Editorials

Editorial Preventing stroke: what is the real progress? At last, stroke prevention is high on the political and public health agenda MJA 1999; 171: 285-286 National Stroke Awareness Week (27 September - 3 October) is a pertinent time to review recent progress in stroke prevention and awareness in the past few years. In Australia, stroke continues to be a major public health issue.1 More than 40 000 Australians each year experience a stroke, nearly a third of which are fatal.1,2 Another third of stroke sufferers become disabled, and stroke victims make up nearly one in four of Australia's chronic disabled population.1 The annual total cost of caring for stroke victims is at least $1.67 billion,2 a figure which will continue to rise with ageing of Australia's population. It is estimated that there will be at least 70 000 new stroke patients each year by 2016.2Nevertheless, real progress has been made in the past few years in several areas: The emergence, and application in clinical practice, of sound evidence for the effectiveness of several stroke-prevention strategies in people at high risk; A decline in stroke incidence due to effective prevention measures; and A willingness of Federal, State and Territory governments to take a more active role in stroke prevention. Strategies for reducing the social and economic burden of stroke are summarised in the Box. The effectiveness of primary stroke prevention in the entire population is difficult to ascertain. Mortality statistics are the only routinely collected data for measuring and monitoring the burden of stroke nationally, and between 1986 and 1997 the stroke mortality rate for Australian men and women fell by 3.2% and 3.5% per year, respectively. Since 1970 there has been a 68% overall reduction in stroke mortality.1,3 The recent Perth Community Stroke Study (PCSS)4 found that the decline in stroke mortality was due to a reduced incidence of stroke rather than an improvement in survival or a change in casemix (eg, a reduced proportion of lethal intracerebral haemorrhages). This fall in stroke incidence is likely to be due to a decline in the prevalence of important causal and modifiable risk factors. The PCSS identified several of these risk factors, many of which are well established, and some of which require confirmation in future studies.5 These include previous stroke or transient ischaemic attack, cigarette smoking, excess alcohol intake (> 60 g daily), a history of hypertension, diabetes mellitus, meat consumption (more than four times weekly), and adding salt to food. Over the past one to two decades, the Australian Institute of Health and Welfare (AIHW) has documented a significant decline in the population prevalence of many of these risk factors (ie, hypertension, smoking, total dietary fat intake, and saturated fat as a proportion of total energy intake).1 Although it is not possible to prove that health promotion programs, government legislation and the decline in prevalence and mean level of risk factors have been directly responsible for the reduction in stroke incidence in Australia, I believe the above data endorse the concept and power of the population approach to stroke prevention. It might be argued that the population approach impinges on all for the benefit of relatively few.3 However, most of us are prepared to adopt lifestyle behaviours (eg, wearing of seatbelts, application of sunscreen lotion) which reduce harm to the population as a whole, and stroke prevention measures would be similar in principle. Moreover, given that the risk of stroke in the next 40 years for a 45-year-old is one in four for men and one in five for women,1 there is also a reasonable chance of individual benefit in adopting lifestyle changes aimed at reducing the risk of stroke. The push for greater stroke awareness in our society has received a considerable boost in recent years from a greater involvement of governments in promoting awareness of stroke and facilitating educational programs aimed at reducing the risk of stroke. The involvement is exemplified by: Establishment of the National Stroke Foundation, which published a National Stroke Strategy and Victorian Stroke Strategy in 1997;9 Establishment by the New South Wales Health Department of the NSW Stroke Project;10 Endorsement by Australian health ministers of heart, stroke and vascular disease as one of the five National Health Priority Areas (NHPAs). The recent NHPA report, Cardiovascular Health 1998,11 highlights the strategies that are in place (and to be developed) to prevent stroke by improving awareness, lifestyle behaviours, and risk factor profiles of Australians, and improving outcomes for those with symptomatic disease through optimal diagnosis, management, rehabilitation, and community care.11 It also emphasises the ongoing role of the AIHW in operating a national system to monitor stroke incidence, pathology, risk factors, treatments, care, outcome (for patients and carers) and costs. At last, stroke is high on the political and public health agenda, but it is crucial that the commitment be maintained to measuring, monitoring and reducing the burden of stroke by widespread adoption of evidence-based practices and other strategies outlined in the NHPA report.11 Otherwise, we will soon experience a needless epidemic of stroke, with its legacy of death, disability and mounting cost. Graeme J Hankey Consultant Neurologist, and Head of Stroke Unit, Royal Perth Hospital Clinical Associate Professor, Department of Medicine, University of Western Australia, Perth, WA Email: gjhankeyATcyllene.uwa.edu.au Australian Institute of Health and Welfare (AIHW). Heart, stroke and vascular diseases, Australian facts. Canberra: AIHW/Heart Foundation of Australia, 1999. (AIHW Catalogue No. CVD 7; Cardiovascular Disease Series No. 10.) National Health and Medical Reseach Council (NHMRC). Clinical Practice Guidelines. Prevention of stroke: the role of anticoagulants, antiplatelet agents and carotid endarterectomy. Canberra: NHMRC/Australian Government Publishing Service, 1997: 3-4. Rose G. The strategy of preventive medicine. Oxford: Oxford University Press, 1992: 29-52, 64-106. Jamrozik K, Broadhurst R, Lai N, et al. Trends in the incidence, severity and short-term outcome of stroke in Perth, Western Australia. Stroke 1999. In press. Jamrozik K, Broadhurst RJ, Anderson CS, Stewart-Wynne EG. The role of lifestyle factors in the etiology of stroke. A population-based case-control study in Perth, Western Australia. Stroke 1994; 25: 51-59. Hankey GJ. Stroke: how large a public health problem, and how can the neurologist help? Arch Neurol 1999; 56: 748-754. Hankey GJ, Warlow CP. Treatment and secondary prevention of stroke: evidence, cost, and effects on individuals and populations. Lancet 1999. In press. Gorelick PB, Sacco RL, Smith DB, et al. Prevention of a first stroke. A review of guidelines and a multidisciplinary consensus statement from the National Stroke Association. JAMA 1999; 281: 1112-1120. National Stroke Strategy. Melbourne: National Stroke Foundation, 1997. Stroke in NSW. Priorities and strategies for better care. Sydney: NSW Health Department, 1997. Commonwealth Department of Health and Aged Care and Australian Institute of Health and Welfare. National Health Priority Area Report: Cardiovascular Health 1998. Canberra: Australian Institute of Health and Welfare, 1999. (Catalogue No. PHE9.) Strategies for reducing the burden of stroke and stroke recurrence (in increasing order of potential impact)6,7 Effective treatment of acute stroke6,7 Organised care in a stroke unit by a multidisciplinary team Aspirin 300 mg for acute ischaemic stroke tPA (may be effective, but possibly hazardous, and therefore is not currently registered in Australia or Europe for stroke treatment6) Secondary prevention of recurrent stroke in patients with transient ischaemic attacks (TIAs) and stroke (in decreasing order of cost-effectiveness)7* Treatment of high blood pressure with a diuretic or β-blocker Aspirin, aspirin + dipyridamole, or clopidogrel for patients in sinus rhythm Anticoagulation with warfarin for patients with atrial fibrillation Carotid endarterectomy for patients with severe stenosis of the internal carotid artery on the symptomatic side Primary prevention of stroke among people at high risk of stroke (eg, those with severe hypertension or atrial fibrillation)3,8 Treatment of high blood pressure with a diuretic or β-blocker "Statins" to lower serum cholesterol levels in patients with symptomatic coronary artery disease or hypercholesterolaemia Anticoagulation with warfarin for patients with atrial fibrillation and specific risk factors (age > 65 years, diabetes, hypertension, TIA or stroke), or patients with recent myocardial infarction who have atrial fibrillation, decreased left ventricular ejection fraction, or left ventricular thrombus Primary prevention of stroke in the general population by reducing risk factors3,6Reducing consumption of meat, salt, saturated fat and alcohol Reducing prevalence of smoking Reducing prevalence of obesity Increasing physical activity Controlling hypertension and hypercholesterolaemia Controlling diabetes mellitus *Randomised trials of the effect of smoking cessation, other antihypertensive agents, and 3-hydroxy-3-methylglutaryl coenzyme A (HMGCoA) reductase inhibitors ("statins") in secondary stroke prevention are either still in progress or yet to be undertaken. Back to text

Graeme J Hankey

Editorial Nurses in Australia: their role today and tomorrow The old stereotypes are long gone and the new nurse is developing swiftly MJA 1996; 164: 520-521 May 12 is International Nurses' Day, in tribute to nurses and the role they play in delivering health care. In Australia, the nature of this role has changed significantly over the past three decades. The momentum for this change has come in response to forces from both within and without the profession: the women's movement of the 1970s dramatically altered expectations of work for this once almost totally female workforce;1 in the 1980s, tertiary education was introduced; and in the 1990s, nursing has not escaped the impact of deregulation of the labour market, multiskilling and the drive towards greater efficiency and productivity in the face of economic pressures. Impact of tertiary education Newly qualified nurses are now the product of a liberal education, quite different from the hospital-based education of the past. Indeed, all nurses have embraced the tertiary opportunities that the transfer of nurse education has provided. The demand for places to convert certificate or diploma qualifications to degrees remains strong in the 34 universities with faculties or schools of nursing in Australia.2 So, too, does the demand for places for graduate diplomas and higher degrees; about half the schools of nursing offer doctoral programs3 and the number of nurses who have gained doctorates is increasing. This has in turn led to the creation of more chairs of clinical nursing (18 as of March 1996, with more pending [Professor S McKinley, Secretary to the Australian Professors of Clinical Nursing Association, personal communication]). As well as providing education, universities have promoted and stimulated research that is contributing to the developing knowledge base for nursing practice. This work, together with hospital-based research and that of newly established nursing research centres, is crucial to the evolution of the nurse's role and to the provision of evidence-based care unique to nursing. In fact, increased scientific knowledge and resulting new technologies and treatment methods are increasing the complexity of nursing practice. And in the constant interplay between education and research, education to maintain and develop new practical skills has become a critical necessity. Other influences Influences apart from those of education and research have led to further developments in the role of nurses. At times, blurred boundaries with the roles of other health workers have resulted, with accompanying dilemmas. For example, economic forces have led to the increasing employment of less skilled workers who have taken on some of the work of nurses, mostly outside the regulatory framework that governs nurses -- grave questions about accountability and duty of care need to be answered. For example, to whom and for what are personal care attendants, with no knowledge of drugs, accountable in administering prescribed medications without supervision? Indeed, the general decline in resources and the restructuring of service delivery systems will continue to impact on the role of nurses. Advancing technology is also associated with yet-to-be-resolved legal and ethical dilemmas in the role of nurses (as for all health practitioners) -- dilemmas, such as euthanasia and assisted suicide, that are no longer remote but immediate and omnipresent. Expanding roles The expansion of the nurse's role is challenging the existing statutory limitations on nursing practice. For example, nurses in intensive care units are at the cutting edge of technological innovation and often undertake activities once thought to be the sole province of medical practitioners.4 Nurses in remote areas have long been expected to act outside the boundaries of the nurse's role and have articulated the case for an expanded role (e.g., the right to prescribe some medications or to order pathological tests).5,6 Further, nurses in women's health services in most States and Territories find the absence of such rights (including also the right to refer clients to specialist services) prevents delivery of optimal patient care.7 A review of existing nursing roles with new and expanded boundaries is almost complete in New South Wales.8 The Nurse Practitioner Review, sponsored by the New South Wales Health Department, started in November 1993 and has included 10 pilot projects to evaluate three models of nursing roles with expanded responsibilities: Nurse Practitioner Remote Area, Nurse Practitioner General Practice and Nurse Practitioner Area and District Health. Within the context of each practice, extra responsibilities include ordering diagnostic procedures, prescribing and receiving or making referrals. The scope that the nurse practitioner role offers for advanced practice in nursing is a major attraction for nurses. And, given the developments in their preparation and the growth of nursing knowledge, it is a role that nurses are ready to fulfil. Within the wider context of all health care professions, nurses wish to work collaboratively, as team members, and to be consulted about their views on people's health care needs. They wish to be acknowledged for the contribution they make to patient recovery and to maintaining people's health and for the care and support they give to the dying; nurses are arguably the health professionals most intimate with people's lives and they recognise their resulting position of privilege and trust. And, in the challenging climate of change continually impacting on so many aspects of the nursing role, at least one aspect will persist: nurses will continue to support the values of caring and comfort that have always underpinned their practice. Elizabeth C Percival Executive Director, Royal College of Nursing, Canberra, ACT Helen M Hamilton Project Officer, Royal College of Nursing, Canberra, ACT Beaumont M. The professional role of a national nursing organisation. In: Gray G, Pratt R, editors. Issues in Australian nursing 2. Melbourne: Churchill Livingstone, 1989; 247-261. Report of the national review of nurse education in the higher education sector: 1994 and beyond. Canberra: AGPS, 1994: 143. Royal College of Nursing, Australia. Directory of higher education nursing courses. Sydney: New Hobson Press, 1996. Bucknall T, Thomas S. Clinical decision making in critical care. Aust J Adv Nurs 1995; 13 (2): 10-17. Kreger A. Remote area nursing practice: a quest for education. Report to the Council of Remote Area Nurses Inc. CRANA, 1991: 57-60. Buckley P, Gray G. Across the spinifex: registered nurses working in rural and remote South Australia. Adelaide: School of Nursing, Flinders University, 1993: 143. New South Wales Health Department. Role and function of nurse practitioners in New South Wales. Discussion paper. Sydney: NSW Health, 1992: 7, 13-17. (NSW State Health Publication No. [NB] 93-120.) New South Wales Health Department. Nurse Practitioner Review Stage 2. Vol 2. Sydney: NSW Health, 1993. A1/1-A5/1-20. (NSW State Health Publication No. [NB] 93-120.) ©MJA 1999 © 1999 Medical Journal of Australia.

Elizabeth C Percival · Helen M Hamilton

Editorial Measuring the success of joint replacement surgery Patients need measures that help them make informed choices MJA 1999; 171: 229-230 The United Nations General Assembly designated 1999 as the International Year of Older Persons. Population ageing is a major focus of social and economic planners and policymakers in Australia. One particular concern is to provide equitable, affordable and appropriate health care services to older people.1 In 1998, in Australia, there were 2.3 million people aged 65 years and over, including 976 500 who were aged 75 years and over. The proportion of the population aged 65 and over is projected to increase from 12% to 21% between now and 2031.2 Osteoarthritis, of which the principal symptoms are pain and restricted joint movement, affects about 25% of people over 65 years and contributes to restricted mobility, the most common form of disability among older men and women.3 North American studies have shown that total hip replacement and total knee replacement effectively reduce pain and improve function in patients with advanced osteoarthritis.4,5 Such surgery is associated with significant improvements in health status and quality of life. However, surprisingly little is known about the epidemiology and outcomes of joint replacement surgery for osteoarthritis in Australia. To define the national practice and outcomes of joint replacement surgery, the Australian Orthopaedic Association established the National Joint Replacement Registry in 1998. The Registry has received significant federal funding, is supported by industry and has been defined as a Federal Quality Assurance Activity. Data collected by the Registry from State and Territory health departments indicated that, in 1997-1998, 13 545 primary total hip replacements and 15 599 primary total knee replacements were performed in Australia. Data from a Registry pilot study of 260 patients undergoing these procedures indicated that about 90% were performed for osteoarthritis and about 80% were in people aged 60 years and over (Dr S Graves, Project Director, Australian Orthopaedic Association National Joint Replacement Registry, personal communication). In this issue of the Journal, March and colleagues6 have investigated whether hip and knee replacement restore health-related quality of life (as measured with the Medical Outcomes Study Short-Form 36 [SF-36]) to that of the age-matched general population. They found that total hip replacement reduced pain and improved physical function in those undergoing surgery to that of the age-matched population. Social function and overall vitality were also restored. Although total knee replacement reduced pain and improved physical function somewhat, postoperative scores, particularly among younger patients, were still significantly less than the population norm or scores for patients undergoing total hip replacement. Similar findings have been reported elsewhere7-9March and colleagues have suggested that these findings might be related to factors such as unrealistic expectations or the presence of comorbidities. Others have been unable to explain the apparent difference in outcome between hip replacement and knee replacement as measured by the SF-36. Although it is possible that knee replacement is less effective than hip replacement in improving quality of life, it is also possible that the SF-36 is less responsive to change following knee replacement. Perhaps restoration of hip function allows patients to perform the activities defined on the SF-36 better than restoration of knee function. March et al noted that the general health of the younger patients undergoing knee replacement declined in the year after surgery. It is not clear to what extent the decline in health status was a contributor to or a consequence of the poorer functional outcomes of surgery in this age group. The effect of comorbidities on long-term outcomes after joint replacement surgery requires further investigation. Debate continues over the best way to assess the outcomes of joint replacement surgery. Currently, radiological, functional, health status, quality-of-life and global satisfaction instruments are being used to provide comprehensive assessment. Yet, it appears that the more generic the instrument, the less responsive it is to change following joint replacement surgery.4 There is no clear correlation between improvements in health status and health perceptions after joint replacement surgery.10 Should we use disease-specific or more global quality-of-life measures when trying to assess the value of therapy, particularly in the elderly? Disease-specific measures may provide more relevant information to patients and clinicians than global measures. Patients can be told that, after hip replacement, it is likely they will have less pain and be able to better perform activities of daily living such as dressing, sitting, walking or climbing stairs. The patient can then weigh these benefits against the risks and complications of surgery and make an informed decision. Patients may have more difficulty in making such decisions if outcomes are expressed in terms of improved vitality or sense of well-being, particularly if it is known that such outcomes can be influenced by comorbidities. On the other hand, global measures allow comparisons between hip replacement surgery and treatments of other conditions, which might help a patient to determine treatment priorities. The best instrument is the one that measures the outcome of greatest relevance. Our challenge, in the International Year of Older Persons, must be to define the outcomes of greatest relevance to the elderly. Owen D Williamson Orthopaedic Surgeon Alfred Hospital, Melbourne VIC email: owen.williamsonATbigpond.com Commonwealth Department of Health and Family Services Conference for Older Australians Interim Report. Canberra: The Department, 1998 (Publication No. 2325). Australian Bureau of Statistics. Australian Social Trends 1999. Catalogue No. 4102.1, 1999. Australian Bureau of Statistics. National Health Survey: Summary of Results. Canberra, ABS: 1995 (Catalogue No. 4364.0). Kreibich DN, Vaz M, Bourne RB, et al. What is the best way of assessing outcome after total knee replacement? Clin Orthop 1996; 331: 221-225. Laupacis A, Bourne R, Rorabeck C, et al. The effect of elective total hip replacement on health-related quality of life. J Bone Joint Surg [Am] 1993; 75-A: 1619-1626. March LM, Cross MJ, Lapsley H, et al. Outcomes after hip or knee replacement surgery for osteoarthritis. Med J Aust 1999; 171: 235-238. Hozack WJ, Rothman RH, Albert TJ, et al. Relationship of total hip arthroplasty outcomes to other orthopaedic procedures. Clin Orthop 1997; 344: 88-93. Van Essen GL, Chipchase LS, O'Connor D, Krishnan J. Primary total knee replacement: short-term outcomes in an Australian population. J Qual Clin Practice 1998; 18: 135-142. Birdsall PD, Hayes JH, Cleary R, et al. Health outcome after total knee replacement in the very elderly. J Bone Joint Surgery [Br] 1999; 81-B: 660-662. McGuigan FX, Hozack WJ, Moriarty L, et al. Predicting quality-of-life outcomes following total joint arthroplasty. Limitations of the SF-36 health status questionnaire. J Arthroplasty 1995; 10: 742-747.

Owen D Williamson

Editorial Cluster investigations: are they worth it? The odds are against finding a cause, but we must address community concerns MJA 1999; 171: 172 The unexpected clustering of rare and often fatal diseases in specific localities gives cause for concern. When it happens, members of the public often draw it to the attention of their doctors, who in turn pass on the information to local public health units or other authorities. The outcomes of systematic investigation of such disease clusters rarely see the light of day in peer-reviewed journals. In that regard the report in this issue of the Journal by Westley-Wise and her colleagues of an investigation into a cluster of leukaemia cases among residents near a major steelworks is unusual.1 What is not unusual, however, is the report's failure to produce a persuasive explanation for the observed cluster, although it usefully reports some ambient benzene levels (levels that are orders of magnitude lower than those known to produce health effects and similarly lower than levels inhaled in cigarette smoke). Of the many studies investigating close case aggregations of any type, only a few have come up with a credible explanation of why the disease cluster exists or have added to knowledge of the causes of disease. Such exceptions would include, for example, the links found between angiosarcoma of the liver and vinyl chloride monomer exposure,2or mercury poisoning in Minamata, Japan.3 These instances demonstrated strong associations that hardly required the sophisticated statistical tools of modern epidemiology to be identified as "possible" causal links. Sadly, experience tells us that almost all cluster investigations will fail to produce insights into environmental disease interactions, and no amount of time, effort and money will change this. This is for a number of reasons. Clusters are by definition based on tiny case numbers. As such, they may not represent the "typical" disease and are not amenable to epidemiological analyses. Further, most reported clusters tend to be of conditions where little or nothing is known of the common causes. There are often controversial theories relating to the condition (eg, the hypothesis that proximity to powerlines can cause cancer). Finally, the supposed environmental-disease links are often impossible to investigate satisfactorily because of the lapse of time or because it is simply not clear what to investigate. The tenfold excess of childhood cancers in the United Kingdom near the Sellafield reprocessing plant4 has been under investigation for a decade, to no avail. Why then do we continue to spend time investigating these phenomena? Why indeed does every state health department in the USA have its own "cluster investigation protocol"? And why did my colleagues and I produce a similar protocol in the UK in 1997?5 Most public health doctors know that having a disease cluster to investigate is a thankless task. Not to have an investigation at all would be regarded with deep suspicion, while investigations with negative results can lead to accusations of a cover-up. On balance, it is better to hold an investigation than not. So the optimistic epidemiologist, hoping that unexpected insights will drop out of the investigation and reveal a truly causal association, adopts a careful protocol to maximise the chances of success. The pessimist feels that at least a sound methodological approach will guard against the reproaches that may follow a negative finding. All the professionals involved are aware that a bad cluster investigation generates considerable disquiet among the public and tends to give them a bad press. Most therefore take the process to be as important as the outcome -- hence the various guidelines. Guides to cluster investigation tend to have a common theme of transparency of action and a candid approach to the concerned parties. They usually suggest various strategies for investigation, one of which is to take the local concern about the cause of the disease cluster as a hypothesis to test. Indeed, testing this hypothesis is often the best "outcome" of any investigation. Westley-Wise et al tested the hypothesis that the leukaemia cluster was caused by pollution from the neighbouring coke-making facilities.1 Their negative findings, if they succeed in allaying local concerns about this point, will be something of a positive outcome. It has to be said that clusters can and do occur fortuitously. It is possible to calculate how often chance events play a part in clustering. This explanation for a cluster, however, is the one least likely to have credibility with those closely concerned. Perhaps the only sensible way forward is to address the underlying issue that usually starts a cluster investigation -- what are the significant causes of a condition? That is best tackled, not by a cluster investigation, but by the combined efforts of laboratory-based sciences and large epidemiological investigations -- usually cohort or case-control studies. This type of effort has been made (internationally) to elucidate the possible causes of childhood leukaemia (a frequent target of cluster investigation). The next year or so will see the assembly of combined and very large datasets that might tell us why this condition appears to "cluster". Possible small risks (such as powerlines) can be found or discounted, and more plausible, but complex, biological phenomena relating to infection in early life can be properly investigated. The latter will be the focus of much attention. Ray A Cartwright Director, Leukaemia Research Fund Centre for Clinical Epidemiology University of Leeds, UK Westley-Wise VJ, Stewart BW, Kreis I, et al. Investigation of a cluster of leukaemia in the Illawarra region of New South Wales, 1989-1996. Med J Aust 1999; 171: 178-183. Baxter PJ, Anthony PP. Angiosarcoma of the liver in Great Britain, 1963-73. BMJ 1977; 2: 919-921. Tsuchiqa K. The discovery of the causal agent of Minamata disease. Am J Indust Med 1992; 21: 275-280. Draper GJ, Stiller C, Cartwright RA, et al. Cancer in Cumbria and in the vicinity of the Sellafield nuclear installation 1963-1990. BMJ 1993; 306: 89-94. Arrundale J, Bain M, Botting B, et al. Handbook and guide to the investigation of clusters of diseases. London: Leukaemia Research Fund, 1997.

