short, or had a better outcome, if the error had not occurred. Prevention strategy: Changes in the system in which an error occurred that mayreduce the probability of the error occurring increase the probability that the error would be remedied before an unintentional injury occurredPreventability: Preventability of an AE was assessed by the detection of "an error in management due to the failure to follow accepted practice at an individual or system level"; accepted practice was taken to be "the current level of expected performance for the average practitioner or system that manages the condition in question". Back to textBack to text 3. Examples of categories of causes of adverse events and preventability scoresA. Human error categories Example 1: A 50-year-old man sustained a bowel perforation from colonoscopy for investigation of abdominal pain. Laparotomy required. Category: "Technical performance". Preventability score: 3. Example 2: A 71-year-old man required six operations for femoral hernia repair. Category: "Technical performance". Preventability score: 2. Example 3: A 32-year-old woman had persisting severe back pain after two laminectomies, three myelograms, one decompression/fusion, and three thecal/epidural injections over 18 months. In pelvic traction at the time of review. Category: "Technical performance". Preventability score: 4. Example 4: A failed attempt at percutaneous endoscopic gastrostomy on a 32-year-old woman was followed by an open procedure. The patient died 9 days later. Autopsy revealed acute peritonitis, subphrenic abscess and bilateral pneumonia. There did not appear to have been an antemortem diagnosis of intra-abdominal sepsis, or any specific treatment for it. Category: "Technical performance". Preventability score: 6. B. Delay in diagnosis and/or treatment categories Example 1: Diagnosis of cancer of the colon was delayed until the patient, a 62-year-old woman, presented with a ruptured caecum and peritonitis from an obstructing tumour. In hospital 3 months earlier with a history suggestive of cancer of the colon and iron-deficiency anaemia, but no investigation performed. Categories: Diagnosis delay, violation of protocol or rule; failure to synthesise, decide or act on available information; lack of care/attention. Preventability score: 5.5. Example 2: A 28-year-old man with abdominal pain was treated with cholecystectomy. Gallbladder was macroscopically and histologically normal. Small bowel lymphoma was eventually diagnosed and treated, with resolution of the presenting symptoms. Categories: Diagnosis delay; failure to synthesise, decide or act on available information; failure to request or arrange an investigation, procedure or consultation. Preventability score: 5. C. Treatment categories Example 1: A 52-year-old man with known asthma was prescribed a beta-blocker for hypertension. This resulted in acute respiratory failure leading to artifical ventilation and tracheostomy. Categories: Wrong or inappropriate treatment; misapplication of or failure to apply a rule; failure to synthesise, decide or act on information. Preventability score: 6. Example 2: A 54-year-old man developed gastrointestinal bleeding (haemoglobin level, 45 g/L) while receiving non-steroidal anti-inflammatory drugs and steroids for rheumatoid arthritis. This required hospital admission and blood transfusion, at which time the correct diagnosis of osteoarthritis was made. Categories: Wrong or inappropriate treatment; acting on insufficient information; failure to request or arrange an investigation, procedure or consultation. Preventability score: 5.5. Example 3: Hospitalisation and surgical intervention for septic arthritis that followed steroid injection into a joint. Categories: Unclassified treatment; technical; lack of care/attention. Preventability score: 4.5. D. Investigation categories Example 1: A 75-year-old woman died from acute renal failure after developing gentamicin toxicity. Gentamicin was used to treat an infected pleural effusion, and drug levels were not measured. Categories: Investigation not performed; failure to request or arrange an investigation, procedure or consultation; lack of care/attention. Preventability score: 5. Example 2: A 58-year-old woman had recurrent hospital admissions for chest pain and impaired cardiac function without specific investigation, and hence a reduction in treatment options. Categories: Investigation; violation of protocol or rule; failure to synthesise, decide and/or act on available information. Preventability score: 5. Back to text 4: Contribution of delay, treatment and investigation categories to adverse events (AEs). Values are number (%) of AEsPermanentHighA. Delay categoryFrequencydisabilitypreventabilityDiagnostic delay267 (56.8%)93 (34.8%)231 (86.5%)Treatment delay191 (40.6%)53 (27.7%)172 (90.1%)Administrativedelay12 (2.6%)3 (25.0%)11 (91.7%)Total470 (100%)149 (31.7%)414 (87.9%) B. Treatment categoryNo or inadequatetreatment237 (51.5%)72 (30.4%)176 (74.3%)Wrong/inappropriatetreatment126 (27.4%)35 (27.8%)96 (76.2%)No or inadequateprophylaxis41 (8.9%)9 (22.0%)34 (82.9%)Treatmentunclassified36 (7.8%)7 (19.4%)28 (77.8%)Missed treatment20 (4.4%)4 (20.0%) 16 (80.0%)Total460 (100%) 127 (27.6%)350 (76.1%) C. Investigation categoryInvestigationnot performed198 (78.6%)81 (40.9%)171 (86.4%)Investigationnot acted on39 (15.5%)13 (33.3%)36 (92.3%)Investigationinappropriate9 (3.6%)2 (22.2%)9 (100.0%)Investigationunclassified6 (2.4%)2 (33.3%)5 (83.3%)Total252 (100%)98 (38.9%)221 (87.7%)Back to text 5: Frequency of occurrence of categories of prevention strategies and the proportion of adverse events (AEs) judged as causing permanent disability or having high preventability. Values are number (%) of AEsPermanentHighCategoryFrequencydisabilitypreventabilityNew, better, or better implementedpolicies or protocols884 (23.7%)206 (23.3%)545 (61.7%)More or better formal quality monitoringor assurance processes790 (21.2%)186 (23.5%)486 (61.5%)Better education and training715 (19.2%)160 (22.4%)646 (90.3%)Consultation with other specialistsor peers391 (10.5%)133 (34.0%)294 (75.2%)Don't know341 (9.2%)51 (15.0%)186 (54.5%)Better access to, or transfer of, information135 (3.6%)40 (29.6%)100 (74.1%)Discharge procedures and protocols122 (3.3%)27 (22.1%)100 (82.0%)Other89 (2.4%)22 (24.7%)46 (51.7%)Changes in organisation management88 (2.4%)22 (25.0%)75 (85.2%)Changes in organisation culture77 (2.1%)26 (33.8%)66 (85.7%)More or better personnel72 (1.9%)29 (40.3%)53 (73.6%)More or better equipment or otherphysical resources22 (0.6%)8 (36.4%) 16 (72.7%)Total3726 (100%)*910 (24.4%)2613 (70.1%) * Total is greater than the number of AEs (2351) as the categories were not mutually exclusive. 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Bernadette T Harrison · Robert W Gibberd · John D Hamilton

Viewpoint Aboriginal health: why is reconciliation necessary? Lisa R Jackson and Jeanette E Ward MJA 1999; 170: 437-440 Introduction - Health and land - What is reconciliation? - A populist movement - Acknowledgements - References - Authors' details - - More articles on Aboriginal health Many health professionals are deeply troubled by the persistent health inequities between Aboriginal and non-Aboriginal Australians. From a social and political perspective it is clear that, for there to be appreciable improvement in Aboriginal health, a process of reconciliation which acknowledges the past in the light of the present needs to be adopted across all sectors of society. We give some practical advice for promoting reconciliation. Introduction Before the arrival of Europeans, the Aboriginal peoples of Australia were a strong and healthy race of hunters and gatherers whose active lifestyle promoted good health. Little evidence has been found of widespread illness or disease in Aboriginal people,1 making it unlikely that they suffered from obesity, hypertension, diabetes, renal failure, coronary heart disease, cancer, arthritis or other diseases endemic in Aboriginal people today.2 It is possible that, in 1770, when Cook charted the east coast of Australia, Aboriginal people were healthier than the average person in Britain or other parts of Europe.1 Further, Aboriginal people had a strong oral pharmacopoeia which was passed down from generation to generation.3 The early European colonists, without a means of replenishing their medical supplies, were taught by Aboriginals to use "medicinal plants growing in the new country".4 After at least 50 000 years of a strong and intact culture, the Aboriginal population was decimated by diseases introduced by Europeans, and those remaining were displaced from their lands and forced to change their lifestyle.1 Now, more than 200 years on, and despite attempts to improve Aboriginal health, the health of Aboriginal people is markedly worse than that of other Australians and of the indigenous peoples of New Zealand and the United States.5 While mortality rates for the total Australian population have been improving in recent decades, mortality rates for Indigenous women have not changed and the rates for Indigenous men have fallen only slightly.6 These data are from Western Australia, the Northern Territory and South Australia. Age-specific mortality rates in these three States in 1992-1994 were higher for all age groups of Indigenous people. The difference was most pronounced -- about five to seven times that of non-Indigenous Australians -- for those aged 25-54 years.7 Infant mortality, although