General medicine

Looking Forward Medicare's maturity: shaping the future from the past John S Deeble MJA 2000; 173: 44-47 By any objective standards Medicare has performed extremely well - - More articles on Administration and health services There are almost as many suggestions for reform of Medicare as there are participants in the system. Depending on the perspectives, ideologies and interests of the proponents, these calls for reform range from its extension and consolidation under either Commonwealth or State management, through various permutations of private and public operation, to relegation of Medicare to a welfare safety net. Some people hold any universal program to be "unaffordable", although for whom is rarely made clear. Some see Medicare's open-ended medical insurance as wasteful, while others (and often the same people) view any limits to hospitalisation as a major fault. Doctors complain about fee levels, the Commonwealth and State governments argue over funding shares, and consumers blame "the system" for the fragmentation of their care. None of these viewpoints are surprising. Medicare is an insurance program, but all of the delivery systems it supports are also seen as part of it, and these will rarely meet all the demands of funders, providers and patients. Given the different perspectives of each group, no system ever could, and Medicare's ability to respond is often limited by factors outside the insurer's control. Political scientists like to point out that in public policy the relevant question is rarely "where do we go?" but more often "where do we go from here?". So first we need to explore where we are now. Medicare since 1986 The summary data for Medicare and the services it covers for 1985-86 and 1997-98 (the most recent year for which full information is available) are shown in Box 1. Expenditure for all health services has risen from 7.5% to 8.4% of gross domestic product (GDP), and most of the increase was in the recession years 1990-1992. However, for Medicare-covered services (medical, public hospitals and optometry), the rise has been very small -- only 0.2% of GDP. In 1995, Australia's health spending as a proportion of GDP was in the middle of the range of health spending of comparable First World countries. Medical services: On the medical side, average benefits paid per person rose by 31% (in constant 1997-98 prices) and the number of services increased by an almost identical amount (30% per person).1 Average fees per service were therefore almost constant in relation to general price changes, and fell by only about 2% when compared with consumer prices (ie, much less than is often argued). On average, fees charged were lower than the schedule level in every year,1 despite the common impression of widespread over-schedule billing. The latter is mostly by specialists, largest for insured patients in private hospitals, and a greater problem for private health insurers than for Medicare. Hospital services: Overall hospital admissions per person rose by nearly 50% over the 12-year period. That was an extraordinary rate of growth, mostly occurring after 1992, and all a result of same-day treatments; overnight admissions per person were almost unchanged (Box 2). Total hospital outlays per person increased by 52% in 1997-98 prices, but the public and private sector experiences were quite different. Per person, public hospital expenditures rose 39.5%, comprising a 34.5% increase in admissions and a rise of about 4% in real costs per admission.1 Nearly all of the increases in admissions were in public patient use (Box 2). In contrast, private hospital outlays per person rose by 115%, the product of a 90% increase in admissions per person and a 13% rise in unit costs. About half the increase in usage was a result of private patients switching from the public hospitals to private hospitals. The underlying growth in private hospital admissions was nevertheless substantial, particularly since the proportion of the population covered by private insurance fell by 18%. Financing Apart from complaints from doctors over fees, the main issue has been the roles of the Commonwealth and State governments in public hospital funding, with each party blaming the other for any perceived shortfall. The details are complex, but the essential data are summarised in Box 3. This shows annual changes in public hospital expenditure and changes in the Commonwealth Government's share. The three time periods shown are the five-year Medicare agreement periods, which set the level of Commonwealth funding. There were clear links between the two variables -- when the Commonwealth share was less than 50% the growth in total outlays fell -- and, despite all the rhetoric, that division in source of funding still underlies the system's behaviour. The level of Commonwealth grants is therefore crucial and their inadequacy in one particular period (1988-1993) has been the main destabilising factor. The other and more popular issue is the role of the Medicare levy, which is often criticised for funding only a small proportion of Medicare's costs. But no one ever claimed that it should do otherwise. It was intended to cover only that part of the medical benefits side, which had previously been met by private insurance -- about half of the total amount paid before Medicare was introduced in 1984. The politics of the time demanded a demonstrable linkage between new outlays and the Medicare levy. This still applies. In 1997-98, the yield of $3760 million was almost exactly half the Medicare benefit payout. The hospital side had always been funded from general taxation via grants to the States and that continued, ironically funded partly by the withdrawal of a 30% tax concession on private insurance, very similar to the subsidy reintroduced last year.2 Medicare today By any objective standards Medicare has performed extremely well. As I have said elsewhere,1 in any other context an industry which increased its output by 30%-35%, with almost no increase in its share of the national product, would be acclaimed as a major success story! Costs have risen almost exactly in line with prices generally and, except for pathology and imaging, growth in medical service use has stabilised since 1994. All of this was achieved in a healthcare system which gives patients and providers more freedom than almost any other system worldwide. But the clamour for change continues. Not all of the exploding demand for hospital admissions has been met and the impact of that demand, plus the costs of upgrading private hospital technology, has threatened private insurance viability. The 30% premium subsidy for private health insurance introduced in 1999, and recent changes from community rating to risk rating, attest to this -- no funding system, public or private, could long sustain an annual growth in hospital admissions of 3.5% per person, nearly twice the growth in GDP. The problem is a medicotechnological one, not one for Medicare alone. People do not admit themselves to hospital, doctors do -- and that is where the explanations must be found. However, some groups have contrived to present it as a crisis on which governments must act and which threatens the whole existence of a universal insurance scheme. What should be done As might be guessed, I am not among those supporting major structural changes to the present system. Special interests apart, the most substantive criticisms concern division of responsibilities for management and funding between the Commonwealth and State governments, institutions and professionals. All these predate Medicare. Its acceptance of the delivery systems, payment methods and reward structures of the time has also been criticised. Badly coordinated care, wasteful cost-shifting and weak incentives for efficiency are held to result. For many people, timidity rather than excessive zeal would be the main complaint. There is truth in this contention, although the Australian experience is not unique. No national insurance scheme has greatly changed the culture and practices which preceded it. The historical and constitutional divisions between the Commonwealth and State governments over medical and hospital services, insurance powers and revenue raising are so deeply intrenched that they could never have been resolved within the time frame which political action required, particularly in the circumstances of 1973-75 (see the articles by Scotton, and Hayden). Almost all proposals for payment change have met strong opposition from the medical profession, although some very modest progress has been made with program-based payments to general practitioners. How much this matters is debatable. The governmental (Commonwealth-State) division is certainly complicated, sometimes irrational and the source of much angst over cost shifting. The latter fascinates the bureaucrats and absorbs a disproportionate amount of their time. However, it works both ways, and I am not convinced that divided financial responsibility has as much effect on the fragmentation of services as many critics claim. The recent coordinated-care trials have shown that, at the operational level, pooling funds is not a sufficient condition for high-quality, efficient care.3 Poor management skills, rivalries and professional myopia are equally important problems. At a higher level, it should be possible to separate "desirable" cost rearrangements from stratagems, although distrust between the Commonwealth and States does not help. It would be naive to expect any major realignment of governmental roles in the foreseeable future. However, the climate could be changed if the Commonwealth Government were to take responsibility for all medical costs, including those in public hospitals and medical training. It would mean no more than setting the Federal-State financial division slightly differently, with no immediate implications for budgets or administrative responsibilities -- existing public hospital appointments would continue with only cost-neutral grant adjustments. That would be much more logical than the present situation in which the Commonwealth supports medical costs directly in the private hospitals, but has no role at all in the public sector. Separate government funding for all medical costs is standard practice in the Canadian system, and there are considerable advantages in it. Among other things, it would change much of the debate over cost shifting, but that would be only one of the anomalies addressed. Commonwealth funding of in-hospital medications has already been mooted on the pharmaceuticals side. The efficiency arguments are more fundamental. For the most radical reformers, any system in which providers both select and deliver services must be inherently flawed. In theory, competitive markets achieve efficiency by separating these two functions. Emulating their operation should therefore be the aim, at least as far as possible. The practical manifestations are schemes for separating purchasers from providers (even funder-purchaser-provider splits) with arm's-length dealing and varying degrees of competitive behaviour. Governments are entitled to mandate insurance and how its costs should be borne, but both the insurance function and the supply of services should be diversified. State hospital systems and single insurance authorities like Medicare are incompatible with such models. These are the same arguments and issues as were traversed 25 years ago, and, like most debates in which the evidence is a mixture of empirical data and behavioural assumptions, they can rarely be settled. My view is that, while there are some supporting services in which standards and outcomes can be sufficiently defined and measured for arm's-length dealing, they cannot be applied to healthcare as a whole. The basic problems of uncertainty and inequalities of information between users and providers were first explored by the Nobel Prize-winning economist, Kenneth Arrow, nearly 40 years ago.4 For patients, they imply a level of trust and delegation to providers unparalleled elsewhere, and the same is ultimately true for purchasers on their behalf. The United Kingdom and New Zealand were the first countries to embrace purchaser-provider separation and internal markets within their public systems. Their experience has shown that, at a general level, it is impossible to write contracts which sufficiently define the obligations of each party, and that the information costs of trying to monitor such contracts have been extremely high for very modest gains. Both systems have now been modified considerably. I am therefore sceptical about most market solutions, and equally doubtful about isolating funders from both user and provider contact. In the Australian context, that doubt is particularly relevant to proposals which would create more "independent" authorities outside the present system. It might be worthwhile, but it could also serve to simply shift responsibility. As it is, Medicare depends for adequate funding on a network of political obligations -- on the Commonwealth in return for money collected through the levy, and on the States in return for Commonwealth grants. These commitments could easily be avoided if government contributions became discretionary and there was someone else to blame. What changes are most likely For the foreseeable future, the medical side of Medicare will almost certainly remain, although technology and corporatisation will force some changes. The diagnostic services are prime examples. They are the fastest-growing expenditure group and the least satisfactory subjects for fee-for-service payment. Per person outlays for pathology and imaging have risen by 38% over the past five years, compared with a growth of only 5% for all other medical services.5 Recent attempts to cap growth have had only a limited effect, and, in pathology, a few corporate providers are now so dominant that their relationship with Medicare is more like commercial contracting than professional fee reimbursement. Imaging is heading in much the same way and commercial interests are making inroads into general practice as well. Potential responses by government and the medical profession cannot be canvassed here, but they can not wait too long. It is on the hospital side, and particularly the relationship between the public and private sectors, that there is most controversy. Australia is unique in having substantial private hospital and private insurance industries operating alongside a universal public program. Both Medibank and, originally, Medicare provided subsidies to private hospitals. They and the regulated private insurance were seen as supplementary to the public system for people who valued choice of doctor, hospital and time of treatment, but they were still regarded as a part of the Medicare system. As shown earlier, the result has been a slow decline in the proportion of the population holding private insurance, but not in the absolute number of patients treated privately and, paradoxically, a very large increase in private hospital admissions. Both perceptions and policy have changed significantly in recent years. Rhetorically, the emphasis has been on the competitive independence of private insurance, with a shift in its depiction from being supplementary to Medicare to being first a complement and then, most recently, an alternative to it. That is the thrust of the current recruitment campaign, however obliquely expressed. The purchase of advantage is recognised and an explicitly two-tier system encouraged by such devices as the levy surcharge on uninsured higher income earners and the portrayal of private insurance membership as a civic duty which assists the poor. There are many people who believe that these measures and the $1.7 billion premium rebate are simply precursors to either means testing Medicare or allowing people to opt out of it. Some realities It is hard to predict political decisions. But it is also easy to exaggerate the impact of current policies. In reality, all the present activity will not raise private insurance membership to much beyond a third of the population -- the same as in 1996 -- and the best estimate is that, although savings to the public hospital system in the long run might reach about $450 million (still only 3% of its total outlays), that is a long way off. None of the big-picture parameters will change. However, both costs and hospital use will rise. Costs -- in its rush to facilitate medical gap insurance, the Government's present restriction to "contracting" doctors will be removed. Average charges will inevitably increase (with the 30% Commonwealth funding) and, in the process, challenge the legitimacy of Medicare's whole schedule fee system and cost control. How can two levels of officially sanctioned charges both be right? Hospital use -- utilisation must rise because unrestricted hospital access is what private insurance offers and is bought for. But Australians are already among the highest hospital users in the world. In 1997-98, our rate of overnight admissions was 159 per 1000 population. In Canada it was 105 per 1000, down from 145 per 1000 in 1986.6 In the United States, the 1996 rate was 117 per thousand and falling.6 These are very substantial differences. It would be a pity if expediency and the demon of managed care prevented any serious thinking about their justification and how they came to be. As it is, one side of the Australian system is trying to contain hospitalisation as much as possible, while the other is effectively promoting it. References Deeble JS. Medicare: Where have we been? Where are we going? Aust N Z J Public Health 1999; 23: 563-570. Deeble JS. Health care under universal insurance: the first three years of Medicare. In: Butler JRC, Doessel DP, editors. Health economics: Australian readings. Sydney: Australian Professional Publications, 1989. Department of Health and Aged Care. The Australian Coordinated Care Trials: Interim Technical Report, Canberra: The Department, 1999. Arrow KJ. Uncertainty and the welfare economics of medical care. Am Econ Rev 1963; 53(5): 941-973. Department of Health and Aged Care, Medicare Statistics, 1984-85 to December Quarter 1999. Canberra: The Department, 98, 99, 106. Organisation for Economic Co-operation and Development. OECD health data 99 [on CD-ROM]. Paris, OECD, 1999. Authors' details John Deeble is Adjunct Professor of Economics in the National Centre for Epidemiology and Population Health, at the Australian National University. He was a Senior Research Fellow at the Institute of Applied Economic and Social Research (University of Melbourne) when he and Richard Scotton formulated the first proposals for universal health insurance. During the Medibank period he was a Special Adviser to the Minister for Social Security, Chairman of the Health Insurance Planning Committee and Deputy Chairman of the Health Insurance Commission. From 1977 to 1983, he was Director of the NHMRC Health Economics Research Unit and was appointed Special Adviser to the Minister for Health, Dr Neal Blewett, and Chairman of the Medicare Task Force in 1983-84. Subsequent appointments included Founding Director of the Australian Institute of Health and Welfare, and First Assistant Secretary of the Department of Health and Community Services. He was a Health Insurance Commissioner for 15 years to 1999. National Centre for Epidemiology and Public Health, Australian National University, Canberra, ACT. John S Deeble, AO, PhD, BCom, DipHospAdmin, Adjunct Professor of Economics. Reprints: Professor J S Deeble, National Centre for Epidemiology and Population Health, Australian National University, Canberra, ACT 0200. Make a comment 1: Vital statistics of Medicare, 1985-86, 1997-98* 1985-86 1997-98 Percentage increase Outlays as a percentage of GDP All health services Medicare only 7.5% 3.7% 8.4% 3.9% 0.9% 0.2% Outlays per person (1997-98 prices) Medical At fees charged At schedule fees At benefits paid $277 $300 $250 $386 $391 $328 39% 30% 31% Hospital Total Public Private $575 $483 $92 $875 $678 $197 52% 39% 115% Services per 1000 population Medical 7580 9850 30% Hospital admissions Total Public Private 193 142 51 288 191 97 49% 35% 90% *Data from Deeble 1999.1 GDP=Gross domestic product. Back to text Back to text Back to text

John S Deeble

Looking Forward Medicare: diagnosis and prognosis Frances C Cunningham MJA 2000; 173: 52-55 The system of mixed public-private healthcare funding works well in Australia and offers the best foundation for the future - - More articles on Administration and health services Australians have now experienced 16 years of national health insurance with Medicare, although the program implemented in 1984 was largely a renamed version of its predecessor, Medibank, introduced 25 years ago. How will the healthcare industry and its external environment change over the next 25 years, and what will be the impact on Medicare? How should we best appraise Medicare's strengths and weaknesses, take account of the fundamental changes that have occurred in healthcare delivery, and apply the better intelligence we now have on financial incentives and delivery mechanisms to develop a more effective national health insurance program for the future? Appraising Medicare How do Australians view Medicare? In a 1998 survey conducted to measure public satisfaction with healthcare, only 19% of Australians agreed that, on the whole, the system works well and only minor changes are needed to make it better.1 Forty-nine per cent wanted fundamental changes, and waiting times for specialist care and non-emergency surgery was reported as the most important consumer issue. The survey also revealed a substantial loss of public confidence in the healthcare system compared with a decade earlier, when 34% of Australians felt that the system needed only minor changes. On the plus side, Medicare has established affordable universal coverage for publicly funded, public hospital services and largely publicly funded, privately provided medical and optometrical services. Australians also have excellent coverage for mainstream pharmaceuticals. With a view to controlling health expenditure, at present at $50 billion and 8.4% of gross domestic product (GDP),2 these services were seen by government as the boundaries of publicly funded Medicare. While our health expenditure is at the median for OECD countries, our life expectancy is above the average. Weaknesses in the Medicare public program are evident: universal coverage only includes medical practitioners and optometrists, and the provision of other publicly funded ancillary services and community health services varies substantially within the various State or Territory health systems. Medicare's financial incentives A valid concern with implementing a national health insurance program is that it tends to lock in place the existing healthcare system. In Australia, this has meant the maintenance of the open-ended, traditional fee-for-service approach to financing medical and optometrical services, with little change in the delivery system structure. There are increasing concerns about the geographic maldistribution of medical services, especially in rural areas. With an administered pricing system, it is difficult to get the prices "right", especially with the rapid technological changes affecting healthcare. Moreover, the structure of such systems can have powerful effects (some intended and undesirable) on services delivered. For example, payment of general practitioners under Medicare has created incentives for shorter patient visits and higher patient throughput. In addition, preventive services -- health screening and disease management programs, and patient education and health outcomes monitoring -- tend not to be as effectively implemented in non-managed systems as in managed systems. Although trials of coordinated care have been implemented in Australia in recent years, they have been primarily public-sector oriented, whereas the major overseas examples of long-term, financially viable care management systems are in the private domain. In the United States, in addition to the coverage that private sector managed health insurance firms provide for those with private insurance, the government has contracted extensively with these health insurers to provide care to beneficiaries in government programs as an alternative to traditional coverage. Split responsibilities and inefficiencies Medicare creates a separation of payment of most ambulatory medical care from inpatient care, with non-hospital medical services and pharmaceutical services funded by the Commonwealth, and hospital and day-surgery services funded through the States and through private health insurance. This means that there are major structural impediments to the provision of a "seamless" web of services through all levels of care. This separation of payment has also made it difficult to move away from an emphasis on inpatient care and the resultant high levels of hospital utilisation. In 1997-98, overall Australian hospital utilisation was 1075 bed-days per thousand population (excluding same-day admissions).3 This compares with the 1996-97 rates of 318 and 335 days per 1000 population in the United States for health maintenance organisations (HMOs) and non-HMOs, respectively.4 The 1997-98 Australian hospital admission rate (excluding same-day admissions) of 16%3 was almost three times the 1996 US health insurance rate of 5.7% (for both managed care and non-managed care).5 In the United States, this reduction in acute inpatient care has been accompanied by an increase in subacute, home health and skilled nursing facility care. This has not happened in Australia, with the result that we have excess hospital bed capacity in both the public and private sectors. An important general caveat about measuring service use is that the assumption "more is better" does not necessarily hold true in healthcare consumption. It is inappropriate to assume that more care -- or more costly care -- is better, or that reductions in service use necessarily indicate reductions in quality. Hospital utilisation in Australia thus presents a conundrum: in spite of having such high levels (by international comparisons) of inpatient admissions and bed-day utilisation, as well as excess bed capacity, there are significant problems with public-hospital waiting lists. The solution lies in better care management and in appropriate care at the appropriate level, rather than in funding for additional beds. Reform of private health insurance Although 10% of total health expenditure is funded through private health insurance,2 the role of private health insurance within Australia's healthcare system has not been clearly delineated. Is private health insurance a supplement to or an alternative to the public health system? Initial estimates of the cost of Medicare assumed that at least 40% of Australians would maintain their private health insurance cover.6 Levels of private cover declined from 60% immediately pre-Medicare in 1983 to 30.1% in 1998.7 The legislative changes introduced in 1995 were intended to make insurance better value for money through agreements made between health insurers and hospitals and health insurers and medical practitioners. These changes have resulted in more effective negotiations between insurers and private hospitals. Since coming into power in 1996, the Howard Liberal-National Coalition Government has made significant progress in modernising the regulation of private health insurance. Within a short timeframe, most of the key recommendations of the 1997 Industry Commission Inquiry8 into private health insurance have been introduced, with the exception of the recommendation for a broad public inquiry into Australia's health system. Australians value choice, whether it be in education, airlines or healthcare. Australians also value a fair go. The Howard Government has introduced strategies to ensure that we maintain a viable mixed private and public healthcare system in Australia. Compared with the financial contribution of those relying totally on the public system, the contribution of privately insured Australians was inequitable. The 30% tax rebate on health insurance premiums for consumers is one part of an overall strategy to ensure the continuation of a mixed public and private health system in Australia. There is bipartisan support for the rebate, with the Leader of the Opposition, Kim Beazley, promising its retention by a Labor Government.9 The rebate ensures that there is a fairer, more equitable approach to financing healthcare for those who choose to pay for private cover, in addition to their Medicare levy payments and their contributions through taxable income (estimates for which range from 5% to 10%). The Private Health Insurance Administration Council reports that a record 187 000 Australians have joined health funds in the first three months of this year, with the fastest-growing membership being in the age bracket 30-34 years.7 This means that more than six million Australians now have health insurance, the highest level since 1996. There has also been stronger growth in no-gap cover for hospital-related medical costs, after the Harradine* amendment. The latter requires health insurers to have no-gap products in place by 1 July 2000 in order to offer the 30% rebate to their members. The legislation, just passed by Federal Parliament (the Health Legislation Amendment (Gap Cover Schemes) Act 2000), will allow the private health industry to develop "no gap" or "known gap" schemes which will operate without the need for contracts. The introduction of Lifetime Health Cover on 1 July 2000 is currently resulting in continued growth in private health insurance membership. Major changes relating to the capital adequacy and solvency requirements of health insurers are to be introduced shortly to provide more clearly defined safeguards for consumers. Major impacts over the next 25 years The fundamental challenge for Medicare, with its financing and delivery systems belonging to the last century, will be coping with the impact of key trends envisaged for 2025. Most of these trends will affect the future costs of Medicare. The health insurance system of the future will also be shaped by the wider sociopolitical, moral and ethical environment, in terms of what is politically feasible and acceptable to the electorate. In particular, what will be the trade-off between the extent of public coverage and the tax burden? Also relevant will be our capacity to reduce behavioural risk factors across societal groups to achieve reductions in morbidity and increases in life expectancy. The magnitude of the contribution of the behavioural risk factors to the disease burden in Australia has recently been estimated, with tobacco smoking causing an estimated 10% of the disease burden in Australia, followed by physical inactivity (7%).10 The Internet, electronic commerce and information technology The Medicare system will be strongly affected by information technology and the Internet. At present, a depressingly large fraction of healthcare processes are still mediated by paper (medical records, prescriptions, appointments, bills and claims). According to Goldsmith,11 an eminent US healthcare forecaster and strategist, what the Internet promises healthcare managers and clinicians is a flexible information architecture that can reach down into the dozens, even hundreds, of healthcare information "silos" and extract, analyse, aggregate and redirect the data clinicians or managers require to make decisions. E-commerce also promises to reduce administration costs. Beyond clinical uses, promising Internet applications in healthcare include: Paperless transmission, assessment and payment of medical and hospital claims; Paperless prescribing of and payment for pharmaceutical items; Medical product ordering and inventory management; Outsourcing of data processing and other management functions; and Smart cards will permit the compiling and updating of standardised patient information using a common platform. The challenges in achieving such uses lie in standardising the coding and formats for clinical and health-related data and in standardising patient identification while protecting privacy. The National Health Information Management Advisory Council has developed a national plan of action for information management in the health sector.12 However, gaps in private sector representation on the Council need to be addressed urgently. Further, the Commonwealth must take the lead in legislatively mandating the development of such electronic standardisation requirements. This would accelerate progress to be made in efficiencies from e-commerce and from performance measurement across the health system. Rising consumer expectations As the post-war "baby boomers" become key healthcare consumers, they will demand more for themselves and for their frail, aged parents. Consumers have aggressively embraced the Internet to acquire health information. The Internet will also strengthen the role of consumers in their interactions with practitioners and healthcare institutions, and create a powerful new tool to help people manage their own health risks. These empowered consumers will demand better information to ensure quality and safety in healthcare. Consumerism will also foster a demand for a wide range of choice of new services and products, many of which will not be paid for by public Medicare. Medical advances, technological change and clinical practice Medical advances and new technologies are likely to continue to develop and will put pressure on cost growth. The Human Genome Project will dramatically alter healthcare. In an era of "individual medicine", genetic screening will identify health risks, and new treatments and precisely targeted pharmaceuticals will emerge. Advances will occur with bioengineered organs, organ transplantation, artificial skin and bones, methods of promoting and inhibiting angiogenesis, and new vaccines. Point-of-care testing, such as hand-held blood and saliva analysers, will move testing to the bedside, the clinic and the home. Telemonitoring in the home will alter demand for home health aides. Berwick envisages that, in the information age, medical practice will be a "knowledge producing" enterprise and not the "contact producing" enterprise of the last century.13 That knowledge will include the best evidence for diagnosis and treatments. There will be a greater focus on the development of standards of care, clinical guidelines and protocols, and on prevention, as well as ambulatory or home care. A greying Australia Compared with the uncertainties of other future impacts, the consequences of demographic change are more certain. The Australian Bureau of Statistics14 projects that the share of the population over age 65 will rise from 12.4% in 2001 to 18% in 2021 as the first wave of the "baby boomers" reaches 75 years. In 2021, the median age will be 40.4 years. Under current arrangements, the burden of increased future health costs would fall on the relatively diminished numbers of non-elderly. Combined with the increased burden of social security, the load may be too great. Governments will need to decide what core elements the tax-funded health system will cover. It is likely that some of the increased costs will have to be reallocated to the elderly. It is likely too that they will aim to protect their superannuated livelihoods through long term care insurance as they enjoy longer life expectancy. The ideal future financing model An ideal model for future healthcare financing is outlined in the Box. I have described this model in greater detail elsewhere.15Advocates for one single health funder, while largely driven by ideology, are campaigning for all health services to be funded through a government-run, single government payer system. Debate over whether government funding or private insurance constitutes the ideal financing model is reaching resolution in a number of overseas countries. The answer seems to be both. On average, private insurance pays about 10% of healthcare costs in OECD countries and is growing at a rate of 5%-7% a year. According to the report HealthCast 2010: smaller world, bigger expectations,16 these trends mean that most of the industrialised world will have both a strong publicly funded government health program and a private, market-based one. While acknowledging areas for improvement in both sectors, on balance the mixed public-private system works well in Australia and offers the best foundation for the future. This aspect of the overall framework of Medicare allows for choice by consumers, rather than the alternative of a totally government-controlled, nationalised health system. In addition, with proposals such as that of the Democrats for regional health authorities to pay medical practitioners on a capitation or salaried basis,17 it could be wise for medical practitioners themselves to have the option of another payer. Ideally, within the future Medicare framework, private health insurers should be able to offer their members a comprehensive range of health services, which should include, as a minimum, ambulatory medical services and inpatient services. This would extend the benefits of a mixed system to both consumers and medical practitioners. Footnotes* Brian Harradine, Independent Tasmanian Senator in Federal Parliament (from 1975 to the present). References Donelan K, Blendon RJ, Schoen C, et al. The cost of health system change: public discontent in five nations. Health Affairs 1999; 18(3): 206-216. Australian Institute of Health and Welfare. Australia's health services expenditure to 1997-98. Canberra: AIHW, 1999 (Health and Welfare Expenditure Series -- Health Expenditure Bulletin No. 15). Australian Institute of Health and Welfare. Australian hospital statistics 1997-98. Canberra: AIHW, 1999. (Health Services Series AIHW Catalogue No. HSE 6.) Tu HT, Kemper P, Wong HJ. Do HMOs make a difference? Use of health services. Inquiry 2000; 36(4): 400-410. Weinick RM, Cohen JW. Levelling the playing field: managed care enrolment and hospital use, 1987-1996. Health Affairs 2000; 19(3): 178-184. Australian Department of Health, Housing, Local Government and Community Services. Reform of private health insurance. A discussion paper. Canberra: AGPS, 1993. Private Health Insurance Administration Council. Quarterly statistics. March 2000. Canberra: PHIAC (May 14), 2000 <www.phiac.org.au> (accessed 7 June 2000). Industry Commission. Private health insurance. Canberra: AGPS, 1997. (Report No. 57.) Beazley K. Health insurance rebate. 4QR Radio: 09:00 News, 22 Feb, 2000. Mathers CD, Vos ET, Stevenson CE, Begg SJ. The Australian Burden of Disease Study: measuring the loss of health from diseases, injuries and risk factors. Med J Aust 2000; 172: 592-596. Goldsmith J. How will the Internet change our health system? Health Affairs 2000: 19(1): 148-156. National Health Information Management Advisory Council. Health Online: a health information action plan for Australia. Canberra: AusInfo, 1999 <www.health.gov.au/healthonline> (accessed 7 June 2000). Berwick D. Knowledge always on call. Modern Healthcare 1999; 29(39) Suppl: 2-4. Australian Bureau of Statistics. Population projections: 1997 to 2051. Canberra: ABS, 1998. (Catalogue No. 3222.0.) Cunningham FC. Medicare reform: via managed care or managed competition? Healthcover 1997; February-March: 8-16. PricewaterhouseCoopers. HealthCast 2010: smaller world, bigger expectations. Dallas, Tex: PricewaterhouseCoopers, 1999. Australian Democrats. Health reform: delivering a remedy. Canberra: Australian Democrats (April 17), 2000 <www.democrats.org.au/campaigns/health/> (accessed 7 June 2000). Authors' details Frances Cunningham is the Executive Director of the New South Wales Health Funds Association, and a member of the NSW Private Health Forum. She has a background as a healthcare consultant, health manager, health policy analyst and health services researcher. She was formerly Senior Policy Adviser to two NSW Ministers for Health, and a member of the NSW Senior Executive Service. She headed the Commonwealth Task Force which developed the discussion paper "Health maintenance organisations: a development program under Medicare" for former Federal Minister for Health, Dr Neal Blewett. NSW Health Funds Association, Sydney, NSW. Frances C Cunningham, ScD, Executive Director. Reprints: Dr F C Cunningham, NSW Health Funds Association, PO Box A2572, Sydney South, NSW 1235. francescATtpgi.com.au The views expressed are solely those of the author, and no endorsement by the NSW Health Funds Association is intended or should be inferred. Make a comment A future national health insurance porgram15 The objectives of a national insurance program should include: Universal coverage; A financially stable and viable program; Choice - and adequate information for Australians to make informed choices; and Comprehensiveness of coverage. Comprehensiveness of coverage will need to include: Better coverage for aged healthcare services; Access to quality healthcare; and Affordability for both those covered and those financing the program. Funding of the program should ensure: Macroeconomic efficiency - the costs of healthcare should not exceed an acceptable share of national resources; Microeconomic efficiency - the mix of services chosen should secure health outcomes and consumer satisfaction at minimum cost; and that Funding arrangements are transparent to the public. Financing mechanisms for Medicare will need to be reviewed: the levy, the tax regime, including relevant income-tax credits and debits, the Commonwealth-State grants arrangements; and the Australian Health Care Agreements. Other aspects of the model: Tax-based financing - an appropriate vehicle for those choosing public Medicare could be the existing Medicare levy (essentially an income-tax), although it should be adjusted on a sound actuarial basis to reflect the true health contribution, with an adjustment to financing from general income tax. Health insurance premiums - for those choosing to directly pay for private health insurance, premiums would be paid to health insurers. Financing for them could include a levy exemption or, if they did pay a levy, their risk-adjusted Medicare funds would flow on to the health insurer. Community rating would continue to apply to individual premium contributions. As at present, people would continue to contribute to social support through their general tax dollars. Ultimately, health insurance contributions should probably be a combination of employee and employer contributions, analogous to superannuation. The fringe benefits tax on employer contributions should be removed. Competition - under this model, strong competition would be possible between public and private health funders, both providing coverage for at least a standard comprehensive benefits package. Both sectors would be able to contract on a competitive basis for the most cost-effective quality providers, whether in the public or private sector. Back to text