Ray A Cartwright

Editorial "Smoking is a major cause of blindness" A new cigarette pack warning? MJA 1999; 171: 173-174 Health warnings on Australian tobacco products have been mandated through federal legislation since 1973, being updated in 1987 and 1995. Issue of the current warnings followed a detailed study examining the likely impact of prototypes, particularly on youth.1 The warnings address general health ("Smoking kills"), lung cancer, heart disease, addiction, low infant birthweight, and harm to others through passive smoking. The adoption of health warnings was vigorously opposed by the tobacco industry, whose internal research indicated that many smokers disliked their prominence and more detailed content.2 Internationally, the track record of the tobacco industry has been to oppose more "hard-hitting", specific warnings in favour of blander, more general warnings such as "Smoking reduces your fitness". We propose a new "hard-hitting" cigarette pack warning. Recent population-based cross-sectional data from four countries3-6 including Australia,7 together with data from two large cohort studies,8,9 have consistently identified smoking as the strongest environmental risk factor for age-related macular degeneration (AMD), the leading cause of blindness in Australia.10,11 All of these studies have shown that people who currently smoke are two to five times more likely to develop AMD than non-smokers or past smokers, and several have demonstrated a dose-response relationship with pack-years of smoking,6,8,9 and a decreased risk with longer duration since cessation.4 Evidence of a gradient between amount smoked and AMD severity has also been shown.4,7 Based on data from two large population-based Australian studies,12,13 there are currently around 34 500 Australians aged over 50 years with legal blindness (ie, they qualify for blind pension benefits because visual acuity in both eyes is reduced to < 6/60). In over 80% of these people, blindness is due to AMD.12 Two late stage AMD lesions causing visual loss have been defined: "neovascular AMD", characterised by macular haemorrhage and scarring (responsible for two-thirds of cases), and "geographic atrophy", an atrophic macular lesion which accounts for the remaining third.11 Increasing age is the strongest risk factor for AMD, with the prevalence of late stage lesions rising from under 1% in people aged less than 70 years to over 10% in over-80-year- olds and more than one third in over-90-year-olds.12 To date, longitudinal data relating smoking to the incidence of AMD are less conclusive than cross-sectional population-based studies. Both the Nurses' Health Study8 and the Physicians' Health Study,9 however, relied on self-reported diagnosis of AMD. The Macular Photocoagulation Study report14 did not find an association between a history of current smoking at the start of the trial and incidence of AMD, but there may have been selection bias in the recruitment of patients to a laser treatment trial. Follow-up examinations have now been performed in three of the four population-based cohorts3,4,7 to assess risk factors for AMD. Of these, the Beaver Dam Eye Study is the only cohort yet to report incidence data.15 This study found that, in both men and women, smoking was related to the incidence of large drusen, the principal precursor lesion for late stage AMD lesions.16 Individually, each of the three studies has relatively low statistical power to examine risk factors for incident late stage AMD lesions, so that pooling of data may be useful. Despite the present lack of firm incidence data, all of the recent cross-sectional studies show a consistency of findings that is difficult to ignore. We estimate that there are currently almost 100 000 people with late stage AMD in Australia, of which around 20 000 may have AMD directly attributable to smoking. Further, we estimate that there are currently more than 8200 Australians whose blindness from late stage AMD can be attributed to smoking. These estimates, shown in the Table, are based on Australian data collected in the Blue Mountains Eye Study. Population-attributable risk estimates were derived from odds ratios adjusted for age and sex.7 We repeated the calculations using risk ratios from the Beaver Dam and Rotterdam studies,3,4 and these separately provided evidence that around 10 000 Australians are currently likely to be blind as a result of smoking. As our population ages, the prevalence of AMD and age-related blindness will increase. At present, the only preventable confirmed risk factor for AMD is smoking. We estimate that smoking may now be responsible for around 20% of all cases of blindness in Australians over the age of 50 years. As 80%-90% of blindness in Australia occurs in those over 50 years, there is a similar overall proportion of people blind as a result of smoking. Most Australian smokers are aware that smoking is harmful to health. However, knowledge of the role of smoking in causing many specific diseases is unacceptably low. For example, a Victorian study found that the percentage of smokers able (unprompted) to nominate specific conditions linked to smoking was 54% (lung cancer), 38% (emphysema), 38% (heart attack), 20% (unspecified cancer), 17% (asthma), and 22% (bronchitis/respiratory problems).17 While research has shown dramatic increases in recognition of cigarette pack warnings, only 66% of Australian smokers say that they "at least sometimes notice" the current warnings.18 There is clearly room for improvement. Pack warnings that are novel and targeted at the concerns of specific population subgroups are likely to have greater impact than blander, older and more general warnings.19 As further epidemiological evidence becomes available on the role of smoking in causing specific diseases, it is important that this is reflected in public information campaigns and warnings. For example, on 5 November 1998, the Thai government required "Smoking causes impotence" to be included among the mandated warnings appearing on cigarette packs. There is no treatment for the majority of AMD cases, and support services for blind people are very costly. The eyes are popularly venerated as "mirrors to the soul" and blindness is greatly feared. Everyone can imagine what it would be like to be blind. If "Smoking is a major cause of blindness" were added to the current Australian set of health warnings, some smokers might reconsider their continued tobacco use. Paul Mitchell Associate Professor, Department of Ophthalmology University of Sydney, Sydney, NSW Simon Chapman Associate Professor Department of Public Health and Community Medicine University of Sydney, Sydney, NSW Wayne Smith Senior Research Fellow National Centre for Epidemiology and Population Health Australian National University, Canberra, ACT Email: paulmiATwestmed.wh.su.edu.au Acknowledgement: The Blue Mountains Eye Study was supported by the National Health and Medical Research Council and the Save Sight Institute, University of Sydney Borland R, Hill D. The path to Australia's tobacco health warnings. Addiction 1997; 92: 151-157. <http://www.pmdocs.com/getallimg.asp?DOCID=2504091432/1443> and <http://www.health.su.oz.au/tobacco/Ozdocs.html#Plain packaging> Klein R, Klein BE, Linton KL, DeMets DL. The Beaver Dam Eye Study: the relation of age-related maculopathy to smoking. Am J Epidemiol 1993; 137: 190-200. Vingerling JR, Hofman A, Grobbee DE, de Jong PT. Age-related macular degeneration and smoking. The Rotterdam Study. Arch Ophthalmol 1996; 114: 1193-1196. Klaver CC, Assink JJ, Vingerling JR, et al. Smoking is also associated with age-related macular degeneration in persons aged 85 years and older: The Rotterdam Study [letter]. Arch Ophthalmol 1997; 115: 945. Delcourt C, Diaz JL, Ponton Sanchez A, Papoz L. Smoking and age-related macular degeneration. The POLA Study. Arch Ophthalmol 1998; 116: 1031-1035. Smith W, Mitchell P, Leeder SR. Smoking and age-related maculopathy. The Blue Mountains Eye Study. Arch Ophthalmol 1996; 114: 1518-1523. Hankinson SE, Willett WC, Colditz GA, et al. A prospective study of cigarette smoking and risk of cataract surgery in women. JAMA 1992; 268: 994-998. Christen WG, Manson JE, Seddon JM, et al. A prospective study of cigarette smoking and risk of cataract in men. JAMA 1992; 268: 989-993. Cooper RL. Blind registrations in Western Australia: a five year study. Aust N Z J Ophthalmol 1989; 107: 875-879. Mitchell P, Smith W, Attebo K, Wang JJ. Prevalence of age-related maculopathy in Australia. The Blue Mountains Eye Study. Ophthalmology 1995; 102: 1450-1460. Attebo K, Mitchell P, Smith W. Visual acuity and the causes of visual loss in Australia. The Blue Mountains Eye Study. Ophthalmology 1996; 103: 357-364. Taylor HR, Livingston PM, Stanislavsky YL, McCarty CA. Visual impairment in Australia: distance visual acuity, near vision, and visual field findings of the Melbourne Visual Impairment Project. Am J Ophthalmol 1997; 123: 328-337. Macular Photocoagulation Study Group. Risk factors for choroidal neovascularization in the second eye of patients with juxtafoveal or subfoveal choroidal neovascularization secondary to age-related macular degeneration. Arch Ophthalmol 1997; 115: 741-747. Klein R, Klein BE, Moss SE. Relation of smoking to the incidence of age-related maculopathy. The Beaver Dam Eye Study. Am J Epidemiol 1998; 147: 103-110. Klein R, Klein BE, Jensen SC, Meuer SM. The five-year incidence and progression of age-related maculopathy: the Beaver Dam Eye Study. Ophthalmology 1997; 104: 7-21. Mullins R, Morand M, Borland R. Key findings of the 1994 and 1995 household surveys. Quit Evaluation Studies Number 8, 1994-1995. Melbourne: Centre for Behavioural Research in Cancer, 1996. Borland R. Tobacco health warnings and smoking-related cognitions and behaviours. Addiction 1997; 92: 1427-1435. Fischer PM, Krugman DM, Fletcher JE, et al. An evaluation of health warnings in cigarette advertisements using standard market research methods: what does it mean to warn? Tob Control 1993; 2: 279-285. Reprints: Professor P Mitchell, Department of Ophthalmology, University of Sydney, Hawkesbury Road, Westmead, NSW 2145. Projected estimates of age-related macular degeneration (AMD) and blindness in Australia due to smokingSmoking prevalence §Sex, Age (years)Population at risk (1999)*Estimated no. of AMD cases †Estimated no. blind from AMD ‡FormerCurrentF, 55-59461 6001 385023.5%20.5%F, 60-69728 0204 25930423.8%14.5%F, 70-79601 48019 5476 03128.2%11.6%F, 80+352 52047 09219 20621.1%4.0%M, 55-59476 1600037.7%25.5%M, 60-69714 6201 980055.3%16.5%M, 70-79493 44010 5571 98757.1%13.0%M, 80+189 78014 0912 87434.1%4.5%Total4 017 62098 91130 402Estimated risk of AMD in smokers compared with never smokers (odds ratio) §Sex, age in (years)FormerCurrentAttributable risk for AMD in (former and current) smokers ¶Estimated no. of AMD cases due to smoking**Estimated no. blind from smoking**F, 55-591.25.653.0%7420F, 60-691.25.644.6%1 898136F, 70-791.25.640.1%7 8482 410F, 80+1.25.619.6%9 2253 765M, 55-591.63.161.0%00M, 60-691.63.168.1%1 3470M, 70-791.63.147.0%4 958933M, 80+1.63.125.6%3 610992Total20 4038 236 * Estimated Australian Population in 1999 interpolated from 1996 Census and 2001 projected population. † Based on Blue Mountains Eye Study prevalence estimates,11 using 5-year age-specific prevalence rates. ‡ Based on Blue Mountains Eye Study visual impairment data,12 assuming that 88% of age-related blindness is caused by AMD. § Based on Blue Mountains Eye Study smoking prevalence data.7 ¶ Calculated using formula: (smoking prevalence) x (odds ratio 2 1) {1 + (smoking prevalence) x (odds ratio2 1)}. ** Calculated from estimated numbers (AMD and blind) multiplied by percentage attributable risk. Back to text

Paul Mitchell · Simon Chapman · Wayne Smith

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

>Advances in technology and well documented clinical studies continue to expand the list of disorders amenable to laser therapy. In this issue, Tan and Vinciullo report their study of 186 children and adults with port-wine stains (capillary malformations) treated with a flashlamp-pumped tunable dye laser in Perth, Western Australia. They confirm reports from other countries of its efficacy and safety. Preferential uptake of yellow laser light (wavelength, 585 nm) by haemoglobin, combined with very short (450-µs) laser pulses, ensures maximum damage to small blood vessels with minimum heat transfer to surrounding tissue (selective photothermolysis).1 Good-to-excellent responses were seen in 78% of patients. The results are similar to those of a recent study at Royal Prince Alfred Hospital (RPAH), Sydney, and Flinders Medical Centre, Adelaide.2 Treatment failures may be related to depth and diameter of blood vessels, as the laser beam penetrates only about 1 mm. Given the well documented, sometimes severe but often hidden, psychological impact of a disfiguring port-wine stain, its potential complications and the lack of significant therapeutic alternatives, these results are impressive. However, critical issues apart from efficacy and safety include cost and access to treatment. The RPAH/Flinders study estimated the cost of treating a port-wine stain involving one cheek to be about $700-$1800 in an adult. This cost includes staff and topical or local anaesthesia, but not general anaesthesia, which is needed for most children. We must also add the laser capital costs (currently $150 000-$200 000) and substantial running costs. Will all patients with port-wine stains have access to a treatment now proven to be efficacious and safe? Ideally, all affected patients should be assessed at or soon after birth and treatment begun in the first two years of life and completed before the potential psychological impact of being a "marked child"3 has developed. Until recently at RPAH the estimated time to completion of treatment for children after assessment was 3.5 years. The service has been advertised only to dermatologists, because resources are too limited to treat the estimated potential number of patients, although the recent purchase of a third generation laser may increase the number able to be treated. Public hospital dermatological laser services vary between States and generally range from severely restricted to non-existent. Now that Australian studies have addressed issues of efficacy and cost, it is up to State Governments and the Federal Government to urgently establish appropriate funding arrangements. There is a large backlog of older children and adults who would benefit greatly from treatment. In the medium to long term, even with current technology, these patients could be treated, leaving a steady-state situation with only children in their first 2-4 years needing treatment. Treatment with the yellow-light laser is not confined to port-wine stains, but can be used for many other conditions characterised by a real or apparent excess of small blood vessels close to the surface of the skin. Proliferating or ulcerating capillary haemangiomas that affect vital structures (e.g., eyes, nose, mouth, pharynx and genitalia) in babies and young children have been shown in both Australia and other countries to respond to treatment with the flashlamp-pumped dye laser. This treatment is often urgent or semiurgent, depending on the rate of proliferation of the haemangioma or rate of ulceration and tissue destruction. Has technology in this area gone as far as it can? The answer is no. Newer lasers are now available that are able to operate several times faster than the initial pumped dye lasers and may require less maintenance. We await lasers that are more portable, cheaper and able to treat at a deeper skin level than current technology allows. Timely and affordable access to treatment for any patient, young or old, affected with a port-wine stain is the goal. Whether this is realised depends on a commitment by State and federal health funding bodies to recognise the extent of the problem, acknowledge the long term benefits of early treatment and provide an adequate funding mechanism. Margaret M Stewart Visiting Medical Officer, Department of Dermatology Royal Prince Alfred Hospital, Sydney, NSW Anderson RR, Parrish JA. Selective photothermolysis: precise microsurgery by selective absorption of pulsed radiation. Science 1983; 220: 524-527. Stewart M, Hailey D, Angel A. Yellow light lasers in dermatology. Canberra: Australian Institute of Health and Welfare, 1995: 1-43. Lanigan SW, Cotterill JA. Psychological disabilities amongst patients with port wine stains. Br J Dermatol 1989; 121: 209-215.