decreasing among Aboriginal people over the past decade, also remains a problem, with rates reported in 1996 that are two to four times higher than the national average.7Hospital separation statistics also indicate a greater burden of illness in Indigenous people: during 1992-93, there were 2.5 and 2.7 times more admissions for Indigenous men and women, respectively, than would be expected, based on all-Australian rates.6 Social disadvantage for many Aboriginal people is likely to contribute to their ill-health. At least 20 000 Aboriginal people still live in communities with permanently inadequate or contaminated water supplies.8 Almost a third (29%) of Aboriginal and Torres Strait Islander people older than 15 years who responded to a health survey were worried about having sufficient food.9 Health and land Since the arrival of Europeans there has been very little formal recognition of the profound spiritual links of Aboriginal peoples to their land. The common law principle of Terra Nullius -- a territory belonging to no one -- was applied unilaterally. The British "took possession" of the land because they considered it to be unoccupied. Moreover, unlike the experience of Maori in Aotearoa (New Zealand) or the indigenous peoples in both the United States and Canada, there has never been a formal treaty between the Aboriginal people and the newcomers to Australia. It has been argued that the absence of a treaty with Aboriginal peoples is causally associated with their poor health and social disadvantage.5 Disempowerment has been accepted as a causative factor by the Royal Australasian College of Physicians in its Darwin Declaration (1997): . . . that the health of Aboriginal and Torres Strait Islander Australians is disastrously poor compared with other Australians, and that the fundamental cause is disempowerment, due to various factors including continued dispossession from land, cultural dislocation, poverty, poor education and unemployment.10 To Aboriginal people, ill-health is more than physical illness; it is a manifestation of other factors, including spiritual and emotional alienation from land, family and culture. Aboriginal people have a spiritual link with the land which provides a sense of identity, and which lies at the centre of their spiritual beliefs.11 Land is the crux of Aboriginal health and well-being. In 1990, the National Aboriginal Health Strategy (NAHS) developed a widely accepted definition of health as perceived by Aboriginal peoples: Health does not just mean the physical well-being of the individual but refers to the social, emotional, spiritual and cultural well-being of the whole community. This is a whole of life view and includes the cyclical concept of life-death-life.12 This definition of health places in context our history, the importance to Aboriginal people of their links with the land, and their disenfranchisement, sense of loss and present-day marginalised position within the Australian community. Accordingly, to understand Aboriginal ill-health, one must first acknowledge the impact of dispossession, theft, genocide, lost and stolen generations of families and the attempted decimation of the innumerable cultures of the people inhabiting Australia before 1770 (Box 1). Furthermore, Aboriginal health is not just the domain of the healthcare system. By accepting the need for an approach that is multifaceted and covers all aspects of people's lives, including housing, education, employment and social justice, we can then understand that physical and symptomatic relief of disease will not in itself redress the burden of Aboriginal ill-health. What is reconciliation? There is no agreed definition of reconciliation. It is agreed, however, that reconciliation encompasses reparation, as recommended by the National Inquiry into the Separation of Aboriginal and Torres Strait Islander Children from Their Families.14 In the report, Bringing them home, five components of reparation have been recommended. These have been taken from the van Boven Principles,15 drawn up by the United Nations Commission on Human Rights as guidelines for reparation of victims of gross violation of human rights: Acknowledgement and apology Guarantees against repetition Measures of restitution Measures of rehabilitation Monetary compensation Reconciliation always begins with acknowledgement or, more colloquially, "truth telling". Alexander Boraine, Vice Chair of the Truth and Reconciliation Commission of South Africa, has spoken of the capacity for forgiveness by those who suffered most under apartheid.16 In Australia, there is a need to acknowledge that the benefits now enjoyed by some have been at the expense of incalculable suffering to others. "Truth telling" is unresolved "sorry business" for our nation. If contemporary Aboriginal health is accepted to be a manifestation of a population dying of despair, anger and disillusionment, then reconciliation is fundamental. It has been compellingly argued that "The diseases of anger and despair which wrack Aboriginal communities in Australia clearly have many of their roots in childhood."17 Acknowledgement of the causes of this anger and despair must occur as the first step in the process of reconciliation. Reconciliation is necessary but is not, in and of itself, sufficient to guarantee improved Aboriginal health. Reconciliation becomes the foundation for health services development. The Australian Medical Association has stated that "The process of reconciliation would be incomplete without the provision of substantial additional resources for Indigenous health."18 As we await proper political processes to implement recommendations from the Muirhead Royal Commission into Aboriginal deaths in Custody19 and the National Inquiry into the Separation of Aboriginal and Torres Strait Islander Children from Their Families,14 individuals and organisations can consider their own processes for reconciliation. A populist movement There are many ways reconciliation can be facilitated through a populist movement. The Council for Aboriginal Reconciliation has published eight key issues considered crucial to restoring Aboriginal community and culture.20Box 2 proposes some practical strategies that health organisations and individuals can adopt as part of their commitment to reconciliation with the Aboriginal and Torres Strait Islander peoples of Australia. These processes can be built upon and adapted by healthcare providers according to their needs and expectations and those of their communities. A people's movement of reconciliation is required to encourage and promote better health for Aboriginal Australians. To recognise the link between Aboriginals' burden of illness and their cultural destruction is the first step towards significant and lasting change. Health professionals can consider a proactive partnership to promote reconciliation. Doing what we have always done to improve Aboriginal health will only give us the same health outcomes, and the statistics will continue to show the shameful morbidity and mortality rates of Australia's first peoples. Although the Council of Aboriginal Reconciliation will be disbanded at the end of the year 2000, reconciliation itself will not cease. As many Aboriginal people are currently saying, now is a time for building bridges. It will take an insightful and committed group of people to take on the challenge of restoring the justice which is long overdue. We hope that health professionals adopt reconciliation as a fundamental issue in their workplaces. Acknowledgements We acknowledge the land on which we live and work as belonging originally to Aboriginal people. We thank the generosity of all those who sent us information, read our manuscript and gave us feedback. We also would like to thank the Indigenous Health Workers Network of the CSAHS for their support. This article was written while Lisa Jackson was completing the New South Wales Health Department Public Health Officer Training Program. References Australian Institute of Health. First biennial report of the Australian Institute of Health. June 1988. Canberra: AGPS, 1988: 1-2. Cowlishaw G. Infanticide in Aboriginal Australia. 1978: In: The health of Aboriginal Australia. Reid J, Trompf P, editors. Sydney: Harcourt Brace Jovanovich, 1991: 3. Latz P. Bushfires and bushtucker. Alice Springs: IAD Press, 1995: 44-72. Cribb AB, Cribb JW. Wild medicine in Australia. Sydney: Fontana/Collins, 1981: 10. Ring IT, Firman D. Reducing indigenous mortality in Australia: lessons from other countries. Med J Aust 1998; 169: 528-531. 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: 87-89, 68. (Catalogue No. 4704.0.) Australian Institute of Health and Welfare. Australia's health 1998. Canberra: AIHW, 1998: 29, 32. Dodson M. Linking international standards with contemporary concerns of Aboriginal and Torres Strait Islander peoples. In: Pritchard S, editor. Indigenous peoples, the United Nations and Human Rights. Annandale, Sydney: Federation Press, 1998. Australian Bureau of Statistics. 