Editorials

Editorial General practice research in Australia: a timely reality check Do we need an independent body empowered to oversee general practice research? MJA 2000; 173: 569-570 General practice is the nub of Australia's healthcare. More than 90% of Australians visit a general practitioner each year: in 1997-98 alone, general practice consultations averaged 5.7 per citizen.1 The cost of providing these services, when added to the associated costs of pathology tests, radiology investigations, pharmaceuticals and allied health services, consumed 14% of the total healthcare bill of $42 267 million in 1997-98 and represents 1.2% of our gross domestic product (GDP).1It is entirely reasonable to expect that an industry with this level of impact on GDP would be underpinned by a thriving research and development program. Unfortunately, this is but a pipe dream! In most First World countries, including Australia, general practice research has a low priority. Indeed, a recent report in The Lancet lamented that this research vacuum made general practice ". . . one of the most intellectually underdeveloped disciplines in medicine".2 This underdevelopment stems from a lack of research culture, a heavy service commitment and the late arrival of academic GPs. Despite their Cinderella status, most Australian general practice academic units have actively pursued research for over 25 years. But what are the outcomes? Unless research leads to publication, its quality is essentially unknown. Through exposure to public scrutiny, individual research can be independently assessed. If deemed rigorous and relevant, it joins the living literature and may change clinical practice; if deemed inadequate or irrelevant, it lies buried in the grave of the silent literature. In this context, the report of Ward and colleagues3 in this issue of the Journal is a timely reality check. These investigators identified Australian general practice research published in the 20-year period 1980-1999 and compared selected characteristics of the research in the decades 1980-89 and 1990-99. The most noticeable difference was a nearly fivefold increase in publications in the second decade. The bulk of the research was published in two Australian journals (Australian Family Physician and The Medical Journal of Australia), but there were signs of an emerging international profile. Not surprisingly, the research was conducted mostly by affiliates of academic general practice units and nearly two-thirds of the authors were GPs. The second decade saw an encouraging twofold increase in randomised controlled trials, but they still accounted for less than 5% of publications. Finally, about half the research focused on topics of direct clinical relevance to general practice. What are we to make of all this? It is evident that general practice research in Australia is growing in stature, but, compared with other medical disciplines, is still in its adolescence. The pleasing increase in publications reflects a combination of factors, including the progressive maturity of our academic departments with their growing infrastructure and research staff, and the dedicated funding of general practice through the General Practice Evaluation Program (GPEP). Since 1990, this program has injected $10.5 million into projects evaluating general practice and promoting research.4 However, despite the encouraging report card from Ward et al, Australian general practice research still has some way to go. This was clearly recognised by the General Practice Review Group in their recent report Changing the future through partnerships, which recommended encouraging a general practice research culture; strengthening the infrastructure of academic general practice; and promoting a multidisciplinary approach to research, involving both consumers and the Divisions of General Practice.5 These are laudable recommendations. But any successful partnership requires sensible collaboration and sensitive cooperation. With at least 13 organisations representing general practice in Australia procuring productive partnerships may be a tall order!6 Clearly, a prime priority for nurturing general practice research is to build upon the current strengths of academic units through infrastructure support and realistic research fellowships for both established GPs and those in training. With the many competing concerns of general practice, a sensible approach might be a national independent body empowered to oversee general practice research. Its first task would be to define general practice research and formulate descriptors for monitoring research activity. In an address to the newly constituted National Health and Medical Research Council in 1937, W M Hughes, as then Federal Minister of Health, declared: We ought to be content with nothing less than original research. Australia, priding herself on being a nation, ought not be satisfied to follow, to imitate, to duplicate. She must blaze a track for herself, seek to lead rather than follow: and this calls for the services of specialists of high repute to train, inspire, and guide research along the right lines.7 More than 60 years later this is the very challenge for Australian general practice. Martin B Van Der Weyden Editor, MJA Hynes T. The financing of general practice. General practice in Australia: 2000. Canberra: Commonwealth Department of Health and Aged Care, May 2000: 235-269. Horton R. Evidence and primary care [editorial]. Lancet 1999; 353: 609-610. Ward A, Lopez D, Kamien M. General practice research in Australia, 1980-1999. Med J Aust 2000; 173: 608-611. Hays R, Piterman L. Education and training for general practitioners. General practice in Australia: 2000. Canberra: Commonwealth Department of Health and Aged Care, May 2000: 347-382. Department of Health and Family Services. General practice. Changing the future through partnerships. Report of the General Practice Strategy Review Group. Canberra: The Department, 1998. Kamien M. Academic general practice: past, present and future -- a personal view. General practice in Australia: 2000. Canberra: Commonwealth Department of Health and Aged Care, May 2000: 519-526. Compston JHL. The health of the people. Canberra: Roebuck, 1978: 76. (Roebuck Series No. 19.) Make a comment

Editorial Media and young minds Despite the best efforts of J K Rowling, young Australians this Christmas will be more interested in video games and cyberspace MJA 2000; 173: 570-571 Whether linked with fictional suicides in 18th-century romantic literature or reports of real-world suicides in today's mass media, copycat suicides have generated suspicions that media images may undermine mental health and moral development.1 Suspicions have given way to uneasiness as a growing number of problems -- drug and alcohol abuse, sexual promiscuity, depression and eating disorders -- have been laid at the media's door. Young people's enthusiasm for new electronic media, where the pace of change outstrips current understandings of effects on health and development, has done little to diminish this sense of uneasiness. In this context, Bokey and colleagues2 have studied images of youth in the "old" media, focusing on "Notable Texts" recently recommended by the Children's Book Council of Australia. Suicide, mental disorder and failure were commonplace in portrayals of an insecure and pessimistic young generation. Psychiatrists were predatory or incompetent and offered no reprieve for the distressed. This genre has been termed "social realism" and its rise attributed to the social and economic changes that have aggravated the usual turmoil of adolescence. It is true that with these social changes familiar adult milestones such as stable employment, financial independence, parenthood and home ownership are delayed3 and rates of adolescent emotional and behavioural problems appear high.4 Even so, images of pervasive adversity, mental disorder and suicide are overly pessimistic and do little to destigmatise mental disorder in a group whose access to health services is already poor. Moreover, if these images are to be found in the familiar old media, how much more concerned should we be about the new? Hard answers are elusive. Academic research on the media and youth lags far behind that of marketing. Most work is North American, where the main focus has been on television violence. It is clear that childhood viewing of violence predicts later aggression and criminal behaviour.5 It is also clear that there are many powerful moderating influences. Parents, for example, have traditionally influenced not only what children watch but also the effect of those images on actual behaviour.6 The closer an image is to real-world scenarios, the greater the effect on behaviour.7 For this reason the virtual-reality experiences of the new media may prove particularly powerful. Trends in young people's media use are relevant. Only a third of today's Australian youth read for recreation.8 In contrast, electronic media have become pervasive and the convergence of telecommunication and computer technologies into the Internet has led to a dizzying growth in communication options. The new media offer individualised, two-way, synchronous interactions, and increasingly draw on sound and vision to offer sophisticated virtual environments. The effects are not all negative and the benefits from opportunities for social contact, education, publication and establishment of businesses, regardless of location, can not be dismissed lightly. The media's growing role in shaping youth lifestyles and cultures also deserves consideration. A longer period of full-time education, growing affluence and greater recreational time have made youth a distinct consumer group, with lifestyles shaped increasingly by the media. The new media offer myriad ways to market messages that affect self-concept, body image, sexuality, and drug and alcohol consumption. The tobacco industry has rightly been the main focus, but the health effects of marketing food, alcohol, fashion, pharmaceuticals and entertainment deserve greater attention. What options exist for action? One is to do little and allow the market forces behind the media to drive solutions. The success of the Harry Potter series is one example of market forces in action, as young readers turn away from a "social realism" they find boring.9 However, the dizzying pace of media change, and a mistrust of increasingly global marketing targeting the young, suggest that few will have confidence in this approach. One alternative is to rely on advisory bodies such as the Children's Book Council of Australia. However, with recommendations to librarians, teachers and parents based on artistic merit alone, a body such as the Book Council seems poorly placed to take on the role. It's a fair bet that, despite the best efforts of J K Rowling, young Australians this Christmas will be more interested in video games and cyberspace. Without better information from research, parents, media professionals and young people face difficult choices. For parents, media education may prove useful in overcoming their unfamiliarity with the new media, one reason for their diminishing monitoring role. For professionals working in competitive media and advertising industries, emerging ethical questions deserve expert advice. An encouraging step is the release by the Commonwealth Department of Health of a media resource kit as part of a mental health promotion strategy.10 It marks the beginning of a dialogue between the health professions and the media and one that should go further. Even with the best of parental and technical monitoring, today's young people will be exposed to a greater number and diversity of media images than any previous generation. For this and future generations, the role of media education in both interpreting images and dealing with virtually limitless information is likely to grow. Academic research may or may not tell us whether Harry Potter is a better companion than the cyberheroine Lara Croft, but should help us all make better-informed decisions about the presents we buy for our children in the years to come. George C Patton Professor Susan M Sawyer Associate Professor Centre for Adolescent Health William Buckland House, Melbourne, VIC Phillips DP. The influence of suggestion on suicide: Substantive and theoretical implications of the Werther effect. Am Sociol Rev 1974; 39: 340-354. Bokey KM, Walter G, Rey JM. From Karrawingi the emu to Care factor zero. Mental health issues in contemporary Australian adolescent literature. Med J Aust 2000; 173: 625-628. Furlong A, Cartmel F. Young people and social change: invidualisation and risk in late modernity. Buckingham, UK: Open University Press, 1997: 40-52. Rutter M, Smith D. Psychosocial disorders in young people: time trends and their causes. Chichester: Wiley & Sons, 1995. Cook DE, Kestenbaum C, Honaker LM, Anderson ER. Joint statement on the impact of entertainment violence on chikdren. Congressional Public Health Summit, American Academy of Pediatrics 2000. <http://www.aap.org/advocacy/releases/jstmtevc.htm> (accessed November 2000). Huesmann LR, Eron LD. Television and the aggressive child: a cross-national comparison. Hillsdale, NJ: Lawrence Erlbaum, 1986. Comstock G. Deceptive appearances: television violence and aggressive behaviour. J Adolesc Health Care 1990; 11: 31-44. Australian Bureau of Statistics. How Australians use their time. Canberra: ABS, 1998. (Catalogue No. 4153.0.) Waldren M. Return to Narnia. The Weekend Australian 2000 September 30: C6. Commonwealth Department of Health and Aged Care. Mental Health Promoting Media Strategy. Canberra: The Department, 1999. Make a comment

George C Patton · Susan M Sawyer

Editorial Getting to grips with heroin and other opioid use We now have effective evidence-based treatments for the increasing number of heroin users MJA 2000; 173: 509-510 How great a problem is heroin and other opioid use in Australia? The lack of reliable data has hampered service planning and the development of drug policies. Claims are made that Australia is experiencing a heroin epidemic of unparalleled proportions, with figures of half a million or more heroin users cited. The illegal and covert nature of heroin use makes it difficult to quantify using standard approaches such as general population surveys or analysis of hospital separation data; heroin use is not revealed in a household survey as readily as, say, an interest in Australian football or one's favourite brand of toothpaste. But how do we measure it? In this issue of the Journal, Hall and colleagues grapple with the quantification of heroin dependence.1 On the basis of the number of overdose fatalities and registrations for methadone maintenance therapy (the most common treatment for heroin dependence in Australia), they provide estimates that are remarkably consistent: between 67 000 and 92 000 individuals, or about 0.7% of our population aged 15-54 years. Taking the median value of 74 000, we may conclude that the number of heroin-dependent individuals in Australia has doubled since the mid-1980s. However, dependence does not equate with use, and the use of heroin, especially intravenously, can lead to fatal overdose and acquisition of HIV, hepatitis B and hepatitis C infection. The proportion of heroin users who become dependent has been estimated to be about 25% (compared with 9% for cannabis and 15% for alcohol).2 If this assumption is correct, the number of current heroin users in Australia would be about 300 000. Previous work from household surveys has estimated the total prevalence of current heroin users (both dependent and non-dependent users) to be 0.7% of the total adult population, or about 100 000 people.3,4 Perhaps this difference merely reflects under-reporting, but there is still work to be done to resolve the disparity. There is also a substantial number of people who take prescribed opioids inappropriately. In a related article in this issue, Berbatis and colleagues examine trends in prescribed opioid use,5 and show that these too have increased in Australia over recent years. With methadone syrup (the formulation used for maintenance treatment of heroin dependence), this is entirely predictable. Berbatis et al found that methadone syrup was most commonly prescribed in New South Wales, where the greatest numbers of heroin-dependent individuals live. However, morphine prescribing in Australia has also increased, and pethidine use is very high by world standards. Methadone tablet prescribing was proportionately greater in Queensland, the Northern Territory, South Australia and Tasmania than in NSW, while morphine prescribing was higher in the last three jurisdictions and in Western Australia. Berbatis et al do not attempt to distinguish between appropriate prescribing and that which is fuelling drug dependence. It is impossible to gauge this in a study of total population use, and determining whether prescribing is appropriate from official data is difficult.6 An important question is whether, in some jurisdictions, methadone tablets and morphine are being prescribed for the de facto maintenance of drug-dependent individuals rather than for pain relief. While there has been some prescribing of these drugs for the treatment of dependence, differences in policy and controlled drug legislation probably play a more important role in explaining these variations. If significant amounts of these drugs were being prescribed in these jurisdictions specifically to maintain dependent opioid users, one would expect the proportion of drug users within formal treatment programs to be substantially lower, and the number of non-heroin opioid-related deaths to be higher, than elsewhere. This is not the case: the proportion of heroin users estimated to be in treatment is actually higher in those jurisdictions where more methadone tablets and morphine are prescribed, and non-heroin opioid-related deaths are lower.7 The only exception is the NT, which has not had a formal methadone maintenance program until recently. There, medical practitioners appear to have been treating heroin-dependent people with opioids other than methadone syrup. What are the implications of these surveys for policy and practice? The findings of Hall et al indicate a doubling of the number of heroin-dependent individuals, despite a concerted campaign against drug use since the mid-1980s. It illustrates the difficulties in preventing an upsurge in drug use when market factors such as low price, ready availability and a seemingly secure supply of heroin predominate. From a medical perspective, however, we now have effective evidence-based treatments for heroin-dependent people. The evidence for the benefits of methadone maintenance in reducing mortality and major morbidity (by about 75%) is now compelling.8 Given this and the evidence supporting the value of buprenorphine, a partial agonist, for the maintenance treatment of heroin dependence, we should aim to recruit and retain as many heroin-dependent users as possible in treatment in agonist maintenance programs, for which the greatest evidence for beneficial health outcomes exists. There has been intense media publicity about the supposed advantages and perils of antagonist drugs, such as naltrexone, for the treatment for opioid dependence.9 The Commonwealth Department of Health and Aged Care has funded a National Evaluation of Pharmacotherapies for Opioid Dependence (NEPOD), which is trying to dissect out the conflicting claims. Treatment with naltrexone appears to be an option for some heroin users, but the key issue is how the various pharmacotherapies compare in terms of mortality, morbidity, criminal behaviour, quality of life, social integration, economic productivity, and cost-effectiveness. Should we countenance the wider prescribing of opioid drugs for chronic pain when there is no clearly identified physical cause? If the appropriate regulatory authorities monitor prescribing and dispensing is supervised, does it matter if dependence is perpetuated? The work of Berbatis et al does not indicate major misprescribing of opioids. One could argue that medical prescribing of opioid drugs, properly regulated, would both relieve suffering and reduce "doctor shopping". It would also allow patients to stabilise their lives and take up opportunities for treatments aimed at abstinence when the time is right for them. Should we be concerned about the increase in both licit and illicit opioid use in Australia? Most certainly. In the future we may be able to reduce demand for opioids through educational approaches, developing our sense of community and making our society hostile -- as best we can -- towards commercial drug dealing. Until then, we should take pragmatic steps to treat people who have become dependent on opioid drugs, and that entails selecting what works rather than what feels good. John B Saunders Professor of Alcohol and Drug Studies Department of Psychiatry, University of Queensland, and Director Alcohol and Drug Services of the Royal Brisbane and The Prince Charles Hospital Health Service Districts Queensland Health, Brisbane, QLD Alun H Richards Manager, Drugs of Dependence Unit Queensland Health, Coorparoo DC, QLD Hall WD, Ross JE, Lynskey MT, et al. How many dependent heroin users are there in Australia? Med J Aust 2000; 173: 528-531. Anthony JC, Warner LA, Kessler RC. Comparative epidemiology of dependence on tobacco, alcohol, controlled substances and inhalants: basic findings from the National Comorbidity Survey. Exp Clin Psychopharmacol 1994; 2: 244-268. Australian Institute of Health and Welfare. 1998 National Drug Strategy Household Survey: First Results. Canberra: Australian Institute of Health and Welfare, 1999. Maxwell JC. Drug use in Australia and the United States: a comparison of the 1995 and 1998 national household surveys in both countries. Drug Alc Review. In press. Berbatis CG, Sunderland VB, Bulsara M, Lintzeris N. Trends in licit opioid use in Australia, 1984-1998: compararative analysis of international and jurisdictional data. Med J Aust 2000; 173: 524-527. Richards AH. The use of controlled-release morphine sulphate (MS Contin) in Queensland, 1990-1993. Med J Aust 1995; 163: 181-182. Hall W, Ross J, Lynskey M, et al. How many dependent opioid users are there in Australia? NDARC Monograph No. 44. Sydney: National Drug and Alcohol Research Centre, 2000. Caplehorn JRM, Dalton MSYN, Halder F, et al. Methadone maintenance and addicts' risk of fatal heroin overdose. Subst Use Misuse 1996; 31: 177-196. Hall W, Mattick RP, Saunders JB, Wodak A. Rapid opiate detoxification treatment. Drug Alc Review 1997; 16: 325-327.