Margaret M Stewart

Editorial Vancomycin-resistant enterococci: causes and control? The overriding emphasis should be on control of antibiotic use in humans and animals MJA 1999; 171: 117-118 This issue of the Journal contains three articles on the emergence and control of vancomycin-resistant enterococci (VRE). Clinical infection with VRE was first noted in England and France in 1986,1,2 and was first detected in Australia (in Melbourne) in 1994.3 To September 1998, 69 sporadic and outbreak-associated strains had been identified in patients from most Australian States.4 The spread of VRE brings us ever closer to the appearance of high-level vancomycin resistance in Staphylococcus aureus, lending urgency to efforts to control VRE. How is vancomycin resistance selected and amplified? In all types of antibiotic resistance, bacterial clones that carry the resistance factor are selected and expanded (amplified) by the selective pressure of antibiotic exposure. In the case of VRE, resistance can also be transferred horizontally between animal and human enterococcal strains by transposons4 (see Box). Of even greater concern is the experimentally demonstrated ability of these transposons to transfer vancomycin resistance to the major human pathogen, S. aureus.6 The specific pressures that have led to vancomycin resistance appear to differ between geographical areas and types of resistance. VanA resistance: As summarised by Collignon,7 use of the glycopeptide avoparcin as a growth promoter in farmed animals in Europe, coupled with the presence of the vanA transposon, has fuelled remarkable selection and amplification of VRE in animals. Vancomycin resistance has spread to human populations (and their enterococci) via the food chain. The strength of evidence for this has been assessed at level III-1 (well designed, non-randomised, controlled trials).8 However, a second amplification step through medical use of glycopeptides in humans is necessary for VRE to emerge as a clinical problem, while lowered defence is usually required for enterococci to cause human disease. The low incidence of clinical VRE infections in most European countries appears related to low medical use of glycopeptides and other antibiotics. Alternatively, transferred animal VRE strains may be less able to cause human disease (although outbreaks of vanA VRE disease have occurred in England9). The relatedness of vanA VRE strains across the world has been examined. The coding sequence of the vanA transposon, Tn1546, comprises over 10 000 base-pairs, but, remarkably, only a single nucleotide difference in this sequence has been documented in the many strains examined to date from the United States and Europe.10 This suggests that the vanA transposon emerged through a complex chain of events that occurred only once, and was then transferred to many strains. While the coding sequences of the vanA transposon are strongly conserved, the non-coding insertion sequences (IS) are more variable. Mapping has shown that some US and European vanA strains have identical IS arrangements, indicating a recent common origin.9-11 As vanA VRE appeared in New York soon after their appearance in Europe,12 it is likely they were carried to the US (and later to Australia) from Europe in food, livestock or humans. In the US, avoparcin was never used, and VRE has spread among hospitalised patients, with insignificant community colonisation.13 VanB resistance: The epidemiology of vanB vancomycin resistance is largely unknown. In Europe, vanB VRE have been isolated infrequently from humans and never, as yet, from animals or food.8 A small study comparing US and European vanB strains found their Tn1547 transposons to be distinct by restriction mapping.14 More recent data indicate that there are at least three vanB genotypes (Dr Robin Patel, Mayo Clinic, Rochester, Minn, USA, personal communication). This greater diversity implies that vanB emerged earlier than vanA. What is Australia's position? In Australia, relative use of glycopeptides in humans and animals strongly resembles that in Europe, where avoparcin has been largely responsible for VRE amplification in animals. As yet, there has been very limited study of VRE in local animal populations, and local VRE strains have not been subtyped by transposon mapping nor compared with overseas strains. Nonetheless, given that VRE strains carrying the vanA and vanB transposons have been isolated in Australia,4 and that these transposons do not emerge by mutation, they must have been imported. Once here, enterococci carrying these transposons may well have been amplified in animals exposed to avoparcin, and passed through the food chain to humans in a manner similar to that in Europe. Community-acquired VRE carriage has been observed at a low level in Victoria,15 and at least one study found vanA and vanB VRE in animal populations.16 The extent of community and animal colonisation in Australia urgently needs quantification. In Australia, in contrast to Europe, most documented human VRE colonisation and disease has been with polyclonal vanB strains. The diverse range of strains implies that there has been either widespread amplification and transfer of VRE transposons within Australia or importation of multiple strains. However, in some regions, clonal strains of vanA VRE have been responsible for hospital-related outbreaks, similar to the US17 and UK9 situations. How does cross-infection occur in healthcare settings? Enterococci are ubiquitous gastrointestinal and genital tract bacteria that readily contaminate and persist in hospital environments. Healthcare workers who comply poorly with handwashing are vectors for patient-to-patient transfer of these bacteria. Equipment and contaminated environments have also been identified as important modes of spread in some acute care settings.18,19 Patients receiving antibiotics usually lose normal protective flora, increasing their risk of colonisation with nosocomial strains of enterococci and other resistant bacteria. Intensive care, organ transplant, renal, haematology and oncology patients are particularly at risk from VRE disease and require protection from inadvertent colonisation. How can VRE be controlled? The overriding emphasis must be on control of antibiotic use. In whatever situation, animal or human, use of glycopeptides will amplify vancomycin resistance, increasing the potential for its eventual transfer to S. aureus. Avoparcin restriction: Collignon has highlighted viable alternatives to use of avoparcin in animals, and Australia should act urgently as a precautionary measure to eliminate or at least restrict avoparcin use. Control of human antibiotic use: This should go further than the restrictions on vancomycin recommended by the Hospital Infection Control Practices Advisory Committee.20 Broad-spectrum antibiotics, particularly third-generation cephalosporins, have been identified as independent risk factors for VRE colonisation and also play an important role in amplifying methicillin-resistant S. aureus (MRSA). Use of broad-spectrum antibiotics should be reduced whenever possible. The incidence of nosocomial disease caused by MRSA, VRE and Clostridium difficile is a valuable "ecological" indicator for hospitals, providing early warning of an adverse antibiotic-created environment. Evidence from the US shows the effectiveness of antibiotic control in reducing the incidence of VRE and C. difficile.21 Regular auditing of antibiotic use can assist hospital drug committees to define areas for targeted intervention. Robertson and colleagues examined detailed reasons for vancomycin use in five metropolitan hospitals in Victoria.22 They highlight unnecessarily prolonged use of vancomycin in empirical and prophylactic therapy, both amenable to intervention. Their study should be repeated at other Australian hospitals. VRE infection control procedures: As VRE are already widespread, albeit uncommon, in many animal and human populations, eradication is not possible. To ensure early detection and containment of VRE, a targeted approach is needed among patients most at risk from VRE disease. Grayson and colleagues describe such an approach.23 After identification of clinical vanB VRE infection in a renal patient, their hospital took measures to prevent a potential outbreak. Screening of at-risk groups for faecal VRE colonisation, which found nine additional isolates of vanB VRE, and review of antibiotic use appear to have been successful in containing VRE.22 The temptation to screen for VRE colonisation in low-risk patients should be resisted, as few of those identified will develop disease, but the hospital and patient must carry the considerable respective financial and psychological burdens. In low-risk groups, it is more worthwhile to focus initially on assessment and modification of antibiotic use. John K Ferguson Director of Microbiology and Infectious Diseases John Hunter Hospital, Newcastle, NSW Uttley AH, Collins CH, Naidoo J, George RC. Vancomycin-resistant enterococci. Lancet 1988; 1: 57-58. Leclercq R, Derlot E, Duval J, Courvalin P. Plasmid-mediated resistance to vancomycin and teicoplanin in Enterococcus faecium. N Engl J Med 1988; 319: 157-161. Kamarulzaman A, Tosolini FA, Boquest AL, et al. Vancomycin-resistant Enteroccus faecium infection in a liver transplant recipient [abstract]. Aust N Z J Med 1995: 25; 560. Bell J, Turnidge J, Coombs G, O'Brien F. Emergence and epidemiology of vancomycin-resistant enterococci in Australia. Commun Dis Intell 1998; 22: 249-252. Arthur M, Molinas C, Depardieu F, Courvalin P. Characterization of Tn1546, a Tn3-related transposon conferring glycopeptide resistance by synthesis of depsipeptide peptidoglycan precursors in Enterococcus faecium BM4147. J Bacteriol 1993; 175: 117-127. Noble WC, Virani Z, Cree RGA. Co-transfer of vancomycin and other resistance genes from Enterococcus faecalis NCTC 12201 to Staphylococcus aureus. FEMS Microbiol Lett 1992; 93: 195-198. Collignon PJ. Vancomycin-resistant enterococci and use of avoparcin in animal feed: is there a link? Med J Aust 1999; 171: 144-146. Ferguson JK, Dalton CB, McGettigan P, Hill S. Antimicrobial resistance in animal enteric bacteria and human disease -- a review of the scientific literature. Commissioned report to the Joint Expert Technical Advisory Committee on Antibiotic Resistance. Canberra; National Health and Medical Research Council, 1998. Woodford N, Adebiyi AMA, Palepou MFI, Cookson BD. Diversity of vanA glycopeptide resistance elements in enterococci from humans and non human sources. Antimicrob Agents Chemother 1998; 42: 502-508. Jensen LB. Differences in the occurrence of two base pair variants of Tn1546 from vancomycin-resistant enterococci from humans, pigs, and poultry. Antimicrob Agents Chemother 1998; 42: 2463-2464. Jensen LB, Ahrens P, Dons L, et al. Molecular analysis of Tn1546 in Enterococcus faecium isolated from animals and humans. J Clin Microbiol 1998; 36: 437-442. Frieden TR, Munsiff SS, Low DE, et al. Emergence of vancomycin-resistant enterococci in New York City. Lancet 1993; 342: 76-79. Leclercq R, Courvalin P. Resistance to glycopeptides in enterococci. Clin Infect Dis 1997; 24: 545-555. Dahl KH, Simonsen GS, Olsvik O, Sundsfjord A. Heterogeneity in the vanB gene cluster of genomically diverse clinical strains of vancomycin-resistant enterococci. Antimicrob Agents Chemother 1999; 43: 1105-1110. Lyddy MM, Smith HJ, Baird RW. Isolation of vancomycin-resistant enterococci in community-based patients [abstract]. Microbiol Aust 1998; 19 (4): A92. Butt H, Bell J, Ferguson JK. Are vancomycin-resistant enterococci prevalent in Hunter region farm animals? [abstract]. Microbiol Aust 1997; 18(4): P04.8. Robson J, Allen A, Jennings A, et al. The emergence of vancomycin resistant Enterococcus faecium (VRE) in an Australian hospital -- clinical and epidemiological features [abstract]. Aust N Z J Med 1998; 28: 712. Bonten MJ, Hayden MK, Nathan C, et al. Epidemiology of colonisation of patients and environment with vancomycin-resistant enterococci. Lancet 1996; 348: 1615-1619. Livornese LL, Dias S, Samel C, et al. Hospital-acquired infection with vancomycin-resistant Enterococcus faecium transmitted by electronic thermometers. Ann Int Med 1992; 117: 112-116. HICPAC committee. Recommendations for preventing the spread of vancomycin resistance: recommendations of the Hospital Infection Control Practices Advisory Committee (HICPAC). Am J Infect Control 1995; 23: 87-94. Quale J, Landman D, Saurina G, et al. Manipulation of a hospital antimicrobial formulary to control an outbreak of vancomycin-resistant enterococci. Clin Infect Dis 1996; 23: 1020-1025. Robertson MB, Dartnell JGA, Korman TM, on behalf of the Victorian Drug Usage Evaluation Group. Vancomycin and teicoplanin use in Victorian hospitals. Med J Aust 1999; 171: 127-131. Grayson ML, Grabsch EA, Johnson PDR, et al. Outcome of a screening program for vancomycin-resistant enterococcci in a hospital in Victoria. Med J Aust 1999; 171: 133-136. Genetic basis of vancomycin resistance Four types of vancomycin resistance in enterococci have been described: vanA, vanB, vanC and vanD. The commonest, vanA, is encoded by a complex mobile genetic element (transposon Tn1546) that contains nine genes responsible for high-level resistance to vancomycin and teicoplanin, including the vanA gene.5 The vanB type (medium-level vancomycin resistance, but teicoplanin susceptibility) is encoded similarly on another transposon, Tn1547, which contains the vanB gene in place of vanA. Location of the vancomycin-resistance genes on transposons is significant, as these mobile elements (or "jumping genes") can copy themselves to different locations on the bacterial chromosome, extrachromosomal plasmids and bacteriophages, and can transfer to other bacteria via mechanisms such as conjugation. Back to text

John K Ferguson

Editorial Acne and acne scarring: why should we treat? Reasons for early medical intervention, and options for treatment of scarring MJA 1999; 171: 62-63 Acne is so common that one could argue that it is a normal occurrence in human development. Its prevalence has been estimated at 95%-100% in 16-17-year-old boys and 83%-85% in 16-17-year-old girls.1 The initial presentation is usually comedonal acne, progressing to inflammatory lesions within 2-3 years,2 then rising in incidence and severity to reach its most serious stage between the ages of 14 and 17 years in girls and 16 and 19 years in boys.1 Development of comedonal acne at an early age, in girls at least, appears predictive of more severe disease in later years.3 Acne will mostly resolve by the age of 23-25 years; nevertheless, 1% of men and 5% of women still bear acne lesions at 40 years of age.4So, is acne a disease worthy of treatment, or a normal occurrence that should be ignored, as it will eventually cease to be a problem for most affected individuals? Concern about acne is one of the commonest reasons for young patients to consult a medical practitioner, so the direct cost of consultations and of the diversion of medical services needs to be taken into account in any assessment of the value of treating this apparently "normal" life event. Added to this, we are seeing the development of increasing antibiotic resistance in Propionibacterium acnes,5 a problem exacerbated by long term and widespread use of often suboptimal doses of antibacterial agents. So how can one justify treatment? Firstly, acne as a condition is aesthetically and sometimes physically unpleasant. Severe cystic acne causes pain, recurrent bleeding and purulent discharge. In rare instances, patients with acne develop severe systemic toxicity and require treatment in hospital. Before isotretinoin was introduced, such patients were extremely difficult to treat. Secondly, it can cause great distress in adolescents at a time when they are probably least able to deal psychologically and socially with the unsightliness of active acne. Being so readily visible (affecting the face in 99% of cases6), acne can reduce employment prospects7 and create interpersonal difficulties.8 Affected adolescents report more social isolation and self-consciousness than their unaffected peers8 and experience more embarrassment, social inhibition, unhappiness, anxiety, and dissatisfaction with their facial appearance.9 Finally, acne scarring can cause devastating long term psychic trauma for the sufferer and it has been suggested that such scarring may be a risk factor for suicide, particularly in men.10As current treatments for acne are very effective, scarring could be avoided in many cases by adequate medical intervention early in the course of the disease. Successful treatment of cystic acne with isotretinoin appears to reduce anxiety and depression in patients.11 Anti-androgen hormonal treatments such as cyproterone acetate and spironolactone, topical preparations such as adapalene, azelaic acid, topical antibiotics and retinoic acid may help to replace or augment long term antibiotic therapy, ensuring a sufficient armamentarium to keep the incidence of acne scarring to a minimum. Unfortunately, scarring may affect up to 95% of patients with acne. The degree of scarring is related to the severity and duration of acne before adequate therapy is instituted. One study found that a time delay of up to three years between acne onset and adequate treatment was sufficient to cause facial scarring in either sex, although keloidal or hypertrophic truncal scarring was more common in men.12 The same study established that superficial inflamed papular acne and cystic acne could both produce scarring, a finding with important implications for our healthcare system, which subsidises isotretinoin for failed therapy in nodulocystic disease only. If hypertrophic scarring occurs it should be dealt with by such measures as intralesional steroids, silicone sheeting or vascular laser treatment, as required. However, most scarring in acne is atrophic rather than hypertrophic in nature, with destruction and dissolution of supporting tissues. In the young, most scars will initially improve, the erythema will subside and the scars mature over the first two to three years. After this initial improvement the scarring is quiescent, but, over time, as facial tone declines and facial fat stores are resorbed, the scars will become more noticeable. With ageing, the facial skin starts to sag and seems to literally hang on the scars. The inelastic strands of scars bind the skin, giving it an uneven, cascading appearance. This is amplified by other age-related changes such as the resorption of skeletal and soft tissues. Remedial approaches to acne scarring have improved over the years. The older, less successful treatments such as dermabrasion and chemical peeling have been replaced by the use of resurfacing infrared lasers such as CO2 lasers13 and, more recently, erbium lasers14 to better remove and tighten the skin. An understanding that replacement of the atrophied structures in the dermis and subcutaneous tissues is necessary in severe cases of acne scarring has led to the development of superior dermal and subcutaneous augmentation techniques. Dermal and subcutaneous augmentation is possible by a number of autologous techniques, including dermal grafting,15 lipocytic dermal augmentation,16 fat transfer17 and, more recently, the implantation of autologous collagen and cultured and expanded autologous fibroblasts. Non-autologous augmentation is also possible by way of injections of bovine collagen, fibrin foam, hyaluronic acid or polymethylmethacrylate microspheres. For "punched out" ("ice pick") scars, none of these methods is useful. For these a range of punch techniques is used, involving coring out of scars with an appropriately sized cylindrical instrument, followed by suturing or graft application. Punch techniques can be used to treat many scars at a single operation, and may be combined with resurfacing techniques such as infrared laser treatment.18 Subcision (dermal scarification) is another helpful technique, in which dermal undermining of scars is used to improve the scar tissue by two mechanisms: (i) direct breaking of scar attachments, and (ii) intentional injury of the dermis to induce laying down of new collagen.19 All of these techniques are valuable tools for practitioners seeking to improve the outcome of treating acne scarring, but it would be better still if the problem never arose. A preventable condition such as postacne scarring should be one deserving of the earliest, best and most effective treatment. Gregory J Goodman President, Skin and Cancer Foundation Melbourne, VIC Burton JL, Cunliffe WJ, Stafford I, Shuster S. The prevalence of acne vulgaris in adolescence. Br J Dermatol 1971; 85: 119-126. Lucky AW, Biro FM, Huster GA, et al. Acne vulgaris in early adolescent boys: correlations with pubertal maturation and age. Arch Dermatol 1991; 172: 210-216. Lucky AW, Biro FM, Simbartl LA, et al. Predictors of severity of acne vulgaris in young adolescent girls: results of a five-year longitudinal study. J Pediatr 1997; 130: 30-39. Cunliffe WJ, Gould DJ. Prevalence of facial acne vulgaris in late adolescence and in adults. BMJ 1979; 1: 1109-1110. Cooper AJ. Systematic review of Propionibacterium acnes resistance to systemic antibiotics. Med J Aust 1998; 169: 259-261. Cunliffe WJ. The acnes. London: Dunitz, 1989. Cunliffe WJ. Unemployment and acne. Br J Dermatol 1986; 115: 386. Schachter RJ, Pantel ES, Glassman GM, Zweibelson I. Acne vulgaris and psychologic impact on high school students. N Y State J Med 1971; 24: 2886-2890. Wu SF, Kinder BN, Trunnell TN, Fulton JE. Role of anxiety and anger in acne patients: a relationship with the severity of the disorder. J Am Acad Dermatol 1988; 18: 325-333. Cotterill JA, Cunliffe WJ. Suicide in dermatological patients. Br J Dermatol 1997; 137: 246-250. Rubinow DR, Peck GL, Squillace KM, Gantt GG. Reduced anxiety and depression in cystic acne patients after successful treatment with isotretinoin. J Am Acad Dermatol 1987; 17: 25-32. Layton AM, Henderson CA, Cunliffe WJ. A clinical evaluation of acne scarring and its incidence. Clin Exp Dermatol 1994; 19: 303-308. Goodman GJ. Facial resurfacing using a high-energy, short-pulse carbon dioxide laser. Australas J Dermatol 1996; 37: 125-131. Stuzin JM, Baker TJ, Baker TM. CO2 and erbium:YAG laser resurfacing: current status and personal perspective. Plast Reconstr Surg 1999; 103: 588-591. Goodman GJ. Laser assisted dermal grafting for the correction of cutaneous contour defects. Dermatol Surg 1997; 23: 95-99. Coleman WP 3d. Lipocytic dermal augmentation. In: Klein AW, editor. Tissue augmentation in clinical practice. Procedures and techniques. New York: Marcel Dekker, 1998: 49-62. Coleman SR. Long-term survival of fat transplants: controlled demonstrations. Aesthetic Plast Surg 1995; 19: 421-425. Johnson WC. Treatment of pitted scars: punch transplant technique. J Dermatol Surg Oncol 1986; 12: 260-265. Orentreich DS. Subcutaneous incisionless (subcision) surgery for the correction of depressed scars and wrinkles. Dermatol Surg 1995; 21: 543-549.

Gregory J Goodman

The vilest deeds, like poison weeds, Bloom well in prison air; Oscar Wilde, "The Ballad of Reading Gaol", 1896 More than two years ago, an editorial in this Journal stated: "Prison authorities and governments must realise that the responsibility for the infection of a prisoner with a bloodborne virus, because means for prevention were not available within the prison, rests with them."1 Sadly, there is little improvement to report. Bleach, for cleaning injecting equipment, has been made available since 1995 in most custodial systems. Condoms and dental dams were first introduced into New South Wales prisons in 1997, but are currently provided to prison inmates in only three jurisdictions. The methadone maintenance program began in New South Wales in 1986 and will soon expand through trials in Queensland and South Australian prisons. Methadone withdrawal regimens are provided in Victorian prisons. Three articles in this issue of the Journal highlight some of the continuing health risks faced by inmates in Australian prisons.2-4 These reports raise concerns that inmates are still placed at unnecessary risk by not being offered opportunities to minimise infection with bloodborne viruses, and complement reports of transmission of a wide range of contagious diseases from custodial systems in other countries.5,6 McDonald et al report that control of HIV transmission in the community has protected prisoners, with sustained low levels of identified HIV-antibody-positive individuals entering Australian prisons.2 The evidence for transmission in prison of HIV presented by Dolan and Wodak3 and of hepatitis C by Haber et al4 indicate that custodial authorities' commitment to zero tolerance would be better applied to the transmission of these viruses rather than to illicit drugs and injecting equipment within prison. Despite universal support for zero tolerance among Australian custodial authorities, drug use continues after reception into prison. In New South Wales, in 1996, 21% of men and 32% of women reported that they had injected drugs in prison; 18% of men and 11% of women did so in the week before interview. Of those who had injected in prison, 69% of men and 64% of women reported that they had shared needles.7 Zero tolerance is not protecting the lives of prison inmates. Between 1980 and 1998, there were 86 deaths in custody in Australian prisons that were classified as accidents -- overwhelmingly drug related.8 The fear of having illicit drugs confiscated leads to "binge" use. Irregular use and inexperience in assessing dosage and drug purity readily lead to overdosing. Needles and syringes have a higher probability of being infectious in the prison environment, as the prevalence of bloodborne viruses is so high. An environment that inadvertently encourages sharing of equipment actually promotes transmission of bloodborne viruses. Consider the ability of zero tolerance in providing prison workers with a safe work environment. It might be argued that the restrictions on needles and syringes make prisons a safer workplace, but the evidence for this is not compelling. The malicious stabbing of a prison officer with a syringe filled with HIV-contaminated blood in 1990 occurred when needles and syringes were prohibited items. The principle of harm minimisation guides public health efforts to control bloodborne viruses in the community. Why should this not also be applied in the prison environment? No measures should be spared to provide a safer environment for prison inmates, and health and custodial staff. A full range of options need to be available for custodial and health authorities to offer inmates, including drug-free prisons, methadone maintenance and consideration of therapeutic prescription of injectable drugs. With controlled heroin prescribing and provision of syringes and needles, the trafficking of contaminated equipment should decrease. In Switzerland and Germany, programs for therapeutic heroin prescription in a few prisons are currently being evaluated.9 These initiatives will require strong advocates for the health of prison inmates and the general community. For this to occur, prison health services must be brought into the mainstream of clinical medicine and public health.10 This can be accomplished by granting autonomy to prison health authorities, by fostering ties between correctional health programs and academic and public health departments, and by funding research that addresses public policy questions peculiar to the prison environment.11 To accelerate the uniform introduction of health protective measures throughout Australian prison systems, correctional health programs need standards against which their performance can be monitored. Australian prison authorities have devised uniform guidelines of operation, but they are not health standards, and they are not enforceable.12 There are currently over 19 000 inmates in Australian prisons, and the number is increasing by more than 7% each year.13 The importance of the health of prisoners and its impact on the general community can only grow. Since March 1999, the Australian Red Cross has identified imprisonment in the previous 12 months as an unacceptable risk factor for blood donation.14 Two years have been squandered. The evidence mounts that prisons pose a health risk to inmates, to workers within prisons, and to the general community. The statement by Crofts bears repeating: "Prison authorities and governments must realise that the responsibility . . . rests with them."1 Michael H Levy Director, Population Health, Corrections Health Service Matraville, NSW, and Department of Public Health and Community Medicine University of Sydney Crofts N. A cruel and unusual punishment. Med J Aust 1997; 166: 116. McDonald AM, Ryan J, Brown PR, et al. HIV prevalence at reception into Australian prisons, 1991-1997. Med J Aust 1999; 171: 18-21. Dolan K, Wodak A. HIV transmission in a prison system in an Australian State. Med J Aust 1999; 171: 14-17. Haber PS, Parsons SJ, Harper SE, et al. Transmission of hepatitis C within Australian prisons. Med J Aust 1999; 171: 31-33. Taylor A, Goldberg D, Emslie J, et al. Outbreak of HIV infection in a Scottish prison. BMJ 1995; 310: 289-292. Valway SE, Richards SB, Kovacovich J, et al. Outbreak of multi-drug-resistant tuberculosis in a New York State prison, 1991. Am J Epidemiol 1994; 140: 113-122. Preliminary findings of the Inmate Health Survey. Sydney: Corrections Health Service, 1997. Dalton V. Prison homicide in Australia: 1980 to 1998. Trends and issues in crime and criminal justice. No. 103. Canberra: Australian Institute of Criminology, 1999. Vumbuca G. Finding a better way. Canberra: The Winston Churchill Memorial Trust of Australia, 1999. Prisoners: an end to second class health care? BMJ 1999; 318: 954-955. Correction of attitudes to prison medicine [editorial]. Lancet 1998; 351: 1371. Standard Guidelines for Corrections in Australia 1996. The Corrective Services Ministers' Conference. 1995. Australian Bureau of Statistics. Corrective Services, Australia. Canberra: ABS, 1998. (Catalogue no. 4512.0.) Australian Red Cross Blood Service. Donor Questionnaire. March 1999.