1994 National Aboriginal and Torres Strait Islander Survey: Detailed findings. Canberra: AGPS, 1994: 10, 11, 13. (Catalogue No. 4190.0.) Royal Australasian College of Physicians. CommuniquŽ of the 1997 Cottrell Conference hosted by the Royal Australasian College of Physicians: Statement on the Delivery of Specialist Services to Remote and Rural Aboriginal and Torres Strait Islander Communities, 1997. http://www.racp.edu.au/open/cottrell.htm Woodward AE. Aboriginal Land Rights Commission Report. Canberra: AGPS, 1974. National Health and Medical Research Council. Promoting the health of Indigenous Australians. A review of infrastructure support for Aboriginal and Torres Strait Islander health advancement. Final report and recommendations. Canberra: NHMRC, 1996: part 2: 4. Independent Commission on International Humanitarian Issues. Proceedings of Conference, 1987: In: The health of Aboriginal Australia. Reid J, Trompf P, editors. Sydney: Harcourt Brace Jovanovich, 1991: xi. Human Rights and Equal Opportunity Commission. Bringing them home. Report of the National Inquiry into the Separation of Aboriginal and Torres Strait Islander Children from Their Families. Sydney: Sterling Press, 1997. Van Boven T. Revised set of basic principles and guidelines on the right to reparation for victims of gross violations of human rights and humanitarian law. United Nations Commission on Human Rights, 24 May 1996. (UN Doc: E/CN4/Sub2/1996/17.) McKendrick JH. Aboriginal reconciliation: a role for psychiatrists? Aust N Z J Psych 1997; 31: 617-621. Bartlett B, Legge D. Beyond the maze. Proposals for more effective administration of Aboriginal health programs. Canberra: National Centre for Epidemiology and Population Health, Australian National University, 1994. (NCEPH Working Paper Number 34.) Australian Medical Association. Australia Day Statement: Greater commitment to indigenous health would boost reconciliation. Media release. Canberra: AMA, 1999. Royal Commission into Aboriginal Deaths in Custody. Reports Vol 1-5. Canberra: AGPS, 1992. Council for Aboriginal Reconciliation. Eight key issues of reconciliation, the community consultative process. Sydney: Australians For Reconciliation, 1996-1967. Horton D, general editor. The encyclopaedia of Aboriginal Australia [CD-ROM]. Canberra: Aboriginal Studies Press, Australian Institue of Aboriginal and Torres Strait Islander Studies, 1994. Aboriginal and Torres Strait Islander Commission. As a matter of fact: answering the myths and misconceptions about Indigenous Australians. Canberra: Office of Public Affairs, 1998. Office of the Minister for Aboriginal and Torres Strait Islander Affairs. Rebutting the myths: some facts about Aboriginal and Torres Strait Islander affairs. Canberra: Office of the Minister for Aboriginal and Torres Strait Islander Affairs, Parliament House Canberra, 1997. Flood S. Essay for the Theosophical Society. Sydney, Public Defenders Office, 1997. Authors' details Needs Assessment and Health Outcomes Unit, Central Sydney Area Health Service, Sydney, NSW. Lisa R Jackson, RN, MPH, Aboriginal Public Health Officer. Jeanette E Ward, PhD, FAFPHM, Director. Reprints: Associate Professor J E Ward, Needs Assessment and Health Outcomes Unit, Central Sydney Area Health Service, Locked Bag 8, Newtown, NSW 2042. Email: jwardATnah.rpa.cs.nsw.gov.au 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/> 1: Land is the crux of Aboriginal health and well-being Next to shooting Indigenous peoples, the surest way to kill us is to separate us from our part of the Earth. Once separated, we will either perish in body or our minds and spirits will be altered so that we end up mimicking foreign ways, adopt foreign languages, accept foreign thoughts and build a foreign prison around our Indigenous spirits, a prison which suffocates rather than nourishes as our traditional territories of the Earth do. Over time, we lose our identity and eventually die or are crippled as we are stuffed under the name of "assimilation" into another society. A senior official of the World Council of Indigenous Peoples.13 Back to text 2: Practical strategies for promoting reconciliation between Aboriginal and Torres Strait Islander peoples and other Australians 1. Understanding country Understanding the significance of land and sea to Aboriginal and Torres Strait Islander societies Accept that for Aboriginals and Torres Strait Islanders, their cultural identity is bound up by ties to the land and sea. Acknowledge that Aboriginal peoples inhabited Australia for at least 50 000 years before Europeans came. 2. Improving relationships Building new relationships between Aboriginal and Torres Strait Islander peoples and all other Australians Invite Aboriginal or Torres Strait Islander people to give talks to professional and community groups to which you belong. Ensure that the people with whom you work do not have preconceived notions of Aboriginal people, in accordance with recommendation 9a of the Bringing them home report.14 Allow staff to attend cultural awareness sessions presented by Aboriginal and Torres Strait Islanders. Join a local study circle and join the mailing list for the Council for Aboriginal Reconciliation. Work with local Aboriginal people in your area towards a statement of commitment to reconciliation for your external communications (eg, a sentence on faxes and letterheads). Find out if your local hospital has an Aboriginal Liaison Health Worker; if not, give your written support to the organisation to employ one. 3. Valuing cultures Recognising the valuable contribution the cultures of Indigenous people make to the Australian heritage Acknowledge the strength of Australia's Indigenous cultures and their importance to our national pride and our international image and trade. Find out the name of the traditional owners of the land where you live and work. Attend cultural events where the focus is on Aboriginal and/or Torres Strait Islander people and their lifestyles. Obtain a copy of the Aboriginal Australia map, published by the Australian Institute of Aboriginal and Torres Strait Islander Studies (AIATSIS). Borrow or buy a copy of the Encyclopaedia of Aboriginal Australia.21 Read works by Aboriginal authors, such as Sally Morgan, Monty Prior, Ruby Langford Ginibi, Oodgeroo Noonuccal, Kevin Gilbert or James Miller. Understand that Aboriginal people have had, and some continue to have, a strong traditional health practice. 4. Sharing history Understanding that the history of Australia began long before the arrival of Captain Cook in 1770 Read general textbooks about Aboriginal history: A secret country, Unfinished business, Six Australian battlefields, The world of the First Australians or Invasion to embassy. Read the summary of the Muirhead Royal Commission into Aboriginal Deaths in Custody19 and Bringing them home14 (the Report of the National Inquiry into the Separation of Aboriginal and Torres Strait Islander Children from Their Families). Read information documents on contemporary Aboriginal issues such as As a matter of fact22 or Rebutting the myths.23 Encourage Aboriginal and Torres Strait Islanders to share their knowledge and perspective of history. Ensure schools attended by your children have Aboriginal and Torres Strait Islander resources in their classrooms and libraries. Watch videos that tell the story, including Women of the sun, Lousy little sixpence and Around the kitchen table (to name just a few), or see movies made by Aboriginal people such as Radiance. 5. Addressing disadvantage Acknowledging that Indigenous people are the most disadvantaged group in Australian society Acknowledge that inequities in such basic areas as education, health, housing and the justice system are very real to Aboriginal people. Having learned from reading, watching and listening, speak up when others voice myths, errors and prejudices about Aboriginal and Torres Strait Islander peoples. Do not allow people speaking untruths to ever believe that your silence means agreement. Support your children when they make friends with Aboriginal and Torres Strait Islander children. Favour businesses that support reconciliation. Encourage affirmative action in your workplace. 6. Custodial levels Drawing attention to the fact that Aboriginal and Torres Strait Islander people continue to be arrested and imprisoned at a rate far above that of the wider community Find out what has been done in your State or Territory to implement the recommendations of the Muirhead Royal Commission into Aboriginal Deaths in Custody.19 Support efforts by the healthcare sector to implement the recommendations of this report specific to health. 7. Destiny Supporting empowerment of Indigenous peoples -- giving them greater control over their own destiny and a right to self-determination Join a study circle or attend local community consultations to discuss ideas and initiatives for self-determination in the spirit of partnership. Phone your local Members to let them know of your support and that of your organisations. Ask what specific actions they have taken during their term in office. Invite Indigenous people to participate and ensure their voices are heard in the formulation and implementation of policy decisions. 8. Formal document(s) of reconciliation Determining whether reconciliation would be helped by a formal document(s) of reconciliation. Support recognition of the unique position of Aboriginal and Torres Strait Islander peoples as the Indigenous peoples of Australia. Put into policy in your organisation a process of reconciliation with an outcome date. Once the formal documents of reconciliation are available, adapt them for your practice and ensure they enter as policy into your organisation. 9. Native Title Recognising the implications of the Native Title debate Realise that matters such as the current Native Title legislation have significant implications in areas (other than land usage), such as health and social justice. The Public Defender, Sean Flood, in a talk given at the Theosophical Society (Sydney) in November 1997, explained this clearly: The Nation's soul is at risk. Extinguishment of Native Title is extinguishment of Indigenous culture and ultimately the cause of sickness and death of Indigenous peoples.24 Learn more about Native Title. Acknowledge a component of restitution, as documented in the Bringing them home14 report, which allows Native Title holders the authority under traditional law to define the content and scope of that title. 10. Stolen generations Acknowledging the injustice and the trauma of forcibly removing Indigenous children from their families and communities, as has been done since the earliest days of European colonisation in Australia Recognise and acknowledge the consequences of the past and seek ways to make amends. Participate in Sorry Day, National Aboriginal Day Organising Committee (NADOC) and National Reconciliation Week activities. Speak out against prejudiced views. Support programs that help Aboriginal and Torres Strait Islander individuals and families overcome the trauma they are still suffering. Listen to Aboriginal and Torres Strait Islander people talking about what has happened and ask what you can do. Back to text