John B Saunders · Alun H Richards

Editorial Domestic violence The healthcare sector could become agents of change MJA 2000; 173: 513-514 The recent series of review papers on domestic violence in the Journal has dealt with a number of important themes: the impact of domestic violence on individuals;1 characteristics of perpetrators;2 presentation of domestic violence in clinical settings;3 and what can be done about domestic violence.4 The prevalence of domestic violence is difficult to estimate because of the variability of definitions and ways of measuring it and the lack of systematic epidemiological studies. Rates tend to be high among patients presenting to general practitioners,5 antenatal clinics,6 emergency departments7 and mental health services,8 but in each of these settings detection is poor. While studies are often developed within a feminist frame of reference and have mostly emphasised the impact on women, men may also be subject to violence from women, as may partners in same-sex relationships. Its impact on children is also substantial, both through witnessing violence and experiencing the effects of abused and abusing parents.9 Focusing on physical abuse as the key indicator may fail to identify far more damaging emotional abuse. There are major health and economic costs of domestic violence.10 Both physical and mental health are affected, increasing the risk of suicide-related behaviours, the drain on healthcare resources and negative perceptions of health status.8,10 Domestic violence in a cultural context Cultural factors have an important impact on the prevalence of domestic violence. These include stereotyped attitudes about "ownership" of women and their value and place in the family and in society; attitudes that define social status in terms of power over others; and the belief of some people that violence is a normal and acceptable way to resolve conflict. The phenomenon of psychological "splitting" is relevant in many situations of domestic violence: people in relationships may unconsciously separate their own good and bad qualities, projecting the hated parts of themselves onto their partner, who is then abused. Understanding violence in families should always encompass an understanding of the importance and complexity of intimate relationships, the making and breaking of affectional bonds and the basic human needs they reflect. These attachments are central to human well-being. It is also vital to take into account social determinants and the particular adversities of social disadvantage that will add cumulative risk. Domestic violence and clinical care Patients are more likely to disclose domestic violence if they receive clear signals that their doctor does not condone violence and will approach the problem in a sensitive way.3,4 A number of questionnaires, including one that has been tested in Australian general practice,5 have been developed to screen for domestic violence. However, they tend to focus only on women, and some are too long to serve as a practical screening tool. In some cases, a single question or a few queries may be all that is required to bring about disclosure of domestic violence if the clinician is alert to its possibility. A high index of suspicion is appropriate if a patient presents with low self-esteem, vague somatic complaints, signs of bruising or other injury and a level of defensiveness. The doctor should question the patient about fear, abuse, depression, and suicidal thoughts. Some victims of domestic violence may even be suffering from a form of post-traumatic stress disorder.11,12 Support, protection, and treatment of acute problems are the first priorities. Effective mental health interventions are available, but should not be provided until the person is in a safe situation. It is also important to remember that children are often traumatised by domestic violence, even if not directly subject to abuse. Feelings of powerlessness, helplessness, and shame often make it difficult for victims of violence to speak of their experience, and they may feel that they are somehow to blame or have "deserved" the abuse. The review of perpetrator issues2 highlights the complexity of this behaviour, the lack of adequate data and the need for evidence of effective interventions. Joint counselling for the couple is usually not recommended because of the late recognition of most cases of domestic violence, the entrenched damaging behaviours and the critical requirement for safety. However, partner programs involving early intervention to reduce negative interaction and interpersonal hostility in relationships could be beneficial.13 Barriers to effective clinical identification and management of domestic violence by health professionals include lack of training, fears for the safety of the victim, or even of the self, identification with victims or perpetrators from the doctor's own social group and, above all, deeply entrenched social attitudes about the privacy of the family.4 Health services and social policy Health services have responded to domestic violence with a range of policies.14 The highest priority for health services is to ensure that victims are protected from further harm. Health professionals need to know about the relevant State legislation, contact details for refuges, and local protocols for appropriate responses when domestic violence is suspected or confirmed. They must be well informed about how to make timely and appropriate referrals.15 The effectiveness of current and proposed programs needs to be evaluated. There are a number of social and health-related policies and programs that could potentially influence the prevalence of and response to domestic violence. Policies that focus directly on domestic violence include: The National Campaign Against Violence and Crime.16 This has programs aimed at preventing violence in schools, rural communities and domestic settings, and programs for dealing with perpetrators. Partnerships Against Domestic Violence.17 This is an agreement between the Federal Government and the States and Territories to work together to prevent domestic violence across Australia. Legislation relating to child protection, family law and orders against violence. Specific policies of States and Territories relating to women's services and the provision of care and protection for women and children who are victims of violence. Other, more general initiatives that may have an effect on domestic violence include National Crime Prevention's "Pathways to Prevention",18 the National Action Plan for Mental Health Promotion and Prevention,19 the Stronger Families and Communities Strategy,20 national policies on alcohol and other drugs, and policies aimed at preventing child abuse and neglect. The complex interface of social policy and health is very relevant in this field. Social variables may far outweigh other factors in the aetiology of domestic violence, but the healthcare sector could become the driving force for change. Beverley Raphael Professor, and Director, Mental Health Services New South Wales Health Department, Sydney, NSW Astbury J, Atkinson J, Duke JE, et al. The impact of domestic violence on individuals. Med J Aust 2000; 173: 427-431. Romans SE, Poore MR, Martin JL. The perpetrators of domestic violence. Med J Aust 2000; 173: 484-488. Hegarty K, Hindmarsh ED, Gilles MT. Domestic violence in Australia: definition, prevalence and nature of presentation in clinical practice. Med J Aust 2000; 173: 363-367. Mazza DM, Lawrence JM, Roberts GL, Knowlden SM. What can we do about domestic violence? Med J Aust 2000; 173: 532-535. Hegarty K. Measuring a multi-dimensional definition of domestic violence: prevalence of partner abuse in women attending general practice. Brisbane: Department of Social and Preventive Medicine, University of Queensland, 1999: 246. Webster J, Sweett S, Stolz T. Domestic violence in pregnancy: a prevalence study. Med J Aust 1994; 161: 466-470. Roberts GL, O'Toole BI, Lawrence JM, Raphael B. Domestic violence victims in a hospital emergency department. Med J Aust 1993; 159: 307-310. Roberts GL, Lawrence JM, Williams GM, Raphael B. The impact of domestic violence on women's mental health. Aust N Z J Public Health 1998; 22: 796-801. Campbell JC, Lewandowski LA. Mental and physical health effects of intimate partner violence on women and children. Psychiatr Clin North Am 1997; 20: 353-374. Resnick HS, Acierno R, Kilpatrick DG. Health impact of interpersonal violence. 2: Medical and mental health outcomes. Behav Med 1997; 23: 65-78. Kemp A, Green BL, Hovanitz C, Rawlings EI. Incidence and correlates of posttraumatic stress disorder in battered women: shelter and community samples. J Interpersonal Violence 1995; 10: 43-55. Herman JL. Complex PTSD: a syndrome in survivors of prolonged and repeated trauma. J Trauma Stress 1992; 5: 377-391. Halford WK. Marriage and the prevention of psychiatric disorder. In: Raphael B, Burrows G, editors. Handbook of studies on preventive psychiatry. Amsterdam: Elsevier, 1995: 121-137. Review of NSW Health domestic violence policy. Discussion paper. NSW Health Department, 1999. Roberts GL, Lawrence JM, O'Toole BI, Raphael B. Domestic violence in the emergency department. 2: detection by doctors and nurses. Gen Hosp Psychiatry 1997; 19: 12-15. National Campaign Against Violence and Crime (NCAVAC). Canberra: Attorney-General's Department, 1998. Partnerships Against Domestic Violence. Information available at: <http://padv.dpmc.gov.au>. Accessed 11 October 2000. Pathways to prevention. Canberra: National Crime Prevention, Attorney General's Department, 1999. Mental Health Promotion and Prevention National Action Plan. Canberra: Commonwealth Department of Health and Aged Care, 1998. Stronger Families and Communities Strategy. Canberra: Commonwealth Department of Family and Community Services, 2000. Make a comment

Beverley Raphael

Editorial Depressed Australians: should we worry? Prescribing an antidepressant should be one component of a pluralistic approach MJA 2000; 173: 452-453 The "decade of the brain", as the 1990s were designated, accorded psychiatry a place in the sun, with depressive illness an obvious focus because of its magnitude and potential for improved management. Disability and suicide, two of the consequences of depression, command broad community interest. The World Health Organization Global Burden of Disease Study quantified "unipolar depression" as the leading cause and "bipolar disorder" (or manic depressive illness) the sixth leading cause of disability in 1990.1 The Australian Burden of Disease Study also established depression as the top-ranking cause of non-fatal disease burden in Australia.2 Other recent Australian data in effect established that, over one year, 1 in 16 Australian adults would be expected to meet the criteria for clinical depression,3 while indicative international data suggest a 20% lifetime rate.4In 1996, Australia's National Health Priority Area initiative identified mental health as a priority area, and, currently, a draft Depression Action Plan has been released for community consideration. This year, a National Depression Initiative has been set up, with Jeff Kennett, the former Premier of Victoria, as chairman. Both these processes recognise the magnitude of the problem and the need for management strategies, while indirectly contributing powerfully to destigmatisation. In this issue of the Journal, McManus and colleagues 5 report a tripling in antidepressant prescriptions in the 1990s in Australia and most other developed countries, and illustrate the "diffusion of an innovation", clearly in line with the noted explosion of information about depression. In contrast, when antidepressants were discovered in the late 1950s, companies were reluctant to release them commercially, as the market was judged too small.6 Depression then was a disorder virtually confined to asylums, and only later formally defined. The American Psychiatric Association's DSM-III manual introduced "major depression" in 1980, an entity then quantified as dominating psychiatric practice, and highly prevalent in general practice and the community. Minor depressive disorders were defined and, more recently, entities such as "sub-clinical depression" and "sub-syndromal depression" have appeared. These have been shown to be associated with considerable disability and amenable to intervention, and thus postulated as disorders.7 If such trends continue, depression will soon be destigmatised by virtue of a depressive subtype for everyone! Such extensions raise predictable questions. Where should the line be drawn in determining "caseness"? As a consequence of stigma or other factors, were we previously minimising, misinterpreting and missing depression? Or are we now excessively "pathologising" aspects of human distress? When psychiatry emerged from its quaintness in the 1960s by adopting a dominant biological model, the "barons" advocating the new Zeitgeist joined with the pharmaceutical industry to promote depression as a medical disorder, and a singularly effective treatment modality -- antidepressant drugs. New drugs were then marketed to redress both the clinical and profit limitations of the old antidepressants. But let's not be critical of the pharmaceutical industry for doing its job, and instead question whether its advertised message should be echoed by professionals. In essence, the message has three components: depression is a distinct medical condition, best treated by antidepressant drugs; the new drugs are as effective as their predecessors; and the new drugs have few side effects, are well tolerated and safe. Each of these issues is worth examining. First, is depression a distinct medical condition?8 Not so. Depression can be a normal mood state -- brief, self-remitting, and ubiquitous. It also exists as a disease, now commonly termed "melancholia", having negligible spontaneous and placebo response rates, with strong biological origins mandating physical treatments. More problematic is the group of disorders once termed neurotic or reactive depression, representing the heterogeneous residue left after excluding the melancholic disorders. It has no distinct or defining clinical features, and high placebo and spontaneous remission rates. This group is better viewed as comprising "spectrum disorders", whereby people with certain temperament styles (eg, anxious worrying, introverted, volatile, obsessional) are disposed to develop depression as a consequence of their temperament style when facing certain stressors. As these temperament styles reflect extremes of normal personality dimensions, the non-melancholic conditions are themselves dimensional, allowing disorder status and need for intervention to be arbitrarily defined, and, as detailed by McManus and colleagues,5 providing the growth arena for the new antidepressant drugs. Second, how effective are our current antidepressant drugs? For psychotic melancholia,9 psychotherapies have no primary role. An antidepressant drug alone will benefit only a quarter, an antipsychotic drug alone a third, while their combination (as with electroconvulsive therapy) will benefit 80% -- distinctly differing levels of effectiveness.9 For non-psychotic depression, the dissonance between drug efficacy data and clinical observation is perturbing. A recent review considered 150 efficacy studies involving 160 000 patients with major depression, concluding that the newer and older antidepressants were equally efficacious.10 However, clinical effectiveness data suggest that the older antidepressants (ie, the tricyclics and the irreversible monoamine oxidase inhibitors) are more effective for melancholia, while, for non-melancholic depression, the newer antidepressants appear (overall) to be as effective.11 Thus, by "homogenising" depression as an entity, specificity of drug action is submerged, assisting marginalisation of the older (low-profit) antidepressants. Thirdly, how safe, acceptable and tolerable are the newer antidepressants? Drop-out rates due to adverse effects only slightly favour them,12 with an appreciable percentage of patients experiencing side effects, which range from alarming (serotonergic reactions on commencement, discontinuation reactions, drug-drug interactions) to inconvenient. Perhaps the most-conceded benefits are their clear-cut cardiac advantages and their non-lethality when taken in overdose. But how truly beneficial are the newer antidepressants? The selective serotonin reuptake inhibitors (SSRIs) are generally considered to be safe and well tolerated. Rarely conceded, and often unrecognised, is that they have the potential to modify several personality styles that dispose to non-melancholic depression (eg, anxious worrying).13 This gives SSRIs a powerful prophylactic role, strongly underpinning patient and prescriber acceptability. Their anti-worry role is neither trivial nor worthy of inciting "cosmetic psychopharmacology" claims. For many who develop non-melancholic depression, taking an SSRI is associated with a normalising of worry and a lessening of both anxiety and irritability. Real-world problems remain, but are viewed and addressed more normally, and resilience to stressful events is increased. Such properties of the SSRIs are noteworthy and, in light of the prevalence of "at-risk" temperament styles (let alone depression), offer a strong utilitarian argument for the SSRIs and some other new antidepressant classes. Regrettably, current alternatives for managing non-melancholic depression are few, when practice and training issues are considered along with efficiency and effectiveness. Many chant the utility of cognitive behaviour therapy, but we need to be assured that advocacy is not merely "non-drug" voting. Although cognitive behaviour therapy (CBT) has high treatment credibility, King, after reviewing several major trials, argues that CBT has little treatment specificity for depression, is highly demanding of time and requires well-trained therapists.14 The high non-specific remission rate attests to the importance of CBT having non-specific therapeutic ingredients, which, together with the high spontaneous remission rate, argue for wise counselling for those with non-melancholic disorders. Finally, should we worry about increased prescribing? Alone, the growth of any effective treatment should be welcomed. But the new Zeitgeist may encourage doctors to reach for a prescription pad at the first suggestion of "depression", welcoming the time and cost efficiency. Such a narrow approach may meet the doctor's practice needs, but is rarely welcomed by patients. Mental health literacy data reveal that the public rates antidepressant medication poorly and as addictive, issues which need redressing.15 Any prescription of an antidepressant should be one component of a pluralistic approach, with the prescriber appreciating the patient's world and predicaments, and providing counselling to assist the patient to come to terms with depression's manifestations, consequences and "meanings". Gordon B Parker Professor, School of Psychiatry, University of New South Wales Research Director, Mood Disorders Unit, Prince of Wales Hospital, Sydney, NSW World Health Organization and the World Bank. The Global Burden of Disease: summary. Cambridge, Mass: The Harvard School of Public Health, Harvard University Press, 1996. Mathers CD, Vos ET, Stevenson CE, et al. The Australian Burden of Disease Study: measuring the loss of health from diseases, injuries and risk factors. Med J Aust 2000; 172: 592-596. Andrews G, Hall W, Teeson M, et al. National Survey of Mental Health and Wellbeing. Report 2. The Mental Health of Australians. Canberra: Mental Health Branch, Department of Health and Aged Care, 1999. Kessler RC, McGonagle KA, Zhao S, et al. Lifetime and 12-month prevalence of DSM-III-R psychiatric disorders in the United States. Arch Gen Psychiatry 1994; 51: 8-19. McManus P, Mant A, Mitchell PB, et al. Recent trends in the use of antidepressants in Australia, 1990-1998. Med J Aust 2000; 173: 458-461. Healy D. The antidepressant era. Cambridge, Mass: Harvard University Press, 1997. Judd LL, Paulus MP, Wells KB, et al. Socioeconomic burden of subsyndromal depressive symptoms and major depression in a sample of the general population. Am J Psychiatry 1996; 153: 1411-1417. Parker G. Classifying depression: should paradigms lost be regained? Am J Psychiatry 2000; 157: 1204-1211. Parker G, Roy K, Hadzi-Pavlovic D, et al. Psychotic (delusional) depression: a meta-analysis of physical treatments. J Affect Dis 1992; 24: 17-24. Anderson IM. Selective serotonin reuptake inhibitors versus tricyclic antidepressants: a meta-analysis of efficacy and tolerability. J Affect Dis 2000; 58: 19-36. Parker G, Mitchell O, Wilhelm K, et al. Are the newer antidepressant drugs as effective as established physical treatments? Results from an Australasian clinical panel review. Aust N Z J Psychiatry 1999; 33: 874-881. Mitchell PB. The new antidepressants -- are they worth the cost? Aust Prescriber 1995; 4: 82-84. Andrews W, Parker G, Barret E. The SSRI antidepressants: defining their "other" possible properties. J Affect Dis 1998; 49: 141-144. King R. Evidence-based practice: where is the evidence? The case of cognitive behaviour therapy and depression. Aust Psychol 1998; 33: 83-88. Jorm AF, Korten AE, Jacomb PA et al. Mental health literacy: a survey of the public's ability to recognise mental disorders and their beliefs about the effectiveness of treatment. Med J Aust 1997; 166: 182-186. Make a comment