Michael H Levy

The evidence so far is not promising Since July 1997, the Australian media have uncritically reported therapeutic claims that naltrexone, an orally well-absorbed, long-acting opioid antagonist, can be used to "cure" heroin dependence. Naltrexone displaces heroin from opioid receptors in the brain, blocking the effects of any opioid agonists while the patient continues to take it. It has no opioid agonist effects and hence is "non-addictive". The current media enthusiasm ignores the reported modest success of naltrexone maintenance in the treatment of heroin dependence over almost 20 years.1,2 Research has shown that induction onto naltrexone is difficult, compliance poor, treatment retention disappointing and abstinence an uncommon outcome.1,3,4 More than 20 years ago the consensus was that naltrexone maintenance has a limited role in treatment of opioid-dependent street users, although it may be useful for drug-dependent professionals and parolees.5 Renewed enthusiasm for naltrexone was based on the claim that it can be used to accelerate withdrawal from heroin and other opioids, allowing immediate induction onto naltrexone maintenance. Because naltrexone may precipitate distressing withdrawal symptoms, naltrexone-accelerated withdrawal is performed under general anaesthesia or light sedation (using benzodiazepines and other symptomatic medications). Induction is followed by naltrexone maintenance for six to 12 months. Media enthusiasm for combined naltrexone-accelerated withdrawal and maintenance has not been shared by many addiction specialists in Australia,6 the United Kingdom7 or the United States.8-10 They have been concerned that this type of induction adds to the expense and possibly reduces the safety of a relatively ineffective maintenance treatment. However, professional scepticism was overwhelmed by the media's recitation of yet to be published claims that the combined procedure achieved abstinence rates of 70%-80% at three months. The article by Bell and colleagues11 in this issue of the Journal is the first peer-reviewed Australian report of naltrexone-accelerated withdrawal under light sedation, followed by naltrexone maintenance. It is a pilot study of 30 patients who were followed up for three months. Although there was no comparison group, the results reinforce the concerns expressed by addiction specialists about the efficacy and safety of naltrexone-accelerated withdrawal and maintenance. Three months after treatment, seven patients (23%) were still abstinent from opioids, only two of whom were still taking naltrexone. One patient had died of a heroin overdose, while most returned to heroin use or methadone maintenance (7 and 11, respectively). Of the six (20%) who were still taking naltrexone, four engaged in the risky practice of using heroin after briefly interrupting the naltrexone maintenance. Patient selection may be one explanation for the marked discrepancy between these results and those reported in the media. Most of the patients in Bell and colleagues' study had long histories of heroin dependence, and half were in methadone maintenance treatment. Although none of these characteristics is said to exclude patients from naltrexone treatment, patients treated in private clinics appear to have much shorter dependence careers and stronger family and social support. The death observed in this case series, and other deaths overseas,3 raise concerns about the safety of naltrexone maintenance. These concerns have been dismissed by promoters of naltrexone-accelerated withdrawal, who assert -- without evidence -- that naltrexone is life-saving. The overdose fatality rate in treated heroin addicts has been estimated at a little less than 1% annually.12 There is no evidence that mortality rates in naltrexone-accelerated withdrawal and maintenance are better than this; they may well be worse, as has been reported in one controlled study.3 Strong conclusions should not be drawn about the efficacy of the procedure on the basis of Bell et al's data, even though favourable reports from less rigorously conducted studies have been accepted uncritically. The role of naltrexone (and other agents to assist in opiate withdrawal) in opioid dependence should be clearer on completion in 2001 of controlled trials of the combined procedure, with and without anaesthesia, as part of the National Evaluation of Pharmacotherapies for Opioid Dependence. In the meantime, thanks to an uncritical media, aggressive marketing and political intervention, Australia is in the midst of a large, uncontrolled experiment using naltrexone-accelerated withdrawal and maintenance to treat unselected opioid-dependent people in the absence of systematic national monitoring of efficacy, safety, or adverse events. It is of particular concern that we have no way of monitoring overdose deaths that may occur when patients discontinue naltrexone maintenance and relapse to heroin use, when research indicates that most unselected patients do return to heroin use.1 There are lessons to be learned from the introduction of naltrexone-accelerated withdrawal and maintenance in Australia. Firstly, decision-making about research and service provision for illicit drug dependence requires the same rigour and evidence demanded elsewhere in medicine. In the absence of this evidence, false expectations of cure will continue to be raised and dashed, scarce research and treatment funding will be wasted, and little progress will be made in improving treatment outcomes. Management of drug dependence has more in common with a marathon than a 100 m sprint. Secondly, all new interventions in medicine should be assumed ineffective and possibly unsafe until proven otherwise. No good evidence has yet been presented to challenge the assumption that naltrexone, however packaged, is at best modestly effective, and at worst unsafe, in management of unselected cases of opioid dependence. Wayne D Hall Professor of Drug and Alcohol Studies, National Drug and Alcohol Research Centre, University of New South Wales Sydney, NSW Alex Wodak Director, Alcohol and Drug Service, St Vincent's Hospital, Sydney, NSW Reprints: Professor W D Hall, National Drug and Alcohol Research Centre, University of New South Wales, Sydney, NSW 2052. Mattick RP, Bell J, Daws LC, et al. Review of evidence on the effectiveness of antagonists in managing opioid dependence. National Drug and Alcohol Research Centre Monograph No 34. Sydney: National Drug and Alcohol Research Centre, 1997. Judson BA, Goldstein A. Naltrexone treatment of heroin addiction: One-year follow-up. Drug Alcohol Depend 1984; 13: 357-365. Miotto K, McCann MJ, Rawson RA, et al. Overdose, suicide attempts and death among a cohort of naltrexone-treated opioid addicts. Drug Alcohol Depend 1997; 45: 131-145. San L, Pomarol G, Peri JM, et al. Follow-up after a six-month maintenance period on naltrexone versus placebo in heroin addicts. Br J Addiction 1991; 86: 983-990. Thomas M, Kauders F, Harris M, et al. Clinical experiences with naltrexone in 370 detoxified addicts. In: Julius D, Renault P, editors. Narcotic antagonists: naltrexone. Vol 9. Rockville, MD: National Institute on Drug Abuse, 1976: 88-92. xHall W, Mattick RP, Saunders J, Wodak A. Rapid opiate detoxification treatment. Drug Alcohol Rev 1997; 16: 325-327. Gossop M, Strang J. Rapid anaesthetic-antagonist detoxification of heroin addicts: what origins, evidence base and clinical justification? Br J Intensive Care 1997; 7: 66-69. O'Connor PG, Kosten TR. Rapid and ultrarapid opioid detoxification techniques. JAMA 1998; 279: 229-234. Kleber HD. Ultrarapid opiate detoxification. Addiction 1998; 93: 1629-1633. Helman BH, Czechowicz D. NIDA scientific report of ultra rapid detoxification with anesthesia (UROD). Opinion of the consultants and criteria relating to evaluating the safety and efficacy of UROD. Washington: National Institute on Drug Abuse, 1996. Bell J, Young M, Masterman S, et al. A pilot study of naltrexone-accelerated detoxification in opioid dependence. Med J Aust 1999; 170: 26-30. English D, Holman CJD, Milne E, et al. The quantification of drug caused morbidity and mortality in Australia 1995 edition. Canberra: Commonwealth Department of Human Services and Health, 1995.

Wayne D Hall · Alex Wodak

Editorial Meeting the challenge of adolescent mental health For about one in five teenagers, emotional difficulties are more than a passing phase MJA 1997; 166: 399-400 Since the turn of the century, when the prominent American psychologist G Stanley Hall first described adolescence as a discrete developmental phase, emotional turmoil has been a part of popular conceptions of youth.1 Emotional and behavioural difficulties that would elicit concern at other times in life have been viewed as part of growing up, with an assumption that the adoption of adult social roles in the early twenties would bring emotional control and a "maturing out" of adolescent difficulties. In this context an apparent long neglect of adolescent mental health seems understandable. Views on adolescence and adolescent mental health have recently shifted. Puberty undoubtedly brings adjustments to physical maturity, changing roles within families and with peers, and the emergence of a more independent lifestyle. Most young people negotiate these changes without upheaval. By and large, they also avoid extremes in early experimentation with alcohol and recreational drugs, dieting and sexual activity.2 Given this more sanguine perspective on adolescent development, emerging concerns about adolescent mental health seem at first sight unwarranted. However, around one in five adolescents do pass through a more prolonged phase of emotional difficulties in which experiences of depression and anxiety are common.3 There is evidence that such difficulties have become commoner. Surveys of adults in several Western countries suggest that cohorts since World War II have higher rates of adolescent-onset psychiatric problems. North American studies, for example, have indicated up to a tenfold rise in rates of adolescent depression in more recently born groups.4 As a consequence, the late teens and early twenties appear to be the period of peak incidence for depression.5 Adolescent mental health has assumed importance for other reasons. One derives from the continuities between adolescent and adult psychopathology. Prospective studies indicate that adolescent depression, far from subsiding in early adulthood, substantially elevates the risk of a later disorder.6 A second reason lies in links between mental health and other indices of adolescent health status. Trends in health-damaging behaviour parallel those in adolescent mental health problems. The age of onset of alcohol and substance abuse and sexual risk behaviours has fallen, so that they have joined eating disorders and deliberate self-harm as adolescent health concerns. These parallel trends have prompted questions about possible causal links between adolescent mental health and behavioural problems. Such a link is probably clearest for suicidal behaviour, in which depressive symptoms are the strongest risk factors for both fatal and non-fatal self-harm.7,8 Risks for suicidal behaviour increase with the level of depressive symptoms. For the most part, adolescent suicidal behaviour does not result from a clear intent to kill oneself. Rather, it is best understood as a maladaptive reaction to the distress, negative self-evaluation and high levels of interpersonal conflict that commonly accompany depression.9 The implications for intervention are great. Self-harming adolescents commonly experience depressive symptoms but many will fall short of meeting criteria for depressive disorder. Preventive and clinical intervention efforts should therefore be broad-based and not restricted to those with a florid mental disorder. For this reason, "population-based" interventions aimed at promoting well-being and reducing depressive symptoms across a whole population, rather than focusing on those at highest risk, seem an attractive but neglected avenue for the prevention of suicidal behaviour.10 Adolescent psychopathology has been linked to other health-damaging behaviours.11,12 Depressive and anxiety symptoms are associated with adolescent alcohol and substance abuse, and their presence predicts progression to dependent patterns of consumption.13 Extreme weight control behaviours,14 adolescent smoking15 and early teenage pregnancy16 are among other behaviours associated with psychological disorders. Clarification of the underlying risk processes may offer strategies for intervention. Self-medication to relieve emotional distress may explain associations with smoking, alcohol and substance abuse, and points to a need to learn alternative means of dealing with emotional distress.15 Susceptibility to peer influences may be another explanation. Loss of self-confidence and social anxiety, which commonly accompany depression, may bring a greater readiness to adopt peer attitudes and behaviours as a means of engaging with a social group. In some instances, where psychopathology and health-damaging behaviour share a common origin, intervention may best focus on antecedent familial or social circumstances. Whatever the risk process, successful interventions for adolescent mental health problems are likely to bring other health benefits. The emerging importance of adolescent mental health carries implications for adolescent health care and health promotion. Within psychiatry this has been recognised in calls for a greater emphasis on the management of adolescent onset disorders.17 However, psychiatric services can deal only with a minority of adolescents with common disorders such as depression and anxiety, so responsibility for early recognition and treatment rests more broadly. General practitioners are likely to play a major role. This has been recognised in the National Health and Medical Research Council guidelines for the treatment of adolescent depression, which are accompanied by guidelines for the general practitioner in the psychological and medical management of adolescent depression.18 These skills are likely to play a central role in dealing with adolescent behavioural problems such as substance abuse, and, when dealing with associated emotional problems, may do much to prevent progression to dependent patterns of use. Meeting the challenge of adolescent mental health must ultimately extend to preventive action. Interventions to support families, schools, youth and community organisations in the creation of social environments which promote mental health and well-being should bring gains in adolescent mental health, which in turn are likely to bring diverse health benefits. George C Patton Associate Professor in Adolescent Psychiatry Centre for Adolescent Health, Department of Paediatrics University of Melbourne, VIC Hall GS. Adolescence: Its psychology and its relations to physiology, anthropology, sociology, sex, crime, religion and education. London: Sidney Appleton, 1905. Hibbert M, Caust J, Patton G, et al. The health of young people in Victoria. Melbourne: Centre for Adolescent Health, 1996. Offer D, Schonert-Reichl KA. Debunking the myths of adolescence: findings from recent research. J Am Acad Child Adolesc Psychiatry 1992; 31: 1003-1014. Burke KC, Burke JD Jr, Rae DS, Regier DA. Comparing age at onset of major depression and other psychiatric disorders by birth cohorts in five US community populations. Arch Gen Psychiatry 1991; 48: 789-795. Kessler RC, McGonagle KA, Zhao S, et al. Lifetime and 12-month prevalence of DSM-III-R psychiatric disorders in the United States. Results from the National Comorbidity Survey. Arch Gen Psychiatry 1994; 51: 8-19. Harrington R. The natural history and treatment of child and adolescent affective /disorders. J Child Psychol Psychiat 1992; 33: 1287-1302. Patton GC, Harris R, Carlin JB, et al. Adolescent suicidal behaviours: a population based study of risk. Psychol Med 1997; 27. In press. Brent DA. Depression and suicide in children and adolescents. Pediatrics Rev 1993; 14: 380-388. Kienhorst I, de Wilde EJ, Diekstra RFW, Wolters WHG. Adolescents' image of their suicide attempt. J Am Acad Child Adolesc Psychiatry 1995; 34: 623-628. Rose G. The strategy of preventive medicine. Oxford: Oxford University Press; 1992. Fergusson DM, Horwood LJ, Lynskey MT. The comorbidities of adolescent problem behaviours: A latent class model. J Abnormal Child Psychol 1994; 22: 339-353. Feehan M, McGee R, Raja SN, Williams SM. DSM-III-R disorders in New Zealand 18-year-olds. Aust N Z J Psychiatry 1994; 28: 87-99. Jones P, Rodgers B, Murray R, Marmot M. Child developmental risk factors for adult schizophrenia in the British 1946 birth cohort. Lancet 1994; 344: 1398-1402. Patton GC, Carlin JB, Shao Q, et al. Adolescent dieting: health weight control or borderline eating disorder? J Child Psychol Psychiatry 1997; 38: 299-306. Patton GC, Hibbert MH, Rosier MJ, et al. Is smoking associated with depression and anxiety in teenagers? Am J Pub Health 1996; 86: 225-300. Kovacs M, Krol RS, Voti L. Early psychopathology and risk for teenage pregnancy among clinically referred girls. J Am Acad Child Adolesc Psychiatry 1994; 33: 106-114. McGorry P. The Centre for Young People's Mental Health: blending epidemiology and developmental psychiatry. Australasian Psychiatry 1996; 4: 243-247. Quality of Care and Health Outcomes Committee. Clinical practice guidelines: depression in young people. Canberra: NHMRC, 1997. © 1999 Medical Journal of Australia.

George C Patton

Editorial Caesarean section: a matter of choice? Women need more information, whether or not it leads to a decrease in caesarean section rates MJA 1999; 170: 572-573 With 20% of all births in Australia being by caesarean section (CS), we have one of the highest rates among First World countries.1 There are, of course, variations from State to State and between the public and private sectors, but this high average rate is of ongoing concern to obstetricians, health administrators and consumer groups. Many reasons for these high rates have been advanced, including better survival prospects for very preterm infants; the threat of litigation leading to earlier intervention in labour; fewer operative vaginal deliveries; and routine abdominal delivery for breech presentation. The widespread use of electronic fetal monitoring and epidural analgesia, and the need for repeat CS, have also been cited. Despite much discussion, the appropriate CS rate for any population has yet to be defined; for instance, the target CS rate set by the US Department of Health and Human Services of 15% of births by the year 2000 is an arbitrary figure widely questioned by obstetricians in the United States.2,3In this issue of the Journal, Turnbull et al present the results of a cross-sectional survey of South Australian women who underwent CS.4 Their aim was to determine the extent of women's involvement in the decision to perform the operation. Although more than 80% of women having elective CS and 50% of those having emergency CS reported such involvement, 20%-50% of women overall were not completely satisfied either with the decision, their input into it, or the amount of information provided to them. Turnbull and colleagues concluded that giving women more information might contribute to a drop in CS rates. Certainly, it is desirable that all pregnant women receive adequate information about the possible course of labour and the reasons why emergency CS might be recommended. Elective CS should probably be regarded differently as far as the decision-making process is concerned -- there is always time to discuss the surgery with medical advisers, partners and friends. But when labour, in particular first labour, has a high chance of ending in CS, women should be better informed of this so that they regard it as a possible normal event, rather than a surprising and disappointing outcome of a planned vaginal birth.5 Several studies have documented an association between emergency CS and subsequent psychological problems, especially postnatal depression.6,7 In the presence of high caesarean rates, such an association would pose a significant health problem for mothers and babies. The psychological sequelae have been linked to a sense of failure on the part of women who anticipated and prepared for a normal vaginal delivery, suggesting that the incidence of attributable postnatal depression might decline if women were more prepared for CS as a possible mode of delivery. Turnbull's article also raises the question of whether, given adequate information, most women who have had a previous CS will opt for an attempt at vaginal delivery in a subsequent pregnancy. Several studies indicate that about 70% of these women will be able to deliver vaginally; this is usually a happy outcome for the woman concerned, and uses fewer health dollars than a repeat CS. However, the 30% of women who will not achieve a vaginal birth also need to be considered; among these will be some with resulting severe psychological problems, as well as those sustaining complications, such as uterine rupture requiring hysterectomy. Although uterine rupture is uncommon, it is more likely to occur with trial of labour than with a repeat CS.2,3,8,9 Women considering vaginal delivery after a CS birth need full, unbiased information about all alternatives if they are to make an informed choice. There is evidence that there are some women who feel quite positive about CS, even requesting the operation when medical indications are slight or non-existent.3,10 More than 25% of the women in Turnbull's study indicated that they had "insisted on", or were "keen to have", a caesarean delivery. Mould et al, in a study of 102 women undergoing CS in a London hospital, found that more than 10% felt the decision for surgery to be entirely their own, and that 50% would opt for CS in a further pregnancy.11 How these women who insist on a CS would respond to extra information is unknown. Al-Mufti and colleagues surveyed the personal responses of London obstetricians (a highly informed group) to various hypothetical pregnancy situations: 31% of female obstetricians, and 8% of male obstetricians, would choose elective CS, for themselves or their partners, for an uncomplicated singleton cephalic presentation at term; higher percentages favoured CS for relatively minor indications. Possible stress incontinence, anal sphincter damage and compromised sexual function following vaginal delivery were among the reasons given. Al-Mufti rather archly suggests that perhaps CS should be offered to all pregnant women, "an option apparently available to all obstetricians".12 Turnbull's study is to be commended as an attempt to quantify the reasons for the decision to have a CS, and as a step towards providing the most appropriate and accurate information for women. However, certain assumptions were made in assessing the degree of satisfaction of the women surveyed, and there was no comparison with women experiencing a spontaneous vaginal delivery. Furthermore, Turnbull's final recommendation -- a randomised controlled trial of an information "package" -- would pose considerable methodological problems, including accruing sufficient participants; blinding the intervention (with some participants getting an information package and some not); and ensuring that patients in the control arm did not independently obtain the same information elsewhere. Regrettably, not all questions in medicine, especially those concerned with counselling, are answerable by randomised controlled trials.13-15 For the moment, it is clear that we must continue to monitor and assess Australian CS rates, and that women must be as well informed as possible about CS, especially emergency CS, long before labour. Many women may opt for a vaginal birth after a previous caesarean delivery, others will not, and others still may request CS for relatively minor indications. We must remember that providing full, unbiased information about birth and CS is not merely to enable health administrators to reach arbitrary targets, but to allow women to make a considered choice (even though that choice may be deplored by other groups of consumers or healthcare providers). Caroline M de Costa Senior Lecturer in Obstetrics and Gynaecology North Queensland Clinical School, University of Queensland, Cairns, QLD Day R, Sullivan E, Lancaster P. Australia's mothers and babies 1996. Sydney: Australian Institute of Health and Welfare National Perinatal Statistics Unit, 1999. (Perinatal Statistics Series No. 7.) Sachs BP, Kobelin C, Castro MA, Frigoletto F. The risks of lowering the cesarean delivery rate. N Engl J Med 1999; 340: 54-57. What is the right number of caesarean sections? [editorial] Lancet, 1997; 349: 815. Turnbull D, Wilkinson CS, Yaser A, et al. Women's role and satisfaction in the decision to have a caesarean section. Med J Aust 1999; 170: 580-583. Hillan EM. Issues in the delivery of midwifery care. J Adv Nurs 1992; 17: 274-278. Boyce PM, Todd AL. Increased risk of postnatal depression after emergency caesarean section. Med J Aust 1992; 157: 172-174. Fisher J, Astbury J, Smith A. Adverse psychological impact of operative obstetric interventions: a prospective longitudinal study. Aust N Z J Psych 1997; 31: 728-738. McMahon M, Luther E, Bowes W, Olshan A. Comparison of a trial of labor with an elective second cesarean section. N Engl J Med 1996; 335: 689-695. Paul RH. Towards fewer cesarean sections -- the role of a trial of labour [editorial]. N Engl J Med 1996; 335: 735-736. Grant JM. Women are satisfied with caesarean section [editorial]. Br J Obstet Gynaecol 1996; 103: vii-viii. Mould TAJ, Chong S, Spencer JAD, Gallivan S. Women's involvement with the decision preceding their caesarean section and their degree of satisfaction. Br J Obstet Gynaecol 1996; 103: 1074-1077. AI-Mufti R, McCarthy A, Fisk NM. Obstetricians' personal choice and mode of delivery [letter]. Lancet 1996; 347: 544. Brewin CR, Bradley C. Patient preferences and randomised controlled trials. BMJ 1989; 229: 313-315. Knottnerus JA, Dinant GJ. Medicine based evidence, a prerequisite for evidence based medicine [editorial]. BMJ 1997; 315: 1109-1110. Solomon MJ, McLeod RS. Surgery and the randomised controlled trial: past, present and future. Med J Aust 1998; 169: 380-383. Photo courtesy Dr P Mason, Department of Obstetrics and Gynaecology, Cairns Base Hospital, QLD