Lisa R Jackson · Jeanette E Ward

Medical Research Perspectives The Menzies School of Health Research offers a new paradigm of cooperative research John D Mathews The Menzies School has addressed problems in Aboriginal and tropical health through research that requires cooperation between disciplines as well as improved communication and trust between researchers, Aboriginal people and the wider community. MJA 1998; 169: 625-629 Introduction - The politics of Aboriginal health - Success in interdisciplinary and crosscultural collaboration - Some research highlights of medical importance - The Menzies School's work in central Australia - Research highlights in tropical and international health - Resources and links - Cooperation is the secret of success - Looking ahead - Acknowledgements - References - Author's details - - More articles on Aboriginal health Introduction The Menzies School of Health Research, in the Northern Territory, has been a surprisingly successful research investment. The dividends since 1985 include increased understanding of Aboriginal and tropical health problems, the transfer of knowledge and skills into training and improved health services, and some 70 research publications each year. The Menzies School is a brave and cooperative venture of the Northern Territory Government, the Menzies Foundation (commemorating the name of our longest-serving prime minister), and the University of Sydney. I was appointed as Foundation Director and we moved to Darwin in January 1985, in quixotic mood, and not knowing what to expect. My wife had found a Thomas Keneally quote: . . . the north is littered with the detritus of great hopes, and Darwin is still an outpost . . . but with a sense of destiny that would have done Athens credit.1 We were naive enough to ignore the implicit warning, and to dream of Athens in the north. To Darwin I brought a research background in medicine and epidemiology; experience from New Guinea, the Walter and Eliza Hall Institute and Oxford; and 10 years as an NHMRC Fellow at the University of Melbourne. My first dream for the Menzies School was to establish a centre of research excellence. The second dream was to somehow make a difference in Aboriginal health. The potential nightmare was to work out how to realise each dream without jeopardising the other. The politics of Aboriginal health Countries with the least education and income tend to have the poorest health, and within any one country persons with the least education and income tend to have the worst health. Box 1 shows the causal linkages between education, income and health in any society, and Box 2 shows how the social dislocation suffered by Aboriginal Australians since colonisation has specifically contributed to their poor health.2 The poor health of Aboriginal Australians is primarily due to social and environmental disadvantage. It is not due to any absolute lack of knowledge about the causes of their ill-health (Box 3), but to the fact that Aboriginal people have had limited access to health resources and knowledge because of their own poverty and educational disadvantage. There has also been limited understanding of Aboriginal health issues by those responsible for funding decisions, compounded by inadequate knowledge and training of health advisers and providers. Unfortunately, the poor state of Aboriginal health has also been perpetuated by disagreements about what should be done and how, who should do it, and who should pay for it. This lack of consensus, amounting to a modern Babel (Box 4), is only now beginning to be resolved. The Menzies School has contributed to the debate on Aboriginal health by helping to fill gaps in understanding, communication and implementation. It has attracted expert staff to the Northern Territory, driven research to identify areas of unmet health need, tested innovative health interventions, and been an evaluator, critic and advocate for Aboriginal health policy. Success in interdisciplinary and crosscultural collaboration The success of the Menzies School has been driven by the quality of our staff, the challenges faced, and by the added value that comes from collaboration and communication between diverse disciplines. Above all, success would have been impossible without the expertise and commitment of Aboriginal staff and colleagues. Major contributions have been made by Lorna Fejo, Jessica Bujevich, the late Sally Ross, Louisa Collins, Daisy Yarmirr, Josie Crawshaw, Annie Bonson, Geoffrey Angeles, Mai Katona and many others. Their achievements have been to communicate the health priorities and values of Aboriginal people to non-Aboriginal researchers, to facilitate research projects in a culturally appropriate manner, and to work with other Aboriginal people to show how knowledge and research findings can be fed back to communities and applied to achieve practical health benefits. Recently, the Tiwi Health Board has played a key role in codifying the many sensitive issues that arise in crosscultural research and providing a framework for future research in a Legal Agreement signed with the School (Box 5). Some research highlights of medical importance (See also Box 6) Understanding streptococcal infection and rheumatic fever At any one time, up to 60% of Aboriginal children in bush schools have skin sores infected with group A streptococci, and there are occasional epidemics of acute poststreptococcal glomerulonephritis. Bart Currie, Jonathan Carapetis and colleagues have shown that the same communities suffer from the highest rates of rheumatic fever in the world. To overcome the limited awareness of rheumatic fever and the low rates of compliance with penicillin prophylaxis, Geoffrey Angeles, Norma Benger and other members of our Aboriginal Unit have developed The Rheumatic Fever Story, a successful education program (booklets, songs and videos) for patients, relatives, health workers and the wider community. K S Sriprakash, a talented molecular geneticist, has led molecular studies of group A streptococci, detecting as many as 13 immunologically distinct types present at the same time in a single bush community of a few hundred children, with a total of about 100 different types circulating through Aboriginal communities in northern Australia, many that have never been identified elsewhere. Candidate nephritogenic strains have recently been identified. This work is linked to studies of the epidemiology and population biology of group A streptococci in Aboriginal communities, to studies of treatment efficacy, and to studies directed towards vaccine development with Michael Good and the Cooperative Research Centre for Vaccine Technology in Brisbane. Understanding endemicity of respiratory bacteria For Aboriginal children, persistent otitis media is a major cause of illness, hearing loss and educational disadvantage. Amanda Leach, Judith Boswell, Terry Nienhuys and others have shown that otitis media develops in all Aboriginal infants within a few weeks of birth immediately after nasopharyngeal colonisation with Streptococcus pneumoniae and Haemophilus influenzae. Although each infection seems to be eventually cleared by the host response, there are some 30 different serotypes of pneumococcus and at least 50 types of haemophilus which can queue up to infect every child in every community. The persistence of nasal infection and respiratory disease is associated with the persistent colonisation by such multiple bacterial strains into adult life. Cross-infection is driven by overcrowding, poor hygiene and the large numbers of bacterial strains circulating. Detailed modelling suggests that each strain is maintained indefinitely, even in relatively small populations, because there are always a few carriers of each strain left to infect susceptible newborn infants. Furthermore, with the carriage of multiple serotypes or strains at the same time by the same host individual, some of the strains are "hidden" from the immune system, giving them an extra survival advantage. Likewise, antibiotic-resistant strains "hide" behind sensitive strains, only to be revealed by antibiotic treatment. Understanding scabies in dogs and people Skin infections associated with scabies