Frances C Cunningham

Recommendations from the Australasian Society of Thrombosis and Haemostasis Abstract The anticoagulant effect of warfarin should be kept at an international normalised ratio (INR) of about 2.5 (desirable range, 2.0-3.0), although a higher level may be better in a few clinical conditions. The risk of bleeding increases exponentially with INR and becomes clinically unacceptable once the INR exceeds 5.0. Warfarin therapy should be continued for around six weeks for symptomatic calf vein thrombosis, and for 3-6 months after proximal deep vein thrombosis (DVT) that occurs after surgery or limited medical illness. Therapy for six months or longer could be considered for DVT occurring without an obvious precipitating factor, proven recurrent venous thromboembolism (VTE), or if there are continuing risk factors. Oral anticoagulants prevent ischaemic stroke in atrial fibrillation (AF). Maximum efficacy requires an INR > 2.0, but some benefit remains at an INR of 1.5-1.9. Patients aged over 75 years are at greatest risk of intracranial bleeding during warfarin therapy for AF, and the target INR may be reduced to 2.0-2.5, or perhaps as low as 1.5-2.0, in such patients. Warfarin should be withheld if it is more likely to cause major bleeding than to protect from stroke (eg, in young people with isolated AF where the annual baseline risk of stroke is < 1%). In patients with AF, aspirin is less effective than warfarin (much less effective after such patients have had a stroke or transient cerebral ischaemia). In people with prosthetic heart valves, an INR of 2.5-3.5 is probably sufficient for bileaflet or tilting disc valves, but a higher target INR is necessary for caged ball or caged disc valves. The addition of aspirin (100 mg/day) further decreases the risk of embolism but increases the risk of gastrointestinal bleeding. Warfarin is used for preventing and treating venous or arterial thrombosis and embolism. It is a potentially hazardous drug, causing major bleeding in 1%-2% of people treated, and intracranial bleeding in about 0.1%-0.5% during each year of therapy. These risks are well recognised, but strong recent evidence that many otherwise healthy people with atrial fibrillation (AF) or venous thromboembolism (VTE) can benefit from long term warfarin therapy has led to a major increase in its use. These consensus guidelines offer advice on the selection of patients for warfarin therapy and management of such patients. The recommendations draw on proceedings of the Fifth American College of Chest Physicians Consensus Conference on Antithrombotic Therapy,1 and are consistent with the most recent Guidelines on oral anticoagulation developed for the British Society for Haematology.2 Warfarin therapy and management of complications The INR The INR (international normalised ratio) is a good indicator of effectiveness and risk of bleeding during warfarin therapy and is best kept at about 2.5, with a target range of 2.0-3.0, for most clinical indications, although higher levels may be better for certain patients (Box 1). The lower limit of this target range recognises a threshold level for effectiveness, while the upper limit is set to minimise bleeding. Starting and maintaining warfarin therapy The daily maintenance dose of warfarin differs greatly between individuals, commonly between 0.5 mg/day and 15 mg/day, and often fluctuates over time. The average maintenance dose is about 4.5 mg/day, although this is lower in the elderly. The drug is rapidly and completely absorbed and immediately blocks further hepatic synthesis of the functional vitamin K-dependent haemostasis factors (II, VII, IX, X, protein C, protein S). However, its impact on the INR is delayed until preformed coagulation factors are removed, so dose adjustment must allow for these delayed effects. The plasma half-life of warfarin is about 36 hours.3 In the past, it was customary to use a loading dose of 10 mg. However, for most situations, a reduced starting dose of 5 mg per day will achieve an INR of 2.0 in four to five days.4 INR is measured daily or every second day during the first week of treatment, with the dose of warfarin (taken in the evening) titrated against the morning's INR. It is then measured at increasing intervals depending on response. Many patients, once the dose is stable, can be well controlled with 4-6-weekly testing and dose adjustment, but others need more frequent assessment. An empirical approach to warfarin dosing can be smooth and effective but published dose-adjustment tables can help.2 Old age, reduced body weight, and impaired cardiac or liver function all predict a smaller than average dose requirement. Multiple comorbidities and a need for many drugs increase the risk of an unstable anticoagulant response. The effect of warfarin is subject to multiple interactions. These include the dietary content or extent of absorption of vitamin K, the absorption of warfarin and its effect on the liver (which are increased or decreased by many other drugs), and the clearance of blood-clotting factors.1,3 Intercurrent illness, starting or stopping therapy with other drugs (especially antibiotics and amiodarone) and changes in diet or bowel function can all influence the INR. Rechecking the INR within a few days of any change in medication or clinical condition is prudent. Bleeding is minimised by regular monitoring to avoid an excessive INR and by educating patients about how warfarin works, why their dose requirement may change, and the likely settings and symptoms of bleeding complications. Successful warfarin therapy requires a partnership with patients, who should be encouraged to have their INR checked soon after any change in their normal routine. Clinics should periodically audit their results with warfarin therapy and review exceptional cases. Between 50% and 75% of INRs are likely to fall into their designated therapeutic range.5 Two recent Australian case reports are reminders that bioequivalence has not been formally demonstrated for Coumadin and Marevan (both from Boots Healthcare Australia, Sydney, NSW), the two locally available formulations of warfarin.6 Warfarin and bleeding Major bleeding has been reported in 1.1%-8.1% of patients during each year of long-term warfarin therapy (1.1%-2.7% by anticoagulant clinics managing patients with prosthetic heart valves,7-9 1.3% in atrial fibrillation trials, and 2.8%-8.1% after a stroke or transient ischaemic attack10-12). Risk factors include old age, serious illness (cerebral, cardiac, kidney or liver disease), cerebrovascular or peripheral vascular disease, and an unstable anticoagulant effect. Forgetfulness, non-steroidal anti-inflammatory drugs and alcohol abuse may also contribute.7,9,13-15 Warfarin appears to be especially hazardous after a transient ischaemic attack or minor stroke; in one trial, 14 months of warfarin therapy with a relatively high target INR of 3.0-4.5 increased major bleeding from 0.9% to 8.1%, intracranial bleeding from 0.5% to 4.1%, and fatal intracranial bleeding from 0.2% to 2.6% (relative to low dose aspirin therapy).12 Bleeding is most likely during the first three months of treatment, and often follows trauma or unmasks a previously unsuspected comorbidity.8,13-15Age alone is not a contraindication to warfarin therapy. Although one report showed that each decade above the age of 40 raised the risk of major bleeding by almost 50%, with a maximum effect above 70 years,7 others have found that age below 70 years has no influence.8,15 The INR is the dominant determinant, whether bleeding is expressed as the absolute risk per annum (Box 2) or as relative risk. In a 1996 study, the bleeding rate was doubled as the INR increased from 2.0-2.9 to 3.0-4.4, quadrupled between 4.5-6.0, and was multiplied by five when the INR was above 7.0.15 There is a consistent increase in major bleeding (including intracranial bleeding16) when the INR exceeds 4.0-5.5.7,11,14 A 1997 trial found that each increase in INR by 0.5 multiplied the risk of major bleeding (mostly intracranial) by 1.43.12 Managing an excessively prolonged INR or bleeding caused by warfarin therapy An INR above 5.0 requires close monitoring and often needs intervention, as determined by the level of the INR and the presence or absence of bleeding (Box 3). The INR often remains elevated for some days, even if warfarin is withheld, but small amounts of vitamin K1 quickly correct the INR to safer levels. In most patients, 1-2.5 mg of oral vitamin K1 reduces the INR from 5.0-9.0 to 2.0-5.0 within 24-48 hours; this intervention is usually sufficient in the absence of bleeding.17,18 These small doses are obtained by withdrawing the desired amount from a 10 mg vial of injectable vitamin K1 and giving this orally or parenterally. When the INR is > 9.0, then 5 mg vitamin K1 may be more appropriate and can be given orally, subcutaneously or intravenously (very rarely, the last may cause a serious anaphylactoid reaction). In people with a massive accidental or self-inflicted warfarin overdose, the long half-life of warfarin means that the INR may rebound over several days as the effects of vitamin K1 wear off. In any case, the response to vitamin K1 needs to be monitored. Bleeding caused by a warfarin overdose is controlled with clotting factor replacement (Box 3), and this may also be indicated in the absence of bleeding when the risk is very high.19 Bleeding or an unstable dose-response should trigger a review of the need for warfarin. Continued treatment will require closer monitoring of the INR, both to detect the transient warfarin resistance caused by too much vitamin K1, and to avoid further overanticoagulation. Heparin treatment may be required to cover a prolonged period of warfarin resistance. Interrupting warfarin therapy for surgery When there is a need for surgery, the risk of perioperative bleeding under continued warfarin therapy must be balanced against the risk of thromboembolism if warfarin therapy is stopped.20Most surgery, including hip or knee replacement and many thoracic or abdominal operations, can proceed under continued warfarin cover without undue bleeding (provided the INR during and soon after surgery is about 1.5-2.0). Warfarin therapy is a contraindication for regional anaesthesia (eg, spinal, epidural, brachial blocks) and is unacceptable where even minor bleeding might cause critical damage (as in neurosurgery and some plastic surgery). It is also unpopular with most surgeons. However, the absolute daily risk of a serious thromboembolic event is small in most people with AF, previous systemic embolism or a prosthetic heart valve (the hazard is greatest from mitral and older-model prosthetic valves, and in patients with more than one prosthetic valve). Thus, it is safe to stop warfarin therapy for several days before and after surgery in such patients. High-dose heparin cover for these indications is rarely indicated as the risk of bleeding is usually prohibitive.20 The risk of recurrence is greatest during the first four weeks after VTE, so warfarin therapy should not be interrupted during this time if at all possible. If anticoagulants must be stopped for surgery soon after VTE, a vena cava filter can be placed to minimise the risk of life-threatening pulmonary embolism. Specific indications for warfarin therapy Deep vein thrombosis and pulmonary embolism Prevention: Heparins are now usually the preferred drugs for the prevention of perioperative VTE, but warfarin retains a limited role when the risk of thrombosis is very high. Its main role is in long-term therapy. Warfarin is no less effective than low molecular weight heparins after hip or knee replacement, and the risk of bleeding is similar or lower when therapy is started at about the time of surgery and continued at least until patients are fully mobile.21 Treatment: Anticoagulants prevent early thrombus extension and embolism and minimise late recurrence. Heparin treatment can be stopped after a minimum of five days when warfarin therapy is also being given, provided that the two drugs are overlapped for at least four days and the INR has exceeded 2.0 for two or more days.22 Increasingly, deep vein thrombosis (DVT) is now managed at home -- an approach preferred by many patients and made possible by trials which found that initial treatment with low molecular weight heparins given in a fixed dose by subcutaneous injection is no less effective or safe after DVT than standard heparin therapy. Home heparin therapy requires close monitoring to ensure compliance and a safe and effective start for warfarin therapy.23,24 Although warfarin is now usually given for 3-6 months after VTE, there is growing evidence that the optimal duration of treatment is determined by the patient's clinical presentation. Six to 12 weeks of warfarin therapy is probably enough when DVT follows surgery or transient immobilisation ("secondary" DVT), as recurrence is minimised by six weeks of treatment after symptomatic calf vein DVT,7 and by three months of treatment after proximal DVT.25,26 However, warfarin therapy for longer than six months may be required after "idiopathic" DVT, recurrent VTE, or when there is a continuing cause like cancer or an inherited or acquired "hypercoagulable" state.27-30 Whether, in these circumstances, warfarin should be given for 12 months, two years, or longer, remains under active investigation. For individuals, the choice will also be influenced greatly by risk of bleeding. Controversies in the management of DVT and VTE Calf vein thrombosis: Although calf vein DVT poses little immediate threat and is commonly believed to be clinically unimportant, it has the potential to extend and embolise. In a randomised comparison where 51 patients with symptomatic calf DVT were treated for five days with heparin only or with heparin followed by ongoing warfarin therapy, there was a recurrence during the next three months in eight of 28 patients from the first group (23%: seven clinically suspected and confirmed; five with proximal extension and one with embolism), but none in the second.31 Therefore, patients with calf vein thrombosis should be treated with warfarin unless there are contraindications. Accuracy of diagnostic tests for DVT: Venous ultrasonography has now replaced venography as the first-line diagnostic test for clinically suspected DVT. Despite its limited sensitivity to small calf vein DVTs, a negative ultrasound result almost excludes thrombosis when there is a low pretest clinical probability for DVT (a DVT score of zero on a checklist of clinical features obtained before ultrasonography, such as active cancer, immobilisation, major surgery, entire leg swelling, localised tenderness, calf swelling, pitting oedema and collateral superficial veins).32 However, for patients in whom the pretest clinical probability is moderate (DVT score of 1-2) or high (score, > 3), a negative ultrasound result does not exclude a small DVT, and they should have either early venography or further ultrasonography once or twice within the next seven days in case there is proximal extension of an undetected calf thrombus. This approach is validated by extensive clinical follow-up.33 Recurrent or idiopathic DVT or VTE: In a randomised trial of patients presenting with recurrent DVT, oral anticoagulant therapy for six months was followed by a recurrence in 21% during four years of follow-up, compared with 3% when treatment was continued. However, ongoing warfarin therapy increased the rate of major bleeding during the four years from 2.7% to 8.6%, while mortality remained unchanged.27 Similarly, in a separate trial of management after a first "idiopathic" VTE, warfarin therapy for three months was followed by recurrence in 16 of 77 patients during 10 months of follow-up, compared with only one of 76 patients in whom warfarin therapy was continued.30 However, the use of warfarin increased the annual risk of major bleeding from zero to 4%.30 These high rates of bleeding reinforce the need for careful risk assessment when considering patients for long term anticoagulant therapy after VTE. The results of these trials suggest that warfarin therapy should be continued for one year after an "idiopathic" or recurrent VTE if the risk of bleeding is acceptable, and that treatment should be extended to two years if warfarin control is straightforward and the bleeding risk remains low. Atrial fibrillation Warfarin is now widely used to prevent systemic embolism in otherwise healthy patients with atrial fibrillation (AF). In clinical trials, warfarin consistently reduced the annual risk of a first ischaemic stroke (including stroke with a residual functional deficit) by almost 70% (from 7% to 3% per annum) and mortality by 33%, at the cost of a small increase in serious bleeding (from 1.0% to 1.3% per annum).10,34,35 The prevalence of AF rises from about 3% at 65 years to more than 10% by 85 years, and AF accounts for about 1.5% of all strokes in people aged 50-59 years, and almost 25% of strokes in people aged 80-89 years. Age is therefore an important determinant of ischaemic stroke in AF (the relative risk [RR] of stroke in AF rises by 1.4 with each decade).35 Previous stroke or transient ischaemic attack (RR, 2.5), diabetes (RR, 1.7), and treated hypertension (RR, 1.6) also contribute, as do heart failure, ischaemic heart disease, a large left atrium, and left ventricular dysfunction.10 Stroke is unlikely in isolated AF but becomes more likely as additional risk factors accumulate (Box 4). This makes warfarin therapy inappropriate for young people with AF alone and no other cardiac risk factor (isolated AF), as their annual risk of stroke (< 1%) is low enough to ensure that risk of bleeding always equals or exceeds any likelihood of gain. Because of the risk of bleeding, these reports raise important questions about the best target level of INR, and about which patients with AF should be offered long-term warfarin therapy. The incidence of stroke is minimised by an INR > 2.0 and increases exponentially below this level, but some benefit remains while the INR is 1.5-1.9. When considering warfarin therapy for AF, each candidate requires a formal estimate of the relative risks of stroke (Box 4) and bleeding (Box 2). Controversies about the use of warfarin or aspirin to prevent stroke in atrial fibrillation Stroke and the INR: The risk of stroke during warfarin therapy for AF is dictated by the INR. Below 2.0, the relative risk doubles at 1.7, triples at 1.5, sextuples at 1.3, and reaches 18 times once the INR is normal, but nothing is gained by increasing the INR beyond its therapeutic threshold of 2.0.36 Results were similar when warfarin was given for secondary stroke prevention in patients with AF who had already developed a stroke or transient cerebral ischaemia.11 Again, in a randomised trial in which patients with AF plus at least one other risk factor for stroke were given either warfarin in a dose to prolong their INR (INR, 2.0-3.0; median, 2.4) or aspirin combined with a low dose of warfarin (0.5-3.0 mg/day; INR, 1.2-1.5; median, 1.3), the dose aiming for the higher INR was clearly superior.37 Aspirin or warfarin for AF? The 30% risk reduction in stroke from aspirin treatment is well below the 70% achieved with warfarin therapy.10 In a blinded analysis of clinical outcomes when the two drugs were compared, warfarin was better at preventing cardioembolic strokes and strokes of uncertain cause.38 This is consistent with the small effect observed with aspirin for secondary stroke prevention in patients with AF and who have had a stroke or TIA -- warfarin reduced the risk of recurrence by 62%, compared with only 16% for aspirin.39 It may be a useful compromise to reserve aspirin for patients with uncomplicated AF whose baseline risk of embolism is low. Warfarin, INR and aspirin in elderly patients with AF: Age above 75 years and a high INR both increase the hazard from intracranial and other major bleeding during warfarin therapy. Because there is some residual benefit at an INR of 1.5-1.9, this reduced target range may offer an acceptable exchange of safety for benefit in some elderly patients. Where the risk of bleeding is high, aspirin is less effective, but safer than warfarin. Cardioembolic stroke prevention in conditions other than AF There is evidence that cardioversion to correct a recent cardiac arrhythmia should be delayed until after three weeks of anticoagulant cover to prevent systemic embolism.35 Warfarin prevents embolic stroke and other arterial embolism, as well as VTE, after myocardial infarction (MI), and is often given for 3-6 months when MI is followed by intraventricular thrombus formation (risk factors include transmural anterior infarction and ventricular dysfunction).40 A good case also exists for long term warfarin therapy in some patients with ongoing left ventricular dysfunction.41,42Prosthetic heart valves Improved design has greatly reduced the thrombogenicity of mechanical prosthetic heart valves, but the need for effective, lifelong warfarin therapy remains because systemic embolism is still the main source of late mortality and morbidity. The risk is determined by the type of valve and its position (higher for mitral than aortic valves, greatest when both are replaced). Tissue valves, by contrast, are almost free of thromboembolic complications, except during the first three months.43The American College of Chest Physicians recommends an INR of 2.0-3.0 for recent-model bileaflet or tilting disc valves, and 2.5-3.5 for older and more thrombogenic valves that have a caged ball or disc; patients with a newly placed bioprosthetic (tissue) valve require three months of warfarin and an INR of 2.0-3.0.43 However, in our view, because the evidence is incomplete, it remains prudent to retain a target range of 2.5-3.5 for most ("low-risk") prosthetic valves while aiming higher (3.0-4.5) for older and more thrombogenic models, provided there is no contraindication (Box 1). This view is consistent with recent recommendations from the British Society for Haematology.2 Antiplatelet drugs alone are ineffective, but combining dipyridamole or aspirin (100 mg/day) with warfarin reduces the risk of systemic embolism. Meta-analysis suggests that the penalty for adding aspirin is a 2.5-times increase in major gastrointestinal bleeding,44 so the combination is perhaps best avoided, except in patients considered to be at unusually high risk of systemic thromboembolism (more than one mechanical valve, previous embolism, associated AF).43 Special circumstances for anticoagulation Antiphospholipid antibody syndrome and factor V Leiden: Two retrospective surveys of clinical outcomes in patients with antiphospholipid antibody syndrome and venous and/or arterial thrombosis suggest that warfarin therapy fails to prevent recurrent thromboses unless the INR is prolonged above 3.0.45,46 This contrasts with a more recent report of few recurrences while the INR was 2.0-3.5.47 Without better information, and until randomised trials are complete, it is not possible to make a firm recommendation about the optimal target range for this condition. The effect of aspirin alone in preventing thrombosis in the antiphospholipid antibody syndrome is unclear.45-47 There is no current evidence to suggest that patients with factor V Leiden-heterozygous abnormality should require more intense anticoagulation. It is still uncertain whether the duration of therapy should be increased in these patients, as evidence from reports about the risk of recurrent VTE is conflicting.28,29,48 Oral anticoagulants in pregnancy: Oral anticoagulants cross the placenta and should be avoided throughout pregnancy, especially during the first and third trimesters.49 Treatment at 6-12 weeks' gestation causes calcified epiphyses (chondrodysplasia punctata) and a characteristic nasal hypoplasia in offspring,50 while later exposure is associated with central nervous system abnormalities, including microcephaly.51 In one report, almost 30% of children (10 of 35) born to mothers with a prosthetic heart valve were malformed if acenocoumarol was taken through 6-12 weeks' gestation, but none of 19 developed a malformation when this drug was replaced with heparin before the sixth week.52 Continuing warfarin therapy until term also exposes infants to the risk of intracranial and other major bleeding during birth. Heparins do not cross the placenta and do not cause these problems.53-55 It is safe to breastfeed during warfarin therapy as there is minimal excretion into breast milk.56 References Hirsh J, Dalen JE, Anderson D, et al. Oral Anticoagulants. Mechanism of action, clinical effectiveness and optimal therapeutic range. Chest 1998; 114 Suppl: 445S-469S. Walker ID, Machin S, Baglin TP, et al. Guidelines on oral anticoagulation. 3rd ed. Br J Haematol 1998; 101: 374-387. Holbrook AM, Wells PS, Crowther NR. Pharmacokinetics and drug interactions with warfarin. In: Poller L, Hirsh J, editors. Oral anticoagulants. Sydney: Arnold, 1996: 30-48. Crowther MA, Ginsberg JB, Kearon C, et al. A randomized trial comparing 5 mg and 10 mg warfarin loading doses. Arch Intern Med 1999; 159: 46-48. Rose P. Audit of anticoagulant therapy. J Clin Pathol 1996; 49: 5-9. Coumadin and Marevan are not interchangeable. 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Overview of the randomized trials to prevent stroke in atrial fibrillation. Ann Epidemiol 1993; 3: 563-567. Laupacis A, Albers GW, Dalen JE, et al. Antithrombotic therapy in atrial fibrillation. Chest 1998; 114 Suppl: 579S-589S. Hylek EM, Skates SJ, Sheehan MA, Singer DE. An analysis of the lowest effective intensity of prophylactic anticoagulation for patients with nonrheumatic atrial fibrillation. N Engl J Med 1996; 335: 540-546. Stroke Prevention in Atrial Fibrillation Investigators. Adjusted-dose warfarin versus low-intensity, fixed-dose warfarin plus aspirin for high-risk patients with atrial fibrillation: Stroke Prevention in Atrial Fibrillation III randomised clinical trial. Lancet 1996; 348: 633-638. Miller VT, Pearce LA, Feinberg WM, et al. Differential effect of aspirin versus warfarin on clinical stroke types in patients with atrial fibrillation. Neurology 1996; 46: 238-240. European Atrial Fibrillation Trial Study Group. Secondary prevention in non-rheumatic atrial fibrillation after transient ischaemic attack or minor stroke. Lancet 1993; 342: 1255-1262. Cairns JA, Theroux P, Lewis HD Jr, et al. Antithrombotic agents in coronary artery disease. Chest 1998; 114 Suppl: 611S-633S. Fuster V, Gersh BJ, Giuliani ER, et al. The natural history of idiopathic dilated cardiomyopathy. Am J Cardiol 1981; 47: 525-531. Al-Khadra AS, Salem DN, Rabd WR, et al. Warfarin anticoagulation and survival: a cohort analysis from the studies of left ventricular dysfunction. J Am Coll Cardiol 1998; 31: 749-753. Stein PD, Alpert JS, Dalen JE, et al. Antithrombotic therapy in patients with mechanical and biological prosthetic heart valves. Chest 1998; 114 Suppl: 602S-610S. Cappelleri JC, Fiore LD, Brophy MT, et al. Efficacy and safety of combined anticoagulant and antiplatelet therapy versus anticoagulant monotherapy after mechanical heart-valve replacement: a metaanalysis. Am Heart J 1995; 130: 547-552. Rosove MH, Brewer PM. Antiphospholipid thrombosis: clinical course after the first thrombotic event in 70 patients. Ann Intern Med 1992; 117: 303-308. Khamashta MA, Cuadrado MJ, Mujic F, et al. The management of thrombosis in the antiphospholipid-antibody syndrome. N Engl J Med 1995; 332: 993-997. Krnic-Barrie S, O'Connor CR, Looney SW, et al. A retrospective review of 61 patients with antiphospholipid syndrome: analysis of factors influencing recurrent thrombosis. Arch Intern Med 1997; 157: 2101-2108. Eichinger S, Pabinger I, Stumpflen, et al. The risk of recurrent venous thromboembolism in patients with and without Factor V Leiden. Thromb Haemost 1997; 77: 624-628. Ginsberg J, Barron W. Pregnancy and prosthetic heart valves. Lancet 1994; 344: 1170-1172. Koren G, Pastuszak A, Ito S. Drugs in pregnancy. N Engl J Med 1998; 338: 1128-1137. Hall JG, Pauli RM, Wilson KM. Maternal and fetal sequelae of anticoagulation during pregnancy. Am J Med 1980; 68: 122-140. Iturbe-Alessio I, del Carmen Fonseca M, Mutchinik O, et al. Risks of anticoagulant therapy in pregnant women with artificial heart valves. N Engl J Med 1986; 315: 1390-1393. Ginsberg JS, Kowalchuk G, Hirsh J, et al. Heparin therapy during pregnancy. Risks to the fetus and mother. Arch Intern Med 1989; 149: 2233-2236. Fejgin MD, Lourwood DL. Low molecular weight heparins and their use in obstetrics and gynecology. Obstet Gynecol Surv 1994; 49: 424-431. Sanson B-J, Lensing AWA, Prins MH, et al. Safety of low-molecular-weight heparin in pregnancy: a systematic review. Thromb Haemost 1999; 81: 668-672. Orme ML, Lewis PJ, de Swiet M, et al. May mothers given warfarin breast-feed their infants? BMJ 1977; 1: 1564-1565. Background and evidence basis of recommendations The Australasian Society of Thrombosis and Haemostasis Consensus Guidelines for Warfarin Therapy were written on behalf of the Australasian Society of Thrombosis and Haemostasis (ASTH). The writing committee was commissioned by council and consisted of Associate Professor A S Gallus (Chairman), Dr R I Baker, Professor B H Chong, Dr P A Ockelford and Associate Professor A M Street. The guidelines were developed after extensive consultation with the membership of the ASTH, including several workshops and teleconferences. The draft recommendations were open for comment and discussion at the 1998 annual scientific meeting of the ASTH in Sydney. They draw upon review of all available evidence from published studies and from clinical experience. The aim is to provide an Australian perspective on the evidence to guide all practitioners in the safe and effective use of oral anticoagulants in hospital and the community. We are grateful for the help of Dr K McGrath, Dr M Herzberg (Quality Assurance Program in Haematology, Royal College of Pathologists of Australasia), Dr P Montanaro (Royal Australian College of General Practitioners), Dr P Steele (Australia and New Zealand Cardiac Society) and Professor J Fletcher (International Union of Angiology). Authors' details Australasian Society of Thrombosis and Haemostasis, Perth, WA. Alex S Gallus, FRACP, FRCPA, Chairman; Ross I Baker, FRACP, FRCPA; Beng H Chong, FRACP, FRCPA; Paul A Ockelford, FRACP, FRCPA; Alison M Street, FRACP, FRCPA. Reprints will not be available from the authors. Correspondence: Professor A S Gallus, Director, SouthPath, C/- Flinders Medical Centre, Bedford Park, SA 5042. 1: Range of international normalised ratio (INR) recommended for specific applications of warfarin therapy* Condition INR range Preventing DVT (high risk patients, like those who have had hip replacement) 2.0-3.0 Therapy after DVT or pulmonary embolism 2.0-3.0 Preventing systemic embolism Atrial fibrillation Valvular heart disease After myocardial infarction Tissue heart valves (first 3 months) 2.0-3.0 2.0-3.0 2.0-3.0 2.0-3.0 Bileaflet mechanical heart valve (aortic) 2.5-3.5 Mechanical prosthetic heart valve (high risk) 3.0-4.5 Preventing recurrence of myocardial infarction 3.0-4.5 Thrombosis in antiphospholipid antibody syndrome 3.0-4.5 DVT=deep vein thrombosis . *Based largely on the 5th American College of Chest Physicians Consensus Conference1 and consistent with current recommendations of the British Society for Haematology.2 2: Risk of major bleeding (% per annum) and international normalised ratio (INR) - findings of two studies23,30 INR Study 130 Study 223 < 2.0 2.0-2.9 3.0-3.9 4.0-4.9 5.0-5.9 ≥ 6 3% 2%-3% 2%-3% 4% 5% 5%-13% 0 1% 3% 4% 50% 3: Managing overdose and bleeding during warfarin therapy* Clinical setting Action INR >5.0 but < 9.0 (no bleeding) Stop warfarin, give 1-2.5mg vitamin K1, measure INR in 6-12 hours, restart warfarin at reduced dose once INR is < 5 INR ≥9.0 (no bleeding) Stop warfarin, give 5mg vitamin K1, measure INR in 6-12 hours, restart warfarin at reduced dose once INR is < 5, clotting factor replacement? if high risk of bleeding Major bleeding (any level of INR) Stop warfarin, give 5mg vitamin K1, clotting factor replacement, measure INR as required, assess need to restart warfarin INR=international normalised ratio. *Based on Makris et al, 1996.19 ?Blood products available in Australia for clotting factor replacement after warfarin overdose include fresh frozen plasma and Prothrombinex-HT (CSL Limited), a factor II, IX and X concentrate. 4: Risk of ischaemic stroke in patients with atrial fibrillation (AF), grouped by age and other risk factors* (derived from Laupacis et al10) Risk categories Patients affected per annum Lone atrial fibrillation† Age < 60 years Age 60-69 years Age 70-79 years Age ≥80 years 0 1.6% 2.1% 3.0% Age < 65 years No risk factors One or more risk factors 1.0% 4.9% Age 65-75 years No risk factors One or more risk factors 4.3% 5.7% Age >75 years No risk factors One or more risk factors 3.5% 8.1% *Hypertension, diabetes, previous stroke or transient ischaemic attack. †Atrial fibrillation without transient ischaemic attack or stroke, myocardial infarction, hypertension or heart failure.