Editorial Angered patients and the medical profession Changing from "doctor's orders" to "patient's choice" MJA 1999; 170: 576-577 Medical treatment is not entirely risk free. The doctor-patient relationship involves two individuals -- both human, and therefore fallible. One seeks assistance with a problem and the other has the skills to deal with that problem. In this human interaction anything can go wrong. A doctor may be responsible for a negligent act or omission, or a patient may wrongly accuse a doctor of negligence. Preventing things from going wrong is called risk management, which, in Australian medicine, is in its infancy. A term more acceptable to clinicians is "quality assurance". The subtle difference is that quality assurance programs focus on "getting things right", whereas risk management programs focus on "not getting things wrong". Clinical quality assurance programs in Australia largely analyse technical performance, but, unlike most other service industries, rarely focus on consumer satisfaction, or dis-satisfaction. Thus, the article by Daniel et al in this issue of the Journal,1 which reports a survey of 290 complainants to the New South Wales Health Care Complaints Commission (HCCC) in 1996 and 1997, is a welcome addition to the scant literature in this area. There are now multiple avenues in Australia for patients to address complaints or concerns about medical management: the doctor involved or the hospital or practice management, the State-based medical ombudsmen (variously described as Health Rights Commissioners, Health Services Commissioners, and, in New South Wales, the HCCC), the Medical Board, the police, or civil litigation through the courts. The role of the medical ombudsmen -- to conciliate or mediate and not to judge or punish -- is, as Daniel et al found, often misunderstood by aggrieved patients. Daniel et al report the same four motivators for complaints to the HCCC as other studies2 have found: Punishment -- this is largely a function of the criminal courts; Regulation -- this is the responsibility of the registration boards, which exist primarily to protect public safety and not to deliver "justice" to complainants; Compensation -- this is still most commonly sought through civil litigation, but increasingly is negotiated outside litigation, perhaps using the conciliation services of the medical ombudsmen; and Accountability -- this is sought by many complainants, who want to see the "guilty" parties brought to account and systems changed so that what happened to them will not happen to other patients in the future. Doctors are now sensitised, if only by the rising cost of professional liability protection, to the increasing incidence and cost of patient complaint and litigation. However, despite their increased medicolegal anxiety, the medical profession has not adapted to this consumer-driven environment. The same rigorous standards used in the management of disease have not been applied to an examination of the causes -- and hence the prevention -- of patient dissatisfaction. It would appear that many doctors prefer the medical defence organisations, or other professional organisations, to do whatever is necessary to make these problems go away, rather than adapt to them by changing long-established habits of practice. Despite evidence to the contrary from the Harvard Medical Practice Study,3 the belief remains prevalent that most litigation results from gross errors in medical diagnosis and treatment, and that these are best minimised through clinical quality control. While clinical errors are usually involved, the likely precipitant is more likely to be a communication error. It is not sufficient for a doctor to reach a conclusion regarding diagnosis and optimal treatment. This must be conveyed to the patient and then skill exercised to motivate the patient to adopt that same point of view. The patient is the one with the problem and it is for the patient to decide, on the basis of the information provided, whether or not to take the doctor's advice. It is no longer "doctor's orders", it is "patient's choice". Furthermore, "informed refusal" is as important as "informed consent". How much non-compliance is uninformed refusal? The results of the Harvard Medical Practice Study (HMPS)3 not only suggested that if you are sued you are unlikely to have been negligent, but also that if you are negligent you are unlikely to have been sued! In about 300 of the 30 000 New York hospital records reviewed, it was assessed that an adverse outcome had resulted from avoidable negligence -- but in only about one in eight of these had a claim for compensation been made. Conversely, of all the legal actions commenced against the surveyed hospitals in that period, only about a third involved one of those 300-odd files. Two conclusions can be inferred from the HMPS. Firstly, that other intervening factors, such as communication failures in the doctor-patient relationship, determine whether or not an adverse event will result in litigation, and, secondly, that a negligent act or omission is a necessary, but not the sole, condition for a successful claim in negligence. A third possible conclusion, of course, is that patients do not sue when they have no inkling that their adverse outcome arose from a negligent error! The Bristol case4 shows that, even when a negligent error is reported, instead of facilitating communication the first response of the medical community may be to suppress the information by "killing the messenger". The factors driving a patient to sue were surveyed in a 1994 study in the United Kingdom of 227 patients who had commenced legal action for alleged medical negligence.2 Only about a quarter said their primary motive was money (compensation). The rest were evenly spread between "it was the only way we could find out what really happened" (information/communication), "we wanted someone brought to account for what happened" (acknowledgement/accountability) and "we want to ensure this doesn't happen again" (regulation/discipline). Litigation (seeking compensation through a civil action) can only provide money, and a poultice of money does not cure all ills. These UK and US findings are reflected in the study by Daniel et al, which found that "Only a few [of the complainants] want compensation; more want acknowledgement of the harm done; most want the doctor punished." The study by Daniel et al, however, is not directly comparable with the UK study; they surveyed patients lodging complaints, whereas the UK study was of litigants. Moreover, Daniel's study may not necessarily reflect the experience in other Australian States because of the different roles of the NSW HCCC (includes prosecution) and other States' medical ombudsmen services (principally mediation). It would be interesting to make a comparable survey of complainants finalised through (for example) the Victorian Heath Service Commissioner's office. When something goes wrong in any area of human endeavour, the instinctive response is to ask, "What happened?" and "How did it happen?". If answers to these questions are not provided quickly, anger explodes and the questions become "Whose fault was it?" and "Who's going to pay?". The NSW study confirms that anger fuels a demand for retribution. Doctors, being human, rarely, but inevitably, make mistakes. Some of these satisfy the legal test of negligence. But not all result in actions in negligence. A doctor's behaviour after an adverse event, or after receipt of a complaint (Box), is often the major factor determining whether the patient proceeds to litigation or chooses another avenue of complaint or does nothing. Paul Nisselle Chief Executive, The Medical Indemnity Protection Society Melbourne, VIC Daniel AE, Burn RJ, Horarik S. Patients' complaints about medical practice. Med J Aust 1999; 170: 598-601. Vincent C, Young M, Phillips A. Why do people sue doctors? A study of patients and relatives taking legal action. Lancet 1994; 343: 1609-1613. Weiler PC, Hiatt HH, Newhouse JP, et al. A measure of malpractice. Medical injury, malpractice, litigation and patient compensation. Cambridge, Mass: Harvard University Press, 1993. Bolsin SN. Professional misconduct: the Bristol case. Med J Aust 1998; 169: 369-372. What to do when an adverse event occurs Inform the patient as soon as possible If a letter of complaint is received, forward a reply promptly Supply information which is detailed and factual but contains neither positive nor negative "spin" Self-flagellation by the doctor or the hospital involved is inappropriate, but so is denial Acknowledge the effect ("I appreciate how distressing this is to you") Express sincere regret and genuine concern for the patient's welfare ("I'm sorry this has happened to you") Do not admit liability ("I'm sorry I did this to you"). It is inappropriate to admit liability in the heat of the moment; calmer reflection, and after seeking advice, may lead to the conclusion that there is no liability. Back to text

Paul Nisselle

Editorial Primary stenting in acute myocardial infarction: paving the way to arterial patency No matter how enticing the data may be, all the answers are not in MJA 1999; 170: 518-519 Acute myocardial infarction (AMI) remains a major cause of morbidity and the single most common cause of mortality among adult Australians.1 It has been estimated that there is one AMI every half hour and one fatal event every hour among men and women under 70 years of age.1 Despite a decade of remarkable insights into the pathobiology of AMI and innumerable randomised clinical trials evaluating therapeutic approaches, the optimal acute management strategy still remains unclear. It is widely accepted that the primary objective in AMI is early reperfusion,2 which, by preserving myocardial cell viability and contractility, results in improved survival.3-6 However, the main mechanism of achieving coronary artery reperfusion -- intravenous thrombolytic therapy -- is not without its limitations: up to half the patients may be ineligible on clinical grounds, and it is only moderately effective in reinstituting the level of coronary flow necessary for improved survival.7 Other problems include recurrent ischaemia, reinfarction and a small but significant chance of life-threatening haemorrhagic complications.8 Because of these drawbacks, interest in mechanical reperfusion by primary coronary balloon angioplasty (without prior thrombolysis) has steadily increased. Despite its 17-year history, balloon angioplasty is not as widely available or as frequently used9 as perhaps it should be (for reasons beyond the scope of this editorial). However, current evidence for its use in primary treatment of AMI is quite encouraging. A review of 10 randomised clinical trials comparing primary coronary balloon angioplasty with thrombolytic therapy in 2606 patients with AMI found those treated with balloon angioplasty had a 34% lower mortality rate, a lower rate of death and/or non-fatal reinfarction and a significantly lower rate of total and haemorrhagic stroke.10 Other randomised trials have indicated that, by reducing early and late recurrent ischaemia, primary balloon angioplasty may expedite early discharge and thus reduce costs.11,12 Promising as these data might be, they are far from conclusive, in part because of the size of the dataset and the unblinded nature of the clinical trials. Almost 13 000 patients would need to be enrolled in a trial to detect a 20% advantage in 30-day mortality rates of primary coronary balloon angioplasty over thrombolytic therapy (assuming a 7% mortality rate in the thrombolytic therapy group).13 Equally concerning are the incidence of no reflow due to distal thrombus embolisation at the time of balloon dilatation; early recurrent ischaemia and/or reinfarction (5%-10% of patients14) due to elastic vascular recoil and/or platelet and thrombus deposition at the site of balloon-induced intimal disruption (dissection); and late restenosis (30%-50% of patients14) due to a varying mix of neointimal proliferation, unopposed recoil and vascular remodelling. While there have been substantial improvements in operator skills, procedural techniques, equipment design and adjunctive antiplatelet therapies, the issues mentioned above continue to frustrate the proponents of primary coronary balloon angioplasty. It is not surprising, therefore, that they should have become infected and intoxicated by the euphoria surrounding coronary stenting in elective angioplasty. Compared with simple balloon angioplasty, coronary stenting in elective (non-infarct-related) coronary angioplasty has been shown to reduce the rate of periprocedural complications and late restenosis, and to be beneficial in the management of saphenous vein graft lesions and restenotic lesions after balloon angioplasty. The thought of in-situ coronary thrombus and the likely consequences of deploying a metal stent into such an environment in a patient with AMI initially struck fear into the hearts of even the most ardent supporters of primary balloon angioplasty. However, the realisation that antiplatelet therapy could prevent stent-related thrombotic complications and the publication of a bold study of primary infarct stenting without conventional anticoagulation therapy15 strengthened the advocates' resolve. This first study, although small and non-randomised, paved the way for larger feasibility trials,16 and, more recently, randomised controlled trials of primary stenting in AMI.17,18 These studies demonstrate a substantially lower rate of recurrent ischaemia, reinfarction, angiographic restenosis and a reduced need for target-vessel revascularisation compared with good old balloon angioplasty. Unfortunately, neither of the randomised trials had sufficient power to assess effects on mortality. As is often the case with provocative new data, these observations on primary stenting in AMI provide many more questions than answers. Clearly, it is now important to establish in whom and by whom primary stenting should be done. What patient, vessel or lesion characteristics respond best to primary stenting? For example, should primary stenting be the treatment of choice in diabetic patients, who tend to have more diffuse atherosclerotic disease and a higher risk of restenosis? Should only experienced operators attempt primary stenting in AMI? Coronary stenting may add to the complexity and risks of the procedure rather than lessen them, and most of the recently published data16-18 emanate from centres with unparalleled resources and expertise. Furthermore, what if the lesion is not amenable to primary stenting, or, for that matter, even primary angioplasty? The question of a second-line strategy is often not addressed. In this issue of the Journal, Hansen and colleagues19 indeed address some of these important practical issues. In a pilot study, they assessed the feasibility, safety and short term clinical outcomes of a primary stenting strategy (embracing several critical contingency plans) in a consecutive group of patients with AMI and eligible for fibrinolysis. The authors observed that primary stenting was possible in 71% of their cohort, and, by adopting a strategy that included the "fall-back" options of simple balloon angioplasty, emergency or semiurgent coronary artery bypass grafting (CABG) and medical therapy, they achieved successful early revascularisation of the infarct-related artery in 95% of their patients, with a remarkably low rate of early, six-week and six-month cardiovascular events. The immediate questions that come to mind concern, firstly, the costs, and what well-timed thrombolytic therapy might have achieved in this cohort, and, secondly, whether these results can be extrapolated to centres where resources such as CABG might not be as readily available. The study by Hansen et al is limited by being non-randomised and observational and the experience of a single centre. Nonetheless, it provides important local insight into primary stenting in AMI and indicates that this strategy is safe and feasible and can be delivered in a timely fashion in an appropriately equipped Australian hospital. Whether this holds true for patients at remote centres is unknown, and it is not clear whether patients should be denied early lytic therapy at one institution so they may be transferred to another to obtain primary coronary balloon angioplasty/primary stenting. Thrombolytic therapy has an inherent time delay of approximately 45-60 minutes. A modest delay in obtaining primary angioplasty/primary stenting may therefore be acceptable, but has not been formally tested. In summary, there is a growing body of evidence which suggests that primary stenting in AMI may be preferable to primary coronary balloon angioplasty and possibly more efficacious than conventional thrombolytic therapies. However, no matter how enticing the data may be, all the answers are not in. Does it save lives? Is it cost effective? Is it widely applicable? Does it improve myocardial salvage? Are all stents equal or are some more equal than others? Is it better than primary coronary balloon angioplasty with adjunctive glycoprotein IIb/IIIa platelet receptor blockade? These are but a few of the questions that need addressing, and until these issues are resolved primary stenting must be viewed as a procedure undertaken with the best of intentions. And need I mention where the road paved with good intentions might lead? Ian T Meredith Associate Professor; and Director, Cardiac Catheterisation and Interventional Cardiology, Centre for Heart and Chest Research Monash Medical Centre, Melbourne, VIC Email: ian.meredithATmed.monash.edu.au National Heart Foundation of Australia. Heart and stroke facts. Canberra: NHF, 1996: 1. Lange RA, Hillis LD. Thrombolysis -- the preferred treatment. N Engl J Med 1996; 335: 1311-1312. White HD, Norris RM, Brown MA, et al. Effects of intravenous streptokinase on left ventricular function and early survival after acute myocardial infarction. N Engl J Med 1987; 317: 850-855. O'Rourke M, Baron D, Keogh A, et al. Limitation of myocardial infarction by early infusion of recombinant tissue-type plasminogen activator. Circulation 1988; 77: 1311-1315. Gruppo Italiano per lo Studio della Streptochinasi nell' Infarto Miocardico, GISSI. Effectiveness of intravenous thrombolytic treatment in acute myocardial infarction. Lancet 1986; 1: 397-401. ISIS-2 Collaborative Group. A randomized trial of intravenous streptokinase, oral aspirin, both or neither among 17187 cases of suspected acute myocardial infarction: ISIS-2. Lancet 1988; 2: 349-360. The GUSTO Angiographic Investigators. The effects of tissue plasminogen activator, streptokinase or both on coronary artery patency, ventricular function and survival after acute myocardial infarction. N Engl J Med 1993; 329: 1615-1622. Grines CL. Primary angioplasty -- the strategy of choice. N Engl J Med 1996; 335: 1313-1315. Coronary angioplasty in Australia 1995. Canberra: Australian Institute of Health and Welfare, 1995. (Cardiovascular Disease Series No. 8.) Weaver WD, Simes RJ, Betriu A, et al. Comparison of primary coronary angioplasty and intravenous thrombolytic therapy for acute myocardial infarction. A quantitative review. JAMA 1997; 278: 2093-2098. Stone GW, Grines CL, Rothbaum D, et al. Analysis of the relative costs and effectiveness of primary angioplasty versus tissue-type plasminogen activator: The Primary Angioplasty Myocardial Infarction (PAMI) Trial. J Am Coll Cardiol 1997; 29: 901-907. De Boer MJ, van Hout BA, Liem AL, et al. A cost-effective analysis of primary coronary angioplasty versus thrombolysis for acute myocardial infarction. Am J Cardiol 1995; 76: 830-833. Yusuf S, Pogue J. Primary angioplasty compared with thrombolytic therapy for acute myocardial infarction. JAMA 1997; 278: 2110-2111. Stone GW, Grines CL, Topol EJ. Update on percutaneous transluminal coronary angioplasty for acute myocardial infarction. In: Topol E, Serruys P, editors. Current review of interventional cardiology. 2nd edition. Philadelphia, Pa: Churchill Livingstone, 1995: 1-56. Saito S, Hosokawa G, Kim K, et al. Primary stent implantation without coumadin in acute myocardial infarction. J Am Coll Cardiol 1996; 28: 74-81. Stone GW, Brodie BR, Griffin JL, et al. Clinical and angiographic follow-up after primary stenting in acute myocardial infarction. The primary angioplasty in myocardial infarction (PAMI) Stent Pilot Trial. Circulation 1999; 99: 1548-1554. Suryapranata H, van't Hof AWJ, Hoorntje JCA, et al. Randomised comparison of coronary stenting with balloon angioplasty in selected patients with acute myocardial infarction. Circulation 1998; 27: 2502-2505. Antonucci D, Santoro GM, Bolognese L, et al. A clinical trial comparing primary stenting of the infarct-related artery with optimal primary angioplasty for acute myocardial infarction. Results from the Florence randomized elective stenting in acute coronary occlusions (FRESCO) trial. J Am Coll Cardiol 1998; 31: 1234-1239. Hansen PS, Rasmussen HH, Vinen J, Nelson GIC. A primary stenting strategy as an alternative to fibrinolytic therapy in acute myocardial infarction. An analysis of results in hospital and at 6 weeks and 6 months. Med J Aust 1999; 170: 537-540. Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/>

Ian T Meredith

Editorial The hip fracture threat Fighting back with a cheap, safe and neglected weapon -- vitamin D with calcium MJA 1999; 170: 459-460 In Australia (as in other developed countries), fractures of the proximal femur are one of the major hazards of old age, particularly in women, in whom the incidence reaches about 3% per annum in the ninth decade.1 Hip fracture, with its associated significant mortality and high rate of residual disability,2 is widely regarded as the ultimate expression of osteoporosis. In fact, this fracture is as much due to more frequent falls in the elderly as to reduced bone density.2,3 As hip fracture is so clearly a function of ageing, its prevalence is bound to increase with increasing longevity, but the scale of this increase is not widely appreciated. In this issue of the Journal, two reports, one by Sanders et al 4 and the other by Pocock et al 5, predict an alarming virtual doubling in hip fracture incidence in Australia (from about 15 000 to 30 000 per annum) in the next 20 years, assuming age-specific rates remain constant. The scenario presented by these authors is made even more disturbing by Pocock and colleagues' assessment of the scope for a preventive screening program.5 Applying optimistic assumptions of 60% of the target population screened, 60% complying with therapy, and the therapy being 50% effective, they found that the number of hip fractures would still increase by over 50% in the next 20 years. This is not surprising in view of the diversity of risk factors involved in both bone fragility and falls in the elderly. Bone fragility is a function not only of bone density (in which there is a major genetic component6), but also of bone turnover7 and bone architecture.8 Falls are subject to even more risk factors, including impaired vision, muscle weakness, postural hypotension (including the use of diuretics, because of their hypotensive action) and long-acting sedatives. Other risk factors for low bone density or frequent falls include smoking, physical inactivity, low body weight and inadequate exposure to sunlight.9 Most preventive measures for hip fractures in the elderly have been directed at the bone itself, and oestrogens,10 bisphosphonates11 and calcitriol12 have all been shown to reduce fracture rates. However, even if increasing use of these potent and relatively expensive agents could reverse fracture risk in selected individuals, this would have only a limited impact at the population level.9 In this rather bleak scenario, there is one relatively simple approach that should perhaps be pursued more actively than it is at present, namely the greater use of vitamin D and calcium in the elderly, particularly in those who are housebound or in institutions. It is 30 years since histological evidence of vitamin D deficiency in hip fracture patients was first reported in England,13 and over 20 years since this histological evidence was confirmed by demonstrating low serum levels of 25-hydroxyvitamin D in these patients.14 After confirmation of these findings in many other countries, vitamin D insufficiency (ie, a low serum level of 25-hydroxyvitamin D without overt evidence of rickets/osteomalacia) was uncovered in women with hip fractures and in nursing home residents in sunny South Australia.15 Subsequent studies confirmed the poor vitamin D status of nursing home residents in New South Wales16 and Victoria,17 and it is now generally accepted that vitamin D insufficiency, and associated secondary hyperparathyroidism16 with high bone turnover,18 are as common among elderly citizens in Australia as elsewhere, both because physical infirmity reduces exposure to sunlight and because age-related thinning of the skin reduces its capacity to synthesise cholecalciferol.19 Although there is some disagreement about the threshold level of 25-hydroxyvitamin D in plasma that triggers secondary hyperparathyroidism (we find the threshold to be at about 40-50 nmol/L, but thresholds as high as 100 nmol/L have been suggested20), there is consensus that quite mild vitamin D insufficiency stimulates parathyroid hormone secretion. These observations might be regarded as academic were it not for a French trial in which 800 units of vitamin D and 1200 mg of calcium daily for 18 months normalised serum 25-hydroxyvitamin D and parathyroid hormone levels and reduced the hip fracture incidence by 43% in 877 female nursing home residents (compared with 888 controls).21 Although the rapidity of this therapeutic effect could hardly have been due to a change in bone density, it might be explained by a reduction in bone turnover from reduced parathyroid activity, combined with improved muscle strength and a consequent reduction in falls from the action of vitamin D on muscle.22 A subsequent Dutch study, showing that 400 units of vitamin D without calcium given daily for three years had no effect on hip fracture rate in subjects not in institutions,23 does not vitiate the French trial, which used more vitamin D, combined it with calcium and targeted a vitamin D-insufficient population. We do not wish to imply that vitamin D (with calcium) is the be-all and end-all of hip fracture prevention, or to deny that aged-care services need to be strengthened to cope with an ageing population. We do suggest, however, that vitamin D (with calcium) -- a preventive measure that is not only cheap and safe but simultaneously targets both bone and muscle -- is an attractive but neglected weapon in the campaign against hip fractures. Perhaps the time has come to set up task forces at Federal and/or State levels to consider this and other options. Howard A Morris Chief Medical Scientist Allan G Need Divisional Head, and Senior Visiting Physician, Division of Clinical Biochemistry Institute of Medical and Veterinary Science, and Department of Medicine, University of Adelaide, SA B E Christopher Nordin Senior Specialist and Visiting Professor Division of Clinical Biochemistry, Institute of Medical and Veterinary Science, and Department of Pathology, University of Adelaide, SA March L, Chamberlain A, Cameron I, et al. Prevention, treatment and rehabilitation of fractured neck of femur. Health Outcomes Project 1996. Sydney: Public Health Unit, Northern Sydney Area Health Service, 1996. (ISBN 07310 9633 9). Also on the internet <http://www.mja.com.au/public/issues/iprs2/march/fnof.pdf> Brockelhurst JC, Exton-Smith AN, Lempert Barber SM, et al. Fracture of the femur in old age: a two-centre study of associated clinical factors and the cause of the fall. Age Ageing 1978; 7: 7-15. Dargent-Molina P, Favier F, Grandjean H, et al. Fall-related factors and risk of hip racture: the EPIDOS prospective study. Lancet 1996; 348: 145-149. Sanders KM, Nicholson GC, Ugoni AM, et al. Health burden of hip and other fractures in Australia beyond 2000. Projections based on the Geeong Osteoporosis Study. Med J Aust 1999; 170: 467-470. Pocock NA, Culton NL, Harris ND. The potential effect on hip fracture incidence of mass screening for osteoporosis. Med J Aust 1999; 170: 486-488. Slemenda CW, Christian JC, Williams CJ, et al. Genetic determinants of bone mass in adult women: a reevaluation of the twin model and the potential inportance of gene interaction on heritability estimates. J Bone Miner Res 1991; 6: 561-567. Melton LJ, Khosla S, Atkinson EJ, et al. Relationship of bone turnover to bone density and fractures. J Bone Miner Res 1997; 12: 1083-1091. Faulkner KG, Cummings SR, Black D, et al. Simple measurement of femoral geometry predicts hip fracture: the study of osteoporotic fractures. J Bone Miner Res 1993; 8: 1211-1217. Cummings SR. Prevention of hip fractures in older women: a population-based perspective. Osteoporos Int 8 (Suppl 1): S8-S12. Weiss NS, Ure CI, Ballard JH, et al. Decreased risk of fractures of the hip and lower forearm with postmenopausal use of oestrogen. N Engl J Med 1980; 303: 1195-1198. Liberman UA, Weiss SR, Broll J, et al. Effect of oral alendronate on bone mineral density and the incidence of fractures in postmenopausal osteoporosis. N Engl J Med 1995; 333: 1437-1443. Tilyard M, Spears GFS, Thomson J, Dovey S. Treatment of postmenopausal osteoporosis with calcitriol or calcium. N Engl J Med 1992; 326: 357-362. Aaron JE, Gallagher JC, Anderson J, et al. Frequency of osteomalacia and osteoporosis in fractures of the proximal femur. Lancet 1974; 2: 229-233. Baker MR, McDonnell H, Peacock M, Nordin BEC. Plasma 25-hydroxyvitamin D concentrations in patients with fractures of the femoral neck. BMJ 1979; 1: 589. Morris HA, Morrison GW, Burr M, et al. Vitamin D and femoral neck fractures in elderly South Australian women. Med J Aust 1984; 140: 519-521. Brock K, Reid J, Fraser D. Effect of type of accommodation on the vitamin D status of the elderly in Sydney, Australia. In: Norman AW, Bouillon R, Thomasset M, editors. Vitamin D: chemistry, biology and clinical applications of the steroid hormone. Riverside, Calif: University of California, 1997: 885-886. Stein MS, Scherer SC, Walton SL, et al. Risk factors for secondary hyperparathyroidism in a nursing home population. Clin Endocrinol 1996; 44: 375-383. Gallagher JC, Kinyamu HK, Fowler SE, et al. Calciotropic hormones and bone markers in the elderly. J Bone Miner Res 1998; 13: 475-482. Need AG, Morris HA, Horowitz M, Nordin BEC. Effects of skin thickness, age, body fat, and sunlight on serum 25-hydroxyvitamin D. Am J Clin Nutr 1993; 58: 882-885. McKenna MJ, Freaney R. Secondary hyperparathyroidism in the elderly: means to defining hypovitaminosis D. Osteoporos Int 1998; Suppl 8: S3-S6. Chapuy MC, Arlot ME, Duboeuf F, et al. Vitamin D3 and calcium to prevent hip fractures in elderly women. N Engl J Med 1992; 327: 1637-1642. Boland R. Role of vitamin D in skeletal muscle function. Endocrine Rev 1986; 7: 434-448. Lips P, Graafmans WC, Ooms ME, et al. Vitamin D supplementation and fracture incidence in elderly persons. Ann Intern Med 1996; 124: 400-406. Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/> We appreciate your comments.