infestation are frequent in Aboriginal communities, particularly among children. Because dog scabies was thought to be a source of infection for people, scabies control programs have sometimes treated dogs rather than people. Now, using molecular genotyping, Shelley Walton and colleagues have shown that populations of scabies mites from dogs in Australia and America do not overlap with scabies from people in those same areas. This strongly suggests that scabies from dogs are not driving human scabies in remote communities and that control programs for human scabies must focus on people. Jonathan Carapetis and Daisy Yarmirr, in cooperation with Aboriginal and health service colleagues, have shown that community-based treatment with pyrethrin can reduce both scabies and streptococcal impetigo. Understanding renal disease and cardiovascular disease Mortality from renal failure for Aboriginal Australians is very high and rising. Up to 50% of Aboriginal adults have proteinuria and in some communities 2% are receiving renal dialysis to stay alive. Paul van Buynder and colleagues identified obesity, hypertension and non-insulin-dependent diabetes mellitus (NIDDM) as risk factors for proteinuria in Aboriginal communities. Modelling studies with Alison Goodfellow and others suggest that proteinuria develops from very early in life in those with evidence of past infection with group A streptococci. Wendy Hoy and colleagues have shown that low birth weight is predictive of NIDDM, proteinuria, and presumably renal disease, and have suggested that the risk factors for renal disease can also help to explain the high rates of cardiovascular disease in Aboriginal adults. Causes of disease acting from early in life The role of low birth weight as a predictor of poor health in later life has attracted much recent attention, and is of particular importance for Aboriginal Australians. Wendy Hoy and others have shown that the combination of low birth weight with adult obesity appears to confer the highest risk of NIDDM, proteinuria and other disorders. Sue Sayers has shown that high rates of Aboriginal low birth weight are due to intrauterine growth retardation, possibly resulting from maternal malnutrition, infection and substance abuse. Thus, low birth weight may be best regarded as a marker of those adverse influences in pregnancy that are the actual mediators of adverse health effects in later life. This hypothesis would explain how poor health can pass from generation to generation, and may provide another reason why health has been slow to improve for many Aboriginal Australians. Early treatment of renal disease The epidemic of Aboriginal renal disease should eventually be controllable through public health measures such as improved nutrition and infection control, particularly in pregnancy. In the meantime, there is a strong rationale to provide "best-practice" clinical treatment, not previously available for Aboriginal people. Accordingly, Wendy Hoy, as an adjunct to the NHMRC-funded research program, has introduced treatment with ACE inhibitors for Tiwi people with early renal disease. Compliance is good, and treatment markedly reduces the rate of deterioration of kidney function, which will in turn prolong life and reduce the escalating social and financial costs of dialysis services. The Menzies School's work in central Australia We have a small research unit in Alice Springs to complement our major operation in Darwin. Major contributions include those of Tim Rowse (historical, social and nutritional studies), David Scrimgeour, Robyn McDermott, Ilan Warchivker and John Wakerman (evaluation studies), and Komla Tsey (health and education). Research highlights in tropical and international health David Kemp, FAA, joined the School as Deputy Director in 1992, with support from the Wellcome Trust and from the Howard Hughes Institute to continue his fundamental work with falciparum malaria, and to commence new molecular studies of haemophilus, donovanosis, and scabies. This year saw the culmination of his 10-year search, begun at the Walter and Eliza Hall Institute, to find the cytoadherence gene in Plasmodium falciparum that is believed to explain the stickiness of red blood cells in cerebral malaria. The new gene, designated CLAG, was identified and sequenced, and a CLAG knock-out was shown to have lost the stickiness phenotype. The team has subsequently identified additional genes, similar to CLAG, elsewhere in the malaria genome, opening up exciting new possibilities for treatment or prevention of cerebral malaria. Other malaria projects in Indonesia are funded by a grant from the Northern Territory Government to mark the 50th anniversary of Indonesian independence and a US National Institutes of Health grant to Nick Anstey, and are being carried out in cooperation with Emiliana Tjitra and Indonesian colleagues. Resources and links (See also Box 7) The achievements of the Menzies School have depended on the generous financial support of the Northern Territory Government and the Menzies Foundation, competitive grants from the National Health and Medical Research Council and other agencies in Australia and overseas, and private and corporate donations. In 1998, the annual budget was $6 million to support about 100 employees and postgraduate research students. The School has also enjoyed the goodwill and cooperation of Territory Health Services and other arms of government, Aboriginal communities, medical services and organisations, the National Heart Foundation and other non-government organisations, the University of Sydney, the Northern Territory University, and Flinders University Clinical School at the Royal Darwin Hospital. The Menzies School became the lead agency in a successful bid to establish the Cooperative Research Centre for Aboriginal and Tropical Health in 1997. Through its Board, chaired by Dr Lowitja O'Donoghue, and with a majority of Aboriginal members, the Cooperative Research Centre has an agenda to discover and disseminate knowledge about Aboriginal health problems, to provide more research and training positions for Aboriginal people and to facilitate Aboriginal control of the planning and implementation of health research and health services. From 1994, the School has taught postgraduate coursework in public health to help develop skills in the local health workforce. Now, in partnership with the Northern Territory University, the School is promoting a broader vision of public health education through a Faculty of Public Health. This Faculty will continue postgraduate teaching and promote access to accredited courses at multiple levels and to short courses to meet the needs of teachers and educators, administrators, Aboriginal people and others in need of public health knowledge and expertise. Cooperation is the secret of success The Menzies School has become a leader in tropical and Aboriginal health research, not only through the talent and commitment of individuals, but also because of its capacity to encourage cooperation between disciplines, and to build and sustain cooperative partnerships with Aboriginal stakeholders, health services and governments in northern and central Australia. This cooperative research paradigm, linking the laboratory with the clinic and the community, has delivered important understandings and contributed to more effective strategies for training of health staff, and to improved health promotion, prevention and treatment strategies. Despite its short-term opportunity costs, cooperation in health research pays off in the longer term by helping to translate modern scientific knowledge into direct community benefit, just as natural selection has discovered that cooperative processes provide pay-offs in the longer term in most otherwise competitive biological and social systems. Indeed, interactions that balance competition with cooperation turn up in all evolving systems to achieve a balance between short term returns (efficiency) and longer term strategic outcomes. Looking ahead The multidisciplinary focus of the Menzies School of Health Research has more than justified the vision of its founders by delivering value for money to its stakeholders and the wider community. However, as the School faces the new millennium, it needs to serve the community with a broad public health perspective while maintaining the deep biomedical expertise that underpins strategic research to be an academic critic of health policy, while working in partnership with health services to promote necessary improvements to persuade funding agencies to recognise the value of, and to pay the full opportunity costs of, cooperation and collaboration between different disciplines and organisations to maintain its cohesion, corporate identity, shared values and vision for the future. Talent and enthusiasm are always welcome! Acknowledgements This summary is based on the work of many colleagues to whom I am deeply indebted. Special thanks to Coralie Mathews, Bart Currie, Dave Kemp and Lindy Warrell for reviewing the manuscript, and Debra Davis for its preparation. References Keneally T. Outback. Sydney: Coronel Books, 1983. Mathews JD. Historical, social and biological understanding is needed to improve Aboriginal health. Recent Adv Microbiol 1997; 5: 257-334. Author's details Menzies School of Health Research, Darwin, NT. John D Mathews, AM, MD, Professor and Director. Reprints will not be available from the author. Correspondence: Professor J D Mathews, Menzies