Gordon B Parker

Editorial Neglect of bereavement care in general hospitals A family-centred approach is needed in caring for the bereaved in our community MJA 2000; 173: 456 Technological advances in medicine during the 20th century, while achieving marvellous gains in combating disease, have made care of the dying harder.1 At the same time, care of the bereaved has drastically deteriorated with the relative loss of family medicine and increasing emphasis on specialist care.2 Such neglect has occurred particularly in general hospitals in Australia, in which 38 000 deaths (30% of total deaths annually in Australian hospitals) occur each year.3 The morbidity resulting from bereavement contributes substantially to healthcare costs. We are challenged to redress this serious problem by adopting a more family-centred model of care, which should begin to operate from the time of first admission of any index patient. The continual pressure on acute general hospital units can easily lead to neglect of the bereaved, unless the unit leader routinely seeks feedback on bereavement follow-up at multidisciplinary meetings. Fleeting contact with several care providers does not easily permit relationships to become established between staff and patients' relatives. Clearly, continuity of care established with relatives before death could facilitate ease of support following the patient's death. In their article about death in the emergency department (ED) in this issue of the Journal, Williams and colleagues offer guidelines for dealing with bereaved relatives.4 They describe a sensitive approach to the communication of news of tragic death; care of the family as they view the deceased's body and express their grief; and a follow-up program that involves comforting bereaved relatives and maintaining contact with them. This model utilises each member of the multidisciplinary team and reaches out to involve the general practitioner. It promotes continuity of care and takes medical practice beyond the usual patient-centred approach to include the wider community. Bereavement support is indeed a broad community responsibility. Medical resources should be directed to bereaved people at greatest risk of a severe grief reaction, including those for whom the death was unexpected or in some way shocking; those who had an ambivalent or over-dependent relationship with the deceased; those particularly vulnerable to depression or psychiatric illness; and those likely to have poor support networks.5 Careful inquiry from a practitioner adopting a family-centred model of care can help to determine whether particular family members are at high risk. The GP is well placed to sustain regular contact with "at risk" individuals over subsequent months and intervene if complications develop. The manner of death, including death by suicide or homicide, may be associated with stigma, the horror of violence, and a pressing need for relatives to understand the sequence of events leading up to the death.6 In such instances, it is vital that GPs meet with family members to address these issues and that they continue to support the family, referring individuals to psychological or family therapy services if appropriate. Untimely and unexpected death occurs not only in the ED, but also regularly within coronary and intensive care units, and occasionally in obstetric and surgical settings, where the emphasis is on repair and rehabilitation.7 The goal of care in such teams is restitutive,8 and hope of recovery is high. Any relationships between staff and relatives are likely to be brief and tentative. Nevertheless, such units need to have established guidelines, along the lines of those outlined by Williams and colleagues, for responding to unexpected death. Other units (eg, renal, oncology or geriatric services) deal with patients who have chronic illness, with slow but steady progression, sometimes leading to an acceptance of dying in a courageous or heroic manner.9 Emphasis here should be on quality of life and relief of specific symptoms. Generally, staff of these units build good relationships with their patients' relatives and provide a bereavement follow-up program after death. Over the past decade, palliative care services have set up bereavement follow-up programs similar to that described by Williams and colleagues for the ED. They have discovered the importance of a structured approach,10 involving selection of the most appropriate staff member (based on continuity of care) to sustain contact during bereavement, and provision of a written record of outcome. Hospice care has sought to redress the neglect of the dying that can occur when hospitals are focused primarily on the fight for life. The hospice tradition promotes a healthy acceptance of the dying process, encouraging doctors to listen to and care compassionately for the dying and their families. This healing intent must be extended to embrace the care of bereaved relatives, not only in the context of palliative care, but in all other areas. A major cultural shift is needed in many Australian hospitals today to strive for better care of the bereaved in our community. The guidelines proposed by Williams and colleagues4 serve as a model that warrants adoption by the whole hospital system. David W Kissane Professor, and Director of Palliative Medicine Centre for Palliative Care, University of Melbourne, Melbourne, VIC Seale C. Constructing death. The sociology of dying and bereavement. Cambridge: Cambridge University Press, 1998. Parkes CM. Bereavement: studies of grief in adult life. 3rd ed. Madison, Connecticut: International Universities Press, 1998. Australian Bureau of Statistics. Australia now -- a statistical profile. Population, deaths. Canberra: ABS, 2000. Williams AG, O'Brien DL, Laughton KJ, Jelinek GA. Improving services to bereaved relatives in the emergency department: making healthcare more human. Med J Aust 2000; 173: 480-483. Kissane DW. Grief and the family. In: Bloch S, Hafner J, Harari E, Szmukler G, editors. The family in clinical psychiatry. Oxford: Oxford Medical Publications, 1994: 71-91. Hassan R. Suicide in Australia. In: Kellehear A, editor. Death and dying in Australia. Melbourne: Oxford University Press, 2000: 190-207. Field MJ, Cassel CK, editors. Committee on Care at the End of Life, Institute of Medicine. Approaching death: improving care at the end of life. Washington: National Academy Press, 1997. Frank A. The wounded storyteller. Chicago: University of Chicago Press, 1995. Field D. Awareness and modern dying. Mortality 1996; 1: 255-266. Kissane DW. A model of family-centered intervention during palliative care and bereavement: focused family grief therapy (FFGT). In: Baider L, Cooper CL, Kaplan De-Nour A, editors. Cancer and the family. 2nd ed. Chichester: Wiley, 2000: 175-197. Make a comment

David W Kissane

Editorial What's in a name? The labelling of back pain We need a taxonomically correct term for back pain that reassures patients that they can confidently resume normal activities MJA 2000; 173: 400-401 When compiling the second edition of the taxonomy of pain,1 the taxonomy subcommittee of the International Association for the Study of Pain (IASP) wrestled with the diagnosis of spinal pain. It recognised that many diagnostic labels were illegitimate, inappropriate, or fanciful. Nevertheless, it allowed certain labels drawn from the osteopathic, physical medicine, and mainstream literature. In doing so, however, the subcommittee stipulated strict criteria that had to be satisfied if a particular diagnostic label was to be used. The purpose of doing so was to ensure consistent, disciplined and accountable use of terms. However, in many instances, the criteria were such that they could not be satisfied using history and examination alone, or even conventional investigations. The purpose of setting such stringent criteria was to highlight the deficiencies of contemporary practice and to indicate the need for research into the reliability and validity of traditional diagnostic practices. In effect, the exercise established that it was essentially impossible to render any conventional or traditional diagnosis for low back pain. The means to do so were simply not available, not reliable, or not valid. Consequently, the subcommittee argued that the only intellectually and clinically honest diagnosis for most cases of low back pain was "lumbar spinal pain of unknown or uncertain origin".1 This rubric serves well enough for purposes of classification and coding, but it is cumbersome and unappealing for everyday use. Despite its accuracy and honesty, the term is long and conveys the sense that the doctor does not know what is going on. Against this background it is not surprising that general practitioners lack a decent vocabulary for labelling a patient's back pain. The study of Schönstein and Kenny,2 of this issue of the Journal, highlights the implicit difficulties that GPs have in this regard when completing workers compensation certificates. Their sample showed considerable variation in the terms used. Yet, we cannot blame GPs; they are doing as best they can in the absence of a satisfying, official term. Nevertheless, the study reveals the need for standardisation. Diagnostic labels are important in the management of patients. Patients expect a name for their condition. A label shows that the doctor knows what is wrong. But such labels should not be incorrect or specious, lest they lead to therapeutic misadventure. Zygapophysial joint pain and discogenic pain can not be diagnosed clinically3,4 and are, at best, suppositions. Other labels, such as "segmental dysfunction", are only metaphors, with no established biological correlates. Some labels are simply wrong and can have deleterious effects. "Degenerative disc disease" conveys to patients that they are disintegrating, which they are not. Moreover, disc degeneration, spondylosis and spinal ostoearthrosis correlate poorly with pain and may be totally asymptomatic.5 They are age changes and do not constitute diagnoses. For this reason they were not admitted by the IASP.2 "Nominated treating doctors", in recording a diagnosis for back and neck pain, can at least approach standardisation by avoiding these presumptive and specious labels. "Sprain" or "strain" are inferences about what caused the back pain, but are based on what the patient reports. They can not be proven clinically and therefore may or may not be correct inferences. Nevertheless, these labels convey the notion that the pain and its cause are not serious. This is the issue that Schönstein and Kenny raise.2 Because it is not possible to render a pathoanatomical diagnosis of back pain, it becomes imperative to distinguish serious from non-serious conditions. In this regard, it has become conventional to refer to serious conditions as "red flag" conditions, the red flags being aspects of history or examination that should warn doctors of the possibility of a tumour or infection being the cause of pain. Mercifully, these conditions are rare. Another term that has emerged is "yellow flags". This pertains to certain beliefs, attitudes and responses that patients may have to their pain that are counterproductive to recovery. They include believing that activity will make their condition worse, blaming work for their pain, avoiding social activity, and relying on passive therapy.6 These are psychosocial features that are unrelated to the cause of pain, and can occur even with simple causes of pain; but they require attention lest they impede, retard or prevent recovery. What is lacking, however, is a term for back pain that is not associated with red flags or yellow flags. Such a term should be more than taxonomically correct. It should positively reassure patients that they can confidently resume normal activities, without developing fears or inappropriate behaviours. It is such a term that Schönstein and Kenny are looking for.2 In the context of workers compensation certificates such a term would provide more than a convenient label. It would indicate a favourable prognosis and convert the certificate from a disconcerting or confusing document to a propitious and enabling one. The terms "simple back pain" or "uncomplicated back pain" lack these latter properties. The challenge remains to help Schönstein and Kenny, and others, find a new term: one that is palatable to doctors, satisfying to patients, and which not only means that there is nothing seriously wrong, but also conveys the message that the patient has no grounds for fear, and can expect recovery with straightforward, even minimal, management. Nikolai Bogduk Newcastle Bone and Joint Institute University of Newcastle, Royal Newcastle Hospital, Newcastle, NSW mgillamATmail.newcastle.edu.au Merskey H, Bogduk N, editors. Classification of chronic pain. Descriptions of chronic pain syndromes and definitions of pain terms, 2nd edition. Seattle: IASP Press, 1994. Schönstein E, Kenny DT. Diagnoses and treatment recommendations on workers compensation medical certificates. Med J Aust 2000; 173: 419-422. Torgerson WR, Dotter WE. Comparative roentgenographic study of the asymptomatic and symptomatic lumbar spine. J Bone Joint Surg Am 1976; 58: 850-853. Schwarzer AC, Aprill CN, Derby R, et al. The prevalence and clinical features of internal disc disruption in patients with chronic low back pain. Spine 1995; 20: 1878-1883. Schwarzer AC, Aprill CN, Derby R, et al. Clinical features of patients with pain stemming from the lumbar zygapophysial joints. Is the lumbar facet syndrome a clinical entity? Spine 1994; 19: 1132-1137. Kendall NAS, Linton SJ, Main CJ. Guide to assessing psychosocial yellow flags in acute low back pain: risk factors for long-term disability and work loss. Wellington, NZ: Accident Rehabilitation and Compensation Insurance Corporation of New Zealand and the National Health Committee. Make a comment

Nikolai Bogduk

Editorial Lower-limb amputation and diabetes: the key is prevention Education in footcare and regular examination will reduce the burden of diabetes-related amputation MJA 2000; 173: 341-342 Diabetes-related foot problems result in significant social, medical and economic consequences, and constitute the most common reason for hospital admission for people with diabetes.1 Lower-limb amputation is one of the most feared complications of diabetes, but comprehensive Australian data for its current incidence and prevalence in people with diabetes have not been previously available. It is thus timely that the study by Payne is published in this issue of the Journal.2 By analysing the National Hospital Morbidity Database of all hospital separations for the ICD codes which shared diabetes and lower-limb amputation over the financial years 1995-96, 1996-97 and 1997-98, he found a mean of 2629 lower-limb amputations per year. This tragic figure is even more frightening as it most likely represents an underestimate, because of the under-reporting of diabetes on discharge summaries. In all countries, diabetes is the major risk factor for amputation. Data from the United States National Hospital Discharge Survey found an annual average of 110 000 amputations for the period 1989-1992. Of these, 32% were for amputation of toe, 10% foot/ankle, 23% below-knee, and 16% above-knee amputations.3 Of all discharges listing lower-limb amputation, about 51% also listed diabetes, even though people with diabetes represented only 3% of the total US population. The age-adjusted amputation rate calculated for people with diabetes is about 15 to 40 times higher than that for people without diabetes. What are the other risk factors for amputation in people with diabetes? As in Payne's Australian study, the amputation rates in the US are 1.4 and 2.4 times higher for individuals aged 65-74 and aged 75 years and over, respectively, compared with those aged under 65 years.4 Apart from sex, the other major risk factors described are race or ethnic background: a number of US studies have shown higher rates of amputation for black and Hispanic people than for non-Hispanic white people.4 It is unfortunate that Payne was unable to determine this type of demographic data for the Australian population. Other major risk factors include the presence of peripheral neuropathy and lower-limb arterial disease.5,6 In turn, many factors contribute to the development of peripheral vascular disease, including hypertension, smoking and hyperlipidaemia. Finally, duration of diabetes and glycaemic control have been documented as risk factors for amputation and clearly contribute to both peripheral neuropathy and vascular disease.5-8 So, the profile of patients with diabetes at increased risk of amputation is well known. How can we reduce the risk of amputation in people with diabetes? The categorisation of risk of developing diabetes-related foot disease is relatively easily achieved in most people by basic clinical history and examination (Box 1). Self-reported preventive practices in patients have been linked to decreased risk of lower-limb complications.3 However, among individuals with diabetes identified in the 1989 US National Heath Interview Survey, 22% stated they never checked their feet, and 52% checked their feet at least daily. In addition, 53% of patients reported no foot examination by a healthcare professional within the past six months.3 These behaviours need to be changed (Box 2). High-risk foot clinics are also very successful both in healing ulcers and in reducing amputations in patients who have had foot ulcers.11 These multidisciplinary clinics involve specialists from vascular surgery, orthopaedic surgery, endocrinology, infectious diseases, orthotics, and podiatry. Recent advances in prosthetic and orthotic materials, design and manufacturing have improved the ability of clinicians to prevent ulceration in the at-risk foot. Furthermore, advances in orthopaedic techniques now enable the reconstruction of many feet previously considered beyond salvage. What approaches are we taking in Australia to reducing diabetes-related foot problems? The National Diabetes Strategy, published in 1998, identified foot care as a major issue in the National Diabetic Foot Disease Management Program.12 Among the goals set was a 50% reduction in lower-limb amputation by the year 2005, and an 80% level of screening for diabetic foot disease risk factors each year. In addition, an increased availability of podiatry services and specialist foot clinics to provide these services was advocated. Guidelines for non-medical healthcare professionals have been formulated by the Australian Diabetes Educators Association and the Australian Podiatry Council, and Diabetes Australia has produced the Australian Podiatric Guidelines. Most States have established footcare guidelines for doctors, and national guidelines will soon be available. Furthermore, the Australian Diabetes Society position statement on the lower limb in people with diabetes is also published in this issue of the Journal.13 The position statement summarises the major issues and makes recommendations to reduce lower-limb problems for Australians with diabetes. The overriding priorities are to ensure all people with diabetes practise appropriate self-care and that healthcare professionals examine the feet of all people with diabetes regularly to identify people at high risk for ulcer and amputation. Finally, appropriate funding is required to ensure that people at risk are provided with regular podiatry care and education and that people with active foot problems are provided with multidisciplinary foot care. Only when these are achieved will we start to make progress towards reducing this tragic and feared complication of diabetes. Peter G Colman Clinical Associate Professor, and Director Department of Diabetes and Endocrinology Royal Melbourne Hospital, Melbourne, VIC Andrew D Beischer Senior Lecturer Department of Orthopaedic Surgery Royal Melbourne Hospital, Melbourne, VIC Young MJ, Veves A, Boulton AJM. The diabetic foot: aetiopathogenesis and management. Diab Metab Rev 1993; 9: 109-127. Payne CB. Diabetes-related lower-limb amputations in Australia. Med J Aust 2000; 173: 352. Reiber GE, Boyko EJ, Smith DG. Lower extremity foot ulcers and amputations in diabetes. In: Diabetes in America. 2nd ed. Bethesda, Md: National Diabetes Data Group, National Institute of Diabetes and Digestive and Kidney Diseases, 1995; 409-427. Centers for Disease Control and Prevention. Diabetes Surveillance, 1993. Atlanta, GA: US Department of Health and Human Services, 1993; 87-93. Reiber GE, Pecoraro RE, Koepsell TD. Risk factors for amputation in patients with diabetes mellitus. A case-control study. Ann Intern Med 1992; 117: 97-105. Nelson RG, Gohdes DM, Everhart JE, et al. Lower extremity amputations in NIDDM: 12-yr follow-up study in Pima Indians. Diabetes Care 1988; 11: 8-16. Lee JS, Lu M, Lee VS, et al. Lower extremity amputation. Incidence, risk factors, and mortality in the Oklahoma Indian Diabetes Study. Diabetes 1993; 42: 876-882. Klein R. Hyperglycemia and microvascular and macrovascular disease in diabetes. Kelly West Lecture, 1994. Diabetes Care 1995; 18: 258-268. Litzelman DK, Slemenda CW, Langefeld CD, Hays LM. Reduction of lower extremity clinical abnormalities in patients with non-insulin dependent diabetes. Ann Intern Med 1993; 119: 36-41. Malone JM, Snyder M, Anderson G, Bernhard VM. Prevention of amputation by diabetic education. Am J Surg 1989; 158: 520-524. Edmonds ME, Blundell MP, Morris ME, Thomas EM. Improved survival of the diabetic foot: the role of a specialized foot clinic. QJM 1986; 60: 763-771. Colagiuri S, Colagiuri R, Ward J. National Diabetes Strategy and Implementation Plan. Canberra: Diabetes Australia, 1998. Campbell LV, Graham AR, Kidd RM, et al. The lower limb in people with diabetes. Position statement of the Australian Diabetes Society. Med J Aust 2000; 173: 369-372. Make a comment 1: Assessing the risk of diabetic foot disease History Look for a history of: non-traumatic partial or total foot amputation, a diabetic foot ulcer, or admission to hospital for a diabetes-related foot infection. Examination It is not unreasonable to expect these procedures to be performed by medical and non-medical healthcare professionals in the primary care setting: Both feet should be inspected for the presence of obvious deformity and for trophic skin changes. A careful examination should be made for callosities, which may herald incipient ulceration, particularly if present on the plantar aspect of the foot. Peripheral neuropathy, with a loss of protective sensation, can be identified using a 10g Semmes-Weinstein monofilament. Peripheral vascular disease can be detected by palpation of the pedal pulses. Shoes should also be inspected to ensure proper fit and also for unusual wear that may be the result of deformity. Back to text 2: Interventions to improve footcare among people with diabetes A 12-month randomised trial evaluated the effectiveness of comprehensive patient, healthcare provider, and system interventions on risk factors for amputation in 352 patients with type 2 diabetes.9 Patients were randomised to a foot-care group that provided education, and telephone and postcard prompts. Physicians assigned to intervention patients received practice guidelines, information on amputation risk factors and footcare practice and prompts. As a result, physicians detected ulcers in the intervention group more frequently. Similarly, foot self-care behaviours were reported more frequently by intervention patients. A similar prospective randomised study used an intervention in which patients attended a one-hour class and were given written instructions for footcare.10 Clinical care for both groups was identical. After one year of follow-up, there was a threefold excess for both foot amputations and ulcers in the group receiving no education. A case-control study reported the same findings.5 Interestingly, patient education provided at the time of diabetes diagnosis and in hospital settings did not show the same benefit as formal outpatient diabetes education nearer to amputation. Back to text