Alex S Gallus · Ross I Baker · Beng H Chong · Paul A Ockelford

Medicine And The Law Determining the validity of advance directives Paul Biegler, Cameron Stewart, Julian Savulescu and Loane Skene MJA 2000; 172: 545-548 Abstract - Ethics - Legislation - Common law - Duties of treating physicians in determining legal validity of advance directives - Conclusions - References - Authors' details - - More articles on Ethics Abstract We examine the ethical principles underpinning advance directives (ADs) and the legal duties of doctors in determining their validity. A physician attending an incompetent patient with an acute life-threatening illness, and an AD refusing treatment, should ensure that the AD is legally valid before making the treatment decision. Treatment against a patient's wishes, as expressed in a valid AD, compromises patient autonomy and may constitute battery. Conversely, withholding treatment in accordance with an AD that is not legally valid risks substantial harm to the patient and may constitute breach of the duty of care and negligence. Legally valid directives should be respected. If an AD is not legally valid, the patient should be treated in his or her best interests. If uncertain, the physician should treat according to the patient's best interests while seeking legal advice. An advance directive (AD) is a statement by a competent person expressing the intention to refuse medical treatment in the future, at a time when he or she may no longer be competent to make a treatment decision.1 ADs have arisen in the context of an increasing need to respect and promote patient autonomy.2 They have received widespread international support and, in the United States, ADs now have a statutory basis in all 50 States.3 Three Australian States (Victoria, South Australia and Queensland) and two Territories (the Northern Territory and the Australian Capital Territory) now have legislation which provides for ADs (Box 1). Although New South Wales, Tasmania and Western Australia do not have similar legislation, ADs may still be valid under common (judge-made) law in these States. Despite their prevalence in the United States, ADs have, in many instances, failed to guide clinical decision-making, and their utility has been questioned.4 Of particular concern is the dilemma facing clinicians when the AD rules out treatment which the doctor believes is in the patient's best interests.5 Treatment in the presence of a valid AD compromises patient autonomy and may constitute battery.6 However, withholding treatment in accordance with a legally invalid AD risks substantial harm to the patient and may constitute breach of the duty of care and negligence.7 We contend that being equipped with a clear process for determining the legal validity of an AD can reduce the uncertainty of physicians in such situations. Legally valid ADs should be respected. If the AD is not legally valid, or if the physician is uncertain, treatment decisions should be based on an assessment of the patient's best interests.8 We look at the ethical foundations and the Australian law pertaining to ADs and offer recommendations to medical practitioners seeking to ascertain the legal validity of ADs. Ethics "Autonomy" comes from the Greek autos-nomos, meaning "self-rule" or "self-determination". The concept of respect for autonomy was enunciated by John Stuart Mill, who said that the sole justification for interfering in another person's action is if that action will harm others -- "His own good, either physical or moral, is not a sufficient warrant".9 This principle, known as Mill's "harm principle", is the grounds for the moral right of a patient to refuse medical treatment, even if such treatment is life-saving, and for a doctor not to interfere in this action. Mill did have one caveat to his stance. He felt that it was acceptable to restrain a person from causing self-harm if that person's action was not fully informed. Take the example of a person crossing a burning bridge without knowing it is burning. Intervening here would be acceptable and this has been labelled "weak or soft paternalism". Intervening if the person was fully informed about the consequences of his or her actions has been labelled "strong or hard paternalism" and is unacceptable.10 Modern theorists have elaborated the notion of autonomy and concluded that an autonomous decision is one that is freely made, by a competent person, based on his or her most recent set of values. It should also be applicable to the circumstances in question, with a full understanding of the relevant facts.11,12 The relevance to ADs is that, unless a directive expresses an autonomous decision, acting upon it may in fact violate patient autonomy and result in serious harm. An example is a patient with HIV who signs a directive refusing resuscitation or admission to an intensive care unit. The patient has a life-threatening allergic reaction to a drug early in the course of the disease, when the prognosis suggests many good years of life. If the patient did not intend the AD to apply in this circumstance, then to allow this patient to die would be to fail to respect his or her autonomy. Treatment here would be weak paternalism (see also Box 3). The law provides a framework for safeguarding patient autonomy in such situations. Legislation The Australian legislation covering ADs is outlined in Box 1. Common law The validity of ADs at common law is yet to be tested in an Australian court. The case law from other jurisdictions suggests the following factors should be considered. The competence of the decision-maker The patient must have been competent to refuse treatment when the AD was drafted. The test for competence rests on the question of whether the patient understood the nature and purpose of the treatment when he or she made the decision to refuse it.13,14 The true scope and basis for the decision The AD must cover the circumstances that have arisen. The evidence must confirm the true scope and basis of the decision; that is, that the anticipatory decision was based on an informed opinion and was intended to apply to the circumstances which have arisen.6,15 Evidence of a decision which consists of remote, general, spontaneous or casual comments will not support the claim of anticipatory decision-making.16 However, evidence of cogent and serious decision-making which consists of written evidence or eye-witness accounts is usually strong enough to support the veracity of an anticipatory decision.17 Evidence of oral directions can, by itself, support the finding of a valid anticipatory decision.18-20 Undue influence The decision to refuse treatment must be free from the undue influence of others. Undue influence may impair the decision-making process and invalidate the directive. Enquiries must be made as to both the strength of will of the patient and the relationship of the patient with the persuader. If the patient was in pain or under the influence of drugs when the decision was made, or was persuaded by someone with close familial ties, the decision may not have been the result of the patient's free will. Such decisions are not legally binding on doctors.15 Duties of treating physicians in determining legal validity of advance directives In the case of directives completed under a statutory scheme, a physician treating an incompetent patient is not required to investigate whether the patient's decision was voluntary, reasonably informed or that the patient was 18 years or over when the directive was signed. The witnesses to the directive attest to those matters. In Victoria, South Australia and Queensland, the witnesses also attest to the patient's capacity to refuse treatment at the time of completing the AD. The obligations of the treating physician are more onerous in relation to common law directives and legal advice may be required in this setting. A schema for determining the validity of ADs from both the legislative and the common law perspective is outlined in Box 2, and an example is given in Box 3. Conclusions In order to respect patient autonomy, avoid harm to patients and reduce the risk to doctors of civil or criminal liability, physicians need to determine the legal validity of advance directives before making their treatment decision. In cases of uncertainty treatment decisions should be made in the patient's best interests while legal advice is sought as to the validity of the directive. References Robertson GS. Making an advance directive. BMJ 1995; 310: 236-238. Kerridge IH, McPhee J, Lowe M, Flynn B. Advance directives. In: Freckelton I, Petersen K, editors. Controversies in health law. Sydney: The Federation Press; 1999: 302. Tonelli MR. Pulling the plug on living wills. A critical analysis of advance directives. Chest 1996; 110: 816-822. Teno JM, Licks S, Lynn J, et al. Do advance directives provide instructions that direct care? SUPPORT Investigators. Study to understand prognoses and preferences for outcomes and risks of treatment. J Am Geriatr Soc 1997; 45: 508-512. Danis M, Southerland LI, Garrett JM, et al. A prospective study of advance directives for life-sustaining care. N Engl J Med 1991; 324: 882-888. Skene L. When can doctors treat patients who cannot or will not consent? Monash University Law Review 1997; 23 (1): 77. Dix A. Law for the medical profession in Australia. Melbourne: Butterworth-Heinemann, 1996: 563. Luttrell S. Making decisions about medical treatment for mentally incapable adults in the UK. Lancet 1997; 350: 950-953. Mill JS. Utilitarianism, on liberty and considerations on representative government. Everyman library. London: J M Dent and Sons, 1910. Ten CL. Paternalism and levels of knowledge: a comment on Rainbolt. Bioethics 1989; 3: 135-139. Dworkin G. The theory and practice of autonomy. Cambridge: Cambridge University Press, 1988. Savulescu J. Good reasons to die [doctoral dissertation]. Melbourne: Monash University, June 1994. Lord Brandon in Re F (Sterilisation Mental Patient) [1989] 2 Fam 376, 419-420. Gillick v West Norfolk and Wisbech AHA [1986] AC 112. Re T [1992] 2 Fam 458, 473 (Lord Donaldson). Matter of Jobes 529 A 2d 434, 443 (NJ, 1987). Matter of Peter 529 A 2d 419 (NJ, 1987). Re Chad Swan 569 A 2d 1202 (Me, 1990). Leach v Akron General Medical Center 426 NE 2d 809 (Ohio Comm Pl, 1980). Matter of Eichner 420 NE 2d 64 (NY, 1981). Authors' details Emergency Department, Monash Medical Centre, Melbourne, VIC. Paul Biegler, MB BS, FACEM, Staff Specialist. Department of Law and Justice, Division of Law, Macquarie University, Sydney, NSW. Cameron Stewart, BEc, LLB(Hons), GradDipJur, Associate Lecturer. The Murdoch Institute, Royal Children's Hospital, and Centre for the Study of Health and Society, University of Melbourne, Melbourne, VIC. Julian Savulescu, MB BS, PhD, Associate Professor, and Director, Ethics Program. Law School, University of Melbourne, Melbourne, VIC. Loane Skene, LLM (Mon), LLB (Hons), Associate Professor and Reader. Reprints will not be available from the authors. Correspondence: Dr P Biegler, Emergency Department, Monash Medical Centre, 246 Clayton Road, Clayton, VIC 3168. pbieglerATnetlink.com.au Make a comment 1: Legislation in Australia providing for advance directives Victoria Act: Medical Treatment Act 1988 (Vic). Type of advance directive: Refusal of treatment certificate (RTC). Treatment refused must relate to a current condition ("current condition" is not defined by the Act but presumably refers to a condition that the person has at the time of completing the RTC). The document must be in the form prescribed by the Act ("in the form" is also not defined, but presumably means in language consistent with that used in the Act). Legally valid if completed voluntarily by a person of sound mind over 18 years who is informed about their condition. Must be signed by a registered medical practitioner and another person who attest to these matters. The patient does not need to sign. Revoked by patient clearly indicating this wish to another person. Palliative care: The RTC does not cover refusal of palliative care, which is defined as "the provision of reasonable medical procedures for the relief of pain, suffering and discomfort; or the reasonable provision of food and water". Physicians’ liability: Under the Act, a doctor who treats a patient despite a valid certificate may commit the statutory offence of medical trespass. This offence would arise in addition to common law claims of battery. Doctors who comply with an RTC are granted immunity from civil claims, criminal charges or professional misconduct proceedings, provided the doctor acts in good faith and with reasonable care. South Australia Act: Consent to Medical Treatment and Palliative Care Act 1995 (SA). Type of advance directive: An "anticipatory grant" refusing consent to medical treatment. The directive is only effective for patients in the terminal stages of a terminal illness or in a persistent vegetative state, who are not competent to make treatment decisions. "Terminal illness" is defined as "an illness or condition that is likely to result in death" and terminal stage as "the phase of the illness reached when there is no real prospect of recovery or remission of symptoms". Legally valid if made by a patient of sound mind over the age of 18 years. Must be in the prescribed form, signed by the patient and witnessed by one person, who need not be a medical practitioner. Revoked by patient orally or in writing (not stipulated in the Act). Physicians’ liability: Physicians honouring directives under the Act are granted immunity from civil and criminal liability if they act in good faith, without negligence and in accordance with proper standards of professional practice. Australian Capital Territory Act: Medical Treatment Act 1994 (ACT), based on the Medical Treatment Act 1988 (Vic). Type of advance directive: "Direction" refusing treatment generally or treatment of a particular kind. Treatment does not have to relate to a current condition, as it does in Victoria. Legally valid if patients are of sound mind over 18 years. Direction must be in the prescribed form and witnessed by two people, neither of whom needs to be a medical practitioner. It can be signed by the patient or by another person at the patient’s direction, but it does not have to be signed to be valid. Revoked by patient clearly indicating his or her wish to another person. Palliative care: Does not cover refusal of palliative care. Physicians’ liability: A physician honouring a certificate in good faith is protected from civil and criminal liability, as well as claims of professional misconduct. Queensland Act: Powers of Attorney Act 1998 (Qld) Type of advance directive: "Advance health directives." Directions to withhold or withdraw life-sustaining measures cannot operate unless: the patient has a terminal illness or an incurable condition and is not expected to live more than a year, or is in a persistent vegetative state, or is permanently unconscious, or has a severe illness with no reasonable prospect of being able to live without the continued application of life-sustaining measures; and (if the direction concerns artificial hydration or nutrition) the life-sustaining measure would be contrary to good medical practice; and the patient has no reasonable prospect of regaining capacity for health matters. Legally valid if the directive is in the prescribed form, signed by the patient or another person at the patient’s direction and witnessed by two people, one of whom must be a medical practitioner. The witnesses must certify that the patient had the capacity to make the treatment decision at the time of completing the directive. Revoked by patient indicating his or her wish in writing. Physicians’ liability: Physicians are protected from criminal and civil liability if they honour the directive in good faith. Northern Territory Act: Natural Death Act 1988 (NT). Type of advance directive: "Directives" refusing treatment are only effective in the case of terminal illness, which is defined as "Such an illness, injury or degeneration of mental or physical faculties that death would, if extraordinary measures were not undertaken, be imminent; and from which there is no reasonable prospect of a temporary or permanent recovery, even if extraordinary measures were undertaken". Extraordinary measures are defined in the Act as "medical or surgical measures that prolong life, or are intended to prolong life, by supplanting or maintaining the operation of bodily functions that are temporarily or permanently incapable of independent operation". Legally valid if made by patients of sound mind who are over 18 years. Must be in the prescribed form, signed by the patient and witnessed by two people, who need not be medical practitioners. The treating doctor cannot be a witness. Revoked by patient orally or in writing (not stipulated by the Act). Palliative care: Does not cover refusal of palliative care. Physicians’ liability: Physicians complying with directives in good faith are protected from criminal and civil liability. Back to text 2: Schema of obligations of treating physicians Incompetent patient presents with acute life-threatening illness and an advance directive (AD) refusing treatment Step 1: Physician determines whether the AD conforms with State legislative requirements The form of the AD is correct The AD has the required signatures There is no evidence that the AD has been revoked (check with relatives, friends and the patient's GP) Victoria - the presenting condition for which treatment is now required is the same as, or has been caused by, the "current condition" as specified on the refusal of treatment certificate (RTC); Australian Capital Territory - treatment generally or treatment of a particular kind has been refused. There is no evidence that the patient was incompetent at the time of making the directive (witnesses are not required to attest to competence); South Australia - the patient is in the terminal phase of a terminal illness or in a persistent vegetative state; Northern Territory - the patient has a terminal illness. There is no evidence that the patient was incompetent at the time of making the directive (witnesses are not required to attest to competence); Queensland - the patient is suffering from one of the conditions outlined in Box 1, and the directive is not uncertain or contrary to good medical practice (section 106 of the Powers of Attorney Act 1998). If ALL of the criteria for Step 1 are satisfied Step 2: Comply with the AD (if uncertain proceed to Step 6). If ANY of the criteria for Step 1 are not satisfied Step 3: Determine common law validity of the AD. No evidence that the person was incompetent when they made the AD. AD covers the proposed treatment and the circumstances that have arisen. (i) It should not be ambiguous about the nature of the treatment being refused; and (ii) It should have been expressed to refuse treatment in the circumstances that have arisen. No evidence that the AD was procured by undue influence. If ALL of the criteria for Step 3 are satisfied Step 4: Comply with the AD (the difficulty of a physician's rapidly ascertaining these data in the acute setting is acknowledged) (if uncertain proceed to Step 6). If ANY of the criteria for Step 3 are not satisfied Step 5: Set aside the AD and treat according to the patient's best interests. Step 6: Legal advice should be sought if uncertainty exists about Steps 2-5. Faced with a delay in determining the validity of the AD, the physician should commence and continue any treatment deemed to be in the patient's best interests until such time as the AD is determined to be legally valid. Back to text 3: Example of an advance directive (AD) and physicians' decision-making A patient with HIV signs an AD refusing resuscitation or admission to an intensive care unit. The patient has an anaphylactic reaction to a drug early in the disease. Ethics If the AD was not intended to apply in this circumstance, withholding treatment would be to fail to respect this person's autonomy and would constitute a serious harm. Legislation Victoria The directive would be invalid because the presenting condition of anaphylaxis differs from the current condition of HIV as specified on the certificate. South Australia, Northern Territory, Queensland The directive would be invalid because the patient is not in the terminal phase of a terminal illness (SA, NT, QLD); in a persistent vegetative state (SA, QLD); and is not permanently unconscious with no reasonable prospect of regaining capacity for health matters (QLD). Australian Capital Territory The situation in the ACT is more complex. It seems that if the patient's AD was executed under the Medical Treatment Act 1994 (ACT) it may, in fact, be legally valid. However, we have argued that it would be ethically wrong to allow this person to die, and the directive would not be valid under other States' legislation or common law (see below). What should the doctor do? The uncertainty raised by the ACT situation should lead the doctor to act in the patient's best interests, which, in this case, probably favour resuscitation, while seeking legal advice. If in doubt, the patient's best interests must be the foremost consideration. Common Law The directive is unlikely to be valid at common law because the scope of the decision does not cover the circumstances that have arisen. Treatment decisions in these jurisdictions should thus be based on an assessment of the patient's best interests, which, in this case, as mentioned, probably favours treatment. Back to text

Paul Biegler · Cameron Stewart · Julian Savulescu · Loane Skene

Matters Arising Doctors' working hours Three articles (and a controversial cover photo) in our 15 June issue, highlighting the perennial problem of excessive working hours for doctors, have inspired comment from junior and senior doctors, and even doctors' family. MJA 1998; 169: 339-341 Shorter hours reduces training - William B Molloy Family concern - Annie Lee The forgotten generation - Terry G Coupland Treat the cause, not the symptoms - Michaela J Farrall In reply: Long hours are a financial reality - Leslie G Olson Smoking among doctors - Mark C J Craddock In reply: Recollections of smoking among doctors - Martin B Van Der Weyden ª 1999 Medical Journal of Australia.

Editorial Schizophrenia today Improvements in treatment need to be built upon and applied more widely and effectively MJA 2000; 172: 470-471 Schizophrenia Awareness Week (21-27 May) has been running in Australia since 1981. During the past 19 years some of the original goals of the week have been achieved largely thanks to the efforts of the State-based Schizophrenia Fellowships and the mental health advocacy and education organisation SANE Australia. These goals have included getting the word "schizophrenia" into the public domain, educating the community about the treatability of the disorder, and encouraging groups of carers to work together to provide mutual support and to lobby governments for enhanced services for people suffering from psychotic disorders. Today, treatment is much more likely to occur in the community, allowing patients to retain a much-valued independence (although loneliness and ennui often develop in the absence of appropriate social supports). Today, medication options are also wider, with clozapine having been used by nearly 10 000 Australians with treatment-resistant disorders (Clozaril Patient Monitoring System, Mental Health Research Institute, Melbourne, unpublished data), and other dopamine and serotonin antagonist drugs, such as risperidone and olanzapine, finding an important role because of their fewer extrapyramidal side effects and, probably, better neurocognitive outcomes.1,2 Our understanding of the biology of schizophrenia has progressed, despite the absence of a signature pathophysiology. This understanding has evolved in light of growing evidence that the disorder is associated with disturbances of neural connectivity and neurodevelopment, and abnormalities in dopaminergic, serotonergic, GABAergic and glutamatergic neurotransmission, involving particular brain regions, including the hippocampus, ventral striatum, and prefrontal cortex.3,4 Nonetheless, schizophrenia remains one of the most stigmatised of all disorders. That the term often conjures up sentiments of derision rather than compassion is well illustrated by a recent description of the Federal Government's actions towards certain UN committees as ". . . at times, sycophantic, abusive, schizophrenic and downright childish".5 The extensive and enduring impact of schizophrenia and related psychiatric disorders on the lives of affected Australians has been brought into sharp focus by a recent Commonwealth Government-sponsored National Survey of 980 individuals with psychotic disorders, more than 60% of whom had schizophrenia.6 It found that the average duration of symptoms was 15 years; 47% of participants were judged to be seriously impaired, 58% were socially withdrawn and 72% did not have a regular job. In addition, the prevalence of tobacco use (males 73%, females 56%), alcohol misuse or dependence (30%), and dependence on or misuse of street drugs (cannabis 25%; others, including heroin, 13%) was considerably higher than in the general population. However, a significant minority of patients -- approximately 25% -- have only one or two episodes of illness, do not continue to need mental health services, and have lower levels of symptoms, impairment and disability. Other data indicate that the rate of suicide among people with schizophrenia is approximately 10 times higher than that in the general population.7 One troubling response to data such as these has been a call -- based on a prediction that Australian mental health budgets are likely to remain relatively fixed -- for reduced emphasis on the treatment of psychotic disorders because of their chronicity and perceived intractability, and for transfer of resources to disorders such as anxiety and depression, which are associated with better responses to treatment.8 An alternative, and in our view far preferable, response is to concentrate on strategies which use what data we have to press for greater overall funding for mental health. There is a strong case for this, as mental illnesses account for 13% of Australia's health burden, third in importance after heart disease and cancer.9 Further, there are several sources of optimism that such strategies will be successful and that new funding is obtainable. For example, prior to 1993, mental health was almost exclusively the preserve of the States and Territories, with the Commonwealth contributing only to Medicare and pharmaceutical benefits. However, since the First National Mental Health Plan, in 1993, the Commonwealth Government has become a significant contributor to public sector psychiatric programs, allocating more than $595 million to them over the years 1993-2003. Also, the States and Territories increased their funding by more than 14% in real terms between the 1992/93 and 1996/97 financial years.10 Another cause for optimism is that, even with high-disability disorders like schizophrenia, there are many measures that meaningfully improve the quality of life of affected individuals, but which need to be better applied. These include early intervention,11 community-based rehabilitation programs, family psychoeducational programs, a greater but targeted use of the newer antipsychotic drugs,12 and good access to residential disability support services and public housing. General practitioners, especially those able to work in conjunction with specialist mental health teams, are in a position to play key roles in ensuring that their patients are offered such treatments and services. This is because people with psychotic disorders often attend GPs (eg, more than 80% had attended their GP in the 12 months before being interviewed in the National Survey,6 with a median of five attendances during that time). The Consultation Liaison in Primary Care Practice (CLIPP) Program13 is one of a number of successful models of collaboration between GPs and mental health services that provide substantial benefit to patients. Future improvements in the management of schizophrenia will require better communication and coordination between patients and carers, medical practitioners, mental health services, and non-government agencies. It will also require the development of new services, the refinement and strengthening of existing ones, especially in the psychosocial domain, the discovery of prognostic markers, and the introduction of novel pharmacotherapies. Fundamental and applied research will be essential to the successful achievement of many of these outcomes. David L Copolov Director, Mental Health Research Institute of Victoria, and Professor, Department of Psychiatry, University of Melbourne, and Professor, Department of Psychological Medicine, Monash University Bruce S Singh Cato Professor, and Head, Department of Psychiatry, University of Melbourne and Clinical Director, North West Mental Health Program Green MF, Marshall BD Jnr, Wirshing WC, et al. Does risperidone improve verbal working memory in treatment-resistant schizophrenia? Am J Psych 1997; 154: 799-804. Purdon SE, Jones BD, Stip E, et al. Neuropsychological change in early phase schizophrenia during 12 months of treatment with olanzapine, risperidone, or haloperidol. The Canadian Collaborative Group for research in schizophrenia. Arch Gen Psychiatry 2000; 57: 249-258. Harrison PJ. The neuropathology of schizophrenia. A critical review of the data and their interpretation. Brain 1999; 122: 593-624. Copolov DL, Velakoulis D, McGorry PD, et al. Neurobiological findings in early phase schizophrenia. Brain Res Brain Res Rev 2000; 31: 157-165. Lewis P. A McEnroe of a nation, but without the charm [letter]. The Melbourne Age 2000 3 April: 14. Jablensky A, McGrath J, Herrman H, et al. People living with psychotic illness: an Australian study 1997-98, an overview. Canberra: Mental Health Branch, Commonwealth Department of Health and Aged Care, October 1999. Harris EC, Barraclough B. Suicide as an outcome for mental disorders: a meta-analysis. Br J Psychiatry 1997; 170: 205-228. Andrews G. Efficacy, effectiveness and efficiency in mental health service delivery. A N Z J Psychiatry 1999; 33: 316-322. Mathers C, Vos T, Stevenson C. The burden of disease and injury in Australia. Canberra: Australian Institute of Health and Welfare, November 1999. National mental health report 1997: 5th annual report: changes in Australia's mental health services under the National Mental Health Strategy 1996/97. Canberra: Department of Health and Family Services, 1998. McGorry PD, Krstev H, Harrigan S. Early detection and treatment delay: implications for outcome in early psychosis. Curr Opin Psychiatry 2000; 13: 37-43. Lehman AF, Steinwachs DM and the Co-investigators of the PORT Project. At issue: translating research into practice: the schizophrenia patient outcomes research team (PORT) treatment recommendations. Schizophr Bull 1998; 24: 1-10. Meadows G. Establishing a collaborative service model for primary mental health care. Med J Aust 1998; 168: 162-165. Make a comment

David L Copolov · Bruce S Singh

Editorial Illness or disease? The case of chronic fatigue syndrome Not every illness can be defined as a disease before care and treatment should commence MJA 2000; 172: 471-472 Few disorders in modern medical practice generate such uncertainty and controversy as the enigmatic clinical condition known as chronic fatigue syndrome (CFS). Much of the difficulty surrounds the dominant reductionist paradigm of medical practice, which emphasises diagnostic tests, recognised pathophysiology, and established pharmacological and other physical treatments. Broader paradigms, incorporating other cultural and psychosocial perspectives, are crucial for clinicians who treat patients with this challenging disorder. Prolonged fatigue is reported by about 25% of all patients presenting to Australian general practice.1 Such fatigue states represent a continuum of severity ranging from the mild and transient symptoms generally attributable to intercurrent infection or minor mental disorder through to the more rare, severe and prolonged fatigue disorders. In about 1% of patients attending general practice, the fatigue state will meet diagnostic criteria for CFS (Box). Although most people present to their doctors with characteristic symptom patterns, current clinical practice relies heavily on diagnostic tests for accurate recognition of almost all disease states. Consequently, doctors frequently explain the patient's suffering in pathophysiological terms based on test results, and treatments are often provided to "fix the numbers" rather than the problem identified by the patient. While doctors readily provide specific treatments that have a firm evidence base, many have little interest in the kind of medicine that maximises non-specific therapeutic benefits, such as providing complex or aversive treatments and encouraging adherence to non-pharmacological interventions. This makes it difficult for patients with poorly defined disorders, or disorders without simple treatment options, to find suitable care. In addition, the increasing specialisation of medicine creates problems for those patients whose disorders do not fit within distinct subspecialty boundaries. Each of these issues contributes to the current dilemmas in managing people with CFS. Syndromal diagnoses were once common in clinical medicine and still persist in situations where disease processes are complex or obscure, such as systemic lupus erythematosus. Syndromal diagnoses are common in neurology (eg, migraine and other headache syndromes), and in psychiatry (eg, major depression), where there is a strong reliance on patient self-report rather than clinical signs or laboratory markers. Many clinical specialties identify syndromes closely related to CFS, but with varied emphasis on a particular symptom feature, such as musculoskeletal pain in fibromyalgia and gastrointestinal disturbance in irritable bowel syndrome. Clinically, CFS has the characteristics of a neuropsychiatric disorder. Its major symptoms (disturbed perception of fatigue and pain, sleep disturbance, neurocognitive difficulties and mood disturbances) suggest a non-localised disturbance of central nervous system function. However, its pathophysiological basis remains obscure. A diverse array of aetiologies has been proposed (including immunological, infective, metabolic, neuroendocrine and psychiatric hypotheses), but no simple explanatory model has been supported by well-controlled studies. Indeed, the heterogeneity within patient groups labelled as having CFS makes it likely that more than one process is operative.3 Thus, CFS challenges the standard concept of discrete disease categories linked to specific aetiologies. The practitioner is confronted with the challenge of explaining the patient's symptoms without reference to a coherent biomedical model. In these circumstances, doctors often fall back on outdated notions of "psychosomatic disease", which patients generally interpret as "imaginary illness". In the face of medical disinterest or scepticism, patients are frequently driven to seek simplistic "alternative" explanations to legitimise their illness experience, and may be tempted to pursue useless or harmful unproven therapies. How can patients and practitioners engage in a more productive dialogue? To begin with, doctors should be prepared to acknowledge the limitations of our current state of knowledge. In the absence of a clear understanding of the underlying pathophysiology, CFS is best described as an illness rather than a disease.4 Illness is a subjective state of suffering -- physical, psychological and social -- and can only be understood and defined with reference to the sick individual.5 Disability arises when illness interferes with the individual's ability to function normally. People with CFS are clearly ill, and are often disabled, even though an underlying disease process has not yet been identified. Our goal as medical practitioners is not only to identify and treat disease, but also to help relieve suffering and disability, whatever the cause. Unfortunately, medical conditions for which there are limited therapeutic approaches are rarely popular territories for practitioners. Various antiviral, immunoregulatory, metabolic, and antidepressive drug treatments for CFS have been subjected to randomised controlled trials, but none has demonstrated definite efficacy. In disorders associated with broad disturbances of central nervous system function there is commonly an interplay between cultural, personal and biomedical factors. Thus, it is not surprising that cognitive-behavioural approaches have shown benefit in clinical trials,6 but it is not yet clear how generally applicable these findings are. A recent evaluation of patients with chronic fatigue in Hong Kong may provide an important insight for our "Western" medical practice.7 For these patients the notion of having a "medical" versus "psychiatric", or "biomedical" versus "psychosocial", cause of their illness made little sense. Their perception was that, while they were clearly unwell, the potential causes of that suffering could lie across a broad domain of personal, social or medical factors. If Australian patients and their doctors could rediscover this basic concept, and could also accept prolonged fatigue as a legitimate illness experience, there would be no need for the polarisation of aetiological models (and political views) that has become characteristic of medical practice in relation to CFS in the USA and UK. This unnecessary polarisation is intellectually shallow and harmful to patients. To build an effective therapeutic alliance, doctors should endeavour to maximise non-specific treatment effects by adopting an empathic and non-judgemental style, by displaying acceptance of their patient's suffering, and by demonstrating a commitment to continued care. Rejecting the patient's illness experience is likely to promote feelings of alienation and to perpetuate ill-health. The cornerstones of good management include providing information about the illness and its natural history; empirical treatment of disturbances of mood and sleep which commonly co-occur in CFS; and encouraging a rehabilitative approach to the illness, including graded physical activity as well as psychological and social support. Andrew R Lloyd Associate Professor, Inflammation Research Unit School of Pathology, University of New South Wales Ian B Hickie Professor, School of Psychiatry, University of New South Wales Robert H Loblay Associate Professor, Department of Clinical Immunology Royal Prince Alfred Hospital, Sydney Hickie I, Hooker AW, Hadzi-Pavlovic D, et al. Fatigue in selected primary care settings: sociodemographic and psychiatric correlates. Med J Aust 1996; 164: 585-588. Fukuda K, Straus SE, Hickie I, et al. The chronic fatigue syndrome: a comprehensive approach to its definition and study. Ann Intern Med 1994; 121: 953-959. Hickie I, Lloyd A, Hadzi-Pavlovic D, et al. Can the chronic fatigue syndrome be defined by distinct clinical features? Psychol Med 1995; 25: 925-935. Jennings D. The confusion between disease and illness in clinical medicine. Can Med Assoc J 1986; 135: 865-870. Cassell EJ. The nature of suffering and the goals of medicine. New York: Oxford University Press, 1991. Wessely S, Hotopf M, Sharpe M. Chronic fatigue and its syndromes. New York: Oxford University Press, 1998. Lee S, Yu H, Wing YK, et al. Psychiatric morbidity and illness experience of primary care patients with chronic fatigue in Hong Kong. Am J Psychiatry 2000; 157: 380-384. Make a comment Diagnostic criteria for chronic fatigue syndrome2A. Clinically evaluated, unexplained, persistent or relapsing fatigue persistent for six months or more that is of new or definite onset; is not the result of ongoing exertion; is not substantially alleviated by rest; and results in substantial reduction in previous levels of occupational, educational, social or personal activities;andB. Four or more of the following symptoms are concurrent, persistent for six months or more, and must not have predated the fatigue: Impaired short term memory or concentration Sore throat Tender cervical or axillary lymph nodes Muscle pain Multijoint pain without arthritis Headaches of a new type, pattern, or severity Unrefreshing sleep Postexertional malaise lasting more than 24 hours. Back to text