School of Health Research, PO Box 41096, Casuarina, NT 0811 Email: johnATmenzies.su.edu.au 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/> 1: Social determinants of good health Back to text 2: Historical impacts of colonisation upon Aboriginal health Back to text 3: Lessons about Aboriginal health and research Aboriginal health is limited more by the failure to apply knowledge that already exists than by the lack of knowledge itself. Aboriginal people have always understood this, and they have been naturally suspicious of research projects that seem to serve the interests of researchers more than those of Aboriginal people. The most relevant research questions are: How to ensure that existing knowledge is taken up and acted upon by public sector decision-makers and managers and health professionals. How to ensure that Aboriginal people have access to the knowledge and resources that they need to use to improve their own health. How to plan specific research projects to make a difference by finding better ways of working across cultural boundaries. improving access to knowledge, resources, education and health services for Aboriginal people providing social or biomedical insights about better ways to promote health or prevent or treat disease for Aboriginal people. Back to text 4: The modern Babel The biblical Tower of Babel (Genesis, xi) is the traditional metaphor for the schisms in language, beliefs and culture in the modern world. It reminds us that without a common language and shared concepts, we are unable to understand each other. In the Northern Territory in 1985 many different voices were speaking about Aboriginal health. Those on the political right tended to blame the victims, and saw the emergence of Aboriginal control as a threat. There were differences between levels of government. Some officials lacked appropriate expertise and were unused to problem solving, let alone to academia. Some health professionals were escaping from academia, or had a postmodern scepticism about science and medicine. Some romantics said that traditional Aboriginal people should be taught as little as possible about Western culture. Urban Aboriginal people voiced their hurt from discrimination or family experiences as stolen children. At the same time, Aboriginal health workers had strong cultural skills, but only limited health training. Traditional Aboriginal people, with insufficient support to deal effectively with the outside world, saw a progressive erosion of their culture and values. In such a Babel there could be little consensus about how to improve Aboriginal health. Without consensus, our political masters had a continuing excuse to ignore many issues. As a result, the poor state of Aboriginal health has continued to burn into the conscience of Australia. It is likely to be long remembered as the worst-ever failure of our nation. Back to text 5: Creative partnership - Tiwi Health Board and the Menzies School of Health Research Ms Alberta Puruntatameri and Dr Val Asche signing the Legal Agreement between the Tiwi Health Board and the Menzies School of Health Research, 22 October 1998. Back to text 6: Some important research areas at the Menzies School Cultural understandings of Aboriginal illness and death (Tarun Weeramanthri, Ada Parry, Norma Benger, Clifford Plummer, Vicky Nangala-Tippett and others) Education and health Otitis media and hearing disability contribute to poor educational outcomes (Anne Lowell, Terry Nienhuys, Judith Boswell, Joan Koops, Al and Lesley Yonowitz) Poor education contributes to poor health (Komla Tsey)Social and environmental determinants of health Community comparisons (Estrella Munoz, John Mathews and others) Environmental health study (Katherine Henderson, Ross Bailie) Melioidosis and contaminated water supplies (Mark Mayo, Bart Currie and Nick Anstey)Studies of substance abuse and appropriate interventions Evaluations of community interventions for alcohol (Peter d'Abbs, David Scrimgeour) Health effects and interventions for petrol sniffing (David Scrimgeour, Chris Burns and Bart Currie) Health effects of kava drinking and policy implications (John Mathews, Malcolm Riley, Estrella Munoz, Peter d'Abbs, Chris Burns, and Alan Clough)Interventions to improve Aboriginal health Community Nutrition Program at Minjilang (Mandy Lee, Annie Bonson, Daisy Yarmirr and others) Strong Women, Strong Baby, Strong Culture Program Evaluation (Lorna Fejo, Dorothy Mackerass and others) Diagnosis and treatment of donovanosis and sexually transmitted diseases (Frank Bowden, Jenny Carter, David Kemp and colleagues) Improved diagnosis and treatment of otitis media (Amanda Leach, Al Yonowitz, Peter Morris, Harold Koops and colleagues) Treatment of trachoma with azithromycin (Andrew Laming, Annie Bonson and colleagues) Smoking prevention (Rowena Ivers, Ross Bailie and the National Heart Foundation)Health service research and evaluation Best practice procedures (Bart Currie, David Scrimgeour, Peter Morris) Evaluation and planning of service models (David Scrimgeour, Chris Burns, John Wakerman and others) Health economic aspects (Robyn McDermott, Ilan Warchivker, John Wakerman) Coordinated care trials evaluation (Peter d'Abbs, Ross Bailie). See http://www.menzies.su.edu.au for a much more detailed account of the work of the Menzies School over the last five years. See also reference 2. Back to text 7: The Menzies building The Menzies School of Health Research was able to secure generous joint funding from the Northern Territory and Commonwealth governments for its new building in Darwin, opened in November 1996. Back to text

John D Mathews

Medical Research Perspectives The TVW Telethon Institute for Child Health Research The birth and growth of a research institute Fiona Stanley Diverse research workers, variously funded by public and private sources, were drawn together to create an Institute and an opportunity to work together on the complex problems in child health. MJA 1998; 169: 630-633 Introduction - Research origins - Rationale for a multidisciplinary institute for child health research - Growth - Successes - Threats - References - Author's details - - More articles on Aboriginal health Introduction In 1967 two men shared a game of golf and a vision for research to improve child health. Sir James Cruthers, then Managing Director of Channel 7 (TVW, Perth), suggested to Jim Clarkson, then the Chief Executive Officer of the Princess Margaret Hospital for Children (PMH) in Perth, the concept of a "Telethon" to raise money from the community for research at PMH. The Telethon became an annual event and in the first year raised funds for the PMH Children's Medical Research Foundation, which funded two small hospital research groups: a clinical immunology research unit founded by Dr Keven Turner, an immunologist from Adelaide, and a clinical nutrition research group established by Dr Michael Gracey, a paediatric gastroenterologist from Melbourne with a special interest in Aboriginal children and their health. From these beginnings, the TVW Telethon has gone on to fund a range of medical research in Western Australia, ultimately providing the essential infrastructural finance for the Institute for Child Health Research, established in 1990 and now a vigorous multidisciplinary research centre employing nearly 200 people. The Institute's name acknowledges not only this beginning but the continuing support from the TVW Telethon. Sir James Cruthers has only recently stepped down from the Institute's Board of Directors. Research origins The first two research groups funded by the Telethon were based at PMH. In the 1970s, the immunology group was beavering away, almost in isolation, in the neglected area of mucosal immunology, looking particularly at the developing respiratory tree and what role the immune system might play in allergy and asthma. This area of immunology and cell biology has now become of global importance in attempts to explain the epidemic of asthma and allergy sweeping the Western world. The work of Patrick Holt was particularly important at the time and has continued to be pre-eminent in the study of the development of allergic sensitisation and asthma.1,2Meanwhile, I had been fortunate enough to be awarded a National Health and Medical Research Council (NHMRC) overseas training fellowship in epidemiology at London University and at the National Institutes of Health, USA. When I returned to Perth in 1977, I used the $4000 setting-up grant in the last year of my fellowship to establish the Western Australian Cerebral Palsy Register (the only other registers at that time were in Sweden and Denmark) and the first congenital malformations register in Australia (funded by the Commonwealth Government in the wake of the Agent Orange scare). Then, as Senior Medical Officer in Child Health for the Health Department of Western Australia, I and my colleagues developed statewide links with midwives and child health nurses which laid the foundations for the Maternal and Child Health Research Data Base. This population-based, record-linked database has become the best in Australia (and probably the world) and now underpins much of the epidemiological work of the Institute.3 They were great days, as there was so little going on in maternal and child health epidemiology in Australia and we felt like pioneers! In 1980 these databases moved with me into a new NHMRC Unit of Epidemiology and Preventive Medicine at the Queen Elizabeth II Medical