Peter G Colman · Andrew D Beischer

Editorial The medical emergency team: no evidence to justify not implementing change Given the lack of evidence on the effect of the MET system, what should we do? MJA 2000; 173: 228-229 Any senior doctor, on quiet reflection, will recall times as a junior doctor when his or her treatment of an acutely unwell patient in hospital was less than ideal, either because of lack of knowledge, inexperience, or inadequate procedural skills. Many of these patients had delayed diagnosis and treatment, but survived in spite of (our) incompetence; others "did not do well". This reality has provided material for popular entertainment, including Doctor in the house,1The house of God,2 and the more recent television medical dramas. In the real world, the challenge of ensuring appropriate and effective treatment of acutely ill hospital patients has been politely ignored. There is a prevailing culture of acceptance that it has always been thus, and is an unfortunate result of the need for the young doctors to gain experience. This "blind eye" attitude is becoming harder to sustain in the face of growing evidence of the magnitude of the problem. The high rate of preventable adverse events in hospitals has been well documented in studies such as the Harvard Medical Practice Study3 and the Quality in Australian Health Care Study.4 Further, studies of inpatients admitted to intensive care units have shown that suboptimal diagnosis and treatment before admission is common.5-7 In the face of this evidence, various efforts to improve the performance of junior medical staff have been made. More consultant involvement, formal training of junior medical staff, greater development of acute care guidelines, and cross-specialty audit and peer review have also been supported.6,8 Those not wishing to change can claim there is no evidence to justify changing... Those who wish to change can claim there is no evidence to justify not changing. A different approach, which amounts to a "re-engineering" of the treatment process for acutely ill inpatients, has been the development of the medical emergency team (MET).9 This has been simply described as a renaming of the cardiac arrest team, together with a widening of calling criteria, so that the team can be called (by the ward nurse) for any patient who is acutely unwell. This is a useful summary description, although the MET system includes a number of other important aspects. These include development of evidence-based criteria for diagnosing the acutely unwell patient, formalised training and inservicing for both the team and the ward nurses, ongoing audit and quality improvement, and institutional supervision. The system has some similarities to the trauma team concept, which became generally introduced a decade ago. Since the introduction of portable defibrillation, comprehensive efforts to improve survival after inhospital cardiac arrest have been disappointing in their effect.10 The appeal of a strategy of early intervention is hard to deny. The concept of the MET system is intuitively appealing to many, and has attracted interest locally (in the National Demonstration Hospital Program)11 and internationally.12,13 But does it work? In this issue of the Journal, Bristow and colleagues attempt to provide an answer.14 In a complex study using innovative statistical methods, they have compared patient outcomes in three hospitals, one of which has had the MET system in place for six years. The study has not clearly demonstrated any difference in death rates associated with the MET system; they conclude there may be a reduction in unplanned admissions to the intensive care unit (ICU). There are a number of methodological shortcomings in this study. Comparison of performance between hospitals is difficult, and casemix adjustment is imperfect at best. Casemix adjustment does not include socioeconomic differences in patient population, funding levels, staffing ratios, medical and nursing staff expertise, and "cultural" differences between hospitals. It is notable that the casemix-adjusted death rate differs markedly between the two non-MET hospitals in the study, presumably because of these and other factors. This difference is of such magnitude that any effect of the MET team (if there is one) is likely to be overwhelmed. The rate of "do not resuscitate" orders appears to be higher in the MET hospital. Admission criteria for ICU may differ between hospitals. The MET team appears to be underutilised in the intervention hospital, while the control hospitals that chose to participate in the study may already emphasise the importance of responding to acutely ill inpatients, reducing the potential benefit of the MET system. Other outcomes could be considered, including the effectiveness of treatment for non-ICU patients, and stress or satisfaction among nursing and medical staff. Many of these shortcomings are unavoidable, and the authors have attempted to address their hypothesis using appropriate methods. They are to be congratulated on this courageous attempt to provide an answer to the difficult issue of the effectiveness of the MET system. This study has produced neither a positive nor a negative result -- it has shown how difficult getting a clear result will be. This is disappointing, but is not surprising given the complexity of the study. Even with the best methodology, it may not be possible to quantify the effect of the MET system. Hospitals are "chaotic" systems, and may be impervious to analysis using linear methodology. In this and other areas, it may be futile to attempt to go beyond qualitative research, despite the lack of traditional respectability of non-quantitative methods. This problem has been powerfully discussed by Runciman,15 among others. Given this lack of "evidence" that the MET system achieves different patient outcomes to the traditional "system" of responding to acutely ill patients, what should be done? Medical traditionalists will advocate no change. The MET system bypasses the traditional medical hierarchy, and it may be claimed that this will "deskill" the junior medical staff. The cost of the MET system is unclear, but ICUs will claim that it increases their workload (although it may reduce ICU admissions). Other objections may relate to the internal politics of hospitals: the MET system empowers nursing staff to involve medical officers other than those nominally working for the admitting medical officer who "owns" the patient. Those not wishing to change can claim there is no evidence to justify changing. In contrast, those who support the MET system will claim that the inevitable delays in the hierarchical system and the lack of skills among junior medical staff make the traditional system inherently inadequate. The MET system is claimed to be an appropriate way to deal with this, intuitively more rational, and a more efficient system for ensuring rapid and appropriate interventions for acutely ill inpatients. Institutional supervision, audit and quality improvement is facilitated. Those who wish to change can claim there is no evidence to justify not changing. The debate is not just between these two extremes. There are important issues still to be resolved, such as the appropriate composition and leadership of the MET, skill and training requirements, and the relative merits of the various specialties that could be involved. The debate includes passionate views about the skills of medical registrars, the importance of keeping management of the patient under the sole control of the admitting team (which is presumed to be omnipresent), and the potential for improving the current system by better emergency protocols and staff training. The situation is very reminiscent of the controversy and debate about the introduction of the trauma team. The deficiencies of existing in-hospital trauma care were recognised for many years,16 but the introduction of trauma teams was debated with many of the same arguments now used about the MET.17 What would the patients -- the general public -- think? Outside of hospitals, an untrained lay person can summon ambulances, paramedics and even helicopters for an acutely ill person. Their calls are monitored and recorded. On the patient's arrival in the emergency department, a structured patient triage system is used to optimise efficiency and outcomes. The performance of this emergency system is audited and analysed. In recent years questions in Parliament, Commissions of Inquiry, and (perhaps) contribution to a change of government have followed reports of inadequate speed or quality of response by out-of-hospital emergency services, and in emergency departments. The contrast with the traditional in-hospital system, based on a university-trained nurse summoning the most junior medical officer as the start of an emergency response, and without systematic institutional supervision, audit, and quality improvement, seems incongruous. The general public, increasingly aware of reports of the inadequacies of hospitals, may be bemused by the persistence of the traditional model of emergency response in hospitals, which is little changed from a century ago. The current unsatisfactory situation requires action. The available evidence does not provide clear direction. The MET system is a rational and reasonable change that may improve patient care, and is unlikely to make things worse. Those who support the traditional model should produce evidence on which to base their resistance to change. In the absence of such evidence, the widespread introduction of the Medical Emergency Team system should proceed. Ross K Kerridge Anaesthetist, John Hunter Hospital Newcastle, and Editorial Chair Australian Resource Centre for Hospital Innovation (www.archi.net.au) mdrkkATcc.newcastle.edu.au Gordon R. Doctor in the house. London: Michael Joseph, 1952. Shem S. The house of God. London: Bodley Head, 1978. Brennan TA, Leape LL, Laird N, et al. Incidence of adverse events and negligence in hospitalised patients: results of the Harvard Medical Practice Study I. N Engl J Med 1991; 324: 370-376. Wilson R McL, Runciman WB, Gibberd RW, et al. The Quality in Australian Health Care Study. Med J Aust 1995; 163: 458-471. McGloin H, Adam S, Singer M. The quality of pre-ICU care influences outcome of patients admitted from the ward. Clin Intensive Care 1997; 8: 104. McQuillan P, Pilkington S, Allan A, et al. Confidential inquiry into quality of care before admission to intensive care. BMJ 1998; 316: 1853-1858. Smith AF, Wood J. Can some in-hospital cardio-respiratory arrests be prevented? A prospective survey. Resuscitation 1998; 37: 133-137. Leah V, Coats TJ. In-hospital resuscitation -- what should we be teaching? Resuscitation 1999; 41: 179-183. Lee A, Bishop G, Hillman KM, Daffurn K. The Medical Emergency Team. Anaesth Intens Care 1995; 23: 183-186. Varon J, Marik PE, Fromm RE. Cardiopulmonary resuscitation: a review for clinicians. Resuscitation 1998; 36: 133-145. Commonwealth Department of Health and Aged Care. A qualitative review of the National Demonstration Hospital Program Phase 2. Canberra: Commonwealth of Australia, 1999. Available at <http://www.health.gov.au:80/hsdd/acc/ndhp/ pubs/ndhp2review.htm>. Garrard C, Young D. Suboptimal care of patients before admission to intensive care. BMJ 1998; 316: 1841-1842. Singer M, Little R. ABC of Intensive Care: Cutting edge. BMJ 1999; 319: 501-504. Bristow PJ, Hillman KM, Chey T, et al. Rates of in-hospital arrests, deaths and intensive care admissions: the effect of a medical emergency team. Med J Aust 2000; 173: 236-240. Runciman WB. Qualitative versus quantitative research -- balancing cost, yield, and feasibility. Anaesth Intens Care 1993; 21: 502-505. Hoffman E. Mortality and morbidity following road accidents. Ann R Coll Surg Engl 1976; 58: 233-240. Spencer JD. Why do our hospitals not make more use of the concept of a trauma team? BMJ 1985; 290: 136-138. Make a comment

Ross K Kerridge

Editorial Alcohol: the good, the bad and the ugly It may be protective against cardiovascular disease, but alcohol is not all good MJA 2000; 173: 231-232 Many recent studies from various countries have consistently highlighted the good effects of alcohol.1 This protective association with alcohol is fairly specific to cardiovascular disease and does not seem to operate for other causes of death. The studies support the notion that the National Health and Medical Research Council (NHMRC) recommendation of two standard drinks a day for women and four standard drinks a day for men2 is sensible advice. That, however, is not the end of the alcohol story. Virtually all of us, as medical students, were exposed to the "bad" of alcohol. Our texts provided lists of diseases caused by the direct effects of high-risk alcohol consumption, as well as the effects of acute intoxication, dependence and withdrawal. Our experience in the wards reinforced these descriptions. In 1997, 3290 Australians (70% men) died of injury and disease caused by high-risk drinking.3 Most of them died of stroke, alcoholic cirrhosis, road injury, suicide, or alcohol dependence. On average, 19 years of life were lost for each person who died of an alcohol-caused condition. At the same time, high-risk drinking was responsible for 72 300 hospitalisations and 403 795 hospital bed-days in Australia; these were predominantly due to falls, alcohol dependence, assaults, or road injuries.3 As medical students, we also witnessed the havoc wrought by alcohol-associated injuries. Between 1990 and 1997, 31% of all driver and pedestrian deaths on Australian roads were alcohol related.4 More than 70% of people with serious alcohol-related road injuries were male (compared with 56% of people with serious non-alcohol-related road injuries). More than half these men were between the ages of 15 and 24 years. The "ugly" was often not seen by medical students. The psychosocial and economic effects of alcohol were rarely spoken about or observed. The annual cost of alcohol misuse in Australia has been estimated at $3.8 billion -- a substantial amount of this is a result of decreased occupational productivity, often a result of hangover-related absenteeism and poor job performance.5 It is estimated that 75% of men and women who have consumed alcohol report that they have experienced hangovers at least once, and 15% experience hangovers at least monthly.5 The leading causes of burden of disease in 15-24-year-old Australian males include alcohol dependence and harmful use, and three other disorders that are related to alcohol: road traffic accidents, suicide, and self-inflicted injury.6 World-wide, alcohol is the fourth leading cause of disability, involving 15.8 million people. In First World regions it is the leading cause, and in Third World regions it is the fourth largest cause, of male disability.7 The recently published National Survey of Mental Health and Wellbeing8 indicates that most Australians (83% of men and 63% of women) report that they have consumed at least 12 drinks of alcohol in the preceding year, and one in 15 (6.5%) have had an alcohol-use disorder in the past 12 months. More men (9.4%) than women (3.7%) had an alcohol-use disorder in the past 12 months, and this is greatest among 18-34-year-olds (almost 16% of men). There is considerable comorbidity between alcohol use and other mental disorders.8 Forty-eight per cent of Australian women with an alcohol-use disorder also suffer from anxiety, affective or other drug-use disorders, compared with 15% of women without alcohol-use disorder; 34% of men with an alcohol-use disorder have another mental disorder. The relation between alcohol and mental disorders is complex: each may cause the other, or both may be related to some underlying cause. Alcohol can also have a devastating effect on families -- more than two-thirds of domestic incidents are alcohol related. Are we making headway against these problems? The initial good news, that since 1978 alcohol consumption in Australia has been progressively falling, is tempered by the slowing of this fall since 1993, and a slight increase in some States. The 1998 National Drug Strategy Household Survey found evidence of increased binge drinking and a softening of attitudes to drinking and driving. In dealing with the problems of alcohol, we need to be aware of two phenomena: Many alcohol-related problems in the community occur in a very large number of people consuming, on a long term basis, above-average but socially acceptable quantities of alcohol, rather than in the much smaller number of persons consuming very large quantities of alcohol.9 Much of the damaging effect of alcohol, particularly in young people, results from episodic (binge) drinking rather than dependent daily consumption of alcohol. These findings have important public health implications. The first point can be partially but effectively addressed by brief intervention strategies delivered by trained GPs as part of their usual strategies.10 However, the second point requires a greater public health commitment to responsible social drinking. Linking alcohol taxes to the alcohol content of beverages is one useful strategy.11 Our strategies need to recognise that people can drink acutely in damaging fashion even if their average weekly consumption is less than the NHMRC limits. Greg Whelan Professor, Department of Drug and Alcohol Studies St Vincent's Hospital, and Physician, Turning Point Alcohol and Drug Centre Inc, Melbourne, VIC Alan T Gijsbers Physician, Department of Drug and Alcohol Studies St Vincent's Hospital, and Turning Point Alcohol and Drug Centre Inc, Melbourne, VIC Doll R. The benefit of alcohol in moderation. Drug Alcohol Rev 1998; 17: 353-363. Pols RG, Hawks DV. Is there a safe level of daily consumption of alcohol for men and women? 2nd ed. Canberra: AGPS, 1992. Chikritzhs T, Jonas H, Heale P, et al. Alcohol caused deaths and hospitalisations in Australia, 1990-1997. National Alcohol Indicators Bulletin No. 1, December 1999. Chikritzhs T, Stockwell T, Heale P, et al. Trends in alcohol-related road injury in Australia, 1990-1997. National Alcohol Indicators Bulletin No. 2, May 2000. Wiese JG, Shiplak MG, Browner WS. The alcohol hangover. Ann Intern Med 2000; 132: 897-902. Mathers C, Vos T, Stevenson C. Burden of disease and injuries in Australia. Canberra: Institute of Health and Welfare, 1999. Murray CJL, Lopez AD. The Global Burden of Disease: a comprehensive assessment of mortality and disability from diseases, injuries and risk factors in 1990 and projected to 2020. Cambridge, Mass: Harvard University Press on behalf of the World Health Organization and the World Bank, 1996. Teesson M, Hall W, Lynskey M, et al. Alcohol and drug use disorders in Australia: implications of the National Survey of Mental Health and Wellbeing. Aust N Z J Psychiatry 2000; 34: 206-213. Kreitman N. Alcohol consumption and the preventive paradox. Br J Addiction 1986; 81: 353-363. Bien TH, Miller WR, Tonigan JS. Brief interventions for alcohol problems: a review. Addiction 1993; 88: 315-336. Richardson J. Alcohol taxes: the case for reform. Med J Aust 1990: 152: 619-620. Make a comment