Howard A Morris · Allan G Need

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

Charles A Vincent

Editorial Designer insulins: moving closer to convenient and physiological replacement of insulin Heralding a new horizon for people with diabetes MJA 1999; 170: 349-350 Since Banting and Best's development of insulin treatment in 1921, several major advances in production and delivery of insulin have revolutionised the care of people with diabetes. From this beginning, when crude animal insulin extracts and uncomfortable syringes and needles were used, the late 20th century has seen the development of pure genetically engineered human insulin delivered by convenient and almost painless pen delivery devices. These technological advances have been coupled with recent clinical trials that have confirmed the importance of euglycaemia to avoid the chronic complications of diabetes. The Diabetes Control and Complications Trial (DCCT)1 and the most recent United Kingdom Prospective Diabetes Study (UKPDS)2 have clearly shown the benefit of intensive compared with conventional insulin therapy. However, for many people with diabetes, intensive insulin therapy means multiple insulin injections and frequent blood sampling, as well as an increased risk of hypoglycaemia. Insulin analogues, or designer insulins, promise a new era of greater convenience and mastery for people with diabetes by replacing insulin in a more convenient and physiological manner. The first of these analogues available in Australia is insulin lispro (Figure). To make insulin lispro, the order of the amino acids proline and lysine on the B chain at positions 28 and 29 has been reversed.3 This subtle but important conformational change improves the solubility and absorption of the insulin molecule. Unlike conventional regular insulin, the peak insulin response is more rapid, occurring within 60-90 minutes, and the total duration of action is shorter, lasting 5-6 hours. The greatest potential benefits of these new types of insulins are improved blood glucose control with less risk of hypoglycaemia, as the peak of insulin action is more likely to coincide with peak glucose levels. Furthermore, as insulin lispro may be administered immediately before meals, it promises to provide greater convenience and flexibility. In this issue of the Journal, Stocks reports the use of this new insulin in a large cohort of 150 patients with type 1 diabetes managed in a private practice setting; results in 125 patients could be fully analysed.4 Before commencing the study all patients were receiving intensive insulin therapy, with at least four injections of insulin per day. The reported findings are similar to those of several randomised studies comparing regimens of multiple daily doses of lispro and regular insulin in patients with type 1 diabetes.5 As with Stocks' study, most of these have, of necessity, been unblinded, because of the different times of administration of the two insulins, and many have used a crossover design to minimise bias. In Stocks' study, despite the use of an intensive insulin regimen, more than half the patients had glycohaemoglobin values (expressed as %HbA1c) above the acceptable level of 8%. This is not an unusual finding in most clinical reports of type 1 diabetes and reflects the imprecise or unphysiological nature of insulin therapy. So does insulin analogue therapy live up to expectations? After changing to insulin lispro more than half the patients reported less glucose fluctuation. In addition, half experienced a reduction in HbA1c, and in those with initial HbA1c values above 8% this change was highly significant. In most other reported studies, lower HbA1c values are not usually achieved with insulin lispro compared with regular insulin.5 This difference may be explained by the appropriate adjustments made to overnight basal insulin in Stocks' study to ensure that fasting blood glucose levels remained within the target range. Coupled with improved glucose control, there was also a reduction in the number of hypoglycaemic episodes, both during the day and the night. The effect on hypoglycaemic episodes in other lispro studies has varied from no change to a 12% reduction. Intensive insulin therapy has been associated with weight gain,1 but in Stocks' study improvement in blood glucose control was not accompanied by changes in weight. The unblinded nature of this and other studies of lispro, and the use of a non-validated questionnaire, complicates the assessment of its impact on patient quality of life. Nevertheless, most patients reported that they felt better when taking insulin lispro. John Main recently described the nature of clinical practice as the "disorderly world of real medical practice".6 The evidence-based-medicine purists among us may undervalue the importance of the reported findings, as the highest level of evidence -- the double-blind randomised controlled trial -- was not used. Nevertheless, Stocks' study is valuable for several reasons, and the findings may be generalisable to other clinical settings. Firstly, it provides "real world" local outcome data on a large number of patients who would be typically seen in routine practice. Secondly, the study reminds us that biochemical outcomes are only one aspect of good diabetes management. Lifestyle issues, flexibility and convenience must also be considered. The perspective of some physicians may, however, be quite different, focusing on biochemical outcomes that may not be easily achieved without significant detriment to quality of life. With the rise of consumerism, the incorporation of patient values into decision-making is likely to gain further momentum. Lastly, in an age of audit, quality and accountability, as well as good clinical governance, it is heartening to see that serious health-outcomes research can and is being conducted in private practice settings. In the near future there is likely to be a vast array of new designer insulins as well as new methods of delivery.7 Other rapid-acting analogues, such as insulin aspart (aspartic acid replaces proline at position 28), are currently being tested. A neutral protamine lispro has also been developed and mixtures of lispro and neutral protamine lispro are being tested. Research is also progressing towards true basal insulin analogues, long-acting insulins with a prolonged action profile that will be reproducibly absorbed to maintain intermediate metabolism. These designer insulins, coupled with new developments such as inhaled insulin delivery, herald a new horizon for people with diabetes as we approach the 80th year of insulin treatment.7 Steven C Boyages Clinical Associate Professor Department of Diabetes and Endocrinology, Westmead Hospital, Sydney, NSW (Presently, Director Research and Clinical Policy, NSW Health, Sydney, NSW) The Diabetes Control and Complications Trial Research Group. The effect of intensive treatment of diabetes on the development and progression of long term complications in insulin dependent diabetes mellitus. N Engl J Med 1993; 329: 977-986. UK Prospective Diabetes Study Group: Intensive blood glucose control of sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). Lancet 1998; 352: 837-853. Barnett AH, Owens DR. Insulin analogues. Lancet 1997; 349: 47-51. Stocks AE. Insulin lispro: experience in a private practice setting. Med J Aust 1999; 170: 364-367. Lee W, Zinman B. From insulin to insulin analogs: progress in the treatment of type 1 diabetes. Diabetes Rev 1998; 6: 73-88. Main J. Doctors advocating evidence based medicine may be out of touch with real medicine. BMJ 1999; 318: 332. Marks J. Diabetes management in the future: a whiff and a long shot? Clin Diabetes 1998; 16: 3. Reprints: Professor S C Boyages, Department of Diabetes and Endocrinology, Westmead Hospital, Westmead, NSW 2145. Make a comment Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company. Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/> We appreciate your comments. Figure: Structure of insulin lispro Back to text

Steven C Boyages

Editorial Euthanasia consultants or facilitators? Few euthanasia consultants in the Netherlands act as independent evaluators of the patient's situation MJA 1999; 170: 351-352 As the Netherlands alone has long practised legally sanctioned assisted suicide and euthanasia, its experience is of great interest to the rest of the world. Of particular significance have been the Dutch government-sponsored studies conducted by van der Maas and his colleagues in 19901 and 1995.2,3 Those studies relied on data collected from a stratified sample of physicians selected because their practices were likely to involve them in end-of-life decisions. In each of the studies, more than 6000 physicians were surveyed and over 400 were interviewed. Informative data were collected. However, the investigators' analysis of their data has been criticised for emphasising procedural problems in the Dutch system while ignoring more basic substantive flaws, such as whether patients were offered treatment alternatives that might have made euthanasia seem unnecessary.4-6 The same might be said of the article in this issue of the Journal by Onwuteaka-Philipsen et al7, which draws on the individual interviews with physicians conducted in 1995 to discuss the use of consultants, a requirement in the Netherlands in intended cases of assisted suicide and euthanasia. The purpose of consultation is to confirm that the attending physician has followed established guidelines regarding the voluntary, well-considered nature of the patient's decision, the presence of suffering that must be unbearable and hopeless, and the absence of any alternative treatment. In a substantial number of cases, however, a consultation is not obtained. Most of these cases involve violation of another Dutch guideline: although all cases of assisted suicide and euthanasia must be reported to the authorities, most (59%) are not.2 Only a minority of unreported cases involve consultants.3 In the most flagrant violation of Dutch guidelines, consultants are not called: between 900 and 1000 patients' lives are ended without their explicit consent each year.1,2 In the 1995 study, 21% of these patients were competent; in the 1990 study, 37% were competent. A consultant was virtually never called when the lives of competent patients were ended without their explicit consent.1 Onwuteaka-Philipsen et al report that 42% of the interviewed physicians had at some time served as a consultant in an assisted suicide or euthanasia case. More general practitioners than specialists had done so (49% v. 30%). The authors note that, of the physicians who had been a consultant more than once, 50% had previously been consulted by the same physician. In 24% of these cases, the treating physician and the consultant had previously acted as consultants for each other. Recognising that such "pairs" may compromise the independence of the consultants, the authors appropriately suggest appointing independent consultants. The Dutch cases I have reviewed warrant the need for concern. The consultant basically functioned in a pro forma way, asking questions to confirm that the patient wished to go forward with euthanasia.8 The current article indicates that physicians did not actually see the patients in 12% of consultations. This probably reflects the view frequently expressed to me by Dutch physicians that the consultations were for the purpose of meeting legal requirements. The authors point out that most Dutch physicians do not have much experience in consulting in assisted suicide and euthanasia cases. Only 27% of Dutch physicians who have served as consultants have done so more than three times, and only 3% more than 10 times. The authors state that "consultants need to have knowledge relevant to euthanasia and assisted suicide, such as the possibilities of palliative care. Gaining experience as a consultant seems to be important for a physician to become comfortable in this role." No one should assume that experience as a consultant in euthanasia cases would make physicians knowledgeable about palliative care. My own experience with a few physicians in the Netherlands who had performed or been consultants in dozens of euthanasia cases was that they were surprisingly uninvolved in palliative care. Nor did they show sensitivity to the ambivalence that accompanies most requests to die, clearly evident in some of the cases we discussed.8 They seemed to be facilitators of the process rather than independent evaluators of the patient's situation who might be able to relieve suffering so that euthanasia seemed less necessary to the patient. One physician described his role as easing the doubts of physicians who were uncertain whether to go forward with euthanasia. He and the other consultants were certainly knowledgeable in what the authors refer to as the "medicotechnical" aspects of euthanasia -- they could end life quickly and efficiently. The Dutch have been widely criticised for their failure to provide adequate palliative care or hospice care for terminally ill patients.9,10 In recent testimony before the British House of Lords, Zbigniew Zylicz, one of the few palliative care experts in the Netherlands, emphasised Dutch deficiencies in palliative care, attributing them partly to the easier alternative of euthanasia. He saw the lack of hospice care in the Netherlands and the fact that there are only 70 palliative care beds in the country as reflections of this easier option.11 The conclusion in the Dutch studies that physicians in the Netherlands essentially practise euthanasia when there is no other alternative has been challenged.6,9,12,13 As neither the attending doctors, nor the consultants, nor the physician-interviewers in the government-sponsored studies were trained in palliative care, they were not in a position to make such a determination. Dr Zylicz, who has devoted his professional life to relieving the suffering of terminally ill patients and to training individual physicians in palliative care, finds his task complicated by the attitude of a medical establishment that insists on regarding euthanasia as a form of palliative care.14,15 This attitude encourages physicians to find euthanasia, which is far less demanding and challenging than what is ordinarily regarded as palliative care, a suitable alternative. Although the Dutch courts have ruled that unrelievable suffering must be present for a physician to be justified in carrying out euthanasia, it is increasingly accepted in the Netherlands and elsewhere that suffering can be considered unrelievable if patients simply exercise their right to refuse treatment for it. A prominent Dutch investigator sees a shift away from unrelievable suffering towards patient choice as the natural progression of a liberal society's increasing emphasis on autonomy.16 The problem with this position is that it ignores what actually happens when a suffering patient is confronted with a physician who does not know how to relieve that suffering except by euthanasia. If the only alternatives are continued suffering and an early death, patients are not likely to feel they have a choice. Study in the United States has shown that the more physicians know about palliative care, the less they favour legalisation of assisted suicide and euthanasia; the less they know, the more they favour it.17 Caring for people at the end of life is challenging, not only taking considerable skill but also requiring a great deal emotionally of physicians. Medical schools and residency training programs have only begun to prepare physicians to meet this challenge. If they succeed, the question of "euthanasia consultants" may become irrelevant. Herbert Hendin Professor of Psychiatry, New York Medical College, and Medical Director, American Foundation for Suicide Prevention, New York, USA van der Maas PJ, Van Delden JJM, Pijnenborg L. Euthanasia and other medical decisions concerning the end of life. New York: Elsevier Science Inc, 1992. van der Maas PJ, van der Wal G, Haverkate I, et al. Euthanasia, physician-assisted suicide, and other medical practices involving the end of life in the Netherlands, 1990-1995. N Engl J Med 1996; 335: 1699-1705. van der Wal G, van der Maas PJ, Bosma JM, et al. Evaluation of the notification procedure for physician-assisted death in the Netherlands. N Engl J Med 1996; 335: 1706-1711. Hendin H. Seduced by death: doctors, patients, and the Dutch cure. Issues Law Med 1994; 20: 123-168. Keown J. Euthanasia in the Netherlands. In: Keown J, editor. Euthanasia examined: ethical, clinical, and legal perspectives. Cambridge: Cambridge University Press, 1995. Hendin H, Rutenfrans C, Zylicz Z. Physician-assisted suicide and euthanasia in the Netherlands: lessons from the Dutch. JAMA 1997; 277: 1720-1722. Onwuteaka-Philipsen BD, van der Wal G, Kostense PJ, van der Maas PJ. Consultants in cases of intended euthanasia or assisted suicide in the Netherlands. Med J Aust 1999; 170: 360-363. Hendin H. Seduced by death: doctors, patients and assisted suicide. New York: W W Norton & Company, 1998. Zylicz Z. Euthanasia [letter]. Lancet 1991; 338: 1150. Dorrepaal KL, Aaronson NK, Van Dam F. Pain experience and pain management among hospitalized cancer patients. Cancer 1989; 63: 593-598. Matthews H. Better palliative care could cut euthanasia [news]. BMJ 1998; 317: 1613. Gomez C. Regulating death: euthanasia and the case of the Netherlands. New York: Free Press, 1991. Jochemsen H, Keown J. Voluntary euthanasia: under control? Further empirical evidence from the Netherlands. J Med Ethics 1999; 25: 16-21. Admiraal PV. A physician's responsibility to help a patient die. In: Misbin RI, editor. Euthanasia: the good of the patient, the good of society. Frederick, Md: University Publishing Group, 1992. Borst-Eilers E. Euthanasia in the Netherlands: brief historical review and present situation. In: Misbin RI, editor. Euthanasia: the good of the patient, the good of society. Frederick, Md: University Publishing Group, 1992. Van Delden JJM. Slippery slopes in flat countries -- a response. J Med Ethics 1999; 25: 22-24. Portenoy RK, Coyle N, Kash KM, et al. Determinants of the willingness to endorse assisted suicide: a survey of physicians, nurses and social workers. Psychosomatics 1997; 38: 277-287. Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/>

Herbert Hendin

Editorial Research and the acute-care hospital of the future A grand history of failed predictions is an argument for scientific prognostications MJA 1999; 170: 292-293 It is difficult to explain the history of healthcare systems, and the interpretation of contemporaneous events is even more challenging. The hardest enterprise, however, is that of futurist -- if it is to be done well. It involves extrapolating past and present trends, anticipating coming events and painting a cogent picture for posterity. Many people have failed miserably for various reasons.1-3 Lord Kelvin's claim in 1895 that "heavier than air flying machines are impossible" foundered on inadequate modelling. Technological change exposed the conjecture by the Chairman of IBM in 1948 that there was "a world market for about five computers". Arrogance probably led to the insouciant prophecy by the US Secretary of the Navy in 1941 that "[we are] not going to be caught napping". The recent prediction by the Australian Private Hospitals Association that the private health insurance rebate has the potential to "completely eliminate public hospital waiting lists"4 will no doubt be sorely tested. Hillman, in this issue of the Journal,5 combines the skills of historian, contemporary commentator and futurist to survey the acute-care hospital. He expresses views with which many would agree. The hospital sector has emerged in response to a wide range of policies and practices, many of which are no longer relevant. More recently, advances in practice and technology have been impressive, but the sector is exhibiting signs of systems failure,6,7 despite the skills and efforts of the individuals who work within it. Measures such as diagnosis-related groups (DRG) funding, involving clinicians in management, basing decisions on evidence and continuous improvement initiatives represent both a recognition of the problems and an indication that people with different perspectives on the healthcare sector, including policymakers, economists, clinicians and managers, are searching for solutions. Some recent trends seem destined to continue. These include further compression of length of stay, increased outsourcing and privatisation, renewed efforts to manage quality of care, and greater use of care options such as ambulatory care, day-only hospitalisation and home care.8,9 However, mere extrapolation is an insufficient basis for prediction given the many changes in clinical practice that could hardly have been anticipated. Further, in view of the lack of strategic vision of most Australian governments, there is no coherent framework for these trends. Moreover, the trends have been influenced by unfortunate constraints. For example, we have maintained the illogical splits in healthcare financing between the Commonwealth and the States despite 50 years of expert opinion that this system is counterproductive. It similarly makes no sense to separate private and public insurance. To allow privately insured patients to congregate in privately owned hospitals ensures there is little or no helpful competition across ownership types. Exactly how the healthcare delivery system will change is open to debate, which is one of the reasons Hillman's contribution is timely and useful. He paints a plausible picture that will no doubt stimulate valuable discussion and will be validated or invalidated over time. We would do well to heed four main points in the article. One is to consider how the idea of "hospitalist" -- essentially a specialist in acute-care and emergency medicine who releases other specialists from these activities -- would translate from the American to the Australian context. Second, the community health-hospital interface needs to be better integrated. Hillman envisages a more prominent role for general practitioners and community medicine, and the experience of the National Hospital Demonstration Program and the Coordinated Care Trials is of considerable value. Third, there will be challenges ahead for medical education in a more complex system.10 The fourth point is the emerging need for more research on the delivery system. The Health and Medical Research Strategic Review has shown that Australian research support is less than that of other Organization for Economic Cooperation and Development (OECD) countries ($28 per capita, compared with a GDP-weighted OECD average for developed countries of $42).11 There are thus grounds for increased expenditure on health and medical research, but health services research appears to be especially at risk. The Figure shows the most recent National Health and Medical Research Council (NHMRC) data comparing the relative success rate of grant applications by research field. The type of research that Hillman calls for is within the very field for which it is most difficult to secure NHMRC funding, the largest, and in some cases the only, source. Yet there are undoubtedly further gains to be made in delivery efficiency, structure and quality of care by enhancing health services' research efforts. We could head in several directions. At one extreme, there could be an intensification of what we have today -- more pressure to produce, more privatisation, more band-aid attempts to link fee-for-service general practitioners with public hospitals and home care services under strictly capped budgets, and more quarterly worrying about private health insurance, even with the 30% tax rebate. On the other hand, we could shoot for the social democrats' dream -- a single public insurer, all-encompassing area health services, multidisciplinary clinical teams as the prime contractors, increased preventive and community services with hospitals demoted to providers of intensive care beds, and so on. Health services research tools, such as critical historical incidents analysis, policy evaluation, scenario planning, computer modelling, decision analysis and risk assessment, can provide guidance to decision makers. They will help reduce the mistakes of the past, illuminate present problems and make future predictions more precise. Jeffrey Braithwaite Senior Lecturer Don Hindle Professor School of Health Services Management Faculty of Medicine University of New South Wales, Sydney NSW Email: j.braithwaiteATunsw.edu.au Cerf C, Navasky V. The experts speak. New York: Pantheon Books, 1984. Starbuck WH. Strategising in the real world. Intl J Technol Management 1992; 8 (1/2): 77-85. Shoemaker PJH. Scenario planning: a tool for strategic thinking. Sloan Management Rev 1995; Winter: 25-40. Australian Private Hospitals Association. An open letter to all Labor, Democrat, Green and Independent Senators. The Australian 9 December 1998: 9. Hillman K. The changing role of acute-care hospitals. Med J Aust 1999; 170: 325-328. Wilson RM, Runciman WB, Gibberd RW, et al. The Quality in Australian Health Care Study. Med J Aust 1995; 163: 458-471. Bolsin S. Professional misconduct: the Bristol case. Med J Aust 1998; 169: 369-372. Braithwaite J. The 21st-century hospital. Med J Aust 1997; 166: 6. Komesaroff PA, Clunie GJ, Duckett SJ. What is the future of the hospital system? Med J Aust 1997; 166: 17-23. Larkins RG, Martin TJ, Johnston CI. The boundaryless hospital -- a commentary. Aust N Z J Med 1995; 25: 169-170. Health and Medical Research Strategic Review. The virtuous circle: working together for health and medical research. Canberra: Commonwealth of Australia, 1998. URL: http://www.hmrsr.com (accessed 1 March 1999). Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/> Back to text