Centre, and spawned a range of epidemiological studies describing maternal and child health in WA and testing a range of hypotheses, focusing on birth defects, cerebral palsy and low birth weight. Telethon grants in the 1980s funded the Cerebral Palsy Register for nearly 10 years and a case-control study of dietary folate and neural tube defects as well.4,5 We commenced our work in indigenous maternal and child health and employed Aboriginal health workers in research before others had considered it important. The resulting partnerships with Aboriginal communities have grown even stronger since the Institute was established. Towards the middle of the 1980s I sensed that only by collaborating with basic scientists were epidemiologists ever going to get at biological mechanisms, properly elucidate causal pathways and be able to develop effective preventive strategies. Telethon funds appeared less secure at this time as they were being given away to other causes. I discussed these problems with Professor Lou Landau, who in 1984 had just accepted the Chair in Paediatrics in Perth, and we began to think of setting up an institute of child health research at the Children's Hospital, taking those with NHMRC funding with us, trying to get some additional funds for infrastructure and solving complex diseases! We both thought it a wonderful idea and invited Sir Gus Nossal across from Melbourne to address the hospital on "The birth of a research institute" -- this inspiring lecture was given in 1985 and aroused interest among local people in the concept. By this time Dr Wayne Thomas (from the Walter and Eliza Hall Institute in Melbourne), Dr Geoff Stewart (from the United Kingdom) and Dr Ursula Kees (from Switzerland) had all joined the Clinical Immunology Research Unit at Princess Margaret Hospital, and most of them now had "secure" NHMRC funding. Ursula Kees' group worked closely with the oncologists in the hospital, particularly Dr Michael Willoughby, the head of the oncology unit, who was determined that the Children's Cancer and Leukaemia Foundation would provide some secure funding for her laboratory in the new Institute. He could see this was crucial to the success of better identification of childhood cancers, investigating aetiology and discovering new therapies. Were we mad? We planned to set up a world-class institute in an isolated city in the biggest but most deserted State in Australia, in the middle of the crisis over business and political corruption known as "WA Inc" and as a recession was in full swing. We invited a group of Australia's leading researchers to Perth in 1986 and asked them to interview all of the researchers in child health and make an assessment. Despite the difficulties, the committee felt we had the right ingredients and encouraged us to go ahead. With the support of the Princess Margaret Hospital Board, and particularly of Professor Lou Landau, the proposal was developed further. In 1989, encouraged by Sir Gus Nossal, I applied for and was appointed Director of the new Institute. In 1990 we moved into our building -- the old School of Nursing at PMH, which was renovated with donations from the WA Lotteries Commission and the Incorporated Body of PMH. The support from other groups like the Variety Club of WA and the community has been the most crucial aspect of our success in this whole venture. Rationale for a multidisciplinary institute for child health research The problems in child health are now complex -- epitomised by diseases such as asthma, birth defects and other developmental problems, cancers and psychosocial problems. These stem from a complicated series of interactions between genes and environment, with variable causal pathways demanding complex solutions for their management or prevention. Our thinking was that if we brought together scientists from different disciplines under one roof we might be able to unravel the causes more successfully than working away separately in our little research areas. The aims of the Institute were to describe the burden of diseases in children and families in WA, to seek causal pathways using all types of scientific methods, and then to apply any knowledge to prevent disease in the community or to improve treatment at the bedside. We started as 90 scientists in four separate groups in 1989, with little infrastructure support, although our research grants from the NHMRC and other local foundations were adequate. Cell Biology, Molecular Biology and Cancer and Leukaemia moved in under the direction of Patrick Holt, Wayne Thomas and Ursula Kees, respectively, from the old PMH Children's Medical Research Foundation. My group from the NHMRC Unit moved to form the Division of Epidemiology and Biostatistics. Research in all these groups has blossomed at the Institute. Ursula Kees' group is making a seminal contribution on the role of homeobox gene malfunction in childhood leukaemia and has, in close collaboration with the PMH Oncology Unit and the international Children's Cancer Group, made significant contributions to the use of genetic markers to determine the prognosis and treatment for children.6,7Wayne Thomas's group is best known for its detailed work on the structure and immunology of house dust mite allergens, and a molecular approach to developing new types of immunotherapy8,9and the development of a candidate vaccine for all types of Haemophilus influenzae based on a conserved outer membrane protein.10 Patrick Holt's group has continued to describe the immunological mechanisms which operate during the development of tolerance to inhaled antigens,11,12 which are of extreme interest to both fundamental immunologists and allergists alike. Growth 1992 was the year of recruitment! We conducted an international search for a top biostatistician, which paid off with the recruitment of Dr Paul Burton, who became the Institute's senior biostatistician, and his wife, Dr Jenny Kurinczuk, an outstanding perinatal epidemiologist with a special interest in reproductive issues. Dr Burton conducted theoretical biostatistical research in a range of analytical problems (such as the analysis of complex interacting data sets and new methods of randomised trials), supported much of the biostatistical needs of the Institute and of our collaborators and spearheaded our new endeavours in genetic epidemiology. Within two years he became head of our new Division of Biostatistics and Genetic Epidemiology. Also in 1992 we sought an outstanding clinical researcher to establish a new Division of Clinical Sciences, with the brief of not only doing research in the Institute bridging the basic and clinical sciences, but also being a role model and stimulus for clinical research on the PMH campus. Dr Peter Sly was lured from Melbourne by offering him "fame and poverty" (he still has the letter) and he has continued to be a great success, collaborating with many groups in the Institute, the hospital and with fetal physiologists and respiratory researchers locally and internationally. In that year as well we were extremely fortunate in convincing the Health Department of Western Australia to second to us two outstanding clinical psychologists, Dr Steve Zubrick and Sven Silburn, whose research has underpinned the State Policy on Youth Suicide and other strategies in child and adolescent mental health. Dr Zubrick became head of the new Division of Psychosocial Research, with Silburn his very able deputy. The arrival of Australia's first MacFarlane Burnet Fellow, Professor Colin Sanderson, whose work on interleukin-5 was recognised internationally, created our last new division (Molecular Immunology) in 1994. This was an important bit of the jigsaw in our multidisciplinary attack on the complex disease of asthma. Dr Dierdre Coomb also arrived and established a laboratory specialising in the extracellular matrix, adhesion molecules and the mechanisms of inflammation, metastasis and haematopoiesis. As I look back now, some of our recruitment was part of a grand plan and some, as you would understand if you were in such an isolated and remote community, was opportunistic. Whatever the reason, the resulting mix has worked, as shown by our growth (from less than 50 to nearly 130 research staff in eight years), the way that many groups are collaborating in the Institute and the output to meet our goals. Successes A major reason for our success in fundraising from the local business community was that our research was focused on health problems that were well known as major burdens to the community -- asthma, adolescent suicide, birth defects, cerebral palsy, cancers and Aboriginal health. Another major factor was that we have had significant success in translating results into action (see Box); examples include the research on folate and spina bifida, reducing suicidal behaviours, improving outcome following bone marrow transplants in children with leukaemia, influencing the uptake of Haemophilus influenzae type b vaccination (which virtually eradicated the disease) and establishing a successful maternal and child health program for Aboriginal families in Kalgoorlie. Most of these are national and international issues and our Institute is increasingly being seen as a source of information for government and a model of success in multidisciplinary research and in translating research into policy. So, eight years on, have we been successful? How do you measure success in a multidisciplinary Institute? At the end of the first year of