Indigenous health

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

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

Gavin H Mooney · Virginia L Wiseman · Stephen Jan

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

Ian T Ring · David Firman

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

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

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

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

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

Jonathan R Carapetis · Bart J Currie

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

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