Greg Whelan · Alan T Gijsbers

Editorial Psychotropic drugs and preschoolers With little evidence for the safety and effectiveness of these drugs in the very young, doctors are in a difficult position MJA 2000; 173: 172-173 Disturbingly, recent overseas reports suggest that the prescribing of stimulant, antipsychotic, antidepressant and other psychotropic drugs for very young children is increasing.1,2 Of even greater concern is that a significant number of these children may be given more than one psychotropic drug concurrently.3While no systematic data are available to show whether the same phenomena are occurring in Australia, there are indications that prescribing of psychotropics for preschoolers is not uncommon in this country. A survey of 788 parents whose children were treated with stimulants found that 8% were aged under five years when diagnosed with attention deficit hyperactivity disorder;4 presumably, many were given medication. Preliminary data provided by the Pharmaceutical Services Branch of the New South Wales Department of Health (NSW Health) show that in the past decade stimulant treatment was initiated (an authority was given) in NSW for 5819 children younger than six years: 67 (1%) were aged two and 715 (12%) three. There was a 12-fold increase in the number of preschool children treated with stimulants between 1990 and 1999. There are no Australian data about the use of other psychotropic drugs in this age group, but our clinical experience shows that antidepressants, antipsychotics and clonidine are being used. Reports suggesting an increase in the prescribing of clonidine in preschoolers, often concurrently with stimulants, are appearing. The result is a disturbing number of clonidine poisonings in very young children.5,6 ...medication, rightly or wrongly, has become more common in managing problematic behaviour, even in the very young. It is worrying that psychotropics are being prescribed for preschoolers. Firstly, with few exceptions, in most countries these medications are not approved for use in the very young. Secondly, there are very few controlled data showing whether they are effective in this age group.7 Thirdly, psychiatric diagnoses in preschoolers generally lack validity and reliability. This is because preschool-age children have a limited repertoire of emotions and behaviours and a reduced ability to communicate, which leads to a reliance on parental reports. Further complications are an overlap of symptoms with temperamental characteristics, difficulties in establishing the range of age-appropriate behaviours in the context of differences in maturation, and the fact that children of this age are highly reactive to environmental stressors, family conflict and inadequate parenting. Fourthly, there is little knowledge and considerable apprehension about the long-term effect of psychotropics on the developing brain. Fifthly, there are scarce data about the pharmacokinetic and pharmacodynamic characteristics of these drugs in the very young. Finally, rather than placing the best interests of the child first, some practitioners may react to pressure from preschools, childcare services or parents. For all of these reasons, prescribing psychotropics in preschoolers is of concern. The problem is magnified if the child is reviewed infrequently, as seems the case for many of those taking stimulants.3 A review of 624 children hospitalised for any reason in five European countries showed that over two-thirds had received medications that were not licensed for use in children or "off label" (ie, used for indications or in patient groups other than those approved by the regulatory bodies).8 Thus, the prescribing of psychotropics to preschoolers is part of the world-wide pattern of prescribing drugs for children off label. This situation is the result of most drugs' not having been tested in children, let alone preschoolers. Drugs are studied in adults, and physicians assume they will be effective and safe for the young. However, such an assumption is unwarranted, as the experience with tricyclic antidepressants in the treatment of depression in children has shown.9 That experience also shows that clinicians find it difficult to wait for the evidence and, in its absence, may prescribe medications that are not only ineffective but also potentially hazardous. With society and families undergoing rapid change, physicians are confronted with growing numbers of young children with severe behavioural problems, with many parents who have limited parenting skills and with an increasingly demanding public. This is compounded by overwhelmed and inadequate social and mental health services for young people. It is not surprising that medication, rightly or wrongly, has become more common in managing problematic behaviour, even in the very young. At the same time, there are preschool children who present with severe symptoms and impairment who do not respond to appropriate psychosocial treatments.7,10,11 Depriving them of potentially effective medication (eg, stimulants, for which there is ample evidence of effectiveness in older children) may be unwarranted. Clinicians find themselves in an all-too-familiar predicament: urged to prescribe but having no evidence base for doing so. None the less, sympathy with the physician's predicament does not justify potentially unsafe practices. Education in paediatric psychopharmacology -- made more necessary by the large number of new drugs marketed recently -- and increasing awareness of the range of effective, non-pharmacological interventions available7,10,11 are probably better alternatives for minimising unproven practices than greater control of prescribing. These problems are not new. Many were identified in a 1997 report which emphasised that labelling of medications for children was poor, that liability was transferred to prescribers, that lack of research could deprive children of access (including subsidised access) to effective treatments, and that ethical concerns made it difficult to conduct treatment trials in this age group, thus creating a vicious cycle.12 We wonder whether the recommendations in this report have been implemented with the diligence this matter deserves. For example, are all relevant new drugs which are submitted for registration required to include paediatric indications? (This requirement has already been implemented in the United States.) Have disincentives for research and for registration of medications for use in children been reviewed or removed? The NHMRC needs to make funding of research on the use of drugs in children a priority, and to tackle the difficult ethical issues involved. This is not something other stakeholders, like the pharmaceutical industry, are likely to take on. It is clear that clinicians are not the only ones responsible for the current state of affairs. Joseph M Rey Professor, Department of Psychological Medicine University of Sydney and Director of Child and Adolescent Mental Health Services Northern Sydney Health Garry Walter Clinical Lecturer, Department of Psychological Medicine University of Sydney and Acting Director Central Sydney Child and Adolescent Mental Health Services Philip L Hazell Conjoint Professor of Child and Adolescent Psychiatry University of Newcastle and Director of Child and Youth Mental Health Services, Hunter Mental Health Zito JM, Safer DJ, dosReis S, et al. Trends in the prescribing of psychotropic medications to preschoolers. JAMA 2000; 283: 1025-1030. Minde K. The use of psychotropic medication in preschoolers: some recent developments. Can J Psychiatry 1998; 43: 571-575. Rappley MD, Mullan PB, Alvarez FJ, et al. Diagnosis of attention-deficit/hyperactivity disorder and use of psychotropic medication in very young children. Arch Pediatr Adolesc Med 1999; 153: 1039-1045. Hazell P, McDowell MJ, Walton JM. Management of children prescribed psychostimulant medication for attention deficit hyperactivity disorder in the Hunter region of NSW. Med J Aust 1996; 165: 477-480. Erickson SJ, Duncan A. Clonidine poisoning -- an emerging problem: epidemiology, clinical features, management and preventative strategies. J Paediatr Child Health 1998; 34: 280-282. Kappagoda C, Schell DN, Hanson RM, Hutchins P. Clonidine overdose in childhood: implications of increased prescribing. J Paediatr Child Health 1998; 34: 508-512. Hazell P. Attention deficit hyperactivity disorder in preschool children. Adelaide: The Australian Early Intervention Network for Mental Health in Young People, 2000: 15-28. Conroy S, Choonara I, Impicciatore P, et al. Survey of unlicensed and off label drug use in paediatric wards in European countries. BMJ 2000; 320: 79-82. Hazell P, O'Connell D, Heathcote D, et al. Efficacy of tricyclic drugs in treating child and adolescent depression: a meta-analysis. BMJ 1995; 310: 897-901. Barkley RA, Shelton TL, Crosswait C, et al. Preliminary findings of an early intervention program with aggressive hyperactive children. Ann N Y Acad Sci 1996; 794: 277-289. Sanders MR, Gooley S, Nicholson J. Early intervention in conduct problems in children. Adelaide: The Australian Early Intervention Network for Mental Health in Young People, 2000: 43-50. Australian Drug Evaluation Committee. Report of the working party on the registration of drugs for use in children. Canberra: Australian Drug Evaluation Committee, October 1997. Make a comment

Joseph M Rey · Garry Walter · Phillip L Hazell

Editorial SIDS: facts and controversies We need to promote the established risk-reducing behaviours, which are based on strong scientific evidence MJA 2000; 173: 173-174 Over the period 1982-1986, Australian Bureau of Statistics figures show that there were an average of 457 deaths per year from sudden infant death syndrome (SIDS) in Australia (1.89 deaths/1000 live births).1 Ten years later, over the period 1992-1996, SIDS mortality had plummeted to 210 deaths per year (0.81 deaths/1000 live births).1In spite of this dramatic decrease, SIDS still causes more deaths than traffic injuries, congenital anomalies and cancer combined in the 1-4 years age group.1 Here, I briefly discuss the established risk factors for SIDS and current areas of controversy. Sleeping position: Studies dating back to the 1960s, but mostly in the 1980s, had suggested that prone sleeping position was associated with SIDS, but it was not until SIDS prevention campaigns had been successfully run in the Netherlands and New Zealand that the potential for reducing SIDS mortality by modifying this risk factor was recognised.2 In 1991, Australia launched its "Reducing the Risk" campaign, driven by SIDS organisations and supported by Red Nose Day funds. In New Zealand, we observed a close temporal relationship between Red Nose Day education campaigns and reduction in the prevalence of placing infants in the prone sleeping position.3 This illustrates the powerful synergy that can be created when professional and voluntary/parent groups work together. The fall in SIDS mortality can be attributed almost entirely to a change in the prevalence of placing infants in the prone sleeping position,4 supporting the contention that prone sleeping is part of the causal pathway and is a cause of SIDS. Recent evidence suggests that sleeping on the side doubles the risk of SIDS compared with sleeping in a supine position, probably because of infants turning to the prone position ("secondary prone").5 Infants who usually sleep supine but are placed prone (ie, are unaccustomed to the prone position) are at very high risk of SIDS.6,7 Smoking: Maternal smoking is the other major non-controversial risk factor for SIDS.8 Since the reduction in the prevalence of prone sleeping position, there have been eight studies examining maternal smoking and SIDS. The pooled unadjusted (not adjusted for confounders) relative risk (RR) determined from these studies is 4.7, which suggests that infants of mothers who smoke are at an almost fivefold greater risk of SIDS than infants of mothers who do not smoke. Evidence for the effect of environmental tobacco smoke exposure can be obtained by examining the risk of SIDS from paternal smoking where the mother is a non-smoker. There have been six such studies. The pooled unadjusted RR for these studies was 1.4. The increased risk of SIDS with tobacco smoke is probably predominantly due to an in-utero effect of tobacco smoke rather than postnatal environmental tobacco smoke.8 Bedding and clothing: Excess bedding and clothing have been shown to increase the risk of SIDS in infants sleeping prone, but not for infants sleeping on their side or back. As few infants in Australia sleep prone,4advice on the amount of bedding and clothing could be dropped. Some 15%-20% of infants who die of SIDS are found with their head covered by bedding.9 Covering of the head might cause death by forcing an infant to rebreathe expired gases or by creating thermal stress. There have been several suggestions as to how to avoid covering of the head, including tucking bedding in firmly, removing bedding, placing infants at the foot of the cot, using the Dutch sleeping sack, and avoiding the use of duvets. The evidence to support these recommendations is limited. Bed sharing: It is well established that infants who share a bed with mothers who smoked during the pregnancy are at increased risk of SIDS.5 Whether or not there is an increased risk for infants sharing a bed with mothers who were non-smokers has not been firmly established. If there is an increased risk it is likely to be quite small (pooled unadjusted RR, 1.4). Complicating the picture is the fact that in some cultures bed sharing is an established practice. Furthermore, others have advocated bed sharing to improve breastfeeding rates.10 Breastfeeding: Most studies have shown that the incidence of SIDS is lower in breastfed infants. However, breastfeeding in most developed countries is associated with socioeconomic advantage, and, when adjustment is made for socioeconomic factors, the protective effect of breastfeeding is less apparent.11,12 Some have concluded there is no decreased risk from breastfeeding,12 whereas others have argued that breastfeeding has a protective effect.11 Use of pacifier: An unexpected finding of several studies has been that pacifiers are associated with a reduced risk of SIDS.13 However, this benefit needs to be balanced against possible detrimental effects of pacifiers, such as a reduction in breastfeeding and increased incidence of otitis media.14 Vaccinations: In the past there was concern that vaccinations might cause SIDS, as the peak age for SIDS is 2-4 months, which coincides with the age for vaccinations. However, studies have shown that vaccinations are not associated with an increased risk of SIDS -- indeed, some studies have shown a reduced risk of SIDS at the time of vaccinations.15 Despite this, the media from time to time revive this old chestnut. "Toxic gas": The "toxic gas" theory has received considerable media attention in the United Kingdom and New Zealand, but has not been substantiated.16 According to this theory, toxic gases are produced by the fungus Scopulariopsis brevicaulis as it metabolises chemicals containing arsenic, antimony and phosphorus in cot mattresses. Proponents of the theory recommend wrapping cot mattresses in polythene, but this is potentially dangerous advice in view of the evidence that plastic sheeting in a baby's sleeping environment can cause death through suffocation.17 Despite the success of the "Reducing the Risk" campaign, SIDS mortality remains unacceptably high among Indigenous Australians (mortality rates for the period 1992-1996, aggregated for South Australia, Western Australia and the Northern Territory, were 30 deaths per year among Indigenous Australians [5.29 deaths/1000 population] compared with 61 deaths/year among non-Indigenous Australians [0.81 deaths/1000 population]). The cause or causes of SIDS remain largely unknown, although the most likely mechanisms include airway obstruction, rebreathing of expired gases, thermal stress and an "arousal defect" (reduced ability to respond to hypoxia or hypercapnoea by arousing or waking up). There is now little support for the (central) apnoea hypothesis, which was the major mechanism postulated in the 1970s and 1980s. Physiologists need to show how the established risk factors might operate, and researchers need to explore the reasons for the high rate of SIDS in disadvantaged and Indigenous communities. We must also continue to promote the established risk-reducing behaviours, which are based on strong scientific evidence, and ensure that all new mothers receive this information. We need to devise and evaluate innovative methods for delivering these messages and changing behaviour among disadvantaged and Indigenous groups. New theories should be examined, and discredited ideas buried. The media have an important responsibility, as they are in a position either to create controversy and confusion about SIDS or to serve as a powerful force for producing change. Ed A Mitchell Associate Professor in Paediatrics Department of Paediatrics University of Auckland, New Zealand. e.mitchellATauckland.ac.nz Acknowledgement: I am grateful to the Australian Bureau of Statistics for supplying mortality data. Australian Bureau of Statistics website <http://www.abs.gov.au> Engelberts AC, de Jonge GA. Choice of sleeping position for infants: possible association with cot death. Arch Dis Child 1990; 65: 462-467. Mitchell EA, Tonkin S. Publicity and infants' sleeping position. BMJ 1993; 306: 858. Dwyer T, Ponsonby AL, Blizzard CL, et al. The contribution of changes in the prevalence of prone sleeping position to the decline in SIDS in Tasmania. JAMA 1995; 273: 783-789. Scragg RKR, Mitchell EA. Side sleeping position and bed sharing in the sudden infant death syndrome. Ann Med 1998; 30: 345-349. L'Hoir MP, Engelberts AC, van Well GT, et al. Risk and preventive factors for cot death in The Netherlands, a low-incidence country. Eur J Pediatr 1998; 157: 681-688. Mitchell EA, Thach BT, Thompson JMD, Williams S. Changing infants' sleep position increases risk of sudden infant death syndrome. Arch Pediatr Adolesc Med 1999; 153: 1136-1141. Mitchell EA, Milerad J. Smoking and sudden infant death syndrome. In: International consultation on environmental tobacco smoke (ETS) and child health. Geneva: World Health Organization, 1999: 105-129. Beal SM, Byard RW. Accidental death or sudden infant death syndrome? J Paediatr Child Health 1994; 30: 144-150. McKenna JJ, Mosko SS, Richard CA. Bedsharing promotes breastfeeding. Pediatrics 1997; 100: 214-219. Ford RP, Taylor BJ, Mitchell EA, et al. Breastfeeding and the risk of sudden infant death syndrome. Int J Epidemiol 1993; 22: 885-890. Fleming PJ, Blair PS, Bacon C, et al. Environment of infants during sleep and risk of the sudden infant death syndrome: results of 1993-5 case-control study for confidential inquiry into stillbirths and deaths in infancy. Confidential Enquiry into Stillbirths and Deaths Regional Coordinators and Researchers. BMJ 1996; 313: 191-195. Fleming PJ, Blair PS, Pollard K, et al. Pacifier use and sudden infant death syndrome: results from the CEDI/SUDI case control study. Arch Dis Child 1999; 81: 112-116. Hunt L, Fleming P, Golding J. Does the supine sleeping position have any adverse effects on the child? I. Health in the first six months. The ALSPAC Study Team. Pediatrics 1997; 100: E11. Hoffman HJ, Hunter JC, Damus K, et al. Diphtheria-tetanus-pertussis immunization and sudden infant death: results of the National Institute of Child Health and Human Development Cooperative Epidemiological Study of sudden infant death risk factors. Pediatrics 1987; 79: 598-611. Expert Group to Investigate Cot Death Theories: toxic gas hypothesis. Chairman, Lady Limerick. Final report. London: Department of Health. May 1998. Kraus JF. Effectiveness of measures to prevent unintentional deaths of infants and children from suffocation and strangulation. Public Health Rep 1985; 100: 231-240. Make a comment