Jeffrey Braithwaite · Don Hindle

Editorial Shedding light on bowel cancer prevention The time has come for a concerted public education campaign MJA 1999; 170: 244-245 Colorectal cancer (CRC) is the second most common cause of cancer death in Australia.1 While motor vehicle accidents cause one death about every five hours, and breast cancer causes one death every four hours, CRC causes one every two hours. Australia has made a major government-sponsored effort to reduce mortality from motor vehicle accidents, and screening to prevent breast cancer mortality is an accepted government-sponsored initiative. Why then is there still confusion and argument about CRC prevention? There is convincing evidence that finding and removing adenomas in individuals at increased risk for bowel cancer prevents development of subsequent cancer in most.2 This would seem logical given the acceptance of the polyp-cancer sequence.3 In this issue of the Journal, Croese clearly demonstrates the potential for improving mortality.4 Using a community-based open-access colonoscopy service in Townsville, he showed that patients over 50 years of age who had undergone colonoscopy (with polypectomy when necessary) were less likely to be subsequently diagnosed with CRC than the remaining community in the same age group. Most of his repeat-colonoscopy patients had higher than average risk for developing CRC, which he defined as having one or more first-degree relatives with CRC or polyps, or ulcerative colitis, including quiescent pancolitis or active limited colitis. His message is simple: CRC can be prevented if those at increased risk are alerted to the need to enter a colonoscopic surveillance program. The strengths of the study are that it reports the outcome of "real world" colonoscopy practice from a relatively confined geographic area and provides details of cancers occurring during surveillance. The population was isolated, and the author was able to comprehensively cross-check data, making the information particularly valuable. The study's weaknesses -- a heterogeneous, unmatched population and retrospective comparisons -- were comprehensively addressed by the author. Although colonoscopic surveillance of those at higher risk of CRC is justified, surveillance intervals and starting age remain controversial. Timing of repeat colonoscopy will be partly influenced by the possibility of metachronous lesions, although these have been documented to occur in fewer than 1% of patients.5 The age at which to begin colonoscopic surveillance is also debated and, as about 8% of cancers develop in people aged under 50 years, it would not seem reasonable to withhold educational information from this group despite any perceived increase in cost. However, despite the simplicity of the message, many authorities in Australia still disagree on the need to deliver it. We need a coordinated, sponsored public education campaign to inform our community that an important step to reduce mortality from CRC is for those at increased risk (eg, first-degree relatives of people with CRC or polyps) to see a medical practitioner for advice and referral to an appropriate colonoscopic surveillance program. At the moment, the message is confused, as so well illustrated by Ward.6 Can we also shed some light on screening to prevent bowel cancer in the average-risk individual in our community? Setting aside the issue of mass screening for now and focusing on case-finding (ie, giving the appropriate advice to individuals who seek it or who may be receptive to it), there are four options for prevention or, at least, early diagnosis. Screening based on faecal occult blood testing (FOBT) reduces mortality from CRC. Studies showed a 16% reduction in mortality with biennial screening in the United Kingdom7 and Denmark,8 while a 33% reduction was seen with annual screening in the United States.9 Despite this well-designed research, the Australian Health Technology Advisory Committee has recently recommended further pilot studies on the efficacy of FOBT screening in the over-50 years age group. What other evidence they require remains a mystery. Flexible sigmoidoscopy is proposed for screening by many cancer authorities worldwide, usually in conjunction with FOBT. The combined approach recognises the limitations of flexible sigmoidoscopy, which may miss 50% of polyps and CRCs. Several retrospective studies have found that, in patients with proximal colon cancers, only 17%-30% of adenomas are in reach of the flexible sigmoidoscope.10 A prospective colonoscopy study showed that only 35% of 105 patients with proximal colon cancer had adenomas distal to the splenic flexure.11 These studies confirm that rectosigmoid adenomas ("sentinel" polyps) are an insensitive marker for proximal colon cancer, and that most proximal colonic neoplasms are not associated with distal polyps or cancer. These conclusions are supported by recent Australian data.12 Screening by flexible sigmoidoscopy alone would fail to detect 70%-80% of proximal cancers. Addition of annual FOBT would increase the diagnostic yield, but at increased cost. Colonoscopy is the third screening option, but has been criticised because of its cost and the failure to demonstrate that it improves mortality. Croese found that, in people aged over 50 years, the rate of cancer diagnosis in the unscreened population was double that in individuals who had previously had colonoscopy (for whatever reason). Almost half the cancers in the unscreened population were Dukes stage C or D, compared with only 16% in the previous-colonoscopy group.4 Australian data confirm that the cost-effectiveness of colonoscopy at both five- and 10-year intervals is almost identical to that of annual FOBT.13 Flexible sigmoidoscopy, alone or combined with FOBT, was found to be significantly less cost effective. Barium enema remains the fourth cost-effective diagnostic option, although it suffers from the fact that at least 20% of individuals will have a lesion identified which requires subsequent colonoscopy. A cohesive, unified and comprehensive public education campaign about CRC and the potential for its prevention is needed. This should emphasise the common nature of CRC and should target higher-risk groups, who can be offered colonic surveillance. This would be a start in reducing the current high mortality rate. When screening strategies for early diagnosis or prevention of CRC are chosen, compliance, costs and efficacy are all key issues. The fact that we have four effective options now allows the practitioner to offer individuals a menu from which they can select a test, depending on their preference and perceived compliance. Terry D Bolin Associate Professor, Gastrointestinal Unit Prince of Wales Hospital, Sydney, NSW Melvyn G Korman Associate Professor, Gastroenterology Unit Monash Medical Centre, Melbourne, VIC Anti-Cancer Council of Victoria. Canstat 1997; 26: 2. Winawer SJ, Zauber AG, Ho MN, et al. Prevention of colorectal cancer by colonoscopic polypectomy. The National Polyp Study Workgroup. N Engl J Med 1993; 329: 1977-1981. Cotton S, Sharp L, Little J. The adenoma-carcinoma sequence and prospects for the prevention of colorectal neoplasia. Crit Rev Oncol 1996; 7: 293-342. Croese J. Colorectal cancer after open-access colonoscopy: a community and case survey. Med J Aust 1999; 170: 251-254. Leggett BA, Cornwell M, Thomas LR, et al. Characteristics of metachronous colorectal carcinoma occurring despite colonoscopic surveillance. Dis Colon Rectum 1997; 40: 603-608. Ward M. Preventing colon cancer: the problem with guidelines or The perils of prevention. Med J Aust 1997; 166: 201-204. Hardcastle JD, Chamberlain JO, Robinson MH, et al. Randomised controlled trial of faecal-occult-blood screening for colorectal cancer. Lancet 1996; 348: 1472-1477. Kronborg O, Fenger C, Olsen J, et al. Randomised study of screening for colorectal cancer with faecal-occult-blood test. Lancet 1996; 348: 1467-1471. Mandel JS, Bond JH, Church TR, et al. Reducing mortality from colorectal cancer by screening for fecal occult blood. Minnesota Colon Cancer Control Study. N Engl J Med 1993; 328: 1365-1371. Lemmel GT, Haseman JH, Rex DK, Rahmani E. Neoplasia distal to the splenic flexure in patients with proximal colon cancer. Gastrointest Endosc 1996; 44: 109-111. Rex D, Chak A, Sack L, et al. Prospective determination of distal colon findings in patients with proximal colon cancer. Gastrointest Endosc 1998; 47: AB103. Nicholson FB, Stern AI, Korman MG, Hansky J. Colorectal cancer screening -- are proximal polyps missed by using flexible sigmoidoscopy? Digestion 1998 Suppl 3: 730. Bolin TD, Korman MG, Stanton R, et al. Positive cost effectiveness of early diagnosis of colorectal cancer. Colorectal Dis 1999; 1: 2. Reprints: Associate Professor T D Bolin, GI Unit, Prince of Wales Hospital, High Street, Randwick, NSW 2031. More articles on Gastroenterology Reprints: Associate Professor T D Bolin, GI Unit, Prince of Wales Hospital, High street, Randwick, NSW 2031. Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/>

Terry D Bolin · Melvyn G Korman

Editorial Complementary medicine -- where lies its appeal? Patients welcome different perspectives for the treatment opportunities they provide MJA 1999; 170: 247-248 By 1993 it was estimated that Australians were spending almost twice as much on complementary medicines (CMs) ($621 million per year) than their contributions to pharmaceuticals, and were spending a further $309 million on CM practitioners each year.1 Recent government estimates are that each year 57% of Australians and 42% of Americans use CMs.2,3 In 1997 there were more visits by Americans to CM practitioners (629 million) than to primary care physicians (386 million),3 and high levels of use of CM are reported throughout the industrialised world.3,4 Furthermore, the international market for CM products -- worth around $20 billion at retail level in 1996 -- is estimated to be expanding at more than 15% per year.5As substantial numbers of consumers choose CM, professional and regulatory responses have emerged. The United States National Institutes of Health has established the National Center for Complementary and Alternative Medicine, with a current budget of $US50 million ($78 million).6 Government reviews,7,8 new journals, dedicated sections in medical journals,9,10 teaching of basic CM in medical schools,11 and increased media coverage are all evidenced. "Complementary", "alternative" or "unconventional" medicine are umbrella terms that encompass health practices ranging from relatively new modalities (eg, rebirthing and magnetotherapy) to ancient skills of an initiated community (eg, yoga, meditation among Buddhist monks), and traditional practices that are quite orthodox in some cultures (eg, traditional Chinese medicine). Various definitions of CM have been proposed, but these fall short because of both the breadth of the term and the changing profile of activity. Eisenberg's definition of CM as "interventions neither taught widely in medical schools nor generally available in US hospitals" is unsatisfactory, because CM is now taught in up to 60% of US medical schools3,11 and is part of conventional medical practice in Europe. CM has been referred to as "unproven" medicine,12 but this would include a range of conventional health practices. CM should be defined as therapeutic practices based on theory or explanatory mechanisms of action that do not conform with current medical thinking.13 Most researchers in the interim have used a list of common practices to define their meaning of CM. Why are patients choosing CM? The report by Easthope et al in this issue of the Journal14 suggests that acupuncture under Medicare is used more by middle-aged and elderly people as an alternative to other (conventional) treatments and largely for chronic pain. One study found Australian users of CM were a younger, healthier and optimistic group.1 Yet, use of CM is also reported to be high among cancer sufferers (22%).15 A recent government report on Chinese medicine found that more than 75% of patients were being treated for recurrent complaints, often rheumatological or neurological in nature.7 Others propose that people who use CM are more likely to hold postmodern (opposed to scientific rationalism and supportive of individual perspectives), "new age" values,16,17 or are dissatisfied with the orthodox medical encounter.17 This includes a sense of not being valued sufficiently as a person within the medical system. But do the elderly Australians who use acupuncture under Medicare largely hold postmodern values? Is there a greater proportion of postmodern thinkers among sufferers of rheumatic or musculoskeletal disorders or those afflicted with cancer? This would hardly seem the case. The reasons for selecting CM are inevitably more pragmatic. Too often the popularity of CM has been dismissed as a sign of rejection of scientific authority, an expression of new values of natural medicine, or of increased time and personal attention given by CM practitioners. Too often these reasons are given to eclipse the more central purpose consumers shop around for healthcare services. When health consumers develop uncomfortable symptoms and choose CM, they pay for treatment mostly out of their own pockets. It is a time when patients do not consider too actively whether their healthcare practitioner is oozing warm fuzzies, but, rather, target what they believe to be the most effective way to get better. If they believe from direct or indirect experience they are not getting broad enough advice or making adequate progress with conventional medicine, then they will try an approach that might offer other help. This is fundamental pragmatism. CM consumers accept the possibility of a different perspective or understanding of their illness -- in fact welcome it -- as it opens a window of opportunity for treatment not previously apparent. A study of 300 Canadian patients found that patients choose specific kinds of practitioners for particular problems, and use a mixture of practitioners to treat specific complaints.17 The choice of type of practitioner is multidimensional and cannot be explained solely by disenchantment with medicine or by an "alternative ideology". This is supported by US findings that dissatisfaction with conventional medicine does not predict use of CM.16 Porter's historical review of medicine states it quite simply: ". . . regular medicine has ceased to convince the public that it is the only, or the best, means to cure their ills" (my emphasis).19 The recent push to apply the principles of evidence-based medicine to CM is important. For clinicians to feel comfortable in recommending a particular CM approach an acceptable standard of evidence must be demonstrable. However, acceptable levels of evidence for the clinician and patient may differ. In the eyes of the consumer, trying a herbal formula that has been used and documented in classical medical literature for many centuries may not be such a brash step. Consumers may be less convinced by a clinical trial of a new drug that has been applied only to a well-defined sample group. However, to the scientific audience, the latter represents the stronger evidence. The medical profession has approached CM with caution, but it also has an interest and responsibility in understanding and developing new approaches (often sourced from ancient traditions) that can be successfully applied to contemporary healthcare problems. Yet, CM proposes mechanisms of action that are not currently scientifically plausible -- this represents a distinct barrier to its adoption. It is this alternative theoretical understanding of the pathophysiology of disease that defines (and isolates) CMs, but also opens a window of opportunity for successful treatment for some patients. With such high proportions of the population using CMs, specific actions need to be taken. Appropriate structures and mechanisms that reflect the healthcare practices of the community need to be identifiable in government agencies and policies that serve that community. In Australia, no government agency reflects in its structure the high level of use of CM. Consumers deserve support both in terms of statutory regulation of practice where required, and increased relevant research. Applying the principles of evidence-based medicine will bring scientific rigour to the field of CM. There is no conflict here -- CM has always had a clinical-outcomes focus. The medical profession also needs to become more familiar with CM practices. Communication rates across practitioner groups are still too low.7,15 We need to develop less adversarial, more collegial relationships, which can be done through better education. To the scientist, the evidence in support of CM may be weak, but to the patient the instinctive search for a remedy that brings relief knows no such intellectual boundaries. This is a search ruled by pragmatism. The searches are relatively new because so many doors have recently been opened by globalisation (eg, traditional Chinese medicine) and increased public access to health information, coupled with a sensitivity towards traditional cultural practices. Medical practitioners, other healthcare professionals and patients are exploring CM for good reasons. Alan Bensoussan Head, Research Unit for Complementary Medicine University of Western Sydney, Macarthur, NSW MacLennan AH, Wilson DH, Taylor AW. Prevalence and cost of alternative medicine in Australia. Lancet 1996; 347: 569-573. Commonwealth Department of Health and Family Services. Government response to recommendations arising from the Therapeutic Goods Administration Review. Canberra: Commonwealth Government, 1997. Eisenberg DM, Davis RB, Ettner SL, et al. Trends in alternative medicine use in the United States, 1990-1997: results of a follow-up survey. JAMA 1998; 280: 1569-1575. Goldbeck-Wood S, Dorozynski A, Lie LG, et al. Complementary medicine is booming worldwide. BMJ 1996; 313: 131-133. Gruenwald J. The emerging role of herbal medicine in health care in Europe. Drug Information J 1998; 32: 151-153. Jonas WB. Alternative medicine -- learning from the past, examining the present, advancing to the future. JAMA 1998; 280: 1616-1618. Bensoussan A, Myers SP. Towards a safer choice: the practice of traditional Chinese medicine in Australia. Sydney: Faculty of Health, University of Western Sydney, Macarthur, 1996. Steering Committee for the Prince of Wales's Initiative on Integrated Medicine. Integrated healthcare: a way forward for the next five years? London: Foundation for Integrated Medicine, 1997. Alternative medicine [section]. Med J Aust 1998; 169: 573-586. Alternative medicine [theme issue]. JAMA 1998; 280(18): 1549-1640. Wetzel MS, Eisenberg DM, Kaptchuk TJ. Courses involving complementary and alternative medicine at US medical schools. JAMA 1998; 280: 784-787. Fontanarosa PB, Lundberg GD. Alternative medicine meets science. JAMA 1998; 280: 1618-1619. Eskinazi DP. Factors that shape alternative medicine. JAMA 1998; 280: 1621-1623. Easthope G, Gill GF, Beilby JJ, Tranter BK. Acupuncture in Australian general practice: patient characteristics. Med J Aust 1999; 170: 259-262. Begbie SD, Kerestes ZL, Bell DR. Patterns of alternative medicine use by cancer patients. Med J Aust 1996; 165: 545-548. Astin JA. Why patients use alternative medicine: results of a national study. JAMA 1998; 279: 1548-1553. Siahpush M. Postmodern values, dissatisfaction with conventional medicine and popularity of alternative therapies. J Sociol 1998; 34: 58-70. Kelner M, Wellman B. Health care and consumer choice: medical and alternative therapies. Soc Sci Med 1997; 45: 203-212. Porter R. Greatest benefit to mankind. A medical history of humanity from antiquity to the present. London: HarperCollins, 1997; 688. More articles on Complementary medicine Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/>