operation (June 1991) the Institute had $1.4 million in peer-reviewed grants, with a total operating revenue of $3 million (which included ongoing refurbishment costs). By the close of 1997 the Institute had gained $5.9 million in grants (including $2.5 million in NHMRC funding) and a total operating revenue of $8.3 million. You cannot force groups of different disciplines such as immunology and epidemiology and biostatistics to work together; all you can do is recruit thoughtful and good scientists and put them next to each other and hope that they talk! I remember two episodes vividly -- Patrick Holt saying "we have a great hypothesis we have developed in the lab and we need you epidemiologists to test it out for us"; this spawned our multidisciplinary asthma cohort study with Patrick Holt, Paul Burton, Peter Sly, Anne Read and myself testing the hypothesis that early and repeated infections may influence the immune response away from allergy and reduce the risk of asthma. The other episode was Colin Sanderson (head of Molecular Immunology) commenting that one of the best people in the Institute was Steve Zubrick, the head of Psychosocial Research -- given the usual contempt in which psychologists are held by "serious" scientists, this was great praise indeed! Bridges being developed between groups enhance the chances of collaboration. Threats With all this success and delight that we have survived our birth, with the new joint Commonwealth and State government $22.5 million building program heading for an early 2000 completion date, with such community support and government acceptance of our role, why am I concerned for our future? Our vulnerability now relates mainly to research funding and the support for our next generation -- our current students and postdoctoral staff. We are finding that research funding is much better in other countries and in other States and that we cannot offer our senior and rising bright young minds incentives to stay with us or even to stay in full time research. Some are off to overseas positions or into the private sector or into academic jobs with all the toil of teaching but at least some security. Our most recent sadness was that Paul Burton and Jenny Kurinczuk have been head-hunted back to the UK to tenured, well paid (at least double the NHMRC salaries they are currently receiving) academic positions at the University of Leicester. We will miss them greatly, but we can take some pride in having provided an environment for these two outstanding young people to develop their research careers to this level. Our policy of establishing an Institute by asking successful scientists to join us and bring their own salaries (usually NHMRC funded) was our only way of getting things going, but is not the way we can continue. It ensured that we only had peer-reviewed science in the Institute and meant that we could spend our precious and scarce resources on infrastructure and not research salaries. This ensured our survival, but it is not good policy in the longer term. The NHMRC roulette is not conducive to recruiting the brightest and the best. The Board needed little convincing to realise that such vulnerability is unacceptable and we are now looking at ways of securing our best people. Independent institutes are disadvantaged compared with universities because they do not receive direct infrastructure support from the Department of Employment, Education and Youth Affairs. Our Institute cannot match this year's increases in academic salaries as the NHMRC decided not to fund such an increase for research for its grant holders. Yet young scientists cannot be expected to work for low wages when salaries in other similar countries are much higher. We continue to lobby at Federal and State level, and wonder why, with our successes in improving child health, excellent research and scholarship, we are so undervalued in this country. Private funding alone is not the answer. I salute the likes of the visionary Sir James Cruthers and all the past, current and future corporate and private sponsors of research in Australia: what you could now do for us is to become advocates to convince governments to join with you in investing in our brightest and our best. Any less and our capacity to do research and benefit from it will be limited. References Holt PG, Yabuhara A, Prescott S, et al. Allergen recognition in the origin of asthma. Ciba Found Symp 1997; 206: 35-49. Holt PG, Macaubas C. Development of long-term tolerance versus sensitisation to environmental allergens during the perinatal period. Curr Opin Immunol 1997; 9: 782-787. Stanley FJ, Croft ML, Gibbins J, Read AW. A population database for maternal and child health research in Western Australia using record linkage. Paed Perinat Epidem 1994; 8: 433-447. Stanley FJ, Watson L. Methodology of a cerebral palsy register. The Western Australian experience. Neuroepidemiology 1985; 4: 146-160. Bower C, Stanley FJ. Dietary folate as a risk factor for neural-tube defects: evidence from a case-control study in Western Australia. Med J Aust 1989; 150: 613-619. Kees UR, Burton PR, Lu C, Baker DL. Homozygous deletion of the p16/MTS1 gene in pediatric acute lymphoblastic leukemia is associated with unfavorable clinical outcome. Blood 1997; 89: 4161-4166. Salvati PD, Ranford PR, Ford J, Kees UR. HOX11 expression in pediatric acute lymphoblastic leukemia is associated with T-cell phenotype. Oncogene 1995; 11: 1333-1338. Thomas WR, Smith W. House dust mite allergens. Allergy 1998; 53: 821-832. Thomas WR, Smith W, Hales BJ. House dust mite allergen characterisation: implications for T-cell responses and immunotherapy. Intern Arch Allergy Immunol 1998; 115: 9-14. Thomas WR, Flack FS, Callow MG, Chua KY. A high-molecular-weight outer membrane protein that is a potential target for protective immunity to type b and untypeable Haemophilus influenzae. J Infect Dis 1992; 165 Suppl 1: S75-S76. Stumbles PA, Thomas JA, Pimm CL, et al. Resting respiratory tract dendritic cells preferentially stimulate Th2 responses and require obligatory cytokine signals for induction of Th1 immunity. J Exp Med 1998. In press. McMenamin C, Pimm C, McKersey M, Holt PG. Regulation of IgE responses to inhaled antigen in mice by antigen-specific gamma delta T cells. Science 1994; 265(5180): 1869-1871. Author's details TVW Telethon Institute for Child Health Research, Perth, WA. Fiona Stanley, AC, MD, FAFPHM, FRACP, Director, and Variety Club Professor of Paediatrics, The University of Western Australia. Reprints: Professor Fiona Stanley, TVW Telethon Institute for Child Health Research, PO Box 855, West Perth, WA 6872. Email: infoATichr.uwa.edu.au URL: http://www.ichr.uwa.edu.au 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/> Milestones for the TVW Telethon Institute for Child Health Research Year Corporate history Research highlights 1985–1990 Planning for an Institute: including international review Cloning of house dust mite allergens (Wayne Thomas et al, from 1988) 1989 Professor Fiona Stanley appointed Director 5 year NHMRC project awarded to Epidemiology division 1990 Institute opened with a Board of Directors and Scientific Advisory Committee and the following research divisions: Cell Biology (Patrick Holt), Molecular Biology (Wayne Thomas), Epidemiology (Fiona Stanley), Leukaemia and Cancer (Ursula Kees) Cloning of outer membrane protein of all types H influenzae (vaccine candidate) (Wayne Thomas et al) 1991 Affiliation with The University of Western Australia Commonwealth grant to complete laboratories Psychosocial Research (Stephen Zubrick) Clinical Sciences (Peter Sly) Folate confirmed to prevent neural tube defects (Carol Bower and Fiona Stanley) 1992 Affiliation with Princess Margaret Hospital for Children Senior Biostatistician appointed (Paul Burton) Launch of Hib vaccination program World first folate and NTD prevention project launched 1993 New Board and other committees: Intellectual Property, Finance, Fundraising Molecular Immunology (Colin Sanderson) Cell Adhesion Laboratory (Dierdre Coombe) WA Child Health Survey commenced 1994 Biostatistics and Computing (Paul Burton) becomes a division Epidemiology Division now headed by Carol Bower Immune deviation by g/d T cells (Christine McMenamin and Patrick Holt) 1995 Administration and Corporate Services established (Robert Ginbey) State Government pledge for new building "Give every Child a Chance" fundraising campaign ($10 800 000 pledged) International review Child Health Survey Vol 1 (Stephen Zubrick and Sven Silburn) HOX 11 deregulation in T cell leukaemias (Patricia Salvati and Ursula Kees) 1996 Consolidation of infrastructure (UWA, HDWA) New approach to Commonwealth Government for building grant First NHMRC Program for Public Health (Maternal and Child Health) Child Health Survey Vol 2 (Stephen Zubrick and Sven Silburn) Only one case of Hib meningitis reported (after vaccination program) Aboriginal maternal and child health research project in Goldfields becomes a government-funded health service 1997 Joint announcement of Capital Works Grant totalling $22 500 000 from State and Commonwealth Governments Child Health Survey Vol 3 (Stephen Zubrick and Sven Silburn) First reduction in rate of NTD (from average of 2 to 1.2 per 1000) 1998 Commence new building program in September Persistence of fetal Th2 immune responses in atopic versus non-atopic individuals (Susan Prescott and Patrick Holt) 2000 New building complete Second international review

Fiona Stanley