Andrew R Lloyd · Ian B Hickie · Robert H Loblay

Healthcare Clinical pathway for fractured neck of femur: a prospective, controlled study Peter F M Choong, Anna K Langford, Michelle M Dowsey and Nick M Santamaria MJA 2000 172: 423-426 For editorial comment, see Swanson et al Abstract - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Orthopaedic surgery Abstract Objective: To assess outcomes of using a clinical pathway for managing patients with fractured neck of femur. Design: Prospective, pseudorandomised, controlled trial. Setting: St Vincent's Hospital, Melbourne, Victoria (a tertiary referral, university teaching hospital), 1 October 1997 to 30 November 1998. Participants: 111 patients (80 women and 31 men; mean age, 81 years) admitted via the emergency department with a primary diagnosis of fractured neck of femur. Interventions: Management guided by a clinical pathway (55 patients) or established standard of care (control group, 56 patients). Main outcome measures: Timing of referrals and discharge planning; total length of stay; and complication and readmission rates within 28 days of discharge. Results: Patients managed according to the clinical pathway had a shorter total stay (6.6 versus 8.0 days; P = 0.03), even if assessment for placement by the Aged Care Assessment Service was required (9.5 versus 13.6 days; P = 0.03). There were no significant differences in complication and readmission rates between pathway and control patients (complication rates, 24% versus 36%; P = 0.40; readmission rates, 4% versus 11%; P = 0.28). Conclusion: Coordinated multidisciplinary care of patients with fractured neck of femur reduces length of stay without increasing complications. By 2050, a quarter of Australia's population will be aged over 65 years, and the incidence of hip fractures is consequently expected to increase fourfold.1 The logistic challenge posed by this increasing incidence and the fourfold greater resources needed by patients over 65 years compared with the average patient2 will be compounded by the expected continuing decline in bed availability. Improving the efficiency of health service delivery to patients with hip fractures may help improve overall availability of acute hospital beds for other elective surgery. Clinical pathways are proposed as a means of providing high quality care in a timely and cost-effective manner. These pathways consist of treatment protocols that aim to streamline and standardise management with multidisciplinary input from medical, nursing, paramedical and administrative staff. They have been used successfully to improve outcomes after elective hip and knee joint replacement.3 This led us to examine the impact of such a coordinated approach on acute and unpredictable admissions such as in patients with femoral-neck fractures. However, surgery for acute hip fracture differs significantly from hip joint replacement as it is non-elective and patient needs and clinical course are more variable. We conducted a prospective, controlled study to assess the effectiveness of clinical pathways for improving outcomes of patients undergoing surgery for acute fracture of the neck of femur. Specifically, we examined time to mobilisation, length of hospital stay, and complication and readmission rates as indices of outcome. Methods We used a pseudorandomised, controlled study design to compare the outcomes of patients whose management was guided by a clinical pathway with those who received the established standard of care in our orthopaedic unit. As the preparation and implementation of the clinical pathway was a quality improvement initiative, ethics committee approval was deemed unnecessary. Setting and participants The study was conducted at St Vincent's Hospital, Melbourne, Victoria (a tertiary referral hospital affiliated with the University of Melbourne). Participants were all patients who underwent standard surgical treatment for acute fracture of the neck of femur (by internal fixation using compression hip screw and plate or hemiarthroplasty) at the hospital between 1 October 1997 and 30 November 1998. In this period, 126 patients were admitted with a diagnosis of fractured neck of femur. Fifteen were excluded from the study, five because they were transferred to another institution for treatment, eight because of associated medical conditions that precluded surgical intervention, and two because of a decision to undertake non-standard surgery. One hundred and eleven patients were allocated to one of two groups (control or clinical pathway) by an administrative clerk, who was independent of the study and unaware of the study hypothesis. Patients were allocated on the basis of their unit record number -- even numbers to the control group (56 patients), and odd numbers to the clinical pathway group (55 patients). A retrospective analysis of a historical treatment group (n = 118) showed a mean length of stay of 11.8 days (range, 2.6-40.0 days; SD, 7.3). To detect a reduction in length of stay of a third at a significance level of 0.05 with a power of 0.8 would require two groups, each with a minimum of 55 participants. Management regimens Management regimens for the clinical pathway and control groups are compared in Box 1. Options for discharge destinations for all patients comprised rehabilitation in an in-patient rehabilitation facility attached to the hospital or in another hospital, patients' own home (with or without domiciliary care services), hostel or nursing home. Patients were deemed suitable for fast-stream rehabilitation in the on-site rehabilitation facility if they had the potential to regain or improve on their prefracture status, were able to achieve this outcome in less than a month, and had a high probability of returning to their previous living environment. Patients who were not expected to regain their prefracture functional level, were not expected to achieve this level in less than two months or were expected to need a higher level of care than before the fracture were referred to the Aged-Care Assessment Service (ACAS) for placement in slow-stream rehabilitation, nursing home, hostel or special accommodation, depending on patient medical conditions and limitations. This service was mediated by a social worker who, together with a medical registrar, prepared the patient for thrice-weekly assessment by a consultant geriatrician which could take place on three occasions per week. Outcome measures Duration of stay: Times in the various stages of the admission were recorded prospectively. Definitions of times were: To surgery: time between admission and theatre; To mobilisation: time between surgery and the patient first walking with the use of aids; To ACAS assessment: time between submission of the referral to ACAS and first assessment by the geriatrician; and Total length of stay: time from admission to discharge from hospital. Inpatient complications: Patients were assessed daily for confusion (disorientation in time, place or person). Wound infection was defined as all wound erythema lasting longer than 24 hours. Deep vein thrombosis was diagnosed clinically and confirmed by ultrasonography, and urinary tract infection was confirmed microbiologically. Postdischarge complications and readmissions: All patients' medical records were examined 28 days after discharge to identify postdischarge complications or readmissions related to the fracture. This time was chosen as we expected the patient to have recovered significantly from their surgery by then. Statistical analyses Results were analysed using SPSS version 8.0.4 Continuous and normally distributed data were compared with t tests for independent groups. Data that were not normally distributed, such as length of stay, were transformed logarithmically before this analysis; consequently, geometric means are reported for these data. Multiple linear regression with a general linear model was used to test for interactions between groups and the variables age, sex, referral to ACAS and premorbid status. Proportions were compared between groups using the z test. P values < 0.05 were regarded as significant. Results The 111 patients comprised 80 women and 31 men, with mean age 81 years. Control and pathway patients did not differ significantly in median age (82 versus 84 years; P = 0.1), number with premorbid conditions (19 versus 18; P = 0.94), number who did not speak English (16 versus 13; P = 0.6) or were confused on admission (24 versus 22; P = 0.98). Outcomes Durations of stay Durations at various stages of the admission for pathway and control patients are compared in Box 2. No significant differences were found between the groups in mean time in the emergency department or mean time from admission to surgery. Pathway patients walked significantly earlier than control patients, but the difference (1.6 versus 2.0 days) was not clinically important. However, the pathway group had a significantly shorter total length of stay than the control group (mean, 6.6 versus 8.0 days; P = 0.03). This meant that control patients stayed 21% longer than pathway patients. After adjusting the log-transformed length-of-stay values for the possible confounding variables of age, sex, aged-care assessment and premorbid status with multiple linear regression, we found that none of these variables produced significant between-group interactions. Group (pathway versus control) remained the most significant factor influencing total length of stay. Referral for aged-care assessment Fifteen of the 55 pathway patients and 18 of the 56 control patients were referred for ACAS assessment. This referral was preoperative for three pathway and two control patients. Time from referral to first assessment by a geriatrician differed only slightly between pathway and control patients: mean times were 2.5 days for pathway patients (range, 1-8 days) and 2.8 days for control patients (range, 0-8 days). Patients who were referred to ACAS had significantly longer total stays than those who were not referred (11.7 versus 6.5 days; P < 0.001; difference, 5.2 days; 95% CI, 3.0-7.5 days). This difference remained significant when the control and pathway groups were analysed separately. However, mean length of stay was significantly shorter for pathway patients referred to ACAS than for control patients referred to ACAS (9.5 versus 13.6 days; Box 2). We explored the possibility of confounding variables for patients referred to ACAS and found that there were none, suggesting that group membership (pathway or control) was the most influential factor affecting length of stay. Postdischarge destinations were similar in pathway and control groups referred to ACAS: 12/15 pathway patients and 16/18 control patients proceeded to slow-stream rehabilitation. Discharge destinations Discharge destinations are shown in Box 2. Patients in each group were most often discharged into fast-stream rehabilitation, followed in frequency by slow-stream rehabilitation or nursing homes. Complications and readmissions There were no significant differences between pathway and control patients in numbers who were confused postoperatively (23/55 versus 31/56) and in rates of other inpatient complications (10/55 versus 14/56 patients), postdischarge complications (3/55 versus 6/56), or readmission rates (2/55 versus 6/56). Discussion We found that use of a clinical pathway for management of fractured neck of femur reduced mean length of hospital stay from 8.0 to 6.6 days, suggesting that a proactive, multidisciplinary approach can reduce hospital stay for this condition. To date, only a few studies5-7 have reported results of a coordinated, multidisciplinary approach to management of fractured neck of femur in Australia. They found, similarly to our study, that these early-intervention programs reduced the length of stay of elderly patients with this condition compared with standard care.5-7 However, actual length of stay varied greatly between studies (from 11.38 days to 32.55 days). This variation highlights the limitations in management inherent in individual institutions because of variation in local factors such as availability of ACAS and support services and patient characteristics. Length of stay in the pathway group at our hospital, which was two to four times shorter than at other hospitals,5-7 may have benefited from our on-site rehabilitation unit. Although we found that use of a clinical pathway reduced total length of stay, the change (1.4 days) was not dramatic. This may be because the strong culture of continued refinement of care in our orthopaedic department had already reduced length of stay for many classes of orthopaedic conditions, including fractured neck of femur. Nevertheless, the reduction of 1.4 days in the clinical pathway group was encouraging. Unlike a previous study,5 our study included patients with language and cognitive difficulties. This choice was made to minimise any selection bias, as patients susceptible to osteoporotic fractures are in an age group which commonly has cognitive difficulties and as our patient population includes a large proportion of non-English-speaking people. We believed that their inclusion would test the efficacy of clinical pathways in the delivery of multidisciplinary care. We observed no difficulties applying the pathway to patients who had cognitive difficulties or did not speak English. Importantly, while use of clinical pathways reduced total length of stay, we found no significant clinical difference in time to mobilisation or complication or readmission rates between the two groups. This contrasted with our earlier findings on the effect of clinical pathways in elective joint replacement surgery.3 Possible explanations for the difference include the frequent existence of unstable and often untreated premorbid conditions in patients with fractured neck of femur, which require attention during their acute admission. In contrast, patients undergoing elective joint replacement have the benefit of preadmission assessment clinics which may resolve expected medical, allied health or discharge issues before admission. Up to a third of our patients with fractured neck of femur were referred for ACAS assessment for placement. Patients who required this assessment stayed significantly longer than patients who did not, possibly reflecting their respective comorbidities and the shortage of aged-care beds in the community. While the time between ACAS referral and consultation was similar for pathway and control patients, total length of stay was four days shorter for pathway than for control patients. It is likely that the daily review of patients' health status promoted by the clinical pathway optimised their readiness for discharge and prompted more regular reviews of discharge plans by the ACAS team. Interestingly, time between ACAS referral and consultation ranged up to eight days in both pathway and control groups. Reasons for this large range were not recorded and warrant further investigation. Some authors have identified that acute care, convalescence, rehabilitation and surgery accounted for more than 90% of total costs for fractured neck of femur, and that the main factors explaining cost variation were the number of days spent in acute care and convalescence or rehabilitation.9,10 However, our study was not designed to evaluate cost-effectiveness of clinical pathways, and, although use of the clinical pathway reduced length of stay by 1.4 days, we did not quantify costs involved in administering the pathway compared with control care. The net cost-effectiveness of our pathway is therefore unknown. Despite the weakness of a limited study, we showed that a multidisciplinary approach using clinical pathways for fractured neck of femur can reduce length of stay without increasing patient morbidity. Acknowledgements We wish to acknowledge the assistance of a special grant from the Victorian Centre for Ambulatory Care Innovation and Michael Bailey, statistical consultant, Alfred Hospital, Melbourne, Victoria. References Sanders KM, Nicholson GC, Ugoni AM, et al. Health burden of hip and other fractures in Australia beyond 2000. Med J Aust 1999; 170: 467-470. Day RO, Henry DA, Muirden KD, et al. Non-steroidal anti-inflammatory drug induced upper gastrointestinal haemorrhage and bleeding. Med J Aust 1992; 157: 810-812. Dowsey MM, Kilgour ML, Santamaria NM, Choong PF. Clinical pathways in hip and knee arthroplasty: a prospective, randomised controlled study. Med J Aust 1999; 170: 59-62. SPSS Inc. SPSS Base 8.0 for Windows. Chicago, (Ill): SPSS Inc, 1998. Swanson CE, Day GA, Yelland CE, et al. The management of elderly patients with femoral fractures. A randomised controlled trial of early intervention versus standard care. Med J Aust 1998; 169: 515-518. Tallis G, Balla JI. Critical path analysis for the management of fractured neck of femur. Aust J Public Health 1995; 19: 155-159. Cameron I, Lyle D, Quine S. Accelerated rehabilitation after proximal femoral fracture: a randomised controlled trial. Disabil Rehabil 1993; 15: 29-34. Lavernia CJ. Hemiarthroplasty in hip fracture care: effects of surgical volume on short-term outcome. J Arthroplasty 1998; 13: 774-778. French FH, Torgerson DJ, Porter RW. Cost analysis of fracture of the neck of femur. Age Ageing 1995; 24: 185-189. Hollingworth W, Todd C, Parker M, et al. Cost analysis of early discharge after hip fracture. BMJ 1993; 307: 903-906. (Received 2 Aug 1999, accepted 25 Jan 2000) Authors' details Department of Orthopaedics, St Vincent's Hospital, Melbourne, VIC. Peter F M Choong, MD, FRACS, Director of Orthopaedics, Professor of Orthopaedics; Anna K Langford, RN, BN, Clinical Nurse Specialist; Michelle M Dowsey, RN, BN, Clinical Nurse Specialist. University of Melbourne, Melbourne, VIC. Nick M Santamaria, MEdSt, PhD, Senior Research Fellow. Reprints: Professor P F M Choong, Department of Orthopaedics, St Vincent's Hospital, 41 Victoria Parade, Fitzroy, VIC 3065. PeterChoongATc031.aone.net.au Make a comment 1: Treatment regimens for control and clinical pathway patients with fractures of the femoral neck Control groupClinical pathway groupEmergency departmentAssessment X-rays Orthopaedic referral Orthopaedic consultation Transfer to wardAssessment Information checklist (prefracture placement, health status, carer) Preoperative investigations (including x-ray) Orthopaedic referral Transfer to wardWard (preoperative)Schedule surgery Preoperative tests ordered Anaesthetic assessmentOrthopaedic consultation Schedule surgery Anaesthetic assessmentWard (postoperative)Strict bedrest X-ray within 48 hours Physiotherapy referral after x-ray MobiliseX-ray within 24 hours Mobilise day after surgeryDocumentationAd hoc patient progress notesSpecific pathway documentation specifying responsibilities by discipline and time frame, to be signed on task completion Coded data collection sheetMedicationProphylactic antibiotics 24h Thromboprophylaxis until discharge (low molecular weight heparin, thigh length stockings)Prophylactic antibiotics 24h Thromboprophylaxis until discharge (low molecular weight heparin, thigh length stockings)Discharge planningBegun postoperatively Depends on patient progress Discharge phone call and summary to discharge destinationBegun on admission Depends on premorbid independence level Discharge package with information on wound care, expected milestones, contact details, simple exercises, equipment for staple removal. 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Anna K Langford · Michelle M Dowsey · Nick M Santamaria

Personal Perspectives Perspectives from a surgeon turned hospital chaplain Irwin B Faris MJA 2000; 172: 389-391 At the end of January 1999, I retired from my chair of surgery to study theology full time as a candidate for ordination. The change from surgery to theology has been an interesting experience, and I have been pleased at how many of my clinician's skills are directly transferable to my new calling (eg, my ability to deal with people and my knowledge of the ways organisations function). As part of my training in 1999, I undertook a placement in the chaplaincy department of a teaching hospital. I chose this placement quite deliberately for two reasons: it was a hospital where I was unknown, except to some of the surgeons, and it gave me a chance to see a hospital from a totally different perspective from my accustomed one. I believe many doctors would be helped by greater understanding and awareness of the emotional responses of doctor and patient My first impression was how poor were the facilities in many wards. Some wards of special units had been renovated and were quite pleasant and well appointed. Other wards, notably those in the general medical and surgical units, with their high turnover and sick patients, were old and run-down with dingy paintwork and corridors cluttered with equipment. My sense from talking to the staff is that the stresses of working in these wards are considerable, and I could not escape the feeling that patients and staff deserve better in a rich country like ours. The next step was obtaining permission to visit patients. The medical students I have taught have complained from time to time of being refused permission by ward clerks and nursing staff to visit patients. I now have first-hand experience of this -- one ward clerk insisted on asking each patient if they wanted to be visited by a chaplain (access to the patients was easier on the days she was away). However, in most wards, access to patients was easier, particularly when I became known to the staff. It was particularly rewarding when a nurse would say, "Mr X is looking forward to seeing you" or "Mrs Y has some problems at home she might want to tell you about". My contact with patients was very enjoyable. I was surprised and delighted at how often and how readily patients would begin to tell me their life story. In my surgical practice, I prided myself on my ability to form a good relationship with my patients, but in this new role communication was on a much deeper level. There may be several explanations. A visit to a specialist, as I then was, can be quite daunting and, despite my best efforts, patients may have felt inhibited from talking openly. Alternatively, they may have believed (quite reasonably) that the detail was irrelevant to the purpose of the visit. Family doctors may have a different perspective, although I would be surprised if the interaction in a standard consultation is as deep as I experienced as a chaplain. I think a third explanation is most likely: in these visits, in contrast to most encounters with medical, nursing or ancillary staff, the patient was much more in control of the situation. There was no agenda (apart from my need to prepare a report for my supervisor), and patients could talk or not talk as they wished. The result was that almost all were happy to talk freely. Two insights caused me concern because they reflect poorly on our profession. The first was the frequency with which patients would tell me that they did not know what was going on with their treatment. I know the difficulty of communicating with sick patients and their families, particularly in the environment of a teaching hospital, and I know that patients have denied having had detailed explanations of planned procedures even when I have explained them myself. In practical terms, this highlights the need for reinforcement of what patients have been told and for testing of their understanding. It is not always easy to find opportunities for senior staff to talk to patients. It was my habit during the preoperative visit to ask patients if they had any further questions about their procedures. I was generally reassured by a negative response. However, this may have been false comfort if the patient did not understand what was to happen or was afraid to ask. Frequent use of written material given to the patient helped, but I think it would have been better had I directly tested the patient's understanding and provided additional information as needed. Nevertheless, there is another side: many patients take the view that the decision has been made, and the sooner the procedure is carried out the better; it may not be helpful to remind them that the carotid endarterectomy they are about to undergo carries a risk of stroke of about 2%, provided the information has been provided previously. The second issue, which disturbed me at times, was the frequency with which some chaplains expressed negative views of the medical profession. This may have been part of the syndrome "doctors are bastards, but my doctor is good". However, at times I heard sufficient detail of patients who had been hurt emotionally by their encounters with doctors to cause me concern about both our image and the way some of our colleagues appear to function. Although the patients seen by chaplains often have complex and difficult interactions of physical, emotional and spiritual factors, and are clearly not a random sample of the population, if these "difficult" patients are not being dealt with adequately by the medical profession, then we need to look to ways of improving the situation. During most of my time in the hospital, my background was unknown to the staff and patients. An exception, and a highlight of my time in the hospital, was when I took part in the teaching session to introduce a new group of medical students to the work of the chaplaincy. The object of the session was to point out the importance of spiritual factors in healing ("making whole"), and to claim on behalf of the chaplains to be the specialists in this area. My ability to talk to the students in familiar language may have enhanced their appreciation of this point of view. The program of training that I undertook is called Clinical Pastoral Education (CPE). Its aim is to allow non-ordained hospital chaplains and ordination candidates to "develop new awareness of their own humanity and of the needs of those to whom they minister".1 This is now an internationally recognised discipline, which began in the United States in the 1920s. The links with medical teaching go back to its originators, one of whom, Dr Richard Cabot, developed the case-study conference at the Massachusetts General Hospital (S Ames, Clinical Pastoral Educator, Anglican Centre for Clinical Pastoral Education, Melbourne, VIC, personal communication). As currently practised, the major element in CPE is the "verbatim" report, which purports to be a literal report of part of a clinical chaplain-patient encounter. This is written from memory and presented either to the supervisor or to the group, which typically comprises four to six students and two to three supervisors. This report is analysed and discussed in detail, often in a way which confronts students with their own feelings and inadequacies. As far as I can determine, this process has no parallels in medical education, either undergraduate or postgraduate. At least one aspect of the CPE program might be helpful in medical education and practice. I believe many doctors would be helped by greater understanding and awareness of the emotional responses of doctor and patient, which occur in almost every clinical encounter. As doctors, we are trained to act in a detached, "objective" manner with our patients. This may be a necessary part of clinical decision-making, but I suspect that doctors do respond emotionally to patients, often in ways we do not recognise or admit. Explicit acknowledgment of this would enable greater rapport with patients and their families, especially in times of stress. In addition, greater awareness of, and sensitivity to, the patient's feelings and emotions would probably help improve patients' perceptions of doctors. There are important lessons from this CPE program for all clinicians concerning communication with patients and families. The first is the need for reinforcement and testing of understanding in situations such as obtaining consent for procedures. The second is the recognition of emotional responses of patients and doctors to clinical encounters. A greater appreciation of these issues would improve the quality of our communication and enhance our image. Irwin B Faris MD, FRACS, Deacon, formerly Professor of Surgery The University of Melbourne The Geelong Hospital, Geelong, VIC ifarisATozemail.com.au Reprints will not be available from the author. Correspondence: Irwin B Faris, 1 Brendan Court, Highton, VIC 3216. Association for Supervised Pastoral Education in Australia. Standards for clinical pastoral education, 1995: 2. Make a comment

Irwin B Faris

For Debate The hospitalist: a third alternative The role of hospitalist is already evolving in Australia, being filled by Career Medical Officers John M Egan, Mary G T Webber, Michael R D King, Michael Boyd, Gabrielle du Preez-Wilkinson and David Brock MJA 2000; 172: 335-338 The need for the "hospitalist" - The role of the hospitalist - Who best fills this role? - References - Authors' details - - More articles on Administration and health services - More articles on General medicine - More articles on Emergency medicine The hospitalist debate began in the Journal in April 1999, when we published an article by Hillman on how acute-care hospitals are changing. In September 1999, Scott and Phillips suggested that general physicians should take on the role of hospitalist. The start of the debate1 . . . in some countries [there has been] the emergence of a "hospitalist" who has a wide range of expertise, but concentrating more on acute hospital medicine -- more like a general physician, but specialising in acute and serious illness rather than chronic and mainly ambulant medicine. The hospitalist also has advanced resuscitation and procedural skills. They are familiar with the medical comorbidities increasingly associated with surgical patients and understand how different organs fail and interact in acute illness. They are a move back to the generalist physician. The equivalent in Australia is probably the intensive care or emergency physician. The hospitalist also understands about continuity and coordination of patient care, managing the patient's inpatient course and arranging a seamless transition to a community setting. . . . A hospitalist could enable community-based specialists to devote more time to what they do best, rather than being continuously confronted by the dilemma of maintaining a busy professional practice with tight appointment schedules and having seriously ill in-hospital patients who might require their attention day or night in an unpredictable way. Having skilled clinical cover 24 hours a day would also help guarantee patient safety. . . . Australia could explore other ways of achieving the same standards. (Hillman K. MJA 1999; 170: 325-328) The general physician as hospitalist2 . . . patients are more likely to be assured of continuous, integrated and efficient care for a multiplicity of concurrent problems if attended to by general physicians from the time of admission via emergency departments right through to the time of discharge and beyond into ambulatory care. Adequate resourcing of general medical units, greater involvement of general physicians in emergency and intensive care settings, ready access to specialised medical, nursing and allied health expertise as needed . . . (Scott IA, Phillips PA. MJA 1999; 171: 312-314) THERE HAS BEEN AN ONGOING DEBATE in the Journal1-6 on the changing role of the acute-care hospital and, associated with this change, the desirability of a new type of doctor, the hospitalist. It is argued that in the hospital of the near future there will be fewer patients, who will, generally, be more seriously ill than at present.7,8 Leaving aside discussion of the likelihood of this scenario,9 we believe there needs to be a change in the role and experience of doctors who work in this hospital setting: the hospitalist is one suggestion for this change. We argue here that this role is already evolving and currently functioning in a variety of clinical situations in the Australian healthcare system.10The doctor delivering those aspects of seniority, experience and permanence relevant to a hospital generalist is a Career Medical Officer (CMO) (see Box). There are two interrelated parts to this debate: What problems are there with current medical staffing of acute care hospitals? What solutions are available? The need for the "hospitalist" The present model of a Visiting Medical Officer (VMO) who has overall responsibility for the patient and who delegates this responsibility to more junior medical staff in a hierarchical manner (registrars, Resident Medical Officers [RMOs]) while out of the hospital, has a long tradition in medicine. This model, while having some excellent features, may have outlived its usefulness at the beginning of the 21st century. There is increasing evidence of major inadequacies in the functioning of our hospitals.11 This may reflect the way we educate and organise our medical staff. An analysis of the causes of adverse events reported in the Quality in Australian Health Care Study12 showed that human error was involved in 82% of adverse events and that the most common causes were failure in technical performance and cognitive failure: failure to act on available information, failure to consult or investigate, and failure to attend or provide adequate attention. A recent study of critical events (ie, cardiac arrest or unplanned admission to ICU) in an Australian metropolitan teaching hospital13 found that these episodes are frequently preceded by documented clinical instability of the patient and multiple medical review before admission to ICU or cardiac arrest ensued. The authors commented that the patients in their study (generally those with complex medical and surgical conditions) were usually managed initially by the most junior member on the ward (intern or resident). We do not suggest that junior medical officers should not be involved in direct care of the very sick, but there appear to be problems with current hospital practice: the major deficiencies appear to us to be the understandable lack of experience of the junior medical staff and their rapid turnover. This outdated way of organising medical staffing has long caused problems with our nursing colleagues14-16 and others, who assist the overworked and inexperienced medical officers organise their time and energies to most effectively care for and investigate sick patients -- and then repeat this education once again with the next rotation. Is it right to give increasing responsibility to our junior doctors, but leave them at times relatively unsupervised, unsupported and responsible for major medical decisions when their level of training may be inadequate for the task? The Postgraduate Medical Councils in the various states provide increasingly good-quality support for first- and second-year graduates, but this is in a logistical and educational role rather than a directly supportive clinical role. The role of the hospitalist We argue that hospital wards may run more smoothly and there may be greater satisfaction by patients, nursing staff, consultant medical staff and, importantly, junior medical staff if there is rapid access at all times to an onsite experienced medical officer. This senior doctor would be conversant with the dynamics of the ward, have good relationships with and an appreciation of the role of ancillary staff, and have a relatively long-term commitment to the hospital. These attributes would enable him or her to deal with evolving clinical situations before they became major problems. An additional benefit would be the provision of extra educational opportunities for interns and RMOs during their "apprenticeship" years. Hillman1 and Scott and Phillips2 appear to be attempting to address the problems by placing another specialist physician into the increasingly fragmented world of hospital medicine. There are examples of this in the United States,17-19 where the hospitalist is usually (but not always20) a specialist in internal medicine who works predominantly in the hospital setting. Physicians who work outside of the hospital relinquish their responsibility for the patient at the hospital entrance and take it up again on discharge. The unstated but underlying expectation is that the hospitalist would usurp the primary role and responsibility of the attending doctor. We believe this vision of a hospitalist to be fundamentally flawed. On the one hand, it sidelines doctors who should be intimately involved in the inpatient care of patients (including specialist physicians, general practitioners and paediatricians) whose main area of practice remains office based; on the other, it may miss out on providing a "new deal" of care for many patients who are in hospital and whose particular problems might not necessarily fall within the expertise of the intensivist/physician (eg, falls in hospital, paediatric problems, or dementia). Our contention is that this role demands not the narrow focus of the specialist but the broad-based knowledge of the generalist -- someone who can be a "jack of all trades". The preceding contributions to this debate1,2 appear to have as their central vision a hospital filled with medical patients or seriously ill surgical patients who would be better managed by a physician. Most hospitals have, and will continue to have, a much wider range of patients and conditions, including all the major and minor acute problems that one finds in paediatric, gynaecological, obstetric and psychiatric wards. We believe the role calls for a "middle management" doctor who has a breadth of knowledge and experience gained from working in hospitals and who is proficient in as many branches of hospital medicine as possible. The optimal solution is to have someone who is conversant with and experienced in treating seriously ill patients expeditiously, who is quite at home in managing the multiple minor problems that beset hospital patients, and who is used to consulting with a wide range of medical and surgical specialties as needed. The role of hospitalist should be complementary to, not in confrontation with, the established Australian model of inpatient care. That is, it seems to us better to have an experienced doctor "on site" to organise -- not take over -- the management of the hospital inpatient. There is some evidence that hospitalists who have complete control of inpatient care increase, rather than decrease, the length of stay in hospital.21 In the model we propose, the consultant physician, surgeon, paediatrician, gynaecologist, or, increasingly, general practitioner would retain primary responsibility for the patient's management, but would be actively supported by someone who had worked in the hospital system for many years and could competently manage most problems that may arise, at least in the short term. This doctor should also have the trust of, and rapid access to, the consultant staff, and good working relationships with the nursing and paramedical staff (mutual respect of each other's role and abilities) as well as a good understanding of the "mechanics" (eg, layout, routine, and regular practices) of the hospital. Who best fills this role? We believe that Scott and Phillips2 are right in having major reservations about intensivists being responsible for general ward patients. The prevention of a slow deterioration of a general medical or surgical patient to serious illness does not require the considerable skills of an intensivist -- most doctors with experience and education, alerted by protocols that highlight dangerous trends, can quite adequately look after these cases and refer to the intensive care or cardiac care unit if appropriate. The opposite and far more common scenario, that of a relatively minor problem, may well lead to the over-investigation and treatment of a condition that could have been easily handled by a broadly experienced medical officer. Although the general physician may have a better claim to this role (especially rural physicians, who are, by necessity, well-rounded generalists), there is still the problem of a doctor who may be overeducated for some aspects of the work, and undereducated for others. Many of the problems outlined above have in the past been handled by registrars, RMOs and interns. Senior registrars are usually quite able to manage patients without the direct supervision of the VMO; however, this is not necessarily the case with more junior registrars and RMOs. Again, frequent rotation takes well-performing doctors out of the loop just as they attain a level of familiarity and experience with a particular group of patients. Although doctors who performed similar roles had been in the health systems throughout Australia for many years, CMOs were initially brought into service in New South Wales in the early 1980s to maintain experienced medical practitioners in the public hospital system. These doctors were working in posts as unaccredited medical registrars or emergency medical officers, particularly in suburban and rural hospitals. The New South Wales Department of Health10 noted in 1989 that there had been a positive response to the introduction of CMOs: it had increased retention rates of hospital doctors, improved middle grade medical staffing in peripheral hospitals, and addressed the service needs of these hospitals, and the individuals were able to undertake more clinical responsibilities and required less supervision. Many CMOs have now been working in these positions for well over 12 years, and have developed considerable expertise in their area of practice. A recent study in Queensland,22 addressing the training needs and career paths of this cohort of doctors, noted their wide range of practice -- predominantly in emergency medicine ("they make up the majority of the senior emergency work force in Queensland"22), but also in orthopaedics, sexual health, community health, and other areas. The report also pointed out the experience of those who worked in emergency medicine: 73% had worked for more than three years full-time since their third postgraduate year, and 25% had worked for 10 or more years in this capacity. Furthermore, a large proportion (69%) of CMOs had postgraduate qualifications. The study also commented on a major flaw in the Australian Medical Workforce Advisory Committee report The Emergency Medicine Workforce in Australia,23 which totally ignored the role played by CMOs in the staffing of emergency departments. This omission seems to be symptomatic of a "blind spot" by some in the profession to the valuable service provided by these doctors. Many modern private hospitals are turning to CMOs to fill a demand in the medical care of hospitalised patients. In the Sydney area the Hills, Kareena and the Sydney Adventist private hospitals have significant CMO staffing (Dr Stephen Delprado, Deputy Director, Emergency Department, Hills Private Hospital, personal communication), and seven private hospitals in Queensland have CMO cover.22 Most CMOs report that they are quite happy to continue to work in these roles (J M E and M R D K, unpublished survey of 32 rural CMOs in NSW, presented to Directors of Clinical Training meeting, Postgraduate Medical Council, Sydney, May 1996). Recently, some have formed themselves into organised subgroups of the medical workforce. The largest of these (the Career Medical Officers Association) is now taking responsibility for initiating educational and industrial policies for CMOs. Examples of these are the provision of continuing medical education (in association with the Royal College of Pathologists of Australasia); discussions with universities and others about more formal training, qualifications and accreditation; and representations on various committees, including the Hospital Medical Officer Subcommittee of the Medical Training Review Panel. We believe that this broad-based experience and commitment is what makes the CMO the ideal person to take on the role of the hospitalist. Furthermore, the changes necessary to do this are relatively minor and merely a continuation of recent trends in medical workforce utilisation in the modern Australian hospital. In our opinion, CMOs are well able to fulfil such future requirements and do it in the most efficient and cost-effective way. We note the invitation by Scott and Phillips to put the respective views of hospitalist practice to the test in a randomised trial comparing the intensivist or internal medicine models of hospitalist.2 Although we have some misgivings about the applicability of this methodology, we firmly believe that any rigorous evaluation of the various hospitalist models on offer would be incomplete without the inclusion of CMOs. References Hillman K. The changing role of acute-care hospitals. Med J Aust 1999; 170: 325-328. Scott IA, Phillips PA. Hospitals and hospitalists: an alternative view. Med J Aust 1999; 171: 312-314. Denaro CP, Bennett CJ. The changing role of acute-care hospitals [letter]. Med J Aust 1999; 171: 224. Hillman K. Hospitals and hospitalists: an alternative view [letter]. Med J Aust 2000; 172: 299. Sartain JB. Hospitals and hospitalists: an alternative view [letter]. Med J Aust 2000; 172: 299. Phillips PA, Scott IA. Hospitals and hospitalists: an alternative view [letter]. Med J Aust 2000; 172: 299. Komesaroff PA, Clunie GJA, Duckett SJ. What is the future of the hospital system? Med J Aust 1997; 166: 17-22. Braithwaite J. The 21st-century hospital [editorial]. Med J Aust 1997; 166: 6. Braithwaite J, Hindle D. Research and the acute-care hospital of the future. Med J Aust 1999; 170: 292-293. Career Medical Officers (CMOs). Circular no. 89/156. Sydney: NSW Health, 1989. Wilson RMcL, Runciman WB, Gibberd RW, et al. The Quality in Australian Health Care Study. Med J Aust 1995; 163: 458-471. 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. Buist MD, Jarmolowski E, Burton PR, et al. Recognising clinical instability in hospital patients before cardiac arrest or unplanned admission to intensive care. A pilot study in a tertiary-care hospital. Med J Aust 1999; 171: 22-25. Lublin J, Gething L. RNs as teachers of junior doctors. Aust J Advanced Nursing 1992; 10(2): 3-9. Agnew T. Just rewards on the wards. Nursing Times. 1995; 91(34): 19. Junior doctors turn to nurses for help. Nursing Standard 1999; 13(47): 8. Wachter RM. An introduction to the hospitalist model. Ann Intern Med 1999; 130: 338-342. Sox HC. The hospitalist model: perspectives of the patient, the internist, and internal medicine. Ann Intern Med 1999; 130: 368-372. Schroeder SA, Schapiro R. The hospitalist: new boon for internal medicine or retreat from primary care? Ann Intern Med 1999; 130: 382-387. NAIP affiliates with the American College of Physicians. <http://www.naipon line.org/hist.htm>. Accessed 2 March 2000. Jackson JL. The international experience with hospitalists. The Hospitalist 1997; Summer. Available at <http://www.naiponline.org/archives/guest.htm>. Accessed 2 March 2000. Bricknall B, Daly M, Catchpole M. The career paths, training needs and future role of non-specialist senior medical officers in the Queensland public health care system. An exploratory study. Brisbane: Health Advisory Unit, Queensland Health, 1999. Australian Medical Workforce Advisory Committee. The Emergency Medicine Workforce in Australia. Sydney: AMWAC, 1997. Summary available at <http://amwac.health.nsw.gov.au/corporate-services/amwac/emerg.htm>. Accessed 2 March 2000. Authors' details Goulburn Base Hospital, Goulburn, NSW. John M Egan, MB BS, Career Medical Officer, Emergency Department. Kareen Private Hospital, Sydney, NSW. Mary G T Webber, MB BS, Career Medical Officer, Emergency Department, and President Career Medical Officers Association. Coffs Harbour Base Hospital, Coffs Harbour, NSW. Michael R D King, FRACGP, FACRRM, Director of Emergency Services. Camden Hospital, Sydney, NSW. Michael Boyd, MB BS, Co-ordinator of Emergency Department. Prince Charles Hospital, Brisbane, QLD. Gabrielle du Preez-Wilkinson, FRACMA, AFCHSE, Medical Officer, Emergency Department. Tweed Heads Hospital, Tweed Heads, NSW. David Brock, MB BS, Career Medical Officer, Emergency Department. Reprints: Dr J M Egan, PO Box 131, Goulburn, NSW 2580. eganjATinteract.net.au Make a comment What is a Career Medical Officer? Officially, a Career Medical Officer (CMO) is a grade of medical officer employed by the New South Wales Department of Health. Unofficially, and more accurately, CMOs are: "middle management" doctors who increasingly perform in responsible and demanding clinical roles; doctors beyond the second postgraduate year and working in clinical medicine; not general practitioners (although some work in both roles), nor specialists, nor in training for these roles; a distinct subgroup within the wider medical community, with their own aspirations, experience and educational needs. In different parts of Australia doctors in this role have different designations: Senior Medical Officer (SMO: Qld, WA, SA, NT); Hospital Medical Officer (HMO: Vic); Career Medical Officer (CMO: NSW, but this title also known and occasionally used in other states). In practice, awards for these medical officers range from registrar to staff specialist range. How many CMOs are there? No accurate numbers are available. Recent medical workforce surveys show 652 "other hospital career" doctors in NSW. In Queensland, there are 149 funded SMO positions. These figures are almost certainly an underestimate as they do not take into account community CMOs who may be labelled as GPs or specialists, and self-reporting of some hospital CMOs as registrars or staff-specialists. Likely "ball-park" figures are 1000 in NSW, and 2000 Australia-wide, but there may be significantly more. Where do CMOs work? About 60%-70% of CMOs work in emergency departments in rural, suburban and private hospitals. CMOs also work in psychiatry, sexual health, women's health, police forensic, intensive care, neonatal, orthopaedics, and other areas. In rural Queensland and NSW, CMOs are the predominant senior doctors in emergency departments. What education do CMOs have? No formal qualifications are required at present, but at least half have postgraduate qualifications. Many (especially in emergency departments) have early management of severe trauma (EMST), emergency life support (ELS), or advanced paediatric life support (APLS) qualifications. Discussions are in progress with the University of Newcastle regarding more formal postgraduate qualifications for CMOs. The Postgraduate Medical Councils may have an advisory or other role in CMO education and training. The Career Medical Officers Association (CMOA) website <http://www.cmoa.ican.net.au/> has details of current interest for CMOs and others. The information in this Box comes from many sources, including the NSW Medical Labour Force Annual Survey 1998, the CMOA website, the CMOA database, Bricknall et al22 and discussions with CMOs. Back to text

John M Egan · Michael Boyd · David Brock

Research Prevention of perinatal group B streptococcal disease: screening practice in public hospitals in Victoria Mary Connellan and Euan M Wallace MJA 2000; 172: 317-320 For editorial comment, see Oats Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Infectious diseases and parasitology Abstract Objectives: To survey clinical protocols for prevention of early-onset group B streptococcal disease (EOGBSD) of the newborn in public maternity hospitals. Design: Postal questionnaire with telephone follow-up when required. Setting: All hospitals that undertook deliveries in public patients in the State of Victoria, November 1997 to January 1998. Results: The survey was sent to 84 hospitals: 71 responded and 64 met the criteria and provided usable data (76% response rate). These 64 represented 42 784 births (68% of births in Victoria in 1996). Most hospitals (62; 97%) undertook actions that would identify and treat pregnant women at risk of EOGBSD. 48 (75%) performed bacteriological screening for maternal GBS carriage, but only 20 of these had a unified protocol. Screening was mostly by low vaginal swab (15 hospitals) and before 30 weeks' gestation (12 hospitals). Low vaginal swab plus anal swab was used in only one hospital. Bacteriological screening was significantly more common in metropolitan hospitals than in rural hospitals (100% versus 67%; P = 0.007, Fisher's exact test). Targeting of prophylaxis by recognised risk factors was reported by 59 (92%) hospitals, 45 of which also undertook screening. There was considerable variation in the specific risk factors used. Conclusions: While there was clearly widespread awareness of EOGBSD in Victorian public hospitals, prevention programs varied considerably. The development of consensus practice guidelines might improve EOGBSD prevention, reducing morbidity, mortality and costs. Introduction Since the 1970s, group B streptococci (GBS) have been recognised as a major cause of neonatal systemic infection in the first week of life -- so called early-onset group B streptococcal disease (EOGBSD). The reported incidence of this condition varies between 1 and 4 per 1000 livebirths.1 Infants acquire the infection by vertical transmission from an asymptomatic mother during delivery.2 Clinical disease manifests at birth or within 24-48 hours as pneumonia, septicaemia or, less commonly, meningitis.1In Australia, the prevalence of GBS vaginal carriage has been estimated at 12%-15%,3-5 and about 1%-2% of infants born to women carrying GBS develop EOGBSD, with about 6% of cases being fatal.2,5-7The risks of EOGBSD and death are particularly high in preterm infants.2 However, antibiotic prophylaxis given to "at risk" women during labour has been shown to significantly reduce the incidence of EOGBSD, and is an important and worthwhile public health measure.2,7-9 While the value of prophylactic antibiotic intervention in at-risk women is now widely agreed, the best means of targeting these women is perhaps less clear. Comprehensive reviews of the available evidence have been published both in Australia1,5,10 and overseas.2,11-13 There are two broad approaches to targeting prophylaxis -- identification of GBS carriers by bacteriological screening or treating by clinical risk factors. No trials have compared the efficacy of the two approaches. It is therefore perhaps not surprising that, anecdotally, GBS intervention practices differ greatly between public hospitals across the State of Victoria. However, no objective data are available to assess the extent of these differences and the appropriateness of current practice. We surveyed all public maternity hospitals in Victoria to explore what GBS intervention programs were in place and, in particular, to assess whether practice was in line with currently available evidence. Methods The Victorian Perinatal Data Collection Unit, Melbourne, provided contact details of all maternity hospitals in Victoria and identified those that undertook deliveries in public patients. Between November 1997 and January 1998, a six-page survey form containing 18 questions was sent to the Delivery Suite Nursing Unit Manager, or equivalent, in each of these hospitals. The survey was multiple-choice format with some free-text fields. Non-respondents were sent a second copy of the survey form two months later and were telephoned if necessary. Data on deliveries in 1996 were supplied by the Victorian Perinatal Data Collection Unit. Statistical analyses were performed using Statview 4.1.14 Significance was taken as P < 0.05. Results Of the 84 hospitals surveyed, 71 responded and 64 met the criteria and provided usable data, giving a final response rate of 76% (three respondents delivered only private patients, one cared for postnatal women only, and three did not provide GBS screening information). The 64 hospitals that provided usable data accounted for 42 784 births in 1996 (68% of all births and 93% of all births to public patients in Victoria) and comprised 16 hospitals in metropolitan Melbourne and 48 rural hospitals. Of the 64 hospitals, 62 (97%) reported undertaking procedures that would identify and treat at least some women with a baby at risk of EOGBSD; 48 hospitals (75%) undertook routine antenatal screening for maternal GBS carriage, including 45 which also offered antibiotic prophylaxis on the basis of risk factors. Another 14 hospitals (22%) used the latter approach alone. Screening for GBS The hospitals which undertook routine antenatal bacteriological screening accounted for 97% of all deliveries in the 64 responding hospitals. They comprised all 16 metropolitan hospitals and 32 of the 48 rural hospitals, a significant difference in proportions between metropolitan and rural hospitals (P = 0.007, Fisher's exact test). Of the 48 hospitals that undertook screening, 20 had a unified hospital screening protocol, with the remainder using individual-doctor protocols. The 20 with a unified protocol comprised nine of the 16 metropolitan hospitals and 11 of the 32 rural hospitals (P = 0.22, Fisher's exact test). Characteristics of the screening protocols among these 20 hospitals are shown in Box 1. Most protocols (65%) were less than five years old, and 40% were less than two years old. The most common approach to bacteriological screening was to perform a low vaginal swab only (15 of 20 hospitals), or, less commonly, a high vaginal swab only (four hospitals). Only one hospital performed a low vaginal swab combined with an anal swab. All but one hospital screened only once in the pregnancy, either before 30 weeks' gestation (12 hospitals) or between 30 and 34 weeks' gestation (seven). The hospital that screened more than once did not specify gestations. All hospitals that performed bacteriological screening administered intrapartum antibiotics to all women who were GBS-positive. Screening of private patients Bacteriological screening was offered to private patients by some or all obstetricians at 37 of the 64 hospitals. This was a smaller proportion of hospitals than offered screening to public patients, although the difference did not reach significance (P = 0.06, Fisher's exact test). In only 18 of these 37 hospitals did all obstetricians offer screening to their private patients. In 13 hospitals, none offered screening to private patients, and in 14 the respondent did not know if it was offered. Risk-factor-targeted prophylaxis Targeting of prophylaxis by recognised clinical risk factors was reported by 59 of the 64 hospitals (92%). Criteria used are shown in Box 2. Antibiotics were reported to be given most commonly for clinical signs of intrapartum infection (51 hospitals) and pre-labour rupture of the membranes (43 hospitals), although the time from membrane rupture to starting antibiotic administration varied considerably. Only 10 hospitals administered antibiotics to women admitted in preterm labour below a specified gestation. All were metropolitan hospitals that also performed routine bacteriological screening. Only four hospitals (6%) administered antibiotics on the basis of all five recognised criteria. Two of these also undertook screening. With regard to the antibiotic used as chemoprophylaxis, 14 of the 20 hospitals with a unified protocol used penicillin, four amoxycillin and two ampicillin. The 14 hospitals using penicillin all had different treatment regimens. Of the hospitals that lacked a unified protocol, only four reported the antibiotic regimen used -- penicillin in three and amoxycillin in one. Discussion To our knowledge, this is the first survey of GBS screening practices in pregnancy to be reported in Australia. It reveals that prenatal screening and prophylaxis for GBS infection were widely practised in public hospitals in Victoria. However, the specific strategies varied considerably, and, while this variation is understandable (given the lack of robust comparative data for the various possible approaches2,10,12,15), it translated into a less than ideal approach in many centres. Current evidence suggests that the optimum approach to reduce EOGBSD is to offer intrapartum chemoprophylaxis, using penicillin (or erythromycin in women allergic to penicillin) to at-risk mother-infant pairs. These at-risk pairs are identified by bacteriological screening, involving a low vaginal and anal swab performed at 36-38 weeks' gestation and/or by clinical risk factors (Box 3).2,10 In our survey, most hospitals reported targeting prophylaxis through bacteriological screening. However, the varied approaches to this screening revealed that current practice may not be as effective as possible. In addition, while most hospitals undertook screening, only 20 had a unified protocol, while the remaining 28 reported that protocols differed between doctors. This, together with the variable practice for private patients, suggests that it may be useful to develop more uniform Australian guidelines. Indeed, that only two hospitals (3% of respondents) reported a current protocol that would be expected to maximally prevent EOGBSD (targeting prophylaxis by bacteriological screening and by all risk factors shown in Box 3) suggests that the introduction of uniform practice guidelines would be worthwhile. The most common differences between the reported screening protocols and an approach expected to minimise EOGBSD were the maternal sites sampled and the timing of screening. GBS carriage within individuals is not constant. Consequently, bacteriological swabs taken at 28 weeks' gestation have only a 50%-70% positive predictive value for carriage at delivery, while about 5%-10% of women who are GBS-positive at delivery are negative at 28 weeks.3,13,16 Therefore, the closer to delivery that bacteriological screening is undertaken, the greater its utility, both as sensitivity and specificity are increased,2,10,16 and as the costs of screening are saved for the 5% of pregnant women who deliver preterm (and should receive prophylaxis irrespective of the screening result.2,11). Thus, bacteriological screening is probably best undertaken at 36-38 weeks' rather than at less than 30 weeks' gestation, the most popular time in our survey. Nevertheless, despite these theoretical considerations, a significant reduction in the incidence of EOGBSD was recently reported by King George V Hospital, Sydney, where screening is performed at 28 weeks' gestation.17 This result emphasises that bacteriological screening at 28 weeks' gestation is preferable to no screening at all. Detection of GBS is increased by 5%-25% if an anal swab is collected in addition to a vaginal swab.16,18,19 Only one hospital in our survey reported collecting both swabs; most took only a low vaginal swab. It has been suggested that Australian women would find collection of anal swabs unacceptable,20 but no objective evidence has been presented for this. Furthermore, most United States centres surveyed by the Centers for Disease Control took anal swabs,21 suggesting that the practice may be more acceptable than is assumed. It would certainly be worthwhile asking Australian women, and reappraising the method of screening most appropriate for our population. Collection of high vaginal swabs, reported by four hospitals in our survey, is inappropriate for GBS screening. The most cost-effective approach to preventing EOGBSD is to offer antibiotic prophylaxis to women with identified risk factors, without bacteriological screening.15 This approach has been recommended by some Australian groups (Professor James King, Mater Perinatal Epidemiology Unit, Mater Misericordiae Mothers' Hospital, Brisbane, Qld, personal communication). Most hospitals surveyed (92%) offered prophylaxis on the basis of risk factors, but only four (6%) used all recognised risk factors appropriately (Box 3). As the relative risk of EOGBSD is significantly greater in preterm neonates than in babies born at term,7 any EOGBSD prevention program should ideally include intrapartum prophylaxis for any woman labouring before 37 weeks' gestation, irrespective of whether she was screened earlier in pregnancy or of the result of that screening.2,11 It was disappointing that only a minority of the hospitals surveyed had such a policy, particularly as infection per se is a major recognised cause of preterm labour. That no rural hospital had such a policy may reflect that these hospitals transfer such women for level 3 neonatal care, and that preparation for transfer focuses more on tocolytic therapy and corticosteroid prophylaxis. If so, then an educational campaign to encourage early antibiotic treatment instituted at the referring hospital might be worthwhile. We were also surprised that only a few hospitals offered antibiotic prophylaxis to women who had had a previous baby with EOGBSD. Neonatal EOGBSD is a devastating infection, and, in our experience, parents who have had an infected child usually seek interventions to prevent infection in a future delivery. That most clinicians and hospitals do not routinely offer prophylaxis in this situation suggests a lack of awareness that this history is an important risk factor. Similarly, the variable responses to the other accepted risk factors suggest that a significant proportion of health providers are either unaware of the epidemiology of EOGBSD or do not perceive EOGBSD as an important clinical problem. Our survey of Victorian public hospitals showed that, while most are clearly aware of EOGBSD, only a minority currently have a strategy that maximises prevention of EOGBSD and represents most cost-effective practice. However, very minor changes in practice would be expected to improve EOGBSD prevention and significantly reduce costs,15 for both screening and treatment. Accordingly, our data support the case for a comprehensive, statewide, or possibly national, education program, and for the development and introduction of uniform consensus practice guidelines. Acknowledgements The authors would like to thank the participating hospitals as well as Dr Jane Halliday and Ms Sofia Mercer, from the Victorian Perinatal Data Collection Unit. EMW was partly funded by a Charles and Sylvia Viertel Clinical Investigator Fellowship. Disclosure: We are not aware of any conflict of interest arising from performing or reporting this work. References Vigneswaran R, O'Loughlin JA, McDonald HM. Group B streptococcus and pregnancy. Aust N Z J Obstet Gynaecol 1995; 35: 117-119. Prevention of perinatal group B streptococcal disease: a public health perspective. Centers for Disease Control and Prevention. MMWR Morb Mortal Wkly Rep 1996; 45 (RR-7): 1-24. McDonald H, Vigneswaran R, O'Loughlin JA. Group B streptococcal colonization and preterm labour. Aust N Z J Obstet Gynaecol 1989; 29: 291-293. Australasian Study Group for Neonatal Infections. Early-onset group B streptococcal infections in Aboriginal and non-Aboriginal infants. Med J Aust 1995; 163: 302-306. Jefferey HE, McIntosh ED. Antepartum screening and non-selective intrapartum chemoprophylaxis for group B streptococcus. Aust N Z J Obstet Gynaecol 1994; 34: 14-19. Garland SM, Fleigner JR. Group B streptococcus (GBS) and neonatal infections: the case for intrapartum chemoprophylaxis. Aust N Z J Obstet Gynaecol 1991; 31: 119-122. Zangwill KM, Schuchat A, Wenger JD. Group G streptococcal disease in the United States, 1990: report from a multistate active surveillance system. Morb Mortal Wkly Rep CDC Surveill Summ 1992; 41: 25-32. Smaill F. Intrapartum antibiotics for Group B streptococcal colonisation (Cochrane review). The Cochrane Library, 1999: 3. Oxford: Update Software. Schrag SJ, Zywicki S, Farley MM, et al. Group B streptococcal disease in the era of intrapartum antibiotic prophylaxis. N Engl J Med 2000; 342: 15-20. Gilbert GL, Isaacs D, Burgess MA, et al. Prevention of neonatal group B streptococcal sepsis: is routine antenatal screening appropriate. Aust N Z J Obstet Gynaecol 1995; 35: 120-126. Schuchat A. Group B streptococcus. Lancet 1999; 353: 51-56. Rouse DJ, Goldenberg RL, Cliver SP, et al. Strategies for the prevention of early-onset neonatal group B streptococcal sepsis: a decision analysis. Obstet Gynecol 1994; 83: 483-494. Regan JA, Klebanoff MA, Nugent RP, et al, VIP Study Group. Colonization with group B streptococci in pregnancy and adverse outcome. Am J Obstet Gynecol 1996; 174: 1354-1360. Statview 4.1. Berkeley, CA: Abacus, 1994. Garland SM, Kelly N. Early-onset group B streptococcal sepsis: economics of various prevention strategies. Med J Aust 1995; 162: 413-417. Boyer KM, Gadzala CA, Kelly PD, et al. Selective intrapartum chemoprophylaxis of neonatal group B streptococcal early-onset disease. II. Predictive value of prenatal cultures. J Infect Dis 1983; 148: 802-809. Jefferey HE, Lahra MM. Eight-year outcome of universal screening and intrapartum antibiotics for maternal group B streptococcal carriers. Pediatrics 1998; 101: E2. Badri MS, Zawaneh S, Cruz AC, et al. Rectal colonisation with group B streptococcus: relation to vaginal colonisation of pregnant women. J Infect Dis 1977; 135: 308-312. Dillon HC, Gray E, Pass MA, Gray BM. Anorectal and vaginal carriage of group B streptococci during pregnancy. J Infect Dis 1982; 145: 794-799. Prevention of neonatal group B streptococcal sepsis: is routine antenatal screening appropriate? [editorial comment]. Aust N Z J Obstet Gynaecol 1995; 35: 120. Adoption of hospital policies for prevention of perinatal group B streptococcal disease -- United States, 1997. MMWR Morb Mortal Wkly Rep 1998; 47: 665-670. (Received 10 Nov 1999, accepted 14 Feb 2000) Authors' details Monash Medical Centre, Melbourne, VIC. Mary Connellan, RM, MPH, Midwife, Women's Health Program, Southern Healthcare Network; Euan M Wallace, MD, FRACOG, Senior Lecturer, Department of Obstetrics and Gynaecology, Monash University. Reprints: Dr E M Wallace, Department of Obstetrics and Gynaecology, Monash University, Monash Medical Centre, 246 Clayton Road, Clayton, VIC 3168. euan.wallaceATmed.monash.edu.au Make a comment 1: Characteristics of screening for group B streptococcus in 20 hospitals with a unified screening protocol Number of hospitalsYears since screening protocol introduced < 28 (40%) 2-55 (25%) > 5-91 (5%) > 92 (10%) Not known4 (20%) Form of screening Low vaginal swab only15 (75%) High vaginal swab only4 (20%) Low vaginal swab and anal swab1 (5%) Frequency per pregnancy Once only19 (95%) More than once1 (5%)Timing < 30 weeks' gestation12 (60%) 30-34 weeks' gestation7 (35%) Unknown1 (5%)**The hospital that screened more than once did not specify gestations. Back to text 2: Criteria for intrapartum administration of antibiotics in 64 hospitals in Victoria CriteriaNumber of hospitals usingClinical signs of intrapartum infection51 (80%)Pre-labour rupture of membranes43 (67%) < 6h4 (6%) 6-12h0 > 12-18h10 (16%) > 18-24h4 (6%) > 24h21 (33%) Doctor-dependent4 (6%)Previous GBS-affected baby30 (47%)GBS-positive vaginal swab in previous pregnancy22 (34%)Preterm labour10 (16%) Gestation < 37 weeks7 (11%) Gestation < 34 weeks2 (3%) Gestation < 32 weeks1 (2%)GBS=Group B streptococcus. Back to text 3: Key risk factors for early-onset neonatal group B streptococcal disease (EOGBSD) Preterm delivery (< 37 weeks' gestation) Prolonged rupture of membranes (> 18h) Previous infant with EOGBSD GBS bacteriuria during pregnancy Intrapartum maternal pyrexia Back to text

Mary Connellan · Euan M Wallace

Editorial Routine antenatal screening: a need to evaluate Australian practice Are current screening practices evidence-based and cost effective? MJA 2000; 172: 311-312 Screening is defined as a procedure to identify, in an organised way, a specified disease or condition among asymptomatic individuals.1 Before introducing a screening test into pregnancy care, it is imperative that the following criteria be met: there is detailed knowledge of the effect of the condition on both the pregnant mother and her fetus; a highly accurate and specific diagnostic test is readily available to make the definitive diagnosis; the condition is a significant health problem; the test and any actions based on its results are ethically acceptable to the community; and increasingly important in the current climate of restricted healthcare funding, the economic implications of either performing or not performing the test have been evaluated. As in many areas of medical practice, various screening tests have been introduced into obstetric practice without being evaluated according to these criteria, while others which might satisfy the criteria are not widely used. Antenatal screening tests currently recommended by the Royal Australian and New Zealand College of Obstetricians and Gynaecologists (RANZCOG) are shown in the Box. In 1997, I surveyed use of a selection of these tests at the 11 hospitals then belonging to Women's Hospitals Australia (an Australian and New Zealand organisation which represents major women's hospitals; almost a quarter of Australian babies are cared for in member hospitals). This survey revealed that, although all 11 hospitals routinely undertook a blood group and antibody screen, full blood count, tests for rubella antibody status and syphilis serology, and a second-trimester ultrasound examination, use of other tests was more variable. Tests for hepatitis B serology were routine at nine hospitals, urine microscopy and culture at four, measurement of serum α-fetoprotein level at two, and the triple test for Down's syndrome at one. The survey also revealed considerable variation in screening for gestational diabetes: six of the 11 hospitals screened all women, while the others selectively screened women with perceived risk factors (eg, maternal age over 30 years, family history of diabetes, poor obstetric history, maternal obesity, and ethnic group with high prevalence of diabetes). The RANZCOG does not recommend routine screening of all pregnant women for gestational diabetes, contrary to the guidelines of the Australasian Diabetes in Pregnancy Society.3 The place of screening for gestational diabetes and the criteria for its diagnosis are the subject of an international, multicentre project funded by the National Institutes of Health (US) -- HAPO (Hyperglycemia and Adverse Pregnancy Outcome). This should be completed in four years. The low rate of screening for asymptomatic bacteriuria (also not recommended as a routine test by the RANZCOG2) is at variance with the recommendations of Rouse based on his analysis of published studies.4 He reported that, of the 2%-10% of pregnant women who have asymptomatic bacteriuria, 30% will develop acute and potentially serious infections. He concluded that screening and treatment prevents symptomatic infection and is cost effective. Screening later in pregnancy for maternal carriage of group B streptococci (GBS) is also controversial. In this issue of the Journal, Connellan and Wallace describe the variation in GBS screening practices in Victoria.5 They recommend development of consensus practice guidelines to help prevent early-onset GBS disease in neonates (EOGBSD). Such guidelines have been developed in Queensland after a systematic review of the literature and a large Brisbane case-controlled study.6 The recommended strategy is not to perform routine antenatal screening but to consider administering intrapartum antibiotics for defined risk factors (preterm birth before 35 weeks' gestation; membranes ruptured for > 18 hours before delivery; maternal temperature ≥ 38ºC; GBS colonisation or GBS bacteriuria ever detected; or previous infant with EOGBSD) (Professor James King, Mater Perinatal Epidemiology Unit, Mater Misericordiae Mothers' Hospital, Brisbane, Qld, personal communication). The implementation of these evidence-based clinical guidelines is now being evaluated. This process could serve as a template for the evaluation and development of guidelines for all antenatal screening tests. Routine screening for HIV is now recommended by the RANZCOG,2 but most units do not comply with this directive -- in 1995, only 20% of pregnant women were so screened.7 The need to revise current policies, especially as antiretroviral drug therapy can reduce the risk of HIV transmission from mother to child from 30% to below 2%,8 was recently reviewed by Ziegler.9 In addition, calls for routine screening of thyroid function have followed publication of a study that found long-term developmental abnormalities in the offspring of women with even mild degrees of untreated hypothyroidism.10 The prevalence of undiagnosed hypothyroidism was 1.9 per 1000, and the offspring had a mean score on the Wechsler Intelligence Scale for Children four points lower than matched control children. To identify each at-risk fetus, 500 pregnant women would need to be tested. Again, this emphasises the pressing need for full analysis of the clinical and economic implications of such tests before they enter clinical practice. Australia is not alone in the variation in screening practice. In a recent survey of obstetric centres in the United Kingdom, only 24% of births occurred in units with a universal testing policy for hepatitis B.11 Conversely, universal screening for syphilis was the norm, although a number of centres were considering dropping this policy.11 There is a paucity of accurate data on the cost of current antenatal screening practices to the Australian community. However, the economic impact is sure to be substantial. In 1997, 252 370 women gave birth in Australia.12 If the RANZCOG screening recommendations were followed for all, then, based on the Medicare schedule fee structure, the annual cost would be around $48 million for routine haematological, serological, biochemical and cytological screening, and an additional $17 million for the triple test and hepatitis C serology. Furthermore, in 1996-1997, Medicare benefits in excess of $33 million were paid for ultrasound examinations in pregnancy.13 Yates et al estimated in 1991 and 1992 that 97% of pregnant women had at least one ultrasound scan, and that 46% had two or more.14 It is not possible to calculate the cost of "routine screening" scans from these data. However, if all pregnant women have a second-trimester scan, the cost to Medicare is $25.5 million annually, with the cost to the community likely to be higher, as many scans are billed at rates above the Medicare schedule fee. The introduction of first-trimester ultrasound scans of nuchal translucency, which identify up to 85% of fetuses with Down's syndrome15 and, potentially, fetuses with an increased risk of other structural abnormalities, including cardiac defects, will inevitably increase the number of routine ultrasound examinations. However, as these scans also identify fetuses with a low probability of Down's syndrome, they have the potential to reduce the numbers of chorionic villus samplings and amniocenteses performed in women with a high theoretical risk of trisomy 21. In addition, improvements in ultrasound resolution and our understanding of the markers of fetal anomalies may allow this late first-trimester scan to replace the second-trimester scan. Although antenatal screening appears well accepted as a significant healthcare issue in Australia, it has not been subject to systematic assessment. The need for funding to critically evaluate all currently used tests seems self-evident. However, currently such funding has not been granted by the Commonwealth or State governments or Medicare, who carry the major financial burden for antenatal testing. The potential to redirect some of the healthcare dollar to other, needier areas is a further reason for appropriate funding to establish practitioner-credible, evidence-based practice. Jeremy J N Oats Director of Obstetrics and Gynaecology, Mater Misericordiae Mothers' Hospital, Clinical Professor of Obstetrics and Gynaecology University of Queensland, Brisbane, QLD joatsATmater.org.au Reprints: Professor J N Oats, Department of Obstetrics and Gynaecology, Mater Misericordiae Mothers' Hospital, Raymond Terrace, South Brisbane, QLD 4101. Peters TJ, Wildschut HIJ, Weiner CP. Epidemiologic considerations in screening. In: Wildschut HIJ, Weiner CP, Peters TJ, editors. When to screen in obstetrics and gynecology. London: WB Saunders, 1996: 1. Royal Australian and New Zealand College of Obstetricians and Gynaecologists Statements. 2.2. Screening in pregnancy. <http://www.ranzcog.edu.au/open/ statements/2_2.htm> Hoffman L, Nolan C, Wilson JD, et al. Gestational diabetes mellitus -- management guidelines. The Australian Diabetes in Pregnancy Society. Med J Aust 1998; 169: 93-97. Rouse DJ. Asymptomatic bacteriuria in pregnancy. In: Wildschut HIJ, Weiner CP, Peters TJ, editors. When to screen in obstetrics and gynecology. London: WB Saunders, 1996: 163-169. Connellan M, Wallace EM. Prevention of perinatal group B streptococcal disease: screening practice in public hospitals in Victoria. Med J Aust 2000; 172: 317-320. Flenady V, King J, Woodgate P, et al. Early onset neonatal GBS sepsis: a case controlled study. Proceedings of the 2nd Annual Congress of the Perinatal Society of Australia and New Zealand. Alice Springs, NT. 29 Mar-1 Apr 1998. Sydney: PSANZ, 1998. Elford J, MacDonald MA, Gabb RG, et al. Antenatal HIV antibody screening in Australia. Med J Aust 1995; 163: 183-185. Riley LE, Greene MF. Elective cesarean delivery to reduce the transmission of HIV. N Engl J Med 1999; 340: 1032-1033. Ziegler JB. Antenatal screening for HIV in Australia: time to revise policies? Med J Aust 1999; 171: 201-203. Haddow JE, Palomaki GE, Allan WC, et al. Maternal thyroid deficiency during pregnancy and subsequent neuropsychological development of the child. N Engl J Med 1999; 341: 549-555. Newell M-L, Thorne C, Pembrey L, et al. Antenatal screening for hepatitis B infection and syphilis in the UK. Br J Obstet Gynaecol 1999; 106: 66-71. Day P, Sullivan EA, Ford J, et al. Australia's mothers and babies 1997. Perinatal Statistics Series No 9. Sydney: Australian Institute of Health and Welfare National Perinatal Statistics Unit 1999; 7. (AIHW Cat No PER 12.) Simes J. Diagnostic ultrasound: discussion paper. Presented at the Forum on Ultrasound. Sydney; 13-14 June 1998. Canberra: Australian Health Technology Advisory Committee, 1998: 41. Yates JM, Lumley J, Bell RJ. The prevalence and timing of obstetric ultrasound in Victoria 1991-1992: a population-based study. Aust N Z J Obstet Gynaecol 1995; 35: 375-379. Hyett JA, Perdu M, Sharland GK, et al. Increased nuchal translucency at 10-14 weeks of gestation as a marker for major cardiac defects. Ultrasound Obstet Gynecol 1997; 10: 242-246. Make a comment Current recommendations on antenatal screening by the Royal Australian and New Zealand College of Obstetricians and Gynaecologists2 At the first antenatal visit, tests should be offered for: blood group and antibody screen; full blood count; rubella antibody status; syphilis serology; hepatitis B serology hepatitis C serology (if significant risk); HIV serology; and cervical cytology. In addition, the doctor should discuss: the availability of maternal serum screening for Down's syndrome ultrasound examination at 18-20 weeks' gestation Back to text

Viewpoint Medicine for the millennium: the challenge of postmodernism Jonathan J Chan and Julienne E Chan MJA 2000; 172: 332-334 Abstract - Postmodernism - Evidence-based medicine - Clinical pathways and diagnosis-related groups - The future - Acknowledgements - References - Authors' details - - More articles on General medicine Abstract As the new millennium dawns, Australian society is becoming more postmodern, whereas the medical system remains increasingly modernist in its outlook. In this article, we discuss the emerging prevalence of postmodernism and examine current medical education and practice strategies, such as evidence-based medicine, from a postmodern perspective. We argue that if medicine does not respond to the ideas of postmodernism, which challenges the concepts of truth and our ability to be objective, it may become increasingly irrelevant to the needs of a changing society. Examining the state of medicine in a postmodern world is important to a profession increasingly reliant on science and technology within a society increasingly distrustful of such a modernist approach. Does medicine run the risk of becoming outmoded in the face of the postmodern expectations of its patients? Postmodernism This amorphous thing [postmodernism] remains ghostly -- and for some, ghastly -- for the simple reason that the debate around the postmodern has never properly been engaged. Thomas Docherty1 Asking the question "what is postmodernism?" is a (post)modern-day equivalent of trying to capture Proteus, "for the concept is not merely contested, it is also internally conflicted and contradictory . . . Postmodernism is not something we can settle once and for all and then use with a clear conscience".2 The term "postmodernism" itself inevitably leads us back to modernism -- whether it be to replace it, reject it, re-evaluate it or revitalise it. Modernism can, in short, be characterised by belief in the existence of truth, objectivity, determinacy, causality and impartial observation.3 It has been described as "a search for an underlying and unifying truth and certainty, a search for a definitive discourse that makes the world and self coherent, meaningful and masterable".4 Modernism thus seeks to capture, define, understand and control knowledge. To return to postmodernism, definitions abound. It has been variously described as an epoch or historical period;1 a theoretical and representational mood, a cultural epoch and an aesthetic practice;5 a sensibility;6 a consciousness, the cultural logic of late capitalism and the crystallisation of previously independent developments;2 a number of related tendencies, values, procedures and attitudes;7 and the general condition of contemporary Western civilisation.8 These definitions are equally valid, inclusive, exclusive, overlapping, complementary and contradictory. For example, in contrast to descriptions of postmodernism as a historical period, or a consciousness, Bauman argues that the notion of historical succession is an illusion, and that the postmodern era is a philosophical and sociological re-evaluation of modernity.9 Jameson goes further, to suggest the disappearance of a sense of history in favour of perpetual change in a perpetual present.10 While these definitions encompass the historical, the aesthetic, the philosophical, the sociocultural, and the politico-economic, Lyotard has described postmodernism as "also, or first of all, a question of expressions of thought".11 From this perspective, one view of postmodernism is that it is the third stage in the evolution of Western conceptions of knowledge, society and culture. The premodern, or classical, era was based on the spiritual and the mythological, and can be summarised by Anselm's credo "I believe so that I might understand".12 The gods (and later God), not humanity, were the centre of the universe. The modern age of the Enlightenment saw a radical change in perspective as humanity, empowered by science and reason, took centre stage. Descartes' axiom "I think, therefore I am" resounded12 as humankind grabbed the keys and set about unlocking the doors, discovering what lay behind them, and determining the boundaries of knowledge. As humanity's glorious hopes for self-determined science, progress and freedom waned, disappointment and disillusion set in. At the turn of the century, the prospect of the new age of technology heralded hopes for a better world, free of disease and social inequality. Yet, at the dawning of a new millennium, the fact that these promises have not been fulfilled has led to increasing doubt about the ability of science to heal and liberate. Although science has generally improved human health and comfort, scientific advances, such as the prolongation of human life, have resulted in a plethora of other problems which medicine and science have difficulty addressing. The widespread use of unconventional therapies in chronic illnesses such as cancer13 and arthritis14 shows that patients are seeking treatment which conventional scientific medicine cannot provide. Bauman has suggested that Wittgenstein's description of understanding as "knowing how to go on"9 encapsulates this current era. The evolution from believing to knowing the facts leaves us at a point of knowing from experience, with the credo "I experience, therefore I try to make sense". In line with a move away from the overarching themes and theories of the Enlightenment, Lyotard has suggested that postmodernism can be simplified to a disbelief in métarécits, or philosophical metanarratives, such as "Science"and "Truth", in favour of the petit récit, the small narrative based on lived lives, the diverse, the complex and the unique.8 Such an approach acknowledges individuality, complexity and the subjectivity of personal experience. The postmodernist paradigm cannot accept that all things may be understood and mastered through science. The validity of intuition and experience is considered equal to that of traditional methods of observation, induction and experimentation. If society believes that the rational, objective truths and certainties of science and medicine are not as true and not as certain as they once may have seemed, where does that leave a practice of medicine which continues to base itself on a modernist approach? Medicine is resolutely progressing down a path of innate modernity. We discuss two aspects of this trend: evidence-based medicine and clinical pathways. Evidence-based medicine is modernist medicine He's the best physician that knows the worthlessness of most medicines. Benjamin Franklin15 Much has already been written about the benefits and caveats of evidence-based medicine (EBM). EBM considers patient management based on available data and medical literature as conceptually vital and important for best care. Since its inception in the early 1990s, EBM has had widespread impact on the teaching and practice of medicine. A postmodernist would regard EBM and the value it places on what is considered to be "current knowledge" as a modernist concept. A postmodernist would question whether current science and technology have the ability to give us the "evidence" vital to the practice of EBM. Thus, EBM is very likely flawed given that "the evidence is based only on our current value systems, which can dramatically alter with new advances in our understanding of nature".16 Proponents of EBM would argue that the constant search for current data would ensure that the practice of medicine is kept abreast of whatever new trends may occur. However, another disturbing consequence of EBM is not only the quest for the right sort of data, but also the essence of the data itself. EBM journals are edited by combinations of physicians, epidemiologists and other experts, who determine the importance of the research. Currently, 98% of articles reviewed are rejected.17 Already, there is a worrying trend that only well-funded, large, multicentre trials are published in first-rank, high-impact-factor journals. Many recent advances in clinical care have been determined from pharmaceutical trials. How do paradigm shifts occur when the motivation for research is biased, not towards "best evidence", but rather to that which would guarantee high-profile publication or sufficient pharmaceutical sales? The recent furore over a high-profile researcher who was not allowed to publish her findings because they contradicted claims about the therapeutic efficacy of the products of her pharmaceutical funding body is an example of how research is increasingly driven by profit.18 In addition, examination of medical literature shows a paucity of articles which report negative findings or use qualitative research methods. Surely the determination of "best evidence" requires consideration of such data? The question is therefore, not "what is 'best evidence'", but "how is 'best evidence' determined" and "is it really the 'best' evidence"? Most physicians would argue that the practice of medicine is an art -- an ill-defined combination of experience and judicious use of knowledge. EBM teaching emphasises "knowledge" -- learning the "facts" and knowing the "literature". Sackett et al recognised this in their own exhortations that EBM is not "cookbook medicine", and that the "external clinical evidence can inform but not replace individual clinical expertise and it is this expertise that decides whether the external evidence applies to the individual patient at all".19 However, in teaching EBM to medical students, there is a danger of "dumbing-down" medicine to the lowest common denominator of understanding facts and applying treatment algorithms without applying Sackett's caveats. The emphasis placed on acquiring medical knowledge may produce practitioners who have no understanding of the uniqueness of each patient. Clinical pathways and diagnosis-related groups are modernist ideals I am truly horrified by the modern man. Such absence of feeling, such narrowness of outlook, such lack of passion and information, such feebleness of thought. Alexander Herzen20 One of the major arguments against modernism and its advances is the dehumanisation of society. From a postmodernist view, the individual is now a faceless number in the databank of society. Technological advancement and efficiency "ha[ve] left people feeling disconnected with one another".12 Campion, in an editorial on "Unconventional medicine",21 posits that, "though Americans want all that modern medicine can deliver, they also fear it. They may resent the way that visits to physicians quickly lead to pills, tests, and technology . . . [they] also may seek out unconventional healers because they think their problems will be taken more seriously". In an effort to rationalise the growing health budget, Australian health providers are now determining costs through funding by classification of diseases through diagnosis-related groups (DRGs) and clinical pathways. The benefits are obvious: greater efficiency in treatment has meant reduction of hospital waiting lists, reduced hospital stays and reduction of costs. The downside is the dehumanisation feared by the postmodernist. Proponents of the system argue that the benefits of more people being treated outweigh the apparent loss of identity. Yet, the outcome of this method of medicine is far more sinister than it seems. The loss of identity and the classification of admissions as DRGs have resulted in a health system which encourages medical practitioners to focus only on disease and to fail to understand the individuality and uniqueness of each patient. The fact is that DRGs and clinical pathways are preparing a future generation of medical practitioners who will be very specialised in treating patients according to such pathways, but little prepared for significant deviations from them. Clinicians are becoming very adept at procedures and skills determined by diseases and not by the individual patient's signs and symptoms. The future There is an ominous cloud in the distance though at present it be no bigger than a man's hand. Arthur Stanley Eddington22 Medicine is continually changing. It came into existence with the Enlightenment and gained scientific maturity in the modernist age. Yet, the current foundation of medical knowledge (EBM) and its essence of practice (DRGs, clinical pathways) are significant constraints which will inhibit its ability to change with the times. In effect, medicine is becoming a modernist phenomenon which can neither progress nor provide the necessary service to a society which is increasingly postmodernist. In the past, there were fewer alternatives to medical practice. Nowadays, the needs of society are met by allied health professionals, naturopaths and other, similar therapists. The role of the medical practitioner is already changing. Doctors are now "healthcare providers" who administer "health services". Patients are now "clients". It is likely that the medicine we know will become just one part of a holistic health service which includes other practitioners currently regarded as "alternative". Producing medical practitioners who know only clinical pathways and DRGs further widens the gap between the modernist model of dehumanised science (the grand narrative) and the postmodernist model of unique, lived experience (the small narrative). Unless the practice of medicine becomes more focused on the unique individual, with understanding of the limitations of the modern science of medicine, our role runs the risk of becoming less relevant to people today. Acknowledgements Jonathan Chan was supported by the Janssen-Cilag Dermatology Research Fellowship of the Australasian College of Dermatologists and the Amy and Athelstan Saw Postgraduate Research Fellowship of the University of Western Australia. Julienne Chan was supported by an Australian Postgraduate Research Award. References Docherty T. Postmodernism: an introduction. In: Docherty T, editor. Postmodernism: a reader. New York: Harvester Wheatsheaf, 1993: 1-31. Jameson F. Postmodernism, or the cultural logic of late capitalism. London: Verso, 1991. Rosenau P. Post-modernism and the social sciences: Insights, inroads and intrusions. Princeton, New Jersey: Princeton University Press, 1992. Usher R, Bryant I, Johnston R. Adult education and the postmodern challenge: learning beyond the limits. London: Routledge, 1997. Waugh P, editor. Postmodernism: a reader. London: Edward Arnold, 1992. Laclau E. Politics and the limits of modernity. In: Docherty T, editor. Postmodernism: a reader. New York: Harvester Wheatsheaf, 1993: 329-343. Hassan I. Toward a concept of postmodernism. In: Docherty T, editor. Postmodernism: a reader. New York: Harvester Wheatsheaf, 1993: 146-156. Lyotard J-F. The postmodern condition: a report on knowledge. Bennington G, Massumi B, translators. Manchester: Manchester University Press, 1984. Bauman Z. Philosophical affinities of postmodern sociology. Sociological Rev 1990; 38: 411-444. Jameson F. The cultural turn: selected writing on the postmodern, 1983-1993. London: Verso, 1998. Lyotard J-F. Note on the meaning of "post-". In: Docherty T, editor. Postmodernism: a reader. New York: Harvester Wheatsheaf, 1993: 47-50. Utley D. Communicating truth in the post-modern world. Luke's Journal 1998; 3: 8-9. Group CO. New Zealand cancer patients and alternative medicine. N Z Med J 1987; 100: 110-113. Cronan TA, Kaplan RM, Possner I, et al. Prevalence of the use of unconventional remedies for arthritis in a metropolitan community. Arthritis Rheum 1989; 32: 1604-1607. Franklin B. Poor Richard, 1733. In: Labaree LW, editor. The papers of Benjamin Franklin. Vol. 1. January 1706 through December 1734. New Haven: Yale University Press, 1959: 316. Raithatha N. Postmodern philosophy offers a more appropriate system for medicine [letter]. BMJ 1997; 314: 1044. Sackett DL, Richardson WS, Rosenberg W, Haynes RB. Evidence-based medicine. How to practice and teach EBM. Edinburgh: Churchill Livingstone, 1997. Ivinson AJ. A duty to publish. Nature Med 1998; 4: 1089. Sackett DL, Rosenberg WMC, Gray JAM, et al. Evidence based medicine: what it is and what it isn't. BMJ 1996; 312: 71-72. Herzen A. Epilogue 1849. In: From the other shore. Budberg M, translator. Oxford: Oxford University Press, 1979: 145. Campion EW. Why unconventional medicine? N Engl J Med 1993; 328: 282-283. Eddington A. New pathways in science. London: Cambridge University Press, 1935: 163. Authors' details Royal Perth Hospital, Wellington Street, Perth, WA. Jonathan J Chan, MB BS, Dermatology Registrar. University of Western Australia, Nedlands, WA. Julienne E Chan, BA(Hons), PGDipEd, Postgraduate Scholar. Reprints will not be available from the authors. Correspondence: Dr J J Chan, Department of Medicine, University of Western Australia, 4th Floor G Block, QEII Medical Centre, Verdun Street, Nedlands, WA 6009. jjchanATcyllene.uwa.edu.au Make a comment

Jonathan J Chan · Julienne E Chan

Clinical Update Genetic testing for Alzheimer's disease Peter K Panegyres, Jack Goldblatt, Ian Walpole, Carmela Connor, Toni Liebeck and Karen Harrop MJA 2000; 172: 339-343 Abstract - Recommendations for gene testing in Alzheimer's disease - Conclusions - Acknowledgements - References - Authors' details - - More articles on Genetics Abstract Genetic factors are important in the development of Alzheimer's disease (AD). Familial AD can result from rare mutations in some genes. Other genes, such as the apolipoprotein E gene (APOE), operate as risk factors for late-onset sporadic AD. On a background of advances in the genetics of AD we suggest a way in which genetic information may be used in the diagnosis of AD. If there is a positive family history of early-onset dementia and the clinical features suggest AD, patients may be tested for presenilin and amyloid precursor protein gene mutations with appropriate pretest and post-test counselling. Predictive testing should be performed under guidelines developed by the World Federation of Neurology and the Human Genetics Society of Australasia. The usefulness of APOE genotyping as an adjunct to conventional diagnostic tests is unknown; data suggest it has low sensitivity and specificity and may have little predictive value in an individual patient. APOE genotyping should not be performed in asymptomatic individuals, except as part of an ethically approved research project; this recommendation is supported by a number of international consensus statements. APOE testing should not be used as a diagnostic test without adequate pretest and post-test counselling, education and support. APOE testing should not be used as a sole diagnostic test in the work-up of patients with AD. Genetic risk factors other than APOE require validation and should not be used routinely, except as part of an ethically approved research protocol. Alzheimer's disease (AD) is one of the major healthcare problems facing First World countries. In 1995, 130 000 Australians aged over 65 years had moderate to severe dementia, and by 2041 the number of people with dementia in Australia is expected to increase by 254%.1 In recent years there have been major advances in the elucidation of genetic factors in both familial and sporadic AD. Unfortunately, the accumulation of this genetic information has outpaced understanding among the medical and genetic communities of the most appropriate way it can be used clinically. This has led to diagnostic kits for DNA markers having to be withdrawn because of misuse in counselling individuals about future risks.2 Consumer-led demand for diagnostic tests and pressure from companies that make them raise major ethical considerations about the role of genetic testing in managing families at possible risk. These developments have encouraged us to develop evidence-based recommendations on the use of molecular genetic testing in Alzheimer's disease. Background information on the genetics of Alzheimer's disease is provided in Box 1. Recommendations for gene testing in Alzheimer's disease Diagnosis of dementia The diagnosis of AD requires assessment by a clinician skilled in diagnosing dementia, using the criteria established by the National Institute of Neurological and Communicative Disorders and Stroke - Alzheimer's Disease and Related Disorders Association (NINCDS-ADRDA),4 shown in Box 2. The diagnosis can sometimes be difficult, and expertise is required to distinguish AD clinically from other disorders such as frontotemporal atrophy and prion diseases, especially in younger patients. The diagnostic work-up of the patients is best performed in a facility with counselling and support staff to help patient and carer cope with the diagnosis of dementia. Collaboration with a neuropathology laboratory can enhance such a service by providing postmortem confirmation of the diagnosis. Education, counselling, support A multidisciplinary team, including a neurologist or specialist physician, neuropsychologists, social workers, allied health workers (occupational therapists, speech therapists), all working together with the patient's general practitioner, helps patients and their carers understand the diagnosis of AD and its implications. Contact with a caring, multidisciplinary team can support the patient, carer, and family in crises such as the development of intercurrent medical problems requiring hospitalisation and respite for patient or carer. Such a team can advise the patient, carer and family on the suitability and appropriateness of genetic testing. Genetic testing If genetic testing is considered then the staff of the multidisciplinary team must know the implications, risks and limitations of the proposed tests and counsel patients, carers and families accordingly. They must have the expertise to counsel patients, carers and families about psychosocial implications, confidentiality, and issues related to employment and insurability, of the genetic tests requested. Accredited laboratory and DNA result disclosure The laboratory that tests the DNA specimen must be accredited by the National Association of Testing Authorities, Australia, which advises on specimen handling, the maintenance of strict confidentiality, and good laboratory practice (Box 3). The DNA result should be given to the clinician who requested the test, who will disclose the result to the patients and carer in strictest confidence with the help of counsellors. As has been shown with Huntington's disease,34 follow-up by counsellors will help to decrease adverse reactions such as suicide, attempted suicide and psychiatric hospitalisation. Familial early-onset AD If there is a positive family history of early-onset dementia, and pedigree analysis suggests autosomal dominant AD, the patient and family should be referred to a clinician with an interest in familial dementia for confirmation of the diagnosis. The patient and family should then be managed by a multidisciplinary team of experts in genetic neurodegenerative disorders (such as Huntington's disease) and predictive gene testing. Genetic testing should only be offered in a comprehensive, structured, clinico-laboratory program where mutations in PS1, PS2 and APP would be sought in affected individuals. Gene testing is not recommended for sporadic cases of early-onset AD without a definite family history. Predictive testing in unaffected and asymptomatic individuals from families in which causative mutations have been discovered must follow guidelines as developed for Huntington's disease.5-8 Only about 6% of patients at risk of Huntington's disease request the gene test, probably because many at-risk people decide against the test once they receive full information of its implications.35 The likelihood of suicide, attempted suicide or psychiatric hospitalisation after predictive testing is no greater than in the general population with symptomatic Huntington's disease, and this is probably the result of good counselling and support.34 Similar considerations may apply to AD. Like Huntington's disease, AD is an incurable condition with devastating consequences, and there are ethical issues (such as patients not wanting to know, and implications for employment and insurability) relating to predictive gene testing in such situations. These ethical issues probably contribute to the low uptake of testing for Huntington's disease and will probably be relevant to AD also. Other dilemmas in predictive testing for AD relate to performing tests in individuals with 25% risk when an unaffected or undiagnosed parent does not request a gene test; a positive result in such individuals would result in an unwanted gene result for the parent. This represents a difficult situation for predictive gene testing programs. Similar problems arise in twins if only one wants to be tested. For ethical reasons, as in Hungtington's disease, children should not be tested for AD. DNA banking should be considered for individuals with a family history of AD who may not want a test at present, or who may not have any of the recognised mutations -- future testing could be carried out if other mutations are recognised. Sporadic AD In patients with the clinical diagnosis of sporadic AD, gene testing for APOE ε4 status or other genetic factors is not recommended. The clinical usefulness of these tests has not been established, and there is no evidence that they improve the sensitivity and specificity of the clinical diagnosis of AD sufficiently to alter the standard diagnostic work-up of these patients. The APOE ε4 genotype should never be used as a sole diagnostic test for the diagnosis of AD. Conclusions Our recommendations are summarised in Box 4. Acknowledgements A National Health and Medical Research Council fellowship awarded to Dr Panegyres supported this work. References Henderson AS, Jorm AF. Dementia in Australia. Aged and Community Care Service Development and Evaluation Report No. 35. Canberra: AGPS, 1998. Lehrman S. Genetic testing for Alzheimer's disease "not appropriate". Nature 1997; 389: 898. Tanzi RE, Kovacs DM, Kim T-W, et al. The gene defects responsible for familial Alzheimer's disease. Neurobiol Dis 1996; 3: 159-168. McKhann G, Drachman DD, Folstein M, et al. Clinical diagnosis of Alzheimer's disease: report of the NINCDS-ADRDA Work Group under the auspices of the Department of Health and Human Services Task Force in Alzheimer's disease. Neurology 1984; 34: 939-944. World Federation of Neurology: Research Committee. Research Group on Huntington's Chorea. Ethical issues policy statement on Huntington's disease molecular genetics predictive test. J Neurol Sci 1989; 94: 327-332. Went L. Ethical issues policy statement on Huntington's disease molecular genetics predictive test. International Huntington Association. World Federation of Neurology. J Med Genet 1990; 27: 34-38. Guidelines for the molecular genetics predictive test in Huntington's disease. International Huntington Association (IHA) and the World Federation of Neurology (WFN) Research Group on Huntington's Chorea. Neurology 1994; 44: 1533-1536. Walpole I, Bankier A, Blackwell J, et al. Guidelines for DNA predictive testing. Bull Hum Genet Soc Austral 1998; 11: 10-14. Goate AM, Chartier-Harlin MC, Mullan MC, et al. Segregation of a missense mutation in the amyloid precursor protein gene with familial Alzheimer's disease. Nature 1991; 349: 704-706. Blacker D, Tanzi RE. The genetics of Alzheimer disease. Arch Neurol 1998; 55: 294-296. Levy-Lehad E, Wasco W, Podrkaj P, et al. Candidate gene for the chromosome 1 familial Alzheimer disease locus. Science 1995; 269: 973-977. Saunders AM, Strittmatter WJ, Schmechel D, et al. Association of apolipoprotein E allele epsilon 4 with late-onset familial and sporadic Alzheimer's disease. Neurology 1993; 43: 1467-1472. Strittmatter WJ, Saunders AM, Schmechel D, et al. Apolipoprotein E: high-avidity binding to beta-amyloid and increased frequency of type 4 allele in late-onset familial Alzheimer disease. Proc Natl Acad Sci USA 1993; 90: 1977-1993. Gomez-Isla T, West HL, Rebeck GW, et al. Clinical and pathological correlates of apolipoprotein E ε4 in Alzheimer's disease. Ann Neurol 1996; 39: 62-70. Jonker C, Schmand B, Lindeboom J, et al. Association between apolipoprotein E ε4 and the rate of cognitive decline in community-dwelling elderly individuals with and without dementia. Arch Neurol 1998; 55: 1065-1069. Hyman BT, Gomez-Isla T, Briggs M, et al. Apolipoprotein E and cognitive change in an elderly population. Ann Neurol 1996; 40: 55-66. Mayeux R, Saunders AM, Shea S, et al. Utility of the apolipoprotein E genotype in the diagnosis of Alzheimer's disease. N Engl J Med 1998; 338: 506-511. McConnell LM, Sanders GD, Owens DK. Evaluation of genetic tests: APOE genotyping for the diagnosis of Alzheimer's disease. Genet Test 1999; 3: 47-53. American College of Medical Genetics and American Society of Human Genetics Working Group on APOE and Alzheimer Disease. Statement on use of apolipoprotein E testing for Alzheimer disease. JAMA 1995; 274: 1627-1629. McConnell LM, Koenig BA, Greely HT, Raffin TA, and Alzheimer Disease Working Group of the Stanford Programme in Genomics, Ethics and Society. Genetic testing and Alzheimer disease: Has the time come? Nature Medicine 1998; 4: 757-759. National Institute on Aging and Alzheimer's Association Working Group. Apolipoprotein E genotyping in Alzheimer's disease. Lancet 1996; 347: 1091-1095. Post SG, Whitehouse PJ, Binstock RH, et al. The clinical introduction of genetic testing for Alzheimer disease. JAMA 1997; 277: 832-836. Relkin NR, Kwon YJ, Tsai J, Gandy S. The National Institute on Aging/ Alzheimer's Association recommendations on the application of apolipoprotein E genotyping to Alzheimer's disease. Ann NY Acad Sci 1996; 802: 149-171. Jobst KA, Hindley NJ, King E, Smith AD. The diagnosis of Alzheimer's disease: a question of image? J Clin Psychiatry 1994; 55 Suppl: S22-S31. Spinnler H, Della Sala S. The role of clinical neuropsychology in the neurological diagnosis of Alzheimer's disease. J Neurol 1988; 235: 258-271. Zakzanis KK. Quantitative evidence for neuroanatomic and neuropsychological markers in dementia of the Alzheimer's type. J Clin Exp Neuropsychol 1998; 20: 259-269. Bullido MJ, Artiga MJ, Recuero M, et al. A polymorphism in the regulatory region of APOE associated with risk for Alzheimer's dementia. Nat Genet 1998; 18: 69-71. Blacker D, Wilcox MA, Laird NM, et al. Alpha-2 macroglobulin is genetically associated with Alzheimer disease. Nat Genet 1998; 19: 357-360. Kang DE, Saitoh T, Chen X, et al. Genetic association of the low density lipoprotein receptor-related protein gene (LRP), an apolipoprotein E receptor, with late-onset Alzheimer's disease. Neurology 1997; 49: 56-61. Montoya SE, Aston CE, Dekosky ST, et al. Bleomycin hydrolase is associated with risk of sporadic Alzheimer's disease. Nat Genet 1998; 18: 211-212. Lehmann DJ, Johnston C and Smith AD. Synergy between the genes for butyrylcholinesterase K variant and apolipoprotein E4 in late onset confirmed Alzheimer's disease. Hum Mol Genet 1997; 11: 1933-1936. Panegyres PK, Mamotte CDS, Vasikaran SD, et al. Butyrylcholinesterase K variant and Alzheimer's disease. J Neurol 1999; 246: 369-370. Payami H, Schellenberg GD, Zareparsi S, et al. Evidence for association of HLA-A2 allele with onset age of Alzheimer's disease. Neurology 1997; 49: 512-518. Almqvist EW, Bloch M, Brinkman R, et al. On behalf of an international Huntington disease collaborative group. A worldwide assessment of the frequency of suicide, suicide attempts, or psychiatric hospitalization after predictive testing for Huntington's disease. Am J Hum Genet 1999; 64: 1293-1304. Taylor SD. Demand for predictive genetic testing for Huntington's disease in Australia, 1987 to 1993. Med J Aust 1994; 161: 351-354. (Received 2 Aug 1999, accepted 14 Feb 2000) Authors' details Neurosciences Unit, Health Department of Western Australia, Perth, WA. Peter K Panegyres, PhD, FRACP, Neurologist, and NHMRC Fellow, Department of Neuropathology, Royal Perth Hospital. Carmela Connor, MPsychol, Senior Clinical Psychologist. Toni Liebeck, BSW, Senior Social Worker. Genetic Services of WA, King Edward Memorial Hospital for Women, Perth, WA. Jack Goldblatt, MD, FRACP, Director. Ian Walpole, MB BS, FRACP, Consultant Geneticist. Karen Harrop, BSc, Genetic Counsellor. Reprints: Dr P K Panegyres, Department of Neuropathology, Royal Perth Hospital, Wellington Street, Perth, WA 6000. peter.panegyresATrph.health.wa.gov.au Make a comment 1: The genetics of Alzheimer's disease Familial early-onset Alzheimer's disease Studies of families in which Alzheimer's disease (AD) was inherited in an autosomal dominant pattern led to the discovery of three pathogenic loci that account for about 50% of all cases of early-onset AD3 (Table). As the condition is heterogeneous, every family with early-onset AD should be offered investigation as part of a coordinated DNA testing program for neurological disease. Mutations in the amyloid precursor protein gene (APP) were the first mutations related to early-onset AD,9 and account for 10%-20% of familial AD.10 Two presenilin genes, PS1 and PS2, are also associated with early-onset familial AD -- almost 50% of cases result from mutations in PS1,10 while mutations in PS2 are rare.11 As reproducibility in PS1 mutation testing has not been established in some laboratories, caution is warranted. Implications for genetic testing: Gene testing for early-onset AD is probably best performed in the context of well-designed, ethically approved research projects involving large families with clear documentation in multiple-affected members who inherited the condition in an autosomal dominant fashion. In some Australian centres, patients with early-onset AD are routinely tested outside of research protocols. As mutations in the presenilin and amyloid precursor protein genes do not account for all cases of early-onset AD, negative screening results for these mutations in an affected individual would not exclude a genetic cause of the disease. Sporadic late-onset Alzheimer's disease APOE: Over 90% of patients with AD have no family history of the condition. One of the more important discoveries in the understanding of these sporadic late-onset cases was that a polymorphism of the apolipoprotein E gene (APOE) was a risk factor (Table).12,13 APOE has three alleles, designated ε2, ε3 and ε4. The ε4 allele is associated with AD in 20%-30% of the general population and in 45%-60% of patients with AD.14 The homozygous genotype, APOE ε4/ε4, is found in 12%-15% of patients with AD, but in only 2%-3% of the general population.14 While not everyone homozygous for APOE ε4 develops dementia, having this genotype might increase the chance of AD developing at an earlier age.15 Approximately 30% of people homozygous for APOE ε4 develop AD.16 The odds ratio for this, based on analysis of 1899 patients aged over 65 years, is 1.37 (versus 0.53 for the APOE ε2 allele).16 In this same study, the age-adjusted odds ratio for incident dementia in individuals homozygous for the ε4 allele was 1.89, and 25% of cognitively normal subjects had at least one ε4 allele. Further, absence of an ε4 allele does not prevent the development of dementia and AD, and 85% of elderly people with the APOE ε4/ε4 genotype did not have evidence of cognitive decline.16 In a pathologically proven series, a single APOE ε4 allele had a sensitivity of 65% and a specificity of 68% for the diagnosis of AD.17 When used with conventional clinical criteria, APOE ε4 testing might increase the diagnostic sensitivity and specificity by 5%-10%; therefore, its role requires further validation.15,17 Implications for genetic testing: APOE ε4 genotyping should not be used in the routine assessment of patients with suspected dementia, as it does not add significant information to other diagnostic investigations such as computed tomography (CT) and neuropsychological assessment.18 If the DNA test is performed it should not be done without adequate pretest counselling as to its limitations and implications, or without adequate post-test psychosocial support. The results need to be stored confidentially in view of the implications for other, unrelated conditions (eg, APOE allele status was used to predict risk in cardiovascular disease long before its significance in AD was known), insurability, employment and psychosocial coping for affected individuals and at-risk families. Thus, APOE genotyping should only be performed as part of a well-structured, ethically approved research study investigating issues about the role of APOE in the pathogenesis of AD. The evidence does not support using APOE e4 genotyping as a predictive test for the development of AD, as the exact significance of an APOE ε4 allele in asymptomatic individuals has not been confirmed.19-23 APOE ε4 genotyping should not be used as a sole diagnostic test for AD. Diagnosis requires specialist referral for investigations, such as a CT scan (which has a 94% positive predictive value24) and neuropsychological tests (85%-90% positive predictive value for the diagnosis of dementia, with less than 5% overlap of neuropsychology scores between patients and controls25,26). A positive APOE ε4 test is not diagnostic of Alzheimer's disease, as a single APOE ε4 allele has a positive predictive value of 65% and a negative predictive value of 68%. The presence of the APOE ε4 allele does not exclude other causes of dementia. For example, a 1998 study showed that about 5% of patients with clinical criteria for the diagnosis of AD were homozygous for APOE ε4, but did not have pathological features of AD.17APOE ε4 diagnostic kits should not be used in the clinical assessment of dementia. (Although such kits were previously available in the United States, they had to be withdrawn because of misuse.2) Other genetic factors: A number of genetic factors in addition to APOE ε4 have been associated with sporadic AD (Table). These include APOE A/T polymorphism in the promoter region,27α2 macroglobulin 5' splice site deletion on exon 18,28 low-density lipoprotein-receptor-related protein,29 the G/G homozygous state of the bleomycin hydrolase gene,30 butyrylcholinesterase K variant,31,32 and the major histocompatibility A2 antigen.33 The contribution of these factors to the diagnosis of AD requires more research, as they have not been sufficiently validated to be used routinely. Implications for genetic testing: These genetic factors need confirmation and further analysis as to their role in the diagnosis of AD and should not be used as diagnostic or predictive tests outside of research programs. Clinical application of genetic factors in Alzheimer's diseaseChromosomeDiagnostic testing*Predictive testing†Pathogenic loci Presenilin 1 (PS1)14++ Presenilin 2 (PS2)1++ Amyloid precursor protein (APP)21+ + Risk loci Apolipoprotein E (APOE ε4)19± - Apolipoprotein E -491AA19- - α2 Macroglobulin12-- Low-density receptor-related protein12- - Bleomycin hydrolase17-- Butyrylcholinesterase K variant3-- *In symptomatic individuals with clinical evidence of autosomal dominant familial or sporadic Alzheimer's disease, using NINCDS-ADRDA criteria for the diagnosis of Alzheimer's disease.4 †In asymptomatic individuals using guidelines as developed for Huntington's disease.5-8 -491AA=A/A polymorphism at position -491 in the transcription regulation region of APOE. Back to text 2: National Institute of Neurological and Communicative Disorders and Stroke - Alzheimer's Disease and Related Disorders Association (NINCDS-ADRDA) criteria for the clinical diagnosis of Alzheimer's disease4 I. The criteria for the clinical diagnosis of probable Alzheimer's disease include: Dementia established by clinical examination and documented by the Mini-Mental Test, Blessed Dementia Scale, or some similar examination, and confirmed by neuropsychological tests; Deficits in two or more areas of cognition; Progressive worsening of memory and other cognitive functions; No disturbance of consciousness; Onset between ages 40 and 90, most often after age 65; and Absence of systemic disorders or other brain diseases that could account for the progressive deficits in memory and cognition. II. The diagnosis of probable Alzheimer's disease is supported by: Progressive deterioration of specific cognitive functions such as language (aphasia), motor skills (apraxia), and perception (agnosia); Impaired activities of daily living and altered patterns of behaviour; Family history of similar disorders, particularly if confirmed neuropathologically, and laboratory results showing: normal lumbar puncture as evaluated by standard techniques, normal pattern or non-specific changes in an electroencephalogram, such as increased slow-wave activity, and evidence of cerebral atrophy on computed tomography, with progression documented by serial observation. III. Criteria for diagnosis of definite Alzheimer's disease are: The clinical criteria for probable Alzheimer's disease, and Histopathological evidence from a biopsy or autopsy. Back to text 3: Australasian centres where genetic testing for presenilin, APP mutations and APOE genotyping and counselling is available Applied Molecular Biology Unit Biochemistry State Health Laboratory Brisbane, QLD Department of Pathology Royal Brisbane Hospital, Brisbane, QLD Molecular Pathology Laboratory Sullivan Nicolaides Pathology Taringa, QLD Laboratory and Community Genetics Kolling Institute of Medical Research Royal North Shore Hospital St Leonards, NSW Institute of Medical and Veterinary Science [IMVS] Adelaide, SA The Neurosciences Unit, Health Department of Western Australia, and Department of Neuropathology, Royal Perth Hospital, Perth, WA Hollywood Private Hospital Perth, WA Molecular Pathology Laboratory Canterbury Health Laboratories Christchurch, New Zealand Back to text 4: Recommendations for genetic testing in Alzheimer's disease Mutation testing for abnormalities in PS1, PS2 and APP should only be considered where the family history is appropriate and by referral to appropriate comprehensive, predictive testing programs. The absence of known mutations does not protect against the development of other types of dementia. The use of APOE ε4 genotyping as an adjunct to conventional diagnostic measures is unknown and the data suggest that it has low sensitivity and specificity and is of little diagnostic value in an individual patient. It has low predictive value in asymptomatic individuals and its use in this situation should be discouraged, except in well-defined research protocols with appropriate institutional ethics approval. APOE ε4 genotyping should not be used as the sole diagnostic test in patients in whom AD is suspected on clinical grounds. APOE ε4 genotype testing should not be offered without adequate pre-test and post-test counselling, education and support in patients in whom AD is suspected on clinical grounds. Genetic testing should follow carer or patient consent. APOE ε4 genotype analysis should not be performed in asymptomatic individuals. This position is supported by a number of overseas consensus statements.19-23 Other DNA-based genetic risk factors should not be used in the routine assessment of patients, except as part of an ethically approved research protocol. Back to text

Peter K Panegyres · Jack Goldblatt · Ian Walpole · Carmela Connor · Toni Liebeck · Karen Harrop

Viewpoint Transport and health: en route to a healthier Australia? The medical profession can show leadership in promoting "active transport" Chloë Mason MJA 2000; 172: 230-232 Abstract - Introduction - Health impacts of transport - The case for "active transport" - Healthier transport policy and urban design - The health sector's role - References - Author's details - - More articles on Public and environmental health Abstract We have been slow to recognise the impact that decisions about transport, land use and infrastructure have on health. Apart from encouraging a sedentary lifestyle, reliance on motor vehicle transport has a range of adverse health effects (traffic accidents, air and noise pollution, and greenhouse gas emissions). Physical activity equivalent to 30 minutes (in total) of brisk walking on all, or most, days of the week provides preventive and protective benefits for a wide range of health conditions (including cardiovascular disease, diabetes, depression and osteoporosis). "Active transport" -- walking, cycling and/or using public transport instead of car travel -- could have dual health benefits by providing physical activity and reducing the adverse health effects of motor vehicle transport. Doctors, medical administrators and health advocates can encourage the use of "active transport", and influence community-based programs and policy development about land use planning and travel demand management. Introduction In June 1999, at the Third Ministerial Conference on Environment and Health, held in London, ministers responsible for health, environment and transport from 54 countries adopted the World Health Organization (WHO Europe) Charter on Transport, Environment and Health.1 A summary substantiation paper reviewing the evidence of health risks from transport concluded that we have been too slow to recognise the full health impacts of motor vehicle transport (traffic accidents, pollution, noise and psychosocial effects), and to appreciate the benefits to health of walking and cycling as a means of transport.1 While noting that health arguments should be central to the debate about the continuing expansion of motor vehicle transport in Europe (a debate which also applies to Australia and the wider Asian region), the WHO report stresses the complementarity of transport, land-use policies and health issues. I review these developments and consider opportunities for doctors in Australia to engage in the debate about transport and health and to support a new transport agenda. Some practical ways in which doctors can promote this agenda in clinical practice, medical administration, and health advocacy are suggested. Health impacts of transport The British Medical Association's report Road transport and health gives the composite picture of the health impacts of transport ("the movement of people and goods between places").2 This picture has been obscured by the separate consideration of the impact of health issues, such as traffic accident deaths and injuries, the environmental hazards of motor vehicle pollution, and the health risks of a sedentary lifestyle. Measures to reduce these adverse effects have tended to be implemented in isolation3 rather than as part of an improved, integrated transport policy. Over the past 50 years in Western countries, several factors have made the links between transport, health and the environment more apparent: More trips are being made by car, with increases in both the number and length of car trips, while the share of trips made by foot, bicycle or public transport has declined.4 Moreover, the flow of vehicles is given priority, causing difficulties and risks for pedestrians and cyclists. From the 1980s, the proportion of Australian adults who are overweight, obese or inactive has increased in parallel with our greater reliance on car transport.5 There is greater recognition of transport's contribution to global warming, added to the other environmental problems of air and noise pollution, which adversely affect health. Any attempts to moderate these trends, or even to reverse them, by replacing car travel by alternative modes of transport (foot, bicycle, public transport, or even "teleaccess") could have net positive health effects. The case for "active transport" Benefits of daily physical activity Physical activity has been described as "today's best buy in public health".6 Yet a recent analysis of the medical media shows that medical readers, not confined to Australia, are less exposed to research about the benefits of physical activity than they are to the benefits of controlling hypertension, lowering cholesterol levels, and stopping smoking -- the other traditional risk factors for cardiovascular disease.7 Compelling evidence attests to physical activity lending preventive and protective benefits to a wide range of health conditions beyond its well-known benefits for preventing cardiovascular disease.8,9 Other important health benefits of physical activity include decreased mortality (all causes); cancer prevention (particularly colon cancer); improved psychological health (relief of symptoms of anxiety and depression); reduced risk of obesity, adult-onset diabetes, and osteoporosis;10 and better retention of mobility and independence by older people.8,9 People who were fit in early adulthood and become sedentary later in life do not retain the lower risk profiles of their youth. However, it is never too late to become physically active; even people who have a history of being sedentary can obtain a significant health benefit.10 At a recent national symposium11 on the National Health and Medical Research Council's report Acting on Australia's weight, participants supported the strategy of complementing the management of food intake with the promotion of "transport exercise" or "active transport" to prevent weight gain and obesity. Active transport is about walking and cycling, or other physically active ways of travelling, that can be done alone or combined with catching public transport, often involving the benefits of climbing stairs. Active transport modes can displace car travel. Walking and cycling Walking is the main option for increasing physical activity in sedentary populations.12 Brisk walking for 30 minutes on most days of the week fulfils the recommended level of moderate-intensity physical activity and provides a level of protection to confer significant health benefits.9 Walking or cycling can be understood as activities fitting more easily into everyday life and life's tasks than the addition of recreational exercise,14 with its extra time and cost commitments.15 Walking has the further benefit of being available to most people regardless of income, location or age. Walking is highly efficient in its use of urban space and energy, it rarely causes injury and it gives streets vitality and personal security. Many car trips are quite short, less than 2 km, indicating that walking could be a feasible alternative and contribute to reducing the pollution from a cold-start vehicle travelling only a short distance. Physically active transport in childhood, such as cycling to school, can help to establish the use of cycling for transport later in life, as a habitual physical activity,16 with considerable benefits for health.17 Promoting active transport In the United Kingdom, several local programs promote active transport. In Glasgow, "Fit for life and healthy transport" includes a range of programs for cardiac rehabilitation, as well as health promotion in workplaces and secondary schools, to assist car travellers and school students to adopt healthier travel regimens.18 The UK Health Education Authority's guide, Active transport, aims to encourage local initiatives for promoting walking and cycling. It gives some case studies, for example initiatives by general practice surgeries to foster walking or cycling among patients attending an angina management clinic.19 There is a need for similar programs in Australia. Healthier transport policy and urban design Since existing transport infrastructure tends to support car travel over any other mode of transport, transport policy initiatives are needed to ensure that infrastructure can be modified to make walking and cycling an attractive option and a feasible substitute for car travel. A UK Health Education Authority briefing paper20 explains that transport has inherent problems that make the alliance with health invaluable. Health and transport policy-makers now recognise that:20 "It is not possible to build enough roads to meet demand, even if the economic, environmental and health costs were ignored. Consequently, the demand for road space must be managed, and emphasis must be placed on efficient use of existing road space." "The need to travel, or to travel longer distances, should be reduced by landuse planning, so that walking, cycling and public transport can be real choices." The phenomenon of growth in car use is as true for cities and towns in Australia as it is in the United Kingdom. It is this growth that is magnifying the adverse health effects of motor vehicle transport. Implementation of new transport measures needs to be coordinated to secure benefits for health and the environment, as well as a safe arrival at one's destination.21 This "new realism" in transport thinking fosters opportunities for converging interests to protect and promote health.22 Responsibility for changing transport patterns can be shared, as illustrated by a program at the University of New South Wales, a major "trip generator" organisation.23 Australian planners in cities and regions are coming to recognise how land use and appropriate urban design can reduce the need for motor vehicle transport and allow more walking and cycling trips.24-26 Creating neighbourhoods and communities that are less dependent on cars requires a denser pattern of development, with residential areas and services (shops, schools, sports facilities, libraries and clubs) located together (mixed-use neighbourhoods), and good public transport infrastructure linking the communities with employment opportunities. In urban improvement projects (and transport infrastructure development), planners are trying to concentrate employment opportunities around railway stations, provide mixed-use residential areas, and promote the principles of "active transport". These urban design and infrastructure changes can markedly reduce greenhouse gas emissions. The annual car-related emissions per dwelling vary greatly by neighbourhood type: conventional neighbourhoods remote from services and dependent on road transport produce 3.3 tonnes of CO2 per dwelling, while mixed-use neighbourhoods that facilitate the use of public and active transport produce 1.4 tonnes of CO2 per dwelling, a reduction of 57%, with associated health benefits of walking, cycling, and reduced exposure to motor vehicle accidents.27 The health sector's role The WHO Charter1 invites health authorities to examine their own use of transport, and the UK Government encourages all hospitals, as organisations generating motor vehicle trips, to show leadership in "promoting active transport" to their communities, while adopting organisational-based programs for cutting car use by staff members and visitors.28-30The Box outlines ways in which the health sector in Australia can support and foster active transport programs and influence policy development. References World Health Organization (WHO Europe). Charter on Transport, Environment and Health. <www.who.dk/London99/WelcomeE.htm> Accessed 10 Feb 2000. British Medical Association. Road transport and health. London: British Medical Association, 1997. Report of the Road Safety Committee on the Inquiry into the Incidence and Prevention of Pedestrian Accidents. Walking Safely. Parliament of Victoria. Melbourne: Victorian Government Printer, 1999. Bureau of Transport Economics. Urban transport -- looking ahead. Canberra: Bureau of Transport Economics, 1999. (Information Sheet 14.) National Health and Medical Research Council. Acting on Australia's weight: a strategic plan for the prevention of overweight and obesity. Summary report. Canberra: NHMRC/AGPS, 1997. Morris JN. Exercise in the prevention of coronary heart disease: today's best buy in public health. Med Sci Sports Exerc 1994; 26: 807-814. Dupen F, Bauman AE, Lin R. The sources of risk factor information for general practitioners: is physical activity under-recognised? Med J Aust 1999; 171: 601-603. US Department of Health and Human Services. A report of the Surgeon General. Atlanta, Ga: Centers for Disease Control and Prevention, 1996. URL: <http://www.cdc.gov/nccdphp/sgr/sgr.htm> Accessed 10 Feb 2000. NSW Health Department. Physical activity and health: a special communication from the Chief Health Officer, 2nd ed. Sydney: NSW Health, 1996. Commonwealth Department of Health and Family Services. Developing an active Australia: a framework for action for physical activity and health. Canberra: The Department, 1998. Commonwealth Department of Health and Aged Care and the Australasian Society for the Study of Obesity. Symposium on the NHMRC's report Acting on Australia's weight. Children and their families; 1999 Aug 23, Sydney. Morris JN, Hardman AE. Walking to health. Sports Med 1997; 23 (5): 306-332. Pears A. Global warming: cool it! Canberra: Environment Australia, 1997. US National Heart, Lung and Blood Institute. Simple lifestyle changes boost physical activity/cardiovascular health. January 1999. URL: <http://www.nhlbi.nih.gov/new/index.htm> Accessed 10 Feb 2000. NSW Physical Activity Taskforce. Simply active everyday: a plan to promote physical activity in NSW, 1998-2002. Sydney: NSW Health 1998. Gardner G. Identifying potential cyclists. European Transport Conference, 27-29 September 1999. Cambridge, UK. Proceedings Vol B: Transport planning, policy and practice, p 405-414. London: PTRC Education & Research Services Ltd, 1999. Roberts I, Owen H, Lumb P, MacDougall C. Pedalling health: health benefits of a model transport shift. Adelaide: SA Department of Transport, 1996. University of Glasgow, Greater Glasgow Health Board, Glasgow City Council, Strathclyde Passenger Transport. Fit for life and healthy transport. Undated. Davis A. Active transport: a guide to the development of local initiatives to promote walking and cycling. London: UK Health Education Authority; 1999. UK Health Education Authority. Transport and Health: a briefing paper for health professionals and local authorities. London: Health Education Authority; 1998. Dora C. A different route to health: implications of transport policies. BMJ 1999; 318: 1686-1689. Goodwin P. Are transport policies driven by health concerns? In: Fletcher T, McMichael AJ, editors. Health at the crossroads: transport policy and urban health. Chichester: John Wiley & Sons,1997: 271-278. Black J, Mason C, Stanley K. Travel demand management: an application by University of New South Wales (UNSW) as a large trip generator. Transport Engineering in Australia. 1999. In press. NSW Government. Action for Transport 2010: an integrated transport plan for Sydney. Sydney: Department of Transport, 1998. NSW Government. Action for air: NSW Government's 25 year air quality management plan. Sydney: EPA, 1998. NSW Government. Shaping our cities. Sydney: Department of Urban Affairs and Planning, 1998. Greenhouse Neighbourhood Project: the low energy suburb. Summary report. Prepared for Victorian Department of Planning and Development, EPA, and Energy Victoria by Loder & Bayly Consulting Group, RJ Nairn & Partners, Sustainable Solutions, PPK Consultants, 1993. Peden S. Southampton University Hospitals, NHS Trust, UK: traffic demand management in action, European Transport Conference, 27-29 September 1999. Cambridge, UK. Proceedings Vol D: Civilising the city, p 11-18, London: PTRC Education & Research Services Ltd, 1999. Transport 2000 Trust. The Healthy Transport Toolkit: a guide to reducing car trips to NHS facilities. Supported by UNISON, the Department of Health, the Health Education Authority and the Department of Environment, Transport and Regions. London: Transport 2000 Trust, 1998. Hanratty B, Patterson W. Three quarters of delegates drove to conference on impact of environment on health. BMJ 1998; 316: 775. -2004 Australian cycling. The National Strategy. Sydney: Austroads,1999. Authors' details PO Box A973, Sydney, NSW. Chloë Mason, PhD, Consultant in Sustainable Transport. Reprints: Dr C Mason, PO Box A973, Sydney, NSW 1235. chloemasonATbigpond.com Make a comment Walking or cycling 1km to the railway station instead of driving saves 0.2-0.3kg greenhouse gas emissions, other air pollutants, and fuel cost. The traveller's moderate physical activity in walking to the station and climbing the station steps to the train would meet a third to a half of his or her daily requirements for physical activity.13 Practical ways for the health sector to encourage active transport and a new, healthier transport agenda Clinical practice "Prescribe" or encourage active transport, preferably displacing car journeys, at least for some trips. Run demonstration projects on the benefits and applications of "active transport" in coronary rehabilitation, the prevention of obesity or the treatment of depression. Medical administration Doctors' surgeries, hospitals and other health services, and government health departments all function as "trip generators" by attracting people to their sites as patients, visitors, or staff members. Produce a Transport access guide or update Practice information sheets to show access to the site -- public transport services, cycling and walking routes and end-of-trip facilities (eg, cycle parking, showering facilities) -- to inform people about the alternatives to car travel, with emphasis on the benefits to health. Develop "healthy transport plans" for the organisation and ensure practices are consistent with encouraging people to reduce car travel to reach the site for work, to attend conferences, or to visit patients. Health advocacy Doctors can become more actively involved in community education and policy development about land use planning, transport infrastructure, and travel demand management (such as raising car parking charges to discourage car travel) and highlight the health impacts of the transport system. Doctors could support new initiatives, such as "Safe routes to school" schemes, and implementation of Australia's national cycling strategy,31 and support reforms to reduce subsidies for parking and car travel which operate by fringe benefits taxation concessions. Medical professional organisations could produce an Australian version of the BMA's report Road transport and health2 to influence national and regional transport policy. Back to text

Chloe Mason

Editorial William Osler: a model for the 21st century? Osler's teachings are as relevant now as they were 100 years ago Whatever way my days decline, I felt and feel, tho' left alone, His being working in mine own, The footsteps of his life in mine. MJA 1999; 171: 577-579

Michael F O'Rourke

The Weight Debate What should we do about overweight and obesity? The goals of treatment should not necessarily be to normalise weight, but to optimise health MJA 1999; 171: 599-600 Introduction - Why are we getting obese? - Why have we not been effective in treating obesity? - What should we do about obesity? - What has been ignored is our environment - - More articles on Nutrition

Ian D Caterson

The Weight Debate The sources of risk factor information for general practitioners: is physical activity under-recognised? Fiona Dupen, Adrian E Bauman and Rose Lin MJA 1999; 171: 601-603 For editorial comment, see Caterson Abstract - Introduction - Methods - Results - Discussion - Acknowledgement - References - Authors' details - - More articles on General practice and primary care

Fiona Dupen · Adrian E Bauman · Rose Lin

The Weight Debate Obesity and virtue. Is staying lean a matter of ethics? Self-control of one's own weight might be described as a form of bioethics John N Burry MJA 1999; 171: 609-610 Article - References - Authors' details - - More articles on Ethics

John N Burry

Rural Healthcare Accessibility to general practitioners in rural South Australia A case study using geographic information system technology MJA 1999; 171: 614-616 Errol J Bamford, Lyle Dunne, Danielle S Taylor, Brian G Symon, Graeme J Hugo and David Wilkinson Abstract - Introduction - Methods - Results - Discussion - References - Authors' details - - - More articles on Administration and health services

Errol J Bamford · Lyle Dunne · Danielle S Taylor · Brian G Symon · Graeme J Hugo · David Wilkinson

Rural Health Mobile intensive care services in rural South Australia John E Gilligan, William M Griggs, Michael T Jelly, David G Morris, Ross R Haslam, Neil T Matthews, Evan R Everest, Robert L Bryce, Peter B Marshall and Ron A Peisach MJA 1999; 171: 617-620 Synopsis - Introduction - The service - Patient care - Discussion - Acknowledgement - References - Authors' details - - More articles on General practice and primary care Synopsis In the 12 years from 1984 to 1995, Adelaide-based mobile intensive care teams transported 4443 critically ill patients from rural areas in South Australia and adjacent States to tertiary-level hospitals in Adelaide. The SA Ambulance Service undertook communications, support staffing and deployment of transport. Average radial distances in 819 road missions were 71 km, in 808 helicopter missions 122 km, and in 2777 fixed-wing aircraft missions 398 km. The largest groups of patients were neonates (23%) and those with trauma (25%). Rural hospitals made 96% of the requests for intensive care transport; 4% came from ambulance or other emergency service crews at accident locations. Emergency surgical or operative obstetrical procedures were performed on 2.7% of patients before transport. One hundred and thirteen patients (2.5%) died during resuscitation or transport, with one death deemed to be preventable. Introduction South Australia has a rural population of 390 000 in an area of about 984 000 km2. Over 100 communities have populations of less than 5000, and the largest provincial cities have populations below 25 000. In these circumstances regional medical services cannot provide intensive care services locally to all patients. The solution has been to use specialised medical teams travelling by road, helicopter or fixed-wing aircraft to stabilise and transport critically ill patients to tertiary referral centres in the South Australian capital, Adelaide. This system was first reported in the Journal in 1977.1 This article describes the function and outcomes of the mobile intensive care service from 1984 to 1995. The service Intensive care teams and facilities were provided by the Royal Adelaide Hospital, the Women's and Children's Hospital, Flinders Medical Centre and the Queen Elizabeth Hospital. The Lyell McEwen Health Service and Modbury Hospital, two community hospitals on the outskirts of Adelaide, played a minor role in providing teams. Rural hospitals were connected to intensive care units at the tertiary centres by dedicated telephone lines so that rural medical officers could obtain emergency advice, contact other specialists and arrange transfer of patients. Mobile teams consisted of a consultant or senior trainee in intensive care, anaesthesia or emergency medicine and a critical care nurse, commonly assisted by a paramedic or Royal Flying Doctor Service (RFDS) nurse. Other specialists (eg, surgeon, obstetrician) travelled as required. The SA Ambulance Service Communications Centre co-ordinated transport and provided supporting staff. Very high frequency radio and mobile phones linked road ambulances, aircraft, tertiary centres and rural hospitals. A twin-engine, pressurised Super KingAir B200C fixed-wing aircraft of the RFDS, carrying a pilot and up to five cabin crew, two stretchers and a stretcher-loading device,2 was used for most long-distance transfers. Recently, Pilatus PC XII aircraft of similar performance have been used. The helicopter used was a twin-engine Bell 412 helicopter of the State Government Insurance Commission-State Rescue Helicopter Service, with 2-4-stretcher capability, pilot, crewperson and up to three medical crew as needed. The Department of Human Services, Royal Flying Doctor Service (Central Section) Medical Review Committee and the SGIC-State Rescue Helicopter Committee audited the operations of the mobile intensive care service. At times, the service was extended to remote areas in other States. Box 1 shows the range of operations. Patient care We did not attempt to classify all patients according to a universal pathological grouping or severity scoring system -- this would have been difficult with the diverse ages and conditions represented among the patients. Our empirical categorisation (Box 2) is similar to that in other reports of transporting the critically ill.3One hundred and thirteen patients died (2.5%) during resuscitation or in transit. One preventable death resulted from an endotracheal tube displacement in transit, which was managed unsuccessfully by emergency tracheostomy at a nearby hospital. Box 3 lists the procedures performed to stabilise patients before transport. A third of patients required endotracheal intubation. Major biochemical disturbances commonly involved potassium or glucose levels. Hypothermia and hyperthermia were corrected to the degree possible. Box 4 lists emergency surgical and obstetrical procedures undertaken before transporting patients. Discussion Rural general practitioners in Australia have a crucial role in recognition, triage and resuscitation of patients with critical illness, but they treat relatively few critically ill patients and lack resources for their care. Access to specialist assistance can reduce the professional isolation felt by rural doctors. Effective care for critically ill rural patients requires an integrated hierarchy of rural and city hospitals, ambulance services, the RFDS and mobile intensive care. Larger rural hospitals have specialist surgical and anaesthetic services, but may lack tertiary centre services such as neurosurgery, burns, spinal injuries, specialised organ imaging, extensive transfusion facilities and major (level III) intensive care.4,5 Because of the large distances involved, staff at tertiary intensive care units encouraged rural medical officers to start a dialogue early with the retrieval service whenever a patient might require retrieval. Intensive care units provided necessary advice while the team was in transit. After stabilising the patient, treatment in transit was commonly restricted to adjustment of sedation, infusion rates and ventilator settings. The transfer of patients immediately after emergency surgery or obstetric procedures was uneventful. Obstetric conditions requiring transfer included eclampsia and major blood loss. The number of obstetric patients declined from 1984 to 1995 as improved antenatal care identified at-risk pregnancies, with elective movement of mothers to a major centre. A surgeon did not usually accompany the mobile intensive care team, largely because the surgical facilities in small rural hospitals were limited. There were 30 patients with suspected extradural haematoma, for whom a local medical officer commenced burr holes, directed by telephone, pending arrival of the team (accompanied by a neurosurgeon in 16 cases) to complete the procedure and retrieve the patient. Data suggest that such emergency drainage of an extradural haemorrhage is a valid procedure if the patient is more than two hours from a trauma centre.6 Ambulance crews at rural accident sites with multiple victims or patients deteriorating during prolonged entrapment were encouraged to request support when needed from local medical officers and/or retrieval teams. While primary (site) retrieval was requested in 149 instances (13% of trauma cases), distance commonly decreed that teams would attend after patients had been transferred to the local hospital. This contrasts with some overseas services that perform mainly primary retrieval missions by helicopter over shorter distances.7-9 Paramedic services provide a high level of care, but retrieval teams have a different role, with a wider therapeutic armamentarium and the ability to undertake major procedures in rural hospitals. Advanced trainees or consultants in intensive care, anaesthesia or emergency medicine, and their nurse counterparts, provide requisite clinical experience and procedural skills. To be effective, they must also be able to work in unfamiliar hospitals, in vehicles and other restricted sites, and they must have insight into the problems of rural doctors and nurses and the concerns of patients and relatives. Fixed-wing aircraft and helicopter services are complementary. Fixed-wing aircraft mobilisation from Adelaide took 45-60 minutes, commonly for distances beyond 200 km. Executive or passenger jet aircraft complete extended trips (eg, Darwin, 2600 km) in half the time of turboprop aircraft. RAAF services assisted in five early cases. Pressurised aircraft were introduced in 1988, enabling smooth, rapid flight above adverse weather and allowing sea-level cabin pressure (eg, in decompression sickness). The helicopter's rapid mobilisation, ability to land close to an incident, and reduced need of supportive road transport offsets slower airspeed. Helicopter transit times, commonly 50 minutes shorter than road transport, were improved by helipads at tertiary centres. Sports fields, lit at night, proved acceptable helipads in country areas. While road transport was used for shorter trips or if aircraft were unavailable, road transfer by local medical officers or ambulance staff (often with inadequate supportive resources) was commonly less satisfactory than if local staff continued resuscitation in the hospital pending arrival of a team. Safe transport requires compact ventilators, infusion pumps and monitors with modest consumption of medical gases and battery power. Monitoring by the mobile teams included electrocardiography, pulse oximetry, core temperature, end-tidal carbon dioxide and (for neonates) transcutaneous measurement of respiratory gases. Intravascular blood pressure and central venous pressure measurements were especially useful, as pulse oximetry and non-invasive blood pressure measurements have limited reliability in hypothermia, shock10,11 and during transport. Neonatal transport incubators weigh about 100 kg, requiring a stretcher base, ventilator, monitors and heating for all phases of transport,12 as combating hypothermia remains the most necessary component. Early transfer of the critically ill has been associated with improved survival.13 Results of care in larger tertiary units are often better than in smaller, local hospitals, especially for severe trauma,14 neonatal15 and paediatric intensive care.16 See Box 5 for some case histories. For this series of 4443 patients, specialised transport was safe, with only one preventable death (a rate of preventable mortality of 0.02%). Two failed intubations occurred before the mobile intensive care team reached the patients. No other adverse effects of resuscitative procedures were reported. Comparable transport mortality rates of 1/2700 (0.04%) have been reported by retrieval organisations in the UK and Canada, usually over shorter distances.3,17 The 112 other deaths during resuscitation or transport were associated with overwhelming injury (eg, ruptured aortic aneurysm or massive trauma) or lack of local resources plus the effect of distance -- an unavoidable death rate of 2.5%. Acknowledgement We thank Ms Liesl Sawyer, computer slide artist, Medical Illustration Unit, Royal Adelaide Hospital, for production of graphics. References Gilligan JE, McCleave DJ, Nicholson B, et al. Retrieval of the critically ill in South Australia: a coordinated approach. Med J Aust 1977; 2: 849-855. Gilligan JE, Goon P, Maughan G, et al. An airborne intensive care facility (fixed wing). Anaesth Intens Care 1996; 24: 245-253. Runcie C. Principles of safe transport. Chapter 3. In: Morton NS, Pollack MM, Wallace P, editors. Stabilisation and transport of the critically ill. New York, London, Melbourne: Churchill Livingstone: 1997. Faculty of Intensive Care. Australian and New Zealand College of Anaesthetists. Minimum standards for intensive care units (IC-1, 1994). Melbourne: ANZCA, 1994. Report of the AHMAC (Australian Health Ministers Advisory Council) Aeromedical Services Working Party. Canberra: Commonwealth Department of Health, Housing, Local Government and Community Services, 1993: 47. Simpson DA, Heyworth JS, McLean AJ, et al. Extradural haemorrhage: strategies for management in remote places. Injury 1988; 19: 307-312. Grabosch A. Ten years experience in helicopter rescue in West Germany. Proceedings of the First International Assembly on Emergency Services. Washington DC: US Department of Transportation, 1982: 222-228. Poisot D. Presentation du SAMU 33. SAMU 33 1994. Paris: Societé Assistance Medicale d'Urgence, 1994: 5-13. Morley AP. Prehospital monitoring of trauma patients: experience of a helicopter emergency service. Br J Anaesth 1996; 76: 726-730. Clayton DG, Webb RK, Ralston AC, et al. A comparison of 20 pulse oximeters under conditions of poor perfusion. Anaesthesia 1991; 46: 3-10. Rutten AJ, Ilsley AH, Skowronski GA, Runciman WB. A comparative study of the measurement of mean arterial blood pressure using automatic oscillometers, arterial cannulation and auscultation. Anaesth Intens Care 1986; 14: 58-65. Duncan AW. The critically ill child. Chapter 101. In: Oh T, editor. Intensive care manual. 4th ed. London: Butterworth-Heinemann, 1997. Purdie JA, Ridley SA, Wallace PG. Effective use of regional intensive therapy units. BMJ 1990; 300: 79-81. West JG, Cales RH, Gazzaniga AB. Impact of regionalisation: the Orange County experience. Arch Surg 1983; 118: 740-744. Harris BA Jr, Wirtschafter DD, Huddleston JF, Perlis HW. In utero versus neonatal transportation of high risk perinates. A comparison. Obstet Gynecol 1981; 57: 496-499. Pollack MM, Alexander SR, Clarke N, et al. Improved outcomes from tertiary center pediatric intensive care: a statewide comparison of tertiary and non-tertiary care facilities. Crit Care Med 1991; 19: 150-159. Girotti MJ, Pagliarello G, Todd TR, et al. Physician-accompanied transport of surgical intensive care patients. Can J Anaesth 1988; 35: 303-308. (Received 31 Aug 1998, accepted 28 Sep 1999 Authors' details Intensive Care Unit, Royal Adelaide Hospital, Adelaide, SA. John E Gilligan, AO, FFICANZCA, FANZCA, Director of Retrieval and Resuscitation; William M Griggs, FFICANZCA, FANZCA, Director of Trauma Services. Department of Human Services, Adelaide, SA. Michael T Jelly, FRACMA, Chief Medical Officer. Women's and Children's Hospital, Adelaide, SA. David G Morris, FRANZCOG, Head of Obstetrics, Department of Perinatal Medicine; Ross R Haslam, FRACP, Head of Neonatal Medicine, Department of Perinatal Medicine; Neil T Matthews, FFICANZCA, FANZCA, Medical Unit Head, Paediatric Intensive Care. Flinders Medical Centre, Adelaide, SA. Evan R Everest, FRACP, Director, Trauma Services and Specialist, Intensive Care; Robert L Bryce, MSc, PhD, FRANZCOG, Director of Obstetrics, Department of Obstetrics and Gynaecology; Peter B Marshall, FRACP, Director, Neonatal Medicine. The Queen Elizabeth Hospital, Adelaide, SA. Ron A Peisach, FFICANZCA, Director, Intensive Care Unit. Reprints: Dr J E Gilligan, Intensive Care Unit, Royal Adelaide Hospital, Adelaide, SA 5000. jgilligaATmedicine.adelaide.edu.au Make a comment 1: Mobile intensive care service missions, 1984-1995 In 12 years (1 January 1984 to 31 December 1995) there were 4443 rural and interstate mobile intensive care missions (three to provide standby services). Missions were conducted around the clock. They constituted 5% of all rural patient transfers (data from Annual Report of St John Ambulance, South Australia). Most missions were by air, comprising about 10% of medical flights to Adelaide (Ms G Malone, RFDS, personal communication). The other flights were mostly transfers by the RFDS of less critically ill patients. Map showing operational area of mobile intensive care services based in Adelaide, South Australia. Missions were flown throughout South Australia and the Northern Territory, to Broken Hill and Mildura, and to transfer neonates from Adelaide to Melbourne for cardiac surgery Mean duration of missions (hours)All missions*5.1Rural SA4.49Interstate8.51All neonatal missions6.08All trauma missions4.85Radius <300 km4.14Radius <200 km3.78Radius <100 km3.13Roadside accident response†1.84* Stabilisation time in hospitals sometimes exceeded one hour, especially for neonates. †Mostly by road or helicopter. Back to text 2: Condition categories of 4443 retrieved patientsMajor trauma. Includes 48 major surgical procedures before transport: craniotomy (30), laparotomy (15), thoracotomy (3). Tracheostomy performed in 12.1125 (25.3%)Neonatal. Commonly prematurity with respiratory distress.1025 (23.0%)Cardiovascular. (a) Aortic and other major vascular bleeding. (b) Myocardial: recurrent major dysrhythmias; heart block requiring pacing; ventilatory failure after cardiac arrest.561 (12.6%)Central nervous system. Profound coma or uncontrolled fits (eg, from cerebrovascular accident, meningitis; subarachnoid bleed). Tracheostomies performed in three.347 (7.8%)Obstetric emergencies (eg, severe bleeding, eclampsia, obstructed labour). Includes 45 operative interventions: caesarean section (26), forceps (8), breech delivery, removal of retained products (8).226 (5.0%)Postsurgical (non-trauma). Commonly multiple problems following surgery and anaesthesia, such as septic shock, ventilatory failure, renal failure, coagulation defects, inhaled gastric content. 137 (3.0%)Poisoning/envenomation/bites 137 (3.0%)Respiratory (eg, severe asthma, pneumonia; laryngotracheobronchitis and epiglottitis in children). Tracheostomies performed in 5.574 (12.9%)Gastrointestinal. Major haematemesis, melaena. Severe gastroenteritis in children.94 (2.1%)Paediatric (unspecified) 70 (1.6%)Severe burns44 (1.0%)Infection. Septic shock, no obvious cause.32 (0.7%)Diving mishaps. Severe decompression sickness, gas embolism.18 (0.4%)Diabetes. Uncontrolled acid-base disturbance.16 (0.3%)Near-drowning11 (0.2%)Allergy. Severe anaphylactic/anaphylactoid reactions.9 (0.2%)Renal/urinary tract7 (0.2%)Psychiatric3 (0.1%)Heat stroke3 (0.1%)Standby (sieges, bushfires) 3 (0.1%)Unclassified1Back to text 3: Stabilisation measures performed by local medical officers or mobile intensive care teamsInterventionAll patients (n=4443)Trauma (n=1125)Peripheral intravenous access4443 (100%)1125 (100%)Intubation,* controlled ventilation1505 (34%)544 (48%)Invasive arterial pressure monitoring786 (18%)276 (24%)Central venous cannulation518 (12%) 164 (15%)Blood transfusion274 (6%)165 (16%)Inotrope infusion†219 (5%)-Formal pleural drainage200 (4%)166 (15%)Needle thoracostomy4 (0.1%)4 (0.4%)Defibrillation20 (0.5%)-Transvenous pacing19 (0.5%)-Regional nerve block17 (0.4%)17 (1.5%)Military antishock trousers11 (0.2%)0*Usually intravenous anaesthesia-relaxant-narcotic sequence. †Other infusions included thrombolytics, sedatives, relaxants. Back to text 4: Emergency surgical and obstetrical procedures performed before transporting patientsProcedureCasesCraniotomy30Thoracotomy4Tracheostomy20Cricothyrotomy1Operative obstetrics:Caesarean section26Forceps delivery8Various procedures: breech delivery, removal of placenta, curettage11Laparotomy (trauma or other)22Oesophagoscopy, laryngoscopy2Fasciotomy1Reduction of dislocated limb2Total127Back to text 5: Resuscitation and recovery - some case histories Shotgun trauma; thoracotomy A man aged 54 with shotgun wounds of the chest and arm had a thoracotomy by a rural surgeon and anaesthetist to control cardiac tamponade and bleeding. A team then transported him, ventilated and with multiple chest drains, by helicopter 240km for further thoracic and abdominal exploration. Multiple outback casualties Ten people injured in a bus accident 900km from Adelaide were taken 80km to the nearest hospital. They were treated by medical staff in five Royal Flying Doctor Service aircraft, two mobile intensive care retrieval teams and two local medical officers, ambulance and nursing staff. After resuscitation, and in one case after fasciotomy for compartment syndrome, all patients were evacuated. Craniotomy pretransport A 20-year-old man was intubated, ventilated and had a burr hole for suspected extradural bleed performed by local medical officers following advice from an intensive care unit in Adelaide. The team neurosurgeon completed the procedure. The ventilated patient was airlifted 230km for postoperative care. Obstetric emergency A woman, 28 weeks pregnant, had an antepartum bleed 340km from Adelaide. She was given intravenous fluids and tocolytics while her partner drove 100km to collect blood. She developed pulmonary oedema requiring artificial ventilation. An obstetric team delivered the baby by caesarean section in the local hospital, then transported mother, baby and partner to a tertiary centre in a two-aircraft mission. Paediatric epiglottitis A four-year-old child developed progressive stridor and drooling from epiglottitis. The medical team intubated the patient under halothane anaesthesia and transported him to a paediatric intensive care unit in Adelaide. Back to text

John E Gilligan · William M Griggs · Michael T Jelly · David G Morris · Ross R Haslam · Neil T Matthews · Evan R Everest · Robert L Bryce · Peter B Marshall · Ron A Peisach

Rural Healthcare Rural doctors -- who are they? Three rural doctors tell their stories MJA 1999; 171: 621

Medical Education The rise and rise of academic general practice in Australia The Heads of General Practice are excited about partnerships with GPs and the community Kerrie A Lawson, Mabel Chew and Martin B Van Der Weyden MJA 1999; 171: 643-648 Introduction - The struggle for identity - Standing as an academic discipline - Role of academic general practice - Divisions of General Practice - Evidence-based medicine - Improving GP morale - The way forward - Authors' details - - More articles on General practice and primary care

Kerrie A Lawson · Mabel Chew

Doctors' Tales CLINICam The world's first live general practice on the Internet MJA 1999; 171: 671

Michael R Kidd

Clinical Practice Health online: the future isn't what it used to be Over the next 10 years, the healthcare system will change to focus more on preventive medicine and healthcare in the home, with fewer doctors and a new class of home healthcare providers. Healthcare professionals need to debate how best to manage these changes. Peter M Yellowlees and Peter M Brooks MJA 1999; 171: 522-525 Introduction - Changing information presentation - The effects - The solutions - References - Authors' details - - More articles on Informatics and computers Introduction Over the past 30 years the framework in which doctors and other healthcare professionals practise has changed relatively little in comparison with the enormous changes seen in transport, manufacturing and telecommunications. While many doctors and health service managers prefer to ignore the extraordinary changes outside of the health system, they do so at their peril. Healthcare will be very different by 2010; the focus will be on the patient at home rather than the provider in the institution. There are three major drivers for this change.1 The first is the economic imperative to restrain healthcare costs in a setting of an ageing community and escalating costs of institutional care and technology. Our present model of care primarily focused on institutions, be these hospitals or related step-down facilities and nursing homes, is not sustainable. In Australia, we already spend more than $21 billion per year on institutional (hospital and nursing home) care. We have to explore ways of reducing this cost. The second is increasing consumerism, and the evolution of the "informed patient". As the "baby boomer" generation ages it will be increasingly concerned about its own welfare and will focus more and more on health. Every social issue that this generation has touched has changed radically, and there is no reason why healthcare should be exempt. The dynamic, yet often self-centred, approach by the baby-boomers is likely to be translated into a much stronger push for home healthcare. The third is the extraordinary changes in communication technology, and the evolution of the Internet. Knowledge has never been as important and as accessible as it is today -- it is now one of the economic cornerstones of our society. The distribution of knowledge is occurring at a remarkable pace via the Internet, as well as through multiple other media outlets. For some years, clinical care has been increasingly delivered electronically via telemedicine, as well as telephonically. Australia is at the leading edge of these developments.2,3 Changing information presentation Before we can benefit from the new technologies (see Box), we have to solve the problems of information quality and information overload, especially on the Internet.9 A variety of sites are being developed as quality health information portals, such as the National Library of Medicine in the United States,10 HealthInsite in Australia,11 and Omni in the United Kingdom.12 In addition, approaches are being developed to allow clinicians and patients to better assess the reliability and validity of health information.13 A more comprehensive Internet classification and coding system using metadata, as well as the development of sophisticated search engines, needs to emerge as a long term solution for this important problem.9 Only then will doctors be able to effectively obtain good quality decision support information within the time and process of a typical consultation. Within the health industry there have been enormous strides in the past five years in the development of electronic patient records, many using Internet protocols. The health system is, unfortunately and inevitably, still replete with many different types of information systems, most of which have been focused on financial and administrative applications. The challenge in the future will be to get all of these "legacy" systems to talk to the new Internet-based systems. Fortunately, Australia is well placed in this respect with the recent funding by the Federal Government of the Cooperative Research Centre for Distributed Systems Technology,14 which has a long term research program with the Centre for Online Health at the University of Queensland.15 There are many related activities at Monash University,16 the University of New South Wales,17 and in private industry. The national approach taken by the Collaborative Health Informatics Centre18 is greatly assisting the integration of the health and information technology industries. The effects We have a good idea of the illnesses and diseases that will be most prevalent and will cause the greatest disease burden by 2020.19 These are chronic cardiac, respiratory and psychiatric diseases, as well as road traffic accidents. The cardiac, respiratory and psychiatric diseases are all highly amenable to the provision of long term home care, while clearly a much more active approach to prevention and education is required to reduce the impact of road traffic accidents. A changing paradigm If we assume that by 2010 health information will be available in the homes of most Australians, and certainly on every health professional's desktop, then what will be the effects? The health system is already moving away from supporting episodic care to supporting continuity of care, and from a service-provider focus to an informed-patient focus. Increasingly, our past individual approach to treatment will be overtaken by the need for team approaches, underpinned by evidence and outcomes, clinical pathways, and guidelines. "Wellness promotion" will be seen as being more important than illness treatment. There will be a move away from institutional care to community care and to the development of the shared, distributed electronic patient record. Hospitals and health departments will make the shift from being autonomous, slowly-growing empires to becoming fluid and rapidly changing enterprises, as has occurred in industry. Therefore, there will be a need, quite simply, for fewer hospitals and more home care and community support services. Figure 1 shows a mock-up of how a patient's Web browser might look during an online consultation with a general practitioner. This patient-accessible electronic home care record system would allow instant contact with a range of healthcare professionals, information sources and other health services in an electronic distributed environment. The system will involve telemetry, monitoring, video links and automatic ordering systems, all delivered via Internet2. The entire health system will be focused on the patient at home (Figure 2) rather than on providers and institutions. If we can reduce institutional care by just 10%, over $2 billion per year will be made available for redistribution. The traditional doctor-patient relationship will alter, being driven much more intensively by patients. The doctor's role will become more advisory, analytic and interventionist. Doctors will need to be experts in assessing information from many different sources and in clinical reasoning, particularly for patients requiring more than a guidelines-and-pathways approach to care. Healthcare education will also be radically different. Medical schools and other health education institutions need to be thinking today about educating clinicians to work within a distributed, primary care focused environment.20,21 If we are correct in our predictions, there will be a need for fewer doctors beyond 2010. Not only will so much of our present-day medical content, knowledge and expertise be less important, but a group of highly skilled home healthcare professionals will exist, probably evolved from today's nurse practitioners. These healthcare providers will have prescribing and other treatment roles for patients being treated within pathway and guideline protocols. The changes will not stop there. There will also be massive opportunities, particularly for Australia, as it may be possible for Australian physicians to provide very much cheaper electronic healthcare into the US than is available locally within that country, if only because of differences in the cost of living and the strength of the dollar. It is more likely, however, that electronic healthcare will be provided in three main time zones (Figure 3), as it is highly unlikely that a doctor in, say, Australia will be prepared to consistently get up in the middle of the night to treat a patient in, for instance, Saudi Arabia or Brazil. The introduction of global electronic physicians and virtual healthcare systems will raise many important cultural, ethical, legal and legislative issues. These include, for example, the need for international medical registration and medical defence systems, the development of global information and security standards for the Internet, more flexibility in drug licensing across countries, and the need to integrate Eastern and Western styles of medicine when working across cultural boundaries. The solutions What are the implications of these changes for the present Australian healthcare sector? What should be done to prepare for this scenario? The following are suggestions. Cultural and political understanding and attitudes: There is a need for increased awareness of the importance of communications technologies in healthcare. Most global companies assume that 5%-10% of their budget will be spent on communication and information technologies. Research into distributed healthcare, both clinical models and technical solutions, is likely to be just as important as biotechnology in improving our national health profile. The clinical and information management issues are more important than, and have to drive, the technological changes. Once government makes a commitment to the changes looming in the near future, there will be the opportunity to create the necessary cultural and social changes required nationally to enable us to move to a future where information technology underpins healthcare delivery. The healthcare environment: There is a need for urgent, widespread debate about the future of healthcare, about the respective roles of doctors, patients, and other healthcare professionals, and about how best to transform a hospital-focused health system to one centred on patients and home care. If change is not guided from within the health system, it will certainly be enforced by external global and national factors. Technological requirements: There is a need to link the many existing computing systems into an Internet-based future. The necessary technological and information-based research and development programs must be focused on the development of user-friendly interfaces for patients of all ages, as well as for clinicians, and will involve the development of electronic clinical care protocols, whether these be delivered in real time, or by "store-and-forward" email, video mail, video conferencing, telephony or other methods. Specific projects need to be developed in home care, in wireless and collaborative environments, and in the development of improved electronic records. Australia needs closer links to the Internet2 consortium and to the exciting opportunities occurring in other countries, such as the Multi Media Super Corridor in Malaysia.22 Henry Ford, around the start of the 20th century, was quoted as saying that "history is bunk". While we believe strongly that history is of great importance, we also have to be well aware that the range and variety of changes confronting the world at present are greater, and are occurring more rapidly, than has ever been the case in the history of mankind. To quote Dr Rick Satava, an eminent surgeon with NASA: "The future isn't what it used to be."23 References Yellowlees P. Therapy online. Kansas: Telemedicine Today, 1999. Queensland Telemedicine Network. Queensland Health. <http://www.health. qld.gov.au/qtn/home.htm>. Accessed 18 October 1999. Yellowlees PM, Kennedy C. Telemedicine: here to stay. Med J Aust 1997; 166: 262-265. University Corporation for Advanced Internet Development. The Internet2 Project. <http://www.internet2.edu/>. Accessed 18 October 1999. Cairncross F. The death of distance. How the communications revolution will change our lives. Boston: Harvard Business School Publishing, 1997. Virtual Collaborative Clinic. <http://www.nren.nasa.gov/vdoc.html>. Accessed 5 October 1999. Graphics Visualisation and Usability Center, College of Computing, Georgia Tech. Virtual Reality Exposure Therapy. <http://www.cc.gatech.edu/gvu/virtual/Phobia/>. Accessed 5 October 1999. Van Houweling D. Distributed Education. 1998. Telecon '98 Conference, Anaheim, California. Appleyard R. Enhancing internet medical document retrieval with 'medical core metadata'. Health Information on the Internet 1999; 10: 6-8. United States National Library of Medicine. <http://www.nlm.nih.gov/>. Accessed 18 October 1999. HealthInsite. Commonwealth Department of Health and Aged Care. <http://www.healthinsite.gov.au/>. Accessed 18 October 1999. OMNI: Organising Medical Networked Information. <http://omni.ac.uk/>. Accessed 5 October 1999. Discern Online. <http://www.discern.org.uk/>. Accessed 12 October 1999. Distributed Systems Technology Centre. <http://www.dstc.edu.au/>. Accessed 5 October 1999. Centre for Online Health. University of Queensland. <http://www.coh.uq.edu.au/>. Accessed 5 October 1999. Centre of Medical Informatics. Monash University. <http://www.monash.edu.au/informatics/>. Accessed 5 October 1999. Biomedical Systems Laboratory. University of New South Wales. <http://www.bsl.unsw.edu.au/>. Accessed 5 October 1999. Collaborative Health Informatics Centre. <http://www.chic.org.au/main.html>. Accessed 5 October 1999. Murray CJ, Lopez AD, editors. The global burden of disease: a comprehensive assessment of mortality and disability from diseases, injuries, and risk factors in 1990 and projected to 2020. Harvard School of Public Health, 1996. Carlile S, Sefton AJ. Healthcare and the information age: implications for medical education. Med J Aust 1998; 168: 340-343. Coiera E. Medical informatics meets medical education. Med J Aust 1998; 168: 319-320. Mohan J. Malaysia's Telemedicine Vision and Initiatives. 1997. Telemed Asia '97 Conference, Kuala Lumpur, Malaysia. Satava RM. Telemedicine and virtual reality. American Telemedicine Association Annual Meeting, Salt Lake City. 17-21 April 1999. Authors' details Faculty of Health Sciences, University of Queensland, Brisbane, QLD. Peter M Yellowlees, MD, FRANZCP, Professor of Psychiatry, and Director, Centre for Online Health; Peter M Brooks, MD (Monash), FRACP, Professor, and Executive Dean. Reprints will not be available from the authors. Correspondence: Professor P M Yellowlees, Department of Psychiatry, University of Queensland, K Floor, Mental Health Centre, Royal Brisbane Hospital, Brisbane, QLD. P. YellowleesATmailbox.uq.edu.au http://www.coh.uq.edu.au Changing information technologies The technical ability to obtain high quality health information in the home or on the doctor's desktop depends on two things: bandwidth and accessibility. Both are on the point of being transformed to make massive amounts of information easily available to the clinician. The bandwidth issue relates to the development of Internet2 by a consortium of about 200 partners, mainly in North America, and including over 130 universities and more than 40 commercial concerns. Internet2 is expected to be between 100 and 1000 times more powerful than the present Internet. It will use much more efficient methods of information packaging to send more information down an equivalent-sized channel in a given time. This will enable a whole new generation of applications and has the potential to transform our lives in ways we cannot yet imagine.4 The issue of accessibility to information is also being resolved within First World countries, although it is crucial to note that in 1999 two-thirds of the world's population still do not even have access to a telephone.5 There are already over half a million kilometres of fibreoptic cable connecting cities and countries around the world. This will double within the next five years. By the end of 2000, it is expected that the latest of many intercontinental data links, a massively powerful fibreoptic cable weaving from Germany through the Mediterranean, across south-east Asia and on to Japan and Korea, will be installed. Simultaneously, greatly improved interactive satellites are being launched. There are now more than 200 such satellites in low earth orbit, acting like mobile phone towers or repeaters above the earth. Within five years, it is likely there will be more than 1000 such satellites, providing accessible global coverage. Improved bandwidth and accessibility will provide the opportunity to radically change the way we work and conduct business. We will be able to develop fully digitised libraries that include comprehensive video and audio collections, as well as develop cyberclinics such as the NASA-sponsored Virtual Collaborative Clinic.6 There will also be collaborative virtual research laboratories enabling "tele-immersion" - the ability to move inside space, inside the human body and into virtual reality situations. Virtual reality scenarios, where the patients move into a virtual world as part of their treatment process, are already being used to treat patients with specific phobias of heights and spiders.7 Scenarios also exist to allow surgeons to immerse themselves within a virtual middle ear, and teach the anatomy, pathology and surgery of the ear from within that organ.8 Glossary Bandwidth: The data transfer rate of an electronic communications system. Internet: An electronic communications network that connects computer networks and organisational computer facilities around the world. Internet protocol: The communications methods used for the Internet. Metadata: Data about data, such as what field the data relate to, who compiled the dataset, or how the data are formatted. Telemetry: Measurement of data and transmission to another site for storage or analysis. Virtual reality: An artificial environment which is experienced through sensory stimuli (as sights and sounds) provided by a computer and in which one's actions partially determine what happens in the environment. Back to textBack to textBack to textBack to text

Peter M Yellowlees · Peter M Brooks