Alan Bensoussan

Editorial Hyperbaric oxygen for carbon monoxide poisoning Are currently recommended regimens ineffective? MJA 1999; 170: 197-199 In 1950 Pace and colleagues published a report establishing that hyperbaric oxygen (HBO) significantly accelerates the rate of carbon monoxide (CO) elimination from haemoglobin.1 Further studies have shown that, after CO exposure, HBO accelerates the dissociation of CO from cytochrome a,a3 and induces a more rapid return to normal of cytochrome redox state,2,3 reduces brain lipid peroxidation,4 inhibits pathological endothelial leukocyte adhesion5 and prevents intracranial hypertension.6It has therefore been no surprise that clinical observation and published evidence, including that of randomised trials, have supported the clinical efficacy of HBO for CO poisoning.7-12 When HBO is given to individuals with moderate or severe poisoning within approximately six hours of exposure, most published data strongly suggest that it not only induces a more rapid recovery, but also reduces the most-feared complication -- persistent or delayed neurological sequelae. Nevertheless, questions remain. As HBO therapy is not immediately available to all poisoned patients, who should be treated or transported to a hyperbaric facility? How many treatments should be given? There have been few randomised trials of HBO therapy, and no published randomised trial has addressed the question of whether it is effective in the treatment of severely poisoned patients. Therefore, a large trial from a reputable institution is welcome. In this issue of the Journal, Scheinkestel and colleagues13 have addressed the question of whether HBO should be used for CO poisoning. Their study design is among the most rigorous yet published in this area. Nonetheless, methodological questions remain, and some caution is required in accepting the authors' conclusions. In the study, all 191 patients were treated for 100 minutes in a hyperbaric chamber, but were randomised to receive either normobaric oxygen (NBO) or HBO at 2.8 atmospheres absolute (ATA) for 60 of the 100 minutes. All patients received continuous high flow oxygen between treatments, or 100% oxygen if they were intubated. They received one treatment per day for three days, after which they underwent neuropsychological assessment. If, after this, they had clinical or neuropsychological abnormalities, they received an additional three treatments. Most patients in this study were poisoned during an attempted suicide, and 73% were categorised as severe (defined by a carboxyhaemoglobin level >30%, Mini-mental score ≤24, confusion, loss of consciousness, focal neurological deficits, convulsions, pulmonary oedema, electrocardiogram abnormalities or dysrhythmias, hypotension, cardiac arrest or acidosis). Nevertheless, inclusion of mildly poisoned patients and the high average Mini-mental scores suggest that a significant number of patients had only mild central nervous system impairment at the time of presentation. The use of cluster randomisation for patients presenting simultaneously (to minimise the effect of the study on daily practice) engenders the risk of bias, as clusters of patients with similar baseline characteristics are simultaneously assigned to one or other of the groups. Generalised linear models were used to adjust for within-cluster correlation, but the authors have not provided enough information to allow an assessment as to whether the statistical analysis accounted for all of the resulting bias. A confirmatory analysis that would not have incurred this potential bias would have been a reanalysis of the results using only one patient from each cluster. This might have strengthened the report, as would a display of the numbers and sizes of clusters and a listing of the magnitude and consistency of the parameter estimates for the various models. The primary results of the study depend heavily on seven neuropsychological assessments that were performed after treatment and before discharge. Two or more "abnormal" test results represented a poor outcome, which then defined persistent neurological sequelae (PNS). Conclusions based on these tests must be tempered by the fact that, although baseline Mini-mental state tests were done, the study did not make baseline neuropsychological assessments, and hence could not quantify change for these patients. The only statistically significant difference between NBO and HBO patients at the end of treatment was in one of seven neuropsychological scales (Rey auditory verbal learning test), which favoured patients treated with NBO. Considering the multitude of statistical tests performed and the lack of a comprehensive baseline assessment, a single significant test may not be meaningful. In view of the weight of evidence in favour of the use of HBO for acute CO poisoning, how can the conclusions of Scheinkestel and colleagues that there is no difference in efficacy between HBO and NBO be explained? Firstly, it is possible that their method of NBO administration was more effective than in other studies. All their patients received three or six days of high-flow oxygen, and intubated patients might have been given 100% oxygen for six continuous days, a regimen that is considerably more intensive than common clinical practice. Secondly, their HBO regimen may have appeared less effective than in other studies, for several reasons. Depression can confound neuropsychological assessment, and the high proportion of depressed patients in the study may have minimised the apparent effect of HBO treatment and contributed to the high number of patients with a poor outcome. Unfortunately, neither the inspired oxygen concentration in either group nor the exact pressure-time profile of the hyperbaric treatments is provided. However, adding up to six HBO sessions to 100% oxygen for three or six days would be expected to produce a significant degree of pulmonary oxygen toxicity. Also, as Scheinkestel and colleagues point out, repetitive treatments at 2.8 ATA (a pressure higher than many clinicians use for CO poisoning) might have induced a neurotoxic effect14 that offset any potential benefit. Further, there are significant omissions from the article that preclude unfettered acceptance of the authors' conclusions. The surprising observation that there was no significant improvement in Mini-mental score in either group is weakened by the lack of information regarding administration of sedative drugs, especially to intubated patients, which might have confounded the testing. Importantly, other than mortality, no clinical outcomes or self-reported assessments of functional ability are reported. The overall relapse rate at follow-up, defined as new morbidity or deterioration in any neuropsychological test score, was higher in the group treated with HBO, but the relapse rate in the various subgroups of greatest interest (particularly those with short treatment delays) is not detailed. Moreover, the low follow-up rate (46%) makes it difficult to draw valid conclusions. The data regarding comparability of the two groups have two significant omissions -- the numbers of severely affected patients with long delays to treatment, and the number of mildly affected patients. Neither of these subgroups is likely to show a measurable response to treatment using the chosen endpoints. The possibility that both types were significantly represented is suggested by Mini-mental scores that appear disproportionately high for the degree of severity that is implied, as well as the high geometric mean of the delays to treatment (>6 hours). It therefore appears possible that a significant proportion of the patients in this study were treated at a time after CO exposure that HBO is likely to be ineffective.15-17 Including a large number of patients who are unlikely to respond (too mildly affected or treated too late) in a study will reduce the apparent effectiveness of the intervention, and might partly explain the surprisingly high proportion of patients with PNS (74% and 68% of patients, respectively, in the HBO and NBO groups). What might otherwise have been the most important conclusion of this investigation -- that even in the subgroup of severe poisonings treated within four hours, there was no difference between NBO and HBO -- would have been more convincing had the authors provided the observational and statistical details. What new information can be learned from the work of Scheinkestel and colleagues? Their results hint that, in the type of patients studied, prolonged administration of NBO may be more effective than the shorter regimens that are in general use. With respect to the primary question addressed by the investigators,13 we feel that there are still too many unresolved issues in their analysis to discard HBO as a treatment for acute CO poisoning. Richard E Moon Professor of Anesthesiology, and Associate Professor of Pulmonary and Critical Care Medicine Elizabeth DeLong Associate Professor, Division of Biometry Duke University Medical Center, Durham, NC, USA Pace N, Strajman E, Walker E. Acceleration of carbon monoxide elimination in man by high pressure oxygen. Science 1950; 111: 652-654. Brown SD, Piantadosi CA. Reversal of carbon monoxide-cytochrome c oxidase binding by hyperbaric oxygen in vivo. Adv Exp Med Biol 1989; 248: 747-754. Brown SD, Piantadosi CA. Recovery of energy metabolism in rat brain after carbon monoxide hypoxia. J Clin Invest 1992; 89: 666-672. Thom S. Antagonism of carbon monoxide-mediated brain lipid peroxidation by hyperbaric oxygen. Toxicol Appl Pharmacol 1990; 105: 340-344. Thom SR. Functional inhibition of leukocyte 2 integrins by hyperbaric oxygen in carbon monoxide-mediated brain injury in rats. Toxicol Appl Pharmacol 1993; 123: 248-256. Jiang J, Tysseborn I. Cerebrospinal fluid pressure changes after acute carbon monoxide poisoning and therapeutic effects of normobaric and hyperbaric oxygen in conscious rats. Undersea Hyperb Med 1997; 24: 245-254. Myers RAM, Snyder SK, Emhoff TA. Subacute sequelae of carbon monoxide poisoning. Ann Emerg Med 1985; 14: 1163-1167. Norkool DM, Kirkpatrick JN. Treatment of acute carbon monoxide poisoning with hyperbaric oxygen: a review of 115 cases. Ann Emerg Med 1985; 14: 1168-1171. Gorman DF, Clayton D, Gilligan JE, Webb RK. A longitudinal study of 100 consecutive admissions for carbon monoxide poisoning to the Royal Adelaide Hospital. Anaesth Intensive Care 1992; 20: 311-316. Ducasse JL, Celsis P, Marc-Vergnes JP. Non-comatose patients with acute carbon monoxide poisoning: hyperbaric or normobaric oxygenation? Undersea Hyperbar Med 1995; 22: 9-15. Thom S, Taber R, Mendiguren I, et al. Delayed neuropsychologic sequelae after carbon monoxide poisoning: prevention by treatment with hyperbaric oxygen. Ann Emerg Med 1995; 25: 474-480. Hampson NB. Carbon monoxide poisoning in the United States. In: Oriani G, Marroni A, Wattel F, editors. Handbook on hyperbaric medicine. New York: Springer, 1996: 297-304. Scheinkestel CD, Bailey M, Myles PS, et al. Hyperbaric or normobaric oxygen for acute carbon monoxide poisoning: a randomised controlled clinical trial. Med J Aust 1999; 170: 203-210. Holbach KH, Caroli A, Wassmann H. Cerebral energy metabolism in patients with brain lesions at normo- and hyperbaric oxygen pressures. J Neurol 1977; 217: 17-30. Zanetti CL. A review of carbon monoxide poisoning treated at Edgewater Hospital. In: Kindwall EP, editor. Proceedings of the Eighth International Congress on Hyperbaric Medicine. 1984; Aug 20-22; Long Beach, CA. San Pedro, CA: Best Publishing, 1987: 258-262. Goulon M, Barois A, Rapin M, et al. Carbon monoxide poisoning and acute anoxia due to breathing coal gas and hydrocarbons. J Hyperbaric Med 1986; 1: 23-41. Raphael JC, Elkharrat D, Jars-Guincestre MC, et al. Trial of normobaric and hyperbaric oxygen for acute carbon monoxide intoxication. Lancet 1989; 2: 414-419. Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/>

Editorial Hospital in the home: take the evidence and run The time for apathy and cynicism towards home-based care is over MJA 1999; 170: 148-149 Australians are credited with making global contributions in biomedical research,1 and the same can now be said for their contribution to developing acute home-based care. Hospital in the home (HIH) units have been established for more than four years in Australia (mainly in Victoria), yet in this short time important work of international standard has shown that HIH is a safe, effective, acceptable and efficient alternative to acute hospitalisation for certain patients and conditions.2-5 Now, in this issue of the Journal, Caplan and colleagues,6 from New South Wales (a virtual HIH desert), report a randomised controlled trial (RCT) of home versus hospital care, something that has hitherto seldom been reported in the medical literature (the only other similar RCT is an Australian study in patients with cystic fibrosis7). Caplan et al found that frail elderly patients requiring intravenous therapy or low molecular weight heparin deserve active consideration for HIH care: there were fewer geriatric complications and greater patient and carer satisfaction in the HIH group. Although no differences in the rates of adverse events and death were found, the small numbers of patients involved meant that the study's power to draw these conclusions was limited. HIH care around the world has varied widely, and so too have the studies it has generated. Thus, for the Cochrane review of HIH care,8 a meta-analysis was not possible, and for good reason. In HIH studies so far there have been: Variations in intervention models; Non-uniformity of conditions, patients and therapies; and Relatively small patient numbers, allowing only for large effects to be detected. Other factors impeding meta-analysis have included: The impact of dedicated and motivated staff self-selected to care for the intervention groups; The refusal of some patients to consent to remain in hospital when HIH treatment was offered as an option; The need for units to be well established before any trial; and The reluctance of established HIH programs to reduce their throughput. Landmark RCTs of HIH care of patients with deep venous thrombosis have taken four years to complete,9 and RCTs of home-based care in the United Kingdom have really examined postdischarge coordination.10 Americans are educated by their constitution to hold some truths to be self-evident, and the appropriateness of HIH appears to be one of them. They have demonstrated this with an expenditure of 2 billion dollars per annum on HIH programs in the absence of RCT evidence.11,12 If HIH were, for example, an imaging technology, it would have crossed the threshold from the novel and experimental. But hospitals are insecure -- they have difficulty letting go even when the evidence is there. So, let us assume that this issue of the Journal is a defining moment for HIH in Australia, and NSW in particular. Let us assume that hospital administrators will conclude that the time is now right for a concerted move to HIH care, and that to deny appropriate patients this intervention is no longer sustainable and may even be unethical. Let us even fantasise that private insurers will look favourably at the benefits of HIH care now that they will receive an injection of 1.5 billion dollars of public funds (Private Health Insurance Incentives Bill 1998 (Cwlth)). How could these interested groups move on with the development of HIH? They might be forgiven for concluding that models for HIH are somewhat ill-defined. In fairness, HIH units have been influenced by the manner in which they were funded, and the background of the staff who volunteered to take on the task. The studies have concentrated on comparisons with inhospital care rather than between HIH models. A more analytical approach is now required, but some principles have emerged. Firstly, let us get the definition clear. The substitution of acute hospital stay is at the heart of HIH.13 Thus, HIH is the delivery of care and services which, without HIH, can only be provided by admission to hospital. At present, the healthcare interventions suited to HIH are intravenous therapy of all types (including antibiotics, antifungals and antivirals, some chemotherapeutic agents, corticosteroids, inotropes, and blood products), and acute anticoagulation. Acute rehabilitation, insulin initiation and some complex wound care are also included in some HIH programs. Although new applications will be found, it is important that HIH should adhere to the demonstrable substitution of hospital inpatient care and not establish intermediate care programs or duplicate current community services. HIH is probably best established through a stand-alone unit within the hospital, with its own budget and staff. It has its own technologies, such as computerised pumps and peripherally inserted central catheters, and is skilled in the use of pharmaceuticals at home. It has its own body of research. It is expert at assessing people for acute home-based care, with involvement in the actual delivery of that care continually updating its expertise. It accepts patients from all other hospital units, services and disciplines. It is therefore generalist in its approach -- a dangerous attribute in a modern hospital environment -- yet is rapidly accumulating its own core of specialist knowledge. It is able to embrace specialist requirements through direct staffing of nurses with appropriate experience, or through the education of current staff. It is developing specific standards that will allow improvement in quality and benchmarking. Australian Council on Healthcare Standards (ACHS) clinical indicators for HIH care are expected this year.14 HIH units should offer nurse-administered and medically supervised and attended care. The ability to establish venous access and detect, treat or transfer patients with complications of illness or therapy is required. Twenty-four-hour nursing and medical telephone support, with the ability to visit after hours, is mandatory. There should be clear lines of clinical responsibility and continuity within HIH, and between it and the hospital, with a clear link to the hospital (in Victoria patients retain their inpatient status while in HIH). Community-based healthcare service providers may then be able to deliver HIH services. When patients understand and consent to the service level offered, their acceptance is high, as is their subsequent satisfaction.5 Patients who have had nosocomial infections or have chronic or relapsing illnesses best understand the advantages of HIH. There is also a level of community altruism, whereby people understand that, as long as they are cared for appropriately, traditional hospital space should go to those who need it more. To keep this faith, Australian HIHs should reject the notion of these programs being built entirely around self-administration of therapy. Even with all of these inputs, HIH will still offer care equivalent to traditional hospital care at a lower cost.11,15 Future studies of hospital and HIH patients examining costs and quality-of-life measures will acknowledge the additional advantages of HIH care. To date, Australian costing studies of HIH have suffered from the problems described earlier for the conduct of trials, together with inconsistent cost-accounting across different hospitals.16 But, even if HIH offered no cost advantage in direct care, in the context of waiting lists and emergency department backlogs HIH offers capital expansion of the hospital's work at a fraction of the usual cost. Until recently, hospitals have only seen their future as involving exponential growth. The view that the hospital is an Aladdin's cave, where the rich rewards of medical and nursing skill and biotechnology are gathered and bestowed on those who surrender themselves, might be usefully reassessed.17 But the real danger is that any such reassessment will merely result in briefer glimpses of the skills and technology where they are genuinely required. This appears to be the current direction of public hospital reform. Hospitals have been accustomed to taking responsibility for only those within their walls. While understandable, this limits the effective use of the technologies and skills held tight within those walls. HIH urges hospitals to adapt their infrastructure to take responsibility for the delivery of appropriate, high quality acute care in and for their community. State and federal health authorities could assist with genuine, targeted medium to long term incentives. Caplan et al offer the best evidence yet that the time for apathy and cynicism towards HIH should be over. We are at the end of a century of unparalleled advances in medical science and hospital care. Any pause in the speed of advance, or any rationing of access due to the burgeoning costs of acute-care delivery, can allow Western healthcare systems to take stock.18 In their review, the return to home-based care, so prevalent before the early 20th century, should be seen as maximising the quality use of technology to fulfil the wishes of the patients and their families, reasserting their pre-eminent position within the acute-care system into the 21st century. Michael Montalto Director, Frankston Hospital in the Home Executive Member, Australian Home and Outpatient Intravenous Therapy Association, Frankston Hospital, Frankston, VIC Bourke PF, Butler L. Mapping Australia's basic research in the medical and health sciences. Med J Aust 1997; 167: 610-613. Grayson L, Silvers J, Turnidge J. Home intravenous antibiotic therapy: a safe and effective alternative to inpatient care. Med J Aust 1995; 162: 249-252. Lowenthal R, Piaszczyk A, Arthur G, O'Malley S. Home chemotherapy for cancer patients: cost analysis and safety. Med J Aust 1996; 165: 184-187. Montalto M. How safe is hospital in the home? Med J Aust 1998; 168: 277-280. Montalto M. Patient and carer satisfaction with hospital in the home care. Int J Qual Healthcare 1996; 8: 243-251. Caplan G, Ward J, Brennan N, et al. Hospital in the home: a randomised controlled trial. Med J Aust 1999; 170: 156-160. Wolter JM, Bowler S, Nolan P, McCormack J. Home intravenous therapy in cystic fibrosis: a prospective randomized trial examining clinical, quality of life and costs. Eur Respir J 1997; 10: 896-900. Sheppard S, Illife S. Effectiveness of hospital at home compared with inhospital care. Cochrane Review in: The Cochrane Library, Issue 3, 1998. Oxford: Update Software, 1998. Koopman M, Prandoni P, Piovalli F, et al. Treatment of venous thrombosis with intravenous unfractionated heparin administered in the hospital as compared with subcutaneous low molecular weight heparin administered at home. N Engl J Med 1996; 334: 682-687. Richards S, Coast J, Gunnell D, et al. Randomised controlled trial comparing effectiveness and acceptability of an early discharge hospital at home scheme with acute hospital care. BMJ 1998; 316: 1796-1801. Balinsky W. Home care -- current problems and future solutions. San Francisco: Jossey-Bass Publishing, 1994. Tice A, Marsh P, Craven P. Response to a call for a randomised controlled trial. Am J Med 1993; 94: 115. Grayson L. Hospital in the home -- is it worth the hassle? Med J Aust 1998; 168: 262. Clinical indicators for hospital in the home -- Final Report to the Victorian Department of Human Services. Melbourne: ACHS Care Evaluation Program. October 1998. Montalto M, Watts J. Considering the cost of hospital in the home care. Report to the Victorian Department of Human Services. Melbourne: Centre for Health Program Evaluation, 1998. KPMG Consulting Services. KPMG hospital in the home evaluation. Melbourne: Victorian Government Department of Human Services, 1997. Stoeckle J. The citadel cannot hold: technologies go outside the hospital, patients and doctors too. Milbank Q 1995; 73: 3-17. Komesaroff P, Clunie G, Duckett S. What is the future of the hospital system? Med J Aust 1997; 166: 17-22. Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/>

Michael Montalto

Editorial Sceptical medicine To admit to not knowing, or to being unsure until the evidence is gathered or accessed, is the beginning of sceptical wisdom MJA 1999; 170: 99-100 The 1998 Skeptic of the Year, awarded by the Australian Skeptics Inc, is Michael Archer, a palaeontologist and professor of biological science at the University of New South Wales, who has recently been appointed Director of the Australian Museum. His interests listed on his Internet home page include "all aspects of zoology and palaeontology that relate to the development of the Australian biota, particularly mammals", and "pseudoscience such as creation science".1 The award is presented to Australians whose work contributes substantially to the promotion of critical thinking.2 Perhaps there should be an equivalent award given each year to the doctor who has best practised lifelong sceptical medicine! Some confuse sceptical medicine with the practice of a nihilistic, cynical clinical code. But Archer, in a recent radio interview, made a clear distinction between scepticism and cynicism: the former pursues evidence and is built on humility; the latter reflects arrogance and seeks to destroy virtue. The distinction could hardly be plainer. The Health Advisory Committee of the National Health and Medical Research Council and the Menzies Foundation recently convened a workshop* to define the current state of the art of evidence-based medicine, and potential implications of and barriers to an evidence-based approach to healthcare in Australia. The aim was to develop ways of incorporating an evidence-based approach into the Australian healthcare system for the next millennium. Different perspectives were explored, including those of healthcare professionals, consumers, health policymakers, researchers, lawyers and funding agencies. David Pencheon, the UK National Health Service's Associate Director of Research and Development, spoke of a recent encounter with new medical students beginning clinical training in Cambridge after intense preclinical education. He asked them questions about simple clinical observations, and their mechanism and meaning. He recalled that it took a long time before he had exhausted their knowledge and one of them finally uttered that most important of all phrases for the future practice of scientific medicine "I don't know!". To admit to not knowing, or to being unsure until the evidence is gathered or accessed, is surely the beginning of sceptical wisdom. Without it, clinical practice guidelines, and ready access to relevant databases or information about the appropriateness of investigations and treatments, are useless -- because the mind of the clinician is not sceptically engaged. Just as a palaeontologist fails who ceases to look for evidence in fossil deposits, so a clinician who forsakes evidence in favour of intuition or half-remembered ideas runs a significant risk. Learning to say to oneself, one's patients and one's colleagues "I don't know" is a vital element of medical education. Papers presented at the workshop examined how healthcare decisions are made, how evidence is synthesised and disseminated and how evidence-based treatment is implemented, and the impact of using an evidence-based approach. Evidence-based medicine is a provocative term, not least because it begs the question whose evidence? While formal and standard definitions of evidence-based medicine show due deference to patient values and evidence from clinical experience,3 there remains a suspicion in the minds of many that this is a new way for purveyors of randomised controlled clinical trials to take over the world.4 This fear may be as straightforward as a professional territorial concern or as complex as the insight held by patients, members of the community and behavioural and social scientists that there is more to the clinical decision omelet than randomly cracking a few clinical trial eggs. Thus, Ian McDonald (Director, Study of Clinical Practice, St Vincent's Hospital, Melbourne) argued that clinical decisions, if properly understood, have a base of scientific evidence familiar to the biological scientist, but that we often fail to understand that other forms of evidence, from studies in sociology, behavioural science and anthropology, are helpful in achieving a full understanding of medical care. His challenge, echoed by Hilda Bastian (Chairperson, Consumers' Health Forum) and Sophie Hill (PhD student, School of Public Health, La Trobe University), was to a new form of scepticism, questioning the completeness of our definition of evidence-based medicine if it does not include knowledge generated from these other disciplines. Likewise, Sydney University's George Rubin (Professor of Public Health and Community Medicine) reminded participants of the relevance of a scientific understanding of motivators of behavioural change in other human settings (eg, business, which refers regularly to the relevant literature and is based on due scepticism) when contemplating how to encourage behavioural change among clinicians. The Australian National University's Bob Douglas (Director, National Centre for Epidemiology and Public Health) proposed that all health facilities and administrative units employ health information analysts, or "Cochrane-ologists", to assist health professionals to make use of evidence and manage scepticism. Multiple pressures operating on practitioners can lead them to ignore what they know to be best practice in their clinical and public health decision-making. These pressures include well-coordinated commercial interests, time and financial constraints, and the potential for litigation. Workshop participants asked that the Health Advisory Committee consider the following recommendations and develop an action plan to support their implementation: To recognise that systematic reviews underpin evidence-based healthcare. Systematic reviews should be required for all future healthcare-related research. They should be accepted as a legitimate form of research and developed to include a wide range of scientific evidence. Reviews should be eligible for research funding, and recognised in research performance assessment and as accreditation towards postgraduate training. To identify and overcome factors that hinder the generation, transfer and implementation of research knowledge into clinical practice. It is important to establish mechanisms and funding for ongoing communication and structural collaboration among groups involved in this area in Australia and overseas. To encourage the use of evidence-based approaches in areas outside clinical practice. These include the development of health and public health policy and practice and health-related litigation. If, as many believe, there needs to be a cultural shift to greater use of evidence in making not only life-critical but also day-to-day clinical practice and public health decisions, it will be important for the evidence to be immediately accessible either in hard copy or via computer to a range of potential users -- clinicians, consumers and health service planners. There is no point in providing clinical guidelines to clinicians about conditions or problems they will never encounter, or presenting them in a way that they can not be used. As Peter Joseph, immediate past president of the Royal Australian College of General Practitioners, has said, "I want guidelines in the form of charts that I can keep in an A4 folder on my shelf and pull down immediately when I have a patient to whom they refer. Then I can locate the patient in the decision matrix, explain to him or her where we are, and walk through the decisions that we then have to make together" (personal communication). The NHMRC's clinical practice guidelines for the management of early breast cancer5 is a fine example of guidelines prepared in a variety of formats to suit the needs of different end-user groups.6,7 Evidence-based medicine can only operate in a climate of healthy scepticism. Those who worry about their colleagues' scepticism towards evidence-based medicine should wait: if the doubters are genuinely sceptical, and if evidence-based medicine works, it will not be long before they, too, have begun to make the best use of it in an admittedly highly complex setting. Stephen R Leeder Professor, and Dean, Faculty of Medicine, University of Sydney, NSW Chris A Silagy Director, Australasian Cochrane Centre, and Professor of General Practice Department of Evidence-Based Care and General Practice Flinders University School of Medicine, Adelaide, SA George L Rubin Professor of Public Health and Community Medicine, and Director, Effective Healthcare Australia, University of Sydney, NSW http://www.unsw.edu.au/bioscience/archer.htm http://www.skeptics.com.au/ Sackett DL, Rosenberg WMC, Gray JAM, et al. Evidence based medicine: what it is and what it isn't. BMJ 1996; 312: 71-72. Lelorier J, Gregoire G, Benhaddad A, et al. Discrepancies between meta-analyses and subsequent large randomised, controlled trials. JAMA 1997; 337: 536-542. National Health and Medical Research Council. Clinical practice guidelines. The management of early breast cancer. Canberra: NHMRC/AGPS, 1995. National Health and Medical Research Council. Early breast cancer. A consumer's guide. Canberra: NHMRC/AGPS, 1995. National Health and Medical Research Council. All about early breast cancer. Sydney: NHMRC National Breast Cancer Centre, 1996. * Proceedings of the workshop are available on CD-ROM and via the Internet at <www.vicnet.net.au/~menzies> and <www.health.gov.au/nhmrc> Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/>

Stephen R Leeder · Chris A Silagy · George L Rubin