Ed A Mitchell

Editorial Falls in the elderly: what can be done? We need to streamline referral to falls programs and coordinate services within and outside hospitals MJA 2000; 173: 176-177 Falls are often referred to as one of the "geriatric giants", generating diagnostic and rehabilitative dilemmas for a variety of specialists in a range of settings. In older people, falls are associated with significant mortality and morbidity and frequently lead to a decline in physical and/or psychological function, ultimately encroaching on independence and autonomy. In addition to the costs to the individual and immediate carers, falls consume significant resources in terms of hospital admissions, bed utilisation, and use of other health and allied services. With an ageing population, the problems associated with falls and injury will escalate unless there is a coordinated and effective approach to prevention and intervention. Given that most falls result from a dynamic interaction between intrinsic and extrinsic factors, a multidisciplinary approach to their management -- incorporating medical, functional, and environmental assessment -- is likely to be most rewarding. To date, there is limited evidence to support a population-based preventive strategy -- it thus becomes imperative to focus on high-risk groups with the potential to benefit. For any falls prevention strategy to be effective and of direct clinical relevance, it should: be acceptable and applicable to the affected population (applicability); alter outcome in terms of falls and fall-related injury (efficacy); be cost effective (cost-effectiveness); and be readily applicable to everyday practice (practicability). There is increasing evidence to support intervention in specific populations, although caution is advised when extrapolating results from one setting and population to another. Tinetti and colleagues' seminal article showed the benefits of undertaking risk factor modification in older people in the community with specific risk factors for falls,1 while Campbell et al have shown a reduction in risk of falling after individually tailored home exercise programs for women 80 years or older.2 T'ai chi undertaken in a group setting has also been shown to reduce the risk of recurrent falls.3 More recently, Campbell and colleagues reported a significant reduction in falls after withdrawal of psychotropic medication in older people.4 However, within a month of completion of the study, 47% of their patients had recommenced psychotropic medication, highlighting the need to provide continuing support. The role of the occupational therapist and home environment modification has not been established. A recently published study by Cumming et al showed a reduction in falls in patients having a home environment assessment by an occupational therapist on discharge from hospital.5 Interestingly, the observed reduction was for both indoor and outdoor falls, raising questions as to the mechanism of the observed effect. Perhaps modifying the home environment enhances safety awareness generally. It should be remembered that most people who fall do not sustain any injury and do not present to any medical service,6 despite increasing evidence supporting targeted intervention. Older people presenting to emergency departments are an easily identifiable, high-risk population. Studies have reported that, among older people discharged from emergency departments, up to half show an increase in dependency, usually secondary to trauma.7,8 A two-year follow-up of patients for whom a geriatric consultation was requested in the emergency department showed 34% had died and 52% were in a long term care facility.9 Falls contribute significantly to the emergency department workload, as highlighted by Bell and colleagues in this issue of the Journal.10 They report data on older people presenting after a fall to an inner-city teaching hospital in Sydney. Their results emphasise the multifactorial nature of falls. A UK inner-city teaching hospital with comparable baseline demographics has produced evidence of the benefits of a structured interdisciplinary assessment of such patients.11 The high rate of injury and admission reported by Bell et al is not surprising and reflects our own experience -- elderly people are four to five times more likely to be admitted to hospital than younger people -- and this must be taken into consideration in the context of demographic projections for the next 25-30 years. The emergency department represents a key interface between the hospital and the community and, as such, affords a unique opportunity for interdisciplinary and multiprofessional cooperation across health and social care sectors. However, assessment in the emergency department focuses largely on injury and limited time is available for investigating underlying causes or implementing preventive strategies. It is neither practical nor feasible for all older people who fall to undergo a detailed assessment in the emergency department, or to be assessed by geriatricians. However, using derived and easily identifiable predictors of risk, it is possible to streamline referrals to a falls program or clinic, which would be in keeping with an attainable level of service commitment. Predictors of future risk, as identified in the emergency department, include a history of one or more falls in the previous year, a fall occurring indoors, inability to get up from the floor after a fall, and polypharmacy (four or more regularly prescribed medications).12 Only through effective liaison with services within and outside hospital can we improve the outcome for older people presenting with falls. The increasing provision of falls programs fulfilling the effective intervention criteria provides the ideal opportunity to bring together existing, but frequently fragmented, services to enhance the care of older people. Jacqueline C T Close Physician Clinical Age Research Unit Department of Health Care of the Elderly King's College School of Medicine and Dentistry London, UK jacqueline.closeATkcl.ac.uk Ed Glucksman Physician, Department of Accident and Emergency Medicine King's College Hospital, London, UK Tinetti ME, Baker DI, McAvay G, et al. A multifactorial intervention to reduce the risk of falling among elderly people living in the community. N Engl J Med 1994; 331: 821-827. Campbell AJ, Robertson MC, Gardner MM, et al. Randomised controlled trial of a general practice programme of home based exercise to prevent falls in elderly women. BMJ 1997; 315: 1065-1069. Wolf SL, Barnhart HX, Kutner NG, et al. Reducing frailty and falls in older persons: an investigation of Tai Chi and computerized balance training. Atlanta FICSIT Group. Frailty and Injuries: Cooperative Studies of Intervention Techniques. J Am Geriatr Soc 1996; 44: 489-497. Campbell AJ, Robertson MC, Gardner MM, et al. Psychotropic medication withdrawal and a home-based exercise program to prevent falls: a randomized, controlled trial. J Am Geriatr Soc 1999; 47: 850-853. Cumming RG, Thomas M, Szonyi G, et al. Home visits by an occupational therapist for assessment and modification of environmental hazards: a randomized trial of falls prevention. J Am Geriatr Soc 1999; 47: 1397-1402. Graham HJ, Firth J. Home accidents in older people: role of primary health care team. BMJ 1992; 305: 30-32. Gerson LW, Rousseau EW, Hogan TM, et al. Multicenter study of case finding in elderly emergency department patients. Acad Emerg Med 1995; 2: 729-734. Khan SA, Miskelly FG, Platt JS, Bhattachryya BK. Missed diagnoses among elderly patients discharged from an accident and emergency department. J Accid Emerg Med 1996; 13: 256-257. Sinoff G, Clarfield AM, Bergman H, Beaudet M. A two-year follow-up of geriatric consults in the emergency department. J Am Geriatr Soc 1998; 46: 716-720. Bell AJ, Talbot-Stern JK, Hennessy A. Characteristics and outcomes of older patients presenting to the emergency department after a fall: a retrospective analysis. Med J Aust 2000; 173: 179-182. Close JCT, Ellis M, Hooper R, et al. Prevention of falls in the elderly trial (PROFET): a randomised controlled trial. Lancet 1999; 353: 93-97. Close JCT, Ellis M, Hooper R, et al. Predictors of falls -- results from Prevention of Falls in the Elderly Trial (PROFET). Age Ageing 1999, 28 Suppl 1: 14. Make a comment

Ed Glucksman

Editorial Alcohol and cardiovascular disease: still a research priority? MJA 2000; 173: 116-117 More precision in measuring drinking levels and patterns will give a firmer basis for advice about drinking The evidence amassed to date on the link between moderate alcohol intake and reduced risk of dying of cardiovascular disease might be thought already sufficient to bracket sceptics of alcohol's protective effect with doubters of manned lunar missions and members of the Flat Earth Society. Published studies demonstrating this link can now be counted in the hundreds, and no fewer than six plausible underlying biological mechanisms have been identified.1 In this issue of the Journal yet another study reports this link: Simons and colleagues show moderate alcohol intake to be associated with increased survival in elderly people.2 Their study is an elegant example of the genre and drawn from a highly respected prospective study of risk factors for death and illness in the population of Dubbo, New South Wales. The two fields of epidemiology and alcohol studies have much to learn from each other Alternative explanations for the protective effect of moderate alcohol intake, relying on ever more tenuous confounding effects, have been discredited one by one. The apparently protective effect of moderate alcohol consumption has so far survived the use of controls for sociodemographic status,3 for the "sick quitter hypothesis"4 (ie, the suggestion that many abstainers have stopped drinking because of serious illness), for the amount of cholesterol in the diet,5 and even for the degree of social isolation.6 As evidenced in the study by Simons et al,2 the protective effect is fairly specific to cardiovascular disease and does not operate for other major causes of death in older people such as cancer. While a handful of recent studies have failed to find a protective effect for moderate drinking,7,8 these are still heavily outnumbered by those with positive findings.1 In fact, the range of different countries and cultures in which the phenomenon has been documented is also testimony to its robustness, even if different levels of consumption appear to provide the benefit in different drinking cultures.1 So, does medical science need further research on this topic? My contention is that, while the basic protective properties of moderate alcohol consumption appear to have been identified, the precision of the measurement of drinking levels and patterns in these studies needs to be sharpened if we are to have a firmer basis for advising people how to drink to avoid ill-health. The recent major systematic review commissioned by the National Health and Medical Research Council to underpin revisions to Australia's national guidelines on low risk drinking found that nearly all epidemiological studies in this area only attempt to measure one of the important dimensions of alcohol consumption: total volume of drinking, usually expressed as average intake per day.1 Despite recent evidence that pattern of drinking plays a role independent of volume,9 large-scale epidemiological studies rarely include simple items in their questionnaires tapping this dimension, such as frequency of drinking five or more drinks in one day, or maximum amount consumed on one day. Simons et al make a rare contribution to our knowledge by providing an analysis of mortality risk, based not only on average volume of alcohol across all days, but also on usual amount consumed on a drinking day. Clearly, these can be very different measures (eg, seven drinks in a day once a week versus one drink every day of the week).2 While the power of the analyses in Simons et al is limited by sample size, usual consumption of five or more drinks for men and of three or four drinks in a day for women was not associated with a significantly reduced risk of death.2 It should be noted, however, that questions regarding "usual" consumption tend to suffer from a bias towards low-consumption occasions and against less frequent occasions of high intake.10 Forthcoming World Health Organization guidelines on measurement of alcohol consumption advise that a superior method is the "graduated quantity frequency", in which respondents are asked how often they drink at each of different levels of consumption, starting with the highest (eg, "How often do you drink 20 drinks on one day?").10 The same guidelines identify another problem bedevilling attempts to convert the results of alcohol studies into precise advice for drinkers: assumptions about the alcohol content of drinks reported vary between studies and are usually not empirically based. A number of studies from different countries have attempted to document usual-serve sizes employed by random samples of drinkers and found these to vary significantly from those usually assumed by researchers.11,12 One study found that the bias created towards under-reporting of consumption was massive in one particular population subgroup: Afro-American women.13 One striking consequence of a failure to measure pattern of alcohol consumption adequately can be the false identification of special benefits from one type of alcoholic beverage over another. Wine is often reported as being most associated with benefits, but being a wine drinker as opposed to a beer and spirits drinker is a marker for many other things, including a tendency towards a more consistent pattern of daily drinking rather than occasional "bingeing".14 A well known Danish study,3 often cited as evidence for a greater benefit of wine over other drinks, measured alcohol consumption by only asking about how much people usually drank if they drank every day. Because this is a less frequent pattern for heavy drinkers of beer and spirits, many of the latter will have been falsely categorised as light or moderate drinkers, thus significantly biasing against finding protective effects for these beverages. The two fields of epidemiology and alcohol studies have much to learn from each other. If epidemiological studies of risk factors for heart disease do not improve their measurement of patterns and levels of alcohol use, it will remain very hard to give precise advice to drinkers who wish to minimise harms and maximise benefits of alcohol consumption. In reality, despite hundreds of studies into the protective effects of alcohol in relation to heart disease, research into this area has only just begun. Timothy R Stockwell Director National Centre for Research into the Prevention of Drug Abuse Curtin University of Technology, Perth, WA Single E, Ashley MJ, Bondy S, et al. Evidence regarding the level of alcohol consumption considered to be low-risk for men and women. Final report. Canberra: National Health and Medical Research Council, 2000. URL: <http://www.nhmrc.health.gov.au/advice/alc-comp.htm> (accessed 29 June 2000). Simons LA, McCallumJ, Friedlander Y, et al. Moderate alcohol intake is associated with survival in the elderly: the Dubbo Study. Med J Aust 2000; 173: 121-124. Gronbaek M, Deis A, Sorensen TIA, et al. Mortality associated with moderate intakes of wine, beer or spirits. BMJ 1995; 310: 1165-1169. Rehm J, Sempos CT. Alcohol consumption and all-cause mortality: questions about causality, confounding and methodology. Addiction 1995; 90: 493-498. Rehm J, Sempos CT. Alcohol consumption and all-cause mortality. Addiction 1995; 90: 471-480. Murray RP, Rehm J, Shaten J, Connett JE. Does social integration confound the relation between alcohol consumption and mortality in the Multiple Risk Factor Intervention Trial (MRFIT)? J Stud Alcohol 1999; 60: 740-745. Leino EV, Romelsjo A, Shoemaker C, et al. Alcohol consumption and mortality. II. Studies of male populations. Addiction 1998; 93: 205-218. Hart CL, Smith GD, Hole DJ, Hawthorne VM. Alcohol consumption and mortality from all causes, coronary heart disease, and stroke: results from a prospective cohort study of Scottish men with 21 years follow up. BMJ 1999; 318: 1725-1729. Rehm J, Ashley KJ, Room R, et al. On the emerging paradigm of drinking patterns and their social and health consequences. Addiction 1996; 91: 1615-1621. World Health Organization (Substance Abuse Department). International guidelines for monitoring alcohol consumption and harm. Geneva: WHO. In press. Stockwell T. Information provided in Australia about the size of "standard drinks". Med J Aust 1992; 156, 295. Lemmens P. The alcohol content of self-report "standard drinks". Addiction 1994; 89: 593-602. Kaskutas L, Graves K. An alternative to standard drinks as a measure of alcohol consumption. Paper presented at International Conference on the Measurement of Drinking Patterns, Alcohol Problems and the Connection; 2000 April 2-7; University of Stockholm, Sweden. In press. Doll R. One for the heart. BMJ 1997; 315: 1664-1668. Make a comment

Timothy R Stockwell

Editorial Women in rural general practice: conflict and compromise The difficulties of practising in the country and of being a woman compound each other MJA 2000; 173: 119-120 Although women now make up almost 50% of Australian medical graduates,1 they are under-represented in the rural medical workforce. In 1998, only 19% of female general practitioners (GPs) worked in rural areas, compared with 23% of male GPs, while 27% of Australia's population lived in these areas.2Recruitment and retention of women in rural general practice is increasingly important. In rural areas, GPs provide a large proportion of medical services but are in short supply. More women than men are now entering general practice -- 57% of GP registrars who enrolled in the training program of the Royal Australian College of General Practitioners (RACGP) this year were women.3 If rural communities are to have equitable access to health services, then more women must be attracted to and retained in rural practice. In addition, there is evidence that female GPs practise in a style that differs from that of male GPs: they treat different conditions, provide longer consultations and perform fewer procedures.4 The smaller number of female doctors in the rural medical workforce limits the access of rural populations to female practitioners; this is of particular concern to young women in rural areas.5 Until recently, research on factors that affect recruitment and retention of rural GPs has not focused on possible sex differences,6-10 and little has been published on this topic in peer-reviewed journals. In 1997, we undertook a pilot study of factors that affect recruitment and retention of female GPs in rural practice, particularly their social support needs.11 This study involved six focus groups of six to 10 women GPs, followed by a postal survey of 155 female GPs in rural Western Australia and New South Wales. The survey questionnaire was returned by 117; the concerns they identified are shown in the Box. In addition, a number of other reports on this topic have been funded or commissioned by the Federal Government.1,12-14 Recently, the National Rural General Practice Study (NRGPS) identified sex differences in priorities and levels of satisfaction about quality-of-life issues, such as practice and social environments.12 Rural doctors usually work longer hours than urban doctors and provide more after-hours services.13 While both sexes are affected, the impact is compounded for female GPs because of their home and family commitments -- female medical practitioners commonly assume the main responsibility for childrearing and the home, whether or not they have full-time careers.14 Role conflict is thus likely to be a greater problem for female than male rural doctors, although it would also be a problem for male doctors who assume the main responsibility for childrearing and the home. Responsibilities for care of children, as well as remoteness, also limit female rural GPs' attendance at continuing medical education events.11 Involvement in after-hours work contributes to their concerns about personal safety.13 Our 1998 study of violence against rural GPs, which included a postal survey of 314 rural GPs (including 91 women), found that female rural GPs are more apprehensive about the possibility of violence during the course of their work than their male counterparts.15 Our 1997 pilot study also found that the small number of female professionals, particularly doctors, in rural areas compounded the problem of social isolation for female rural GPs.11 Although social isolation may also be a problem for some male rural GPs (eg, solo practitioners), the NRGPS identified "more peer support" as a higher priority for female than male rural GPs.12 Female and male doctors are also attracted to different aspects of rural practice.11,12,14,16For example, female rural doctors rate the opportunity to carry out inpatient care and access to hospital as less important than male doctors.12 A study in Victoria found that women made up 30% of doctors in towns without hospitals, but only 7% in towns with hospitals.16 We asked our focus groups for strategies to address the problems they had raised. Suggestions included: More flexible childcare services and financial subsidies for childcare; Childcare for continuing medical education programs; Support and email chat groups for female rural doctors; Discussion of gender issues in medical practice during undergraduate and postgraduate training; Involvement of Divisions of General Practice in improving the availability of health services for rural doctors; Adequate workplace security at a local and regional level, especially for after-hours services; Suitable continuing medical education programs for female rural doctors that reflect their practice content; and Retraining for rural female doctors returning to the workforce. A number of groups, including Monash University and the University of Newcastle, the NSW Rural Doctors Network, the RACGP and the Australian College of Rural and Remote Medicine, are already developing ways to better support female doctors in rural areas, including some of the suggestions from our pilot study. These include the development of curricula on gender issues in undergraduate medical programs and support groups for female rural GPs. The General Practice Partnership Advisory Council (which advises the Commonwealth Department of Health and Aged Care) is currently acting on recommendations of the 1998 General Practice Strategy Review to increase recruitment and retention of women in rural general practice.17 The recent numbers of women entering the rural training stream of the RACGP training program are encouraging (47% of entrants in 19993). However, to attract and retain more women in rural practice, it needs to be structured to reflect the ways in which women practise medicine. This may involve more flexible models of practice, which accommodate the doctor's home and family commitments, and in which the type of work performed by many female doctors is valued and given practical support. Helen M Tolhurst Senior Lecturer in Rural General Practice Jane M Talbot Senior Lecturer in Rural General Practice Faculty of Medicine and Health Sciences, University of Newcastle Newcastle, NSW Louise L T Baker Program Manager for Education and Workforce NSW Central West Division of General Practice, Cowra, NSW Australian Medical Workforce Advisory Committee and Australian Institute of Health and Welfare. Female participation in the Australian medical workforce. Sydney: AMWAC, 1996: 7. Data supplied by the Australian Institute of Health and Welfare. Unpublished data from the Royal Australian College of General Practitioners. Britt H, Bhasale A, Miles DA, et al. The sex of the general practitioner: a comparison of characteristics, patients and medical conditions managed. Med Care 1996; 34: 403-415. Bryson L, Warner-Smith P. Choice of GP: who do young rural women prefer? Aust J Rural Health 1998; 6: 144-149. Kamien M. Report of the ministerial inquiry into the recruitment and retention of country doctors in Western Australia. Claremont, WA: University of Western Australia Department of Community Practice, 1987. Strasser R. Rural general practice in Victoria: the report from a study of the attitudes of Victorian general practice to country practice and training. Melbourne: Monash University, 1992. Kamien M. Staying in or leaving rural practice: 1996 outcomes of rural doctors' 1986 intentions. Med J Aust 1998; 169: 318-321. Hays RB, Veitch PC, Cheers B, Crossland L. Why doctors leave rural practice. Aust J Rural Health 1997; 5: 198-203. Kamien M, Buttfield IH. Some solutions to the shortage of general practitioners in rural Australia. Part 4. Professional, social and economic satisfaction. Med J Aust 1990; 153: 168-171. Tolhurst H, Bell P, Baker L, et al. Educational and support needs of female rural general practitioners. Bathurst: School of Nursing and Health Administration, Charles Sturt University, 1997. Strasser R, Kamien M, Hays R, Carson D. National rural general practice study -- quality of life. Melbourne: Monash University Centre for Rural Health, 1997. Australian Medical Workforce Advisory Committee. The medical workforce in rural and remote Australia. Sydney: AMWAC, 1996: 8. Australian Medical Workforce Advisory Committee. Influences on participation in the Australian medical workforce. Sydney: AMWAC, 1998: 4. Tolhurst H, Talbot J, Baker L, et al. "An inkling of mayhem": violence against rural general practitioners. Report to the General Practice Evaluation Program, 1999. Campbell D, Strasser R, Kirkbright S. Survey of Victorian rural general practitioners in towns without a hospital. Traralgon (Vic): Monash University Centre for Rural Health, 1996. General practice. Changing the future through partnerships. Report of the General Practice Strategy Review Group. Canberra: Commonwealth Department of Health and Family Services, 1998. Make a comment Concerns of female rural general practitioners Professional experience Pressure to work longer hours than they wish (often full- rather than part-time) Large demand for their involvement in counselling services and women's health services so that other types of work are excluded Under-remuneration for their work, especially long consultations for mental health problems Perception that their work is undervalued by their colleaguesSocial support Limited availability of flexible childcare for after-hours and on-call work Lack of support from a peer groupRole conflict Conflict caused by competing professional and personal obligations Feelings of guilt because of inability to fulfil demands of competing role expectationsContinuing medical education Difficulty attending continuing medical education events because of personal commitments and need for childcarePersonal health and safety issues Concerns about personal safety, particularly while providing after-hours services Difficulty accessing health services for themselves, particularly gynaecological services. 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Helen M Tolhurst · Jane M Talbot

Editorial Evaluating policy and practice: what are the effects of early hospital discharge after childbirth? Large, specific, randomised trials are the only way to answer this question MJA 2000; 172: 524-525 Two years ago the Journal published an article which described early hospital discharge after birth as a major risk factor for postnatal depression.1 There was also a strongly worded editorial supporting that conclusion.2 In this issue the message is reversed, with the finding by Thompson and colleagues that there is no evidence of increased risk.3 This is no trivial disagreement. A quarter of a million women give birth in Australia each year, virtually all of them spending less time in hospital than their mothers did, with close to 40% having an "early discharge" by the definition used in both articles (within 72 hours of birth).4Depression is a distressing and disabling condition for those directly affected, and particularly so in women with a new baby, who have just taken on a 24-hour-a-day, seven-day-a-week job. The effects of maternal depression may flow on to other vulnerable family members. Doctors and midwives, hospitals, policymakers and the general public need to know whether early discharge is safe or not. One problem in answering this question is the paucity of evidence from randomised trials on length of hospital stay after childbirth. Not only are there relatively few trials, but those that have been published have rarely measured maternal health outcomes such as depression, breastfeeding duration, confidence, or breastfeeding problems. The limited evidence from trials shows either no difference in depression between women discharged early and late, or a lower proportion of women becoming depressed after early discharge.5,6 The article by Thompson and colleagues3 is the third Australian population-based study which has shown no relationship between early discharge and depression after birth.7-10 All three of these studies were large enough to detect a twofold increase in the odds of becoming depressed after early discharge, as was found in the Nepean hospital-based study published in the Journal two years ago.1 All three, and the Nepean study, used the Edinburgh Postnatal Depression Scale (EPDS) with the same cut point of a score of more than 12 for probable depression, though the Victorian studies measured the point prevalence with a single score of more than 12 at six or eight months after birth, the ACT group measured the period prevalence from eight through 16 and 24 weeks, and the Nepean group required two or more scores over 12, from six, through 12, 18 and 24 weeks, confirmed by a structured clinical interview to measure the period prevalence of major depression. The difference in findings between the Nepean study and the other three studies is surprising. Thompson and colleagues suggest that an important contributing factor might be the routine provision of a postnatal visit from a midwife and more practical help at home in the ACT than at Nepean.3 However, this was not the case in the 1993/94 Victorian Survey of Recent Mothers, which found that only 66% of women who went home within 48 hours of birth, and only 27% of those going home on the third or fourth day, had a home visit from a midwife8 -- findings much closer to those of the Nepean study. It is also unlikely that temporal factors explain the discrepancy in findings, as the Victorian survey took place at a very similar time to the Nepean study. Public knowledge and expectations about postnatal stay would have been similar in both study populations. In interpreting non-experimental descriptive and observational studies, the key problem is selection bias -- in what ways do women who leave hospital early differ from those who stay longer, and are these differences in themselves factors which have a bearing on women's chances of becoming depressed in the following months? Predictable factors associated with shorter postnatal stays include maternal age less than 25 years, multiparity, unassisted birth, birth at term, low medical risk, birth centre care, and not having private health insurance. Psychological predictors of depression were measured in both the ACT and Nepean studies; they were not significantly associated with length of stay. The six vignettes in the Box describe some groups of women who will be over-represented (A, C, D, E) and under-represented (B, F) among new mothers going home early, despite having uncomplicated vaginal births at term. Young women are often over-represented in group D8 and women from diverse overseas backgrounds in group E.11 As all these women "chose" their length of stay, these vignettes draw attention to problems with the notion of "choice" as a key determinant. Some choices are constrained by factors outside the woman's control, especially social isolation and absence of a partner or other social support, which are common associations of depression at this life stage. We also know that women are not necessarily free to choose their length of stay, as almost a quarter of those discharged early in both the ACT study,3 and in Victoria,8,9 thought their stay had been too short. The vignettes also remind us that the relative proportions of women from groups A, C and E in study populations could easily contribute to, or even explain, the differing associations between length of stay and subsequent depression reported from different studies. Given the inevitability of such selection biases, which are impossible to adjust for, if we really want to know whether shortening postnatal stay is safe and cost-effective, or whether domiciliary midwifery or other postnatal support improves outcomes for mothers and babies, there is no alternative but to test these policies in randomised trials. Judith M Lumley Director Centre for the Study of Mothers' and Children's Health La Trobe University, Melbourne, VIC Hickey AR, Boyce PM, Ellwood D, Morris-Yates AD. Early discharge and risk of postnatal depression. Med J Aust 1997; 167: 244-247. Buist A. Counting the costs of early discharge after childbirth. Med J Aust 1997; 167: 236-237. Thompson JF, Roberts CL, Currie MJ, Ellwood DA. Early discharge and postnatal depression: a prospective cohort study. Med J Aust 2000; 172: 532-536. Day P, Sullivan EA, Ford J, Lancaster P. Australia's Mothers and Babies 1997. (Perinatal Statistical Series No. 9). Sydney: AIHW National Perinatal Statistics Unit, 1997. (AIHW Cat. No. PER 12.) Waldenström U. Early and late discharge after hospital birth: fatigue and emotional reactions in the postpartum period. J Psychosom Obstet Gynaecol 1988; 8: 127-135. Carty EM, Bradley CF. A randomized, controlled evaluation of early postpartum hospital discharge. Birth 1990; 17: 199-204. Small R, Lumley J, Brown S. To stay or not to stay: are fears about shorter lengths of stay justified? Midwifery 1992; 8: 170-177. Brown S, Lumley J, Small R. Reasons to stay, reasons to go. Victorian women talk about early discharge. Melbourne: Centre for the Study of Mothers' and Children's Health, 1995: 27-54. Brown S, Lumley J. Reasons to stay, reasons to go: results of an Australian population-based survey. Birth 1997; 24: 148-158. Brown S, Lumley J, Small R. Early obstetric discharge: does it make a difference to health outcomes? Paediatr Perinat Epidemiol 1998; 12: 49-71. Yelland J, Small R, Lumley J, et al. Support, sensitivity, satisfaction: Filipino, Turkish and Vietnamese women's experiences of postnatal hospital stay. Midwifery 1998; 14: 144-154. Make a comment Examples of scenarios in which women select different lengths of stay Group Description Length of stay Maternal health outcomes A Healthy mother, healthy baby, good or excellent family support Chooses to go home at 24-48 hours to be with her family in a restful atmosphere and establish breastfeeding Likely to be good B Healthy mother, healthy baby, good or excellent family support Chooses to stay in hospital for 5 or more days to establish breastfeeding, recover from the birth and have a good rest Likely to be good C Mother with major responsibilities at home and little or no family support Goes home as soon as she can ? D Mother who dislikes life in hospital Leaves as soon as she can, even despite strong advice to stay ? E Mother who does not find the hospital able to provide her with enough support and is unable to get enough rest there Leaves much earlier than she had planned to Possibly poor F Mother who has had a long, exhausting labour; baby who is difficult to feed; slow establishment of breastfeeding; mother loses self-confidence Stays much longer than she had planned to Possibly poor Back to text

Judith M Lumley

Editorial Cancer in the family: risks and management A recent NHMRC publication addresses the clinical implications of cancer genetics for Australian families MJA 2000; 172: 529-530 A family history of cancer is widely recognised as an important risk factor for common cancers, with 5%-10% of cancers considered attributable to genetic predisposition. A recent National Health and Medical Research Council (NHMRC) publication for health professionals, Familial aspects of cancer: a guide to clinical practice,1 addresses the clinical implications of cancer genetics. Why do we need such a guide, and what does it cover? Cancer genetics Knowledge of the genetic basis of cancer has increased dramatically in the past decade. It is now clear that cancers evolve in Darwinian fashion, exploiting mutations in genes that regulate cellular growth, death and differentiation. The cumulative acquisition of defects in a number of these genes facilitates the progressive selection of cells towards a highly malignant and uncontrolled state of cellular proliferation and immortality. In the majority of cancers, these mutations are acquired in particular cells over a lifetime (somatic mutations). There are, however, families displaying clear inherited predisposition to certain common cancers, including breast, ovarian, colorectal and prostate cancer and melanoma. The affected members of these families carry an inherited (germline) mutation in one of their "cellular fitness" genes. Germline mutations affect all body cells, but give certain tissues a genetic head start down the cascade of genetic errors that results in cancer. Genes prone to such inherited abnormalities are called "cancer susceptibility" genes. The individuals carrying mutations in these genes often carry a very high lifetime chance (> 50%) of developing cancer. Implications for clinical practice The improved ability to detect individuals at high risk of cancer through analysis of family history and/or genetic testing has fortunately been accompanied by major advances in screening, surveillance and prevention. The clinical usefulness of such advances is exemplified in the management of familial adenomatous polyposis (FAP), a condition caused by a dominantly inherited mutation in the adenomatous polyposis coli (APC) gene. Individuals with FAP develop hundreds of adenomatous polyps, of which one or more may, if untreated, become malignant, often at an early age. Until recently, all at-risk individuals required regular screening sigmoidoscopy from the early teenage years. Now, after being genetically tested, only those family members found to carry the mutation need to undergo intensive cancer screening and eventually prophylactic colectomy.2 Similarly, genetic testing for hereditary non-polyposis colorectal cancer has proved to be acceptable to families, and may reduce the cost of unnecessary screening colonoscopy in those family members found not to carry a mutation.3Familial cancer clinics have now been set up in response to the growing public and professional awareness of family history as a risk factor for cancer. These clinics provide pedigree analysis, risk assessment and advice to those at high risk of cancer, and may also carry out genetic testing (if appropriate) in association with genetic counselling. The NHMRC document1 stratifies risk categories for people with a family history of diseases such as breast and colorectal cancer. It identifies those who may benefit from referral to familial cancer clinics and the role of general practitioners and specialists in managing high risk families. In the context of a detailed ethical discussion, an attempt is made to designate those who may benefit from genetic testing (see Box). Why national guidelines? A coordinated national policy on cancer genetics has arisen in response to a number of factors: In recent years there has been heightened public awareness of the problem and increased demand for access to familial cancer services from those at perceived risk of cancer. (At the Familial Cancer Service at Westmead Hospital, for example, referrals, carefully screened for adherence to eligibility criteria, increased from 120 new families in 1996 to almost 300 in 1999); Health authorities have understandable concerns about the potential for proliferation of unregulated, unevaluated genetic testing facilities for cancer, as has occurred in the United States, and the need for public education and guidance in this area; Scientists face considerable challenges in assuring quality for complex, new and constantly evolving diagnostic tests, overcoming difficulties in resource management, and ensuring the timely and appropriate translation of relevant technologies from a research to a diagnostic environment. While similar documents have been produced by other international groups,4-7 these issues need to be addressed in a manner relevant to the Australian population. Guidelines based on US data for breast cancer, for example, may be quite inappropriate for Australia, and specific mutations in melanoma susceptibility genes may be more highly penetrant under the influence of Australian sunlight.8,9 In 1995 the Australian Cancer Network (ACN), in joint sponsorship with the NHMRC National Breast Cancer Centre (NBCC) and the Human Genetics Society of Australasia, convened the ACN Cancer Genetics Working Party to draft national guidelines for clinical practice. The current guidelines are the culmination of an extensive consultation and collaboration process. The future In such a rapidly changing field, future refinements of the guidelines will depend on the availability of high quality Australian data from national epidemiological studies. These studies will provide information on the frequency and penetrance of mutations in cancer susceptibility genes in the Australian population and the effect of local environmental factors on those mutations. A welcome spin-off of the endeavour to compile this guide has been the unification of diverse research interests throughout Australia in well organised, comprehensive consortia investigating the cancer genetics of breast cancer, melanoma and colorectal cancer.* In parallel with these exciting developments in research, we need to improve the accessibility of such information to general practitioners.10 The NBCC and the ACN have already moved toward the provision of more succinct information for GPs with their publications Current best advice about familial aspects of breast cancer11 (under current revision to incorporate familial ovarian cancer) and Advice about familial aspects of bowel cancer: a guide for general practitioners (ACN, in preparation). Consumer information has been developed to accompany these documents. The National Cancer Control Institute is also fostering a national approach to education and data management for families with a genetic predisposition to malignancy. The energy, goodwill and collaborative spirit associated with the preparation of these new guidelines provide a strong basis for the ongoing care of cancer families in Australia. Judy Kirk Senior Staff Specialist Familial Cancer Service and Westmead Institute for Cancer Research Westmead Hospital, Westmead, NSW Richard Kefford Professor of Medicine, Westmead Institute for Cancer Research Westmead Hospital, Westmead, NSW *Breast cancer: The Kathleen Cuningham Consortium for Research on Familial Breast Cancer (kConFab) research project (see <http://www.pmci.unimelb. edu.au/kconfab>), led by Joseph Sambrook, and the Australian Breast Cancer Family Study, led by John Hopper (j.hopperATgpph.unimelb.edu.au). Colorectal cancer: The Australasian Colorectal Cancer Study, led by Jeremy Jass (j.jassATmailbox.uq.edu.au). Melanoma: The Australian Melanoma Family Study, led by Graham Mann (gmannATmail.usyd.edu.au) National Health and Medical Research Council. Familial aspects of cancer: a guide to clinical practice. Endorsed Nov 1999. Available at: <http://www.nhmrc.health.gov.au/publicat/cp-home.htm>. Accessed 2 May 2000. (Catalogue No. 993839X.) Gardner M, St John J. Gene testing and genetic counselling in familial polyposis. Med J Aust 1995; 162: 457. Stanley AJ, Gaff CL, Attomaki AK, et al. Value of predictive genetic testing in management of hereditary non-polyposis colorectal cancer (HNPCC). Med J Aust 2000; 172: 313-316. Burke W, Daly M, Garber J, et al. Recommendations for follow-up care of individuals with an inherited predisposition to cancer. II. BRCA1 and BRCA2. Cancer Genetics Studies Consortium. JAMA 1997; 277: 997-1003. Burke W, Petersen G, Lynch P, et al. Recommendations for follow-up care of individuals with an inherited predisposition to cancer. I. Hereditary nonpolyposis colon cancer. Cancer Genetics Studies Consortium. JAMA 1997; 277: 915-919. Eisinger F, Alby N, Bremond A, et al. Recommendations for medical management of hereditary breast and ovarian cancer: the French National Ad Hoc Committee. Ann Oncol 1998; 9: 939-950. Kefford RF, Newton Bishop JA, Bergman W, Tucker MA. Counseling and DNA testing for individuals perceived to be genetically predisposed to melanoma: a consensus statement of the Melanoma Genetics Consortium. J Clin Oncol 1999; 17: 3245-3251. Cannon-Albright LA, Meyer LJ, Goldgar DE, et al. Penetrance and expressivity of the chromosome 9p melanoma susceptibility locus (MLM). Cancer Res 1994; 54: 6041-6044. Bishop JA, Wachsmuth RC, Harland M, et al. Genotype/phenotype and penetrance studies in melanoma families with germline CDKN2A mutations. J Invest Dermatol 2000; 114: 28-33. Gupta L, Ward JE, Hayward RS. Clinical practice guidelines in general practice: a national survey of recall, attitudes and impact. Med J Aust 1997; 166: 69-72. National Breast Cancer Centre. Current best advice about familial aspects of breast cancer. Sydney: NBCC, 1997. Available at: <http://www.nbcc.org.au/ pages/info/resource/nbccpubs/advice.htm>. Accessed 2 May 2000. Make a comment Familial aspects of cancer: a guide to clinical practice New NHMRC guidelines1 address the following key issues: Importance of an accurate, extended family history in assessing cancer risk Identification of rare families with a genetic predisposition to one of the common malignancies (eg, breast, ovarian, colorectal or prostate cancer, or melanoma) Role of familial cancer clinics in the management of families at risk Evolving role of genetic testing in risk assessment Requirement for genetic counselling in association with genetic testing Ethical issues relating to genetic counselling and testing for cancer predisposition Management, screening and cancer prevention for individuals found to be at high risk or potentially high risk of developing cancer Continued need for national collaborative research in this field Back to text

Judy Kirk · Richard Kefford

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

Sandra J Eades

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

David L Copolov · Bruce S Singh

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

Andrew R Lloyd · Ian B Hickie · Robert H Loblay

Editorial Migraine treatment and mistreatment: primum non nocere Triptans can provide wonderful relief from migraine, but must not be overused as "pseudo-preventives" MJA 2000; 172: 412-413 If the 1990s was the decade of the brain for neuroscientists, then it was the decade of new treatments and renewed hope for sufferers of neurological diseases. Neurology, long the bastion of diagnosis, has become the specialty of the physician that we would all like to be -- one who is able to take a careful history and conduct a meticulous physical examination leading to a diagnosis and management plan. For headache patients, and perhaps neurological patients in general, it is the latter development in neurology, the move to more effective management of the conditions, that has been truly marvellous. We have started to identify the genes involved in causing the problem,1 and by so doing have begun to understand the episodic nature of the attacks in terms of ion-channel dysfunction. We have finally begun to image the primary headaches with functional/anatomical methods that have pointed to the brainstem, in migraine,2 and the posterior hypothalamus, in cluster headache,3 as likely candidates for the basic pathophysiological process. What is misuse and when is good medicine slipping into overtreatment? Best of all, from a clinical perspective, neurotherapeutics leapt ahead. The advent of the triptans (serotonin agonists) was to migraine and cluster headache almost the equivalent of penicillin to bacterial infection! It seems almost outrageous to liken the development of triptans to the discovery of penicillin, but this analogy has been used by at least three of my patients, themselves general practitioners who suffer migraines, to describe the change in their lives. Migraine never threatens life, but, as Professor Jim Lance, the Australian doyen of migraine, taught me, it simply "makes it hell". Disability is the key word to understanding the impact of migraine: inability to work effectively, care for dependants, enjoy recreation or participate in the myriad responsibilities that the non-migraineur takes for granted. What have we learnt from the developments of the past decade and what should we expect for the next decade in terms of therapeutics? The first triptan to be released was sumatriptan, developed in considerable part through the pioneering work of Lance and Anthony at Prince Henry Hospital in Sydney.4 This compound burst on to the clinical scene in the late 1980s,5 proving to be highly efficacious in clinical studies.6 Its development was marked by careful clinical trials methodology and spurred the widespread adoption of the International Headache Society Diagnostic Criteria7 for use in clinical studies. These criteria have been a boon for the clinical scientist and, if more widely used and adapted for primary care, could be useful for both doctors and patients more generally. As it became obvious that sumatriptan heralded a major advance in therapy, other researchers became interested in the field and triptan sons and cousins were soon in gestation. Naratriptan and zolmitriptan are now available in Australia and in Europe we also have rizatriptan; in late development or close to registration are almotriptan, eletriptan and frovatriptan. Do we have enough? For patients who respond to the triptans already available, obviously yes; for those who still suffer, confined like children to a room without a view for no sin other than their parents' genetic gifts, obviously not.8 Triptans are not perfect: a third of patients taking them have recurrence of headache within 24 hours; for some they do not work at all; and for those with significant risk factors for cardiovascular disease they are inappropriate. It has been at once heartening to find patients who show no improvement with one triptan yet respond to another, and disheartening that we have not been able to dissect what it is about the compounds9 that makes such profound differences in their clinical performance in individuals. In medicine almost every sunny day has a cloud on the horizon, and headache therapeutics is no exception. Ten years after the release of sumatriptan for clinical use, we have begun to appreciate the problems of mistreatment with triptans, reinforcing previous observations on mistreatment with other acute attack medications such as ergotamine or compound analgesics. In this context, "mistreatment" implies the inappropriate use of acute attack therapies by patients, either acting independently or under their doctors' instructions. This is referred to in the literature variously as "abuse", "overuse" or "misuse". Patients seldom misuse medications for any gain other than to attempt to function normally, to get to work or to look after their families. Given that acute medicines were designed for relatively infrequent use, and indeed that the triptans were studied explicitly in people having migraine frequencies of six or less per month, I believe that frequent use is a misuse of the medicine and a mistreatment of migraine. Reports of triptan misuse10,11 come as no surprise given the problems with ergotamine over the years,12 and this has sparked renewed interest in the subject of analgesic misuse.13 While the extent to which analgesics, particularly compound analgesics such as those containing codeine, can induce headache is not yet established, it seems clinically plausible that they block the frequency-reducing benefits of headache preventive therapy. What is misuse and when is good medicine slipping into overtreatment? With regard to ergotamine, a recent European consensus statement recommends, with some clearly stated exceptions, that the maximum usage should be 4-6 times a month.14 The tool with which to define this problem is the diary: a simple record of the number of days on which headache is experienced, and which prescription or over-the-counter medications are taken, will soon reveal whether excess medication is being consumed and whether management, including neurological referral, is appropriate. What are the prospects for the future? An understanding of migraine neurobiology will build on what has been done; more genes will be identified; functional imaging will better define and elaborate on the brain areas responsible for the disorder; and experimental laboratory work will put these observations under the modern anatomical and physiological microscope, returning more questions to the clinical scientists. In terms of treatment we need to do both more and less. We need to treat more patients who could benefit from medication but are not receiving adequate treatment. We need to develop new preventives to treat the sufferer of frequent headache whose disability load is truly dreadful, while at the same time guarding against using medications designed for intermittent acute use (triptans, ergotamine and analgesics) as pseudo-preventives -- primum non nocere! Lastly, we must spread the message that migraine is a genetically determined problem which is reasonably well characterised neurobiologically. Migraine involves dysfunction of brainstem and diencephalic areas normally involved in controlling pain and other sensory information and results in activation of very specific trigeminovascular pain pathways which are well defined and understood. The future is bright -- a good history, meticulous physical examination, clear diagnosis and explanation, and management directed at restoring ability to function is exactly what we can offer and, I think, exactly what patients want. Peter J Goadsby Professor of Clinical Neurology, Institute of Neurology University Department of Clinical Neurology National Hospital for Neurology and Neurosurgery Queen Square, London, UK Disclosure statement: In recent times the author has advised, collaborated with, and spoken at meetings organised by various companies, including Allergan, Almiral-Prodesfarma, AstraZeneca, BristolMyersSquibb, GlaxoWellcome, MSD, Pfizer, Pharmacia-Upjohn, Sandoz, and SmithKlineBeecham, which manufacture compounds referred to in this article or have an interest in developing compounds for the treatment of various primary headache syndromes. Ophoff RA, Terwindt GM, Vergouwe MN, et al. Familial hemiplegic migraine and episodic ataxia type-2 are caused by mutations in the Ca2+ channel gene CACNLA4. Cell 1996; 87: 543-552. Weiller C, May A, Limmroth V, et al. Brain stem activation in spontaneous human migraine attacks. Nat Med 1995; 1: 658-660. May A, Bahra A, Buchel C, et al. Hypothalamic activation in cluster headache attacks. Lancet 1998; 351: 275-278. Anthony M, Hinterberger H, Lance JW. Plasma serotonin in migraine and stress. Arch Neurol 1967; 16: 544-552. Doenicke A, Brand J, Perrin VL. Possible benefit of GR43175, a novel 5-HT1-like receptor agonist, for the acute treatment of severe migraine. Lancet 1988; 1: 1309-1311. Ferrari MD. The Subcutaneous Sumatriptan International Study Group. Treatment of migraine attacks with sumatriptan. N Engl J Med 1991; 325: 316-321. Headache Classification Committee of the International Headache Society. Classification and diagnostic criteria for headache disorders, cranial neuralgias and facial pain. Cephalalgia 1988; 8(Suppl 7): 1-96. Goadsby PJ. A triptan too far. J Neurol Neurosurg Psychiatry 1998; 64: 143-147. Goadsby PJ. 5-HT1B/1D agonists in migraine: comparative pharmacology and its therapeutic implications. CNS Drugs 1998; 10: 271-286. Kaube H, May A, Diener HC, Pfaffenrath V. Sumatriptan misuse in daily chronic headache. BMJ 1994; 308: 1573-1574. Limmroth V, Kazarawa S, Fritsche G, Diener HC. Headache after frequent use of new serotonin agonists zolmitriptan and naratriptan. Lancet 1999; 353: 378. Friedman AP, Brazil P. Ergotamine tolerance in patients with migraine. J Am Med Assoc 1955; 157: 881-884. Diener HC. A personal view of the classification and definition of drug dependence headache. Cephalalgia 1993; 13: 68-71. Tfelt-Hansen P, Saxena PR, Dahlof C, et al. Ergotamine in the acute treatment of migraine - a review and European consensus. Brain 2000; 123: 9-18. Make a comment

Peter J Goadsby

Editorial Government policymaking, private health insurance and hospital-efficiency issues Will government subsidies provide a long term solution to declining rates of health insurance coverage? MJA 2000; 172: 413-414 Increased support for private health insurance by subsidising health fund contributions has been featured in all the policy proposals developed by the Liberal/National Coalition parties in Opposition between 1986 and 1993.1 Thus, the current focus on private health insurance by the Howard Government represents a continuation of elements of the Coalition parties' previous policies. Senator Graham Richardson, after he became Minister for Health in the Keating Government in 1993, focused considerable attention on the same issue, but had a different approach. The legislation that Labor introduced in 1995 was designed to facilitate the development of contracts between the health funds, private hospitals and doctors, based, in part, on the use of casemix data. The main reason for Government and Opposition preoccupation with private health insurance has been the alleged threat to the viability of private hospitals posed by the decline in the number of people with private health insurance. It was claimed that, with decreased use of private hospitals, pressures on public hospitals would increase. However, at the time that these initiatives were foreshadowed or implemented by the Keating or Howard governments, there was no evidence to support the proposition that the decline in private insurance coverage posed a threat to either the public or private health sectors. In fact, the decline in health insurance coverage was associated with increased use of the private sector. Between 1993-94 and 1997-98, the proportion of patient-days in private hospitals increased from 24.6% to 26.9% of all acute hospital patient-days.2 The proportion of the population covered by private health insurance declined from 39.4% in June 1993 to 30.1% in December 1998.3 The principal reason for this apparent paradox is that the people who have dropped out of private health insurance have been the younger contributors, who, with the exception of women in their childbearing years, are not heavy users of hospital services.4 There may have been increased pressures on public hospitals in this period, but these can hardly have come from a declining private hospital sector. But why was the evidence on increased use of private hospitals ignored by health policymakers? The interests of influential private sector groups, including the private hospitals, the health funds and some doctors, would be fostered by a policy of supporting private health insurance. Moreover, State governments, in their never-ending quest for additional Commonwealth funding for public hospitals, also had an interest in subscribing to the same doctrine of the threat posed to these hospitals by the decline in private health insurance. The introduction in 1999 by the Howard Government of the 30% rebate on private health insurance contributions was partly a response to these political pressures. However, there is an equity issue arising out of the payment by health fund members of substantial premiums, and of a proportion of their taxation to support public hospitals that they may never use. Discontent among many electors, possibly concentrated in marginal electorates, is the politically relevant outcome of this perceived inequity. The equity issue is complicated by the positive association between private health insurance and income. It can also be argued that subsidising health fund contributions from government revenue means that many people on low incomes are being required to meet part of the costs of more affluent people using private hospitals. As with most arguments about equity, different value judgements will determine which aspect is perceived as being more important. Efficiency issues If private hospitals were more efficient than public hospitals there might be a case for subsidising private health insurance to facilitate a shift of resources from the public to the private sector, or to maintain the existing balance. The article by Duckett and Jackson in this issue of the Journal demonstrates, subject to the limitations of the data and the methods, that, in 1996-97, private hospitals were apparently less efficient than their public counterparts.5Duckett and Jackson use national casemix cost data to quantify the relative technical efficiency in the two types of hospitals, and make careful adjustments for differences in cost structures. They argue that insulating public hospitals from any effects of the decline in private health insurance could have been achieved by making further Commonwealth payments to public hospitals. Duckett and Jackson recognise in passing the political arguments for the subsidy, although not the contentious equity argument. It is of considerable importance for future policymaking that the unadjusted cost relativity between public and private hospitals has changed substantially since the original national casemix costing study was conducted using 1991-92 data. The average cost per separation was $2405 in public hospitals and $1630 in private hospitals.6 One study concluded that private hospitals were probably more efficient than public hospitals. In other words, allowing for casemix and cost structure adjustments was highly unlikely to reduce the cost ratio of 1.48 to less than 1.0.7 Duckett and Jackson's work indicates that, for 1996-97 data, the unadjusted cost ratio of 1.19 ($2319/$1942) is reduced to 1.11 by casemix adjustment, and to 0.91 when the different cost structures are taken into account.8,9 The combination of budget cuts, casemix funding, and benchmarking in the public sector has led, it seems, to considerable efficiency gains for which, to that time, there was no counterpart among private hospitals. What does the future hold? The very modest increase in hospital insurance coverage after the first year of the new policy -- from 30.1% to 31.2% -- casts doubt on whether government subsidies provide any long term solution to the perceived problem. The fundamental contradiction in the current healthcare arrangements in Australia is the provision of free hospitalisation in public institutions, co-existing with what is essentially full cost recovery in the private sector. What is perhaps most surprising is that the decline in private health insurance coverage has not taken place more rapidly. Private hospitals have been successful in competing with public hospitals for patients partly because, as Duckett and Jackson point out, they provide a method of avoiding the queues in public hospitals for a range of non-emergency services. If the decline in private health insurance coverage continues, the pressure to erode one of the cornerstones of Medicare -- the provision of free services in public hospitals without a means test -- may become overwhelming for a Coalition Government if it succeeds in winning a third term. It is this aspect of Medicare that has the most potent influence in undermining the demand for private health insurance for a large majority of the population. A more evidence-based approach to private health insurance policymaking might have been derived from the results of a comprehensive enquiry into all aspects of the healthcare system as recommended by the Industry Commission.10 George R Palmer Emeritus Professor of Health Services Management Faculty of Medicine, University of New South Wales, Sydney, NSW Palmer GR, Short SD. Health care and public policy: an Australian analysis. 3rd ed. Melbourne: Macmillan Education, 2000: 76-78. Australian Institute of Health and Welfare. Australian hospital statistics, 1997-98. Canberra: AGPS, 1999. Private Health Insurance Administrative Council. Industry statistics. Coverage of hospital insurance tables. Year ended 30 June. <www. phiac.org.au> (accessed 7 April 2000). Industry Commission. Private Health Insurance. Canberra: AGPS, 28 February, 1997. (Report No. 57.) Duckett SJ, Jackson T. The new health insurance rebate: an inefficient way of assisting public hospitals. Med J Aust 2000; 172: 439-442. Commonwealth Department of Human Services and Health. National Costing Study. National cost weights project: Final report. Canberra: DHSH, November, 1994. Palmer GR, Hindle D, Lapsley H. Health policy and technical issues in the use of casemix to demonstrate potential savings in private hospitals. Healthcover 1995; 5: 7-11. Commonwealth Department of Health and Family Services. Report on the national hospital cost data collection 1996-97. Canberra: DHFS, 1998. Australian Institute of Health and Welfare. Australian hospital statistics, 1996-97. Canberra: AGPS, 1998. Palmer GR. Evidence-based health policy-making, hospital funding and health insurance. Med J Aust 2000; 172: 130-133. Make a comment

George R Palmer

Editorial Clinical pathways and fractured neck of femur The generalisability and cost effectiveness of clinical pathways need further research MJA 2000; 172: 415-416 The proportion of Australians aged 65 and over is projected to continue increasing for the next 50 years.1 Fractures of the neck of femur are common in this age group and are associated with increased risk of morbidity and mortality, long-term institutionalisation and costly management. Their impact on a public healthcare system funded by an ever-diminishing number of tax-paying workers is a major concern. Increasing attention is being given to improving management of these fractures and rehabilitation of patients.2-5 Morbidity and mortality rates have been reduced through increased surveillance for and treatment of complications, such as wound and other infections, pressure sores and deep venous thrombosis. Early involvement of multidisciplinary teams in patient rehabilitation and early mobilisation have been used in large hospitals to reduce delays and optimise treatment for previously ambulatory patients. These programs result in fewer perioperative complications and enable patients to return home and resume functional independence earlier, reducing the number who need long term residential aged care.2,3 However, these improvements come at a cost -- direct costs, such as salaries of additional staff for multidisciplinary teams,6 and indirect costs, such as when patients are sent home early, and postdischarge care is assumed by family and community.7 Pressure on hospital administrations to contain or reduce costs may result in outcomes of little, if any, benefit to the patient, but which may have a substantial impact on others living with or looking after the patient. Little is known about the nature and extent of this potential impact. Implementation of these efforts needs to be both preceded and accompanied by careful evaluation and assessment. Among strategies that attempt to achieve savings is the development and use of clinical pathways, as outlined by Choong and colleagues8 in this issue of the Journal. A clinical pathway is a type of management plan formulated for a specified condition, which defines expected daily activities, identifies lines of responsibility for those activities, and indicates goals for the patient to achieve along the way.9 These pathways are based on a multidisciplinary perspective and collaboration. Introduction of a clinical pathway requires considerable commitment and investment of time from many departments within the hospital, as well as substantial changes to the medical record. It also raises concerns about the medicolegal implications of non-compliance with the pathway in the event of an adverse outcome. All these issues require further study.10,11 Clinical pathways have been successfully implemented for a variety of conditions and settings, overseas and in Australia. However, patient groups have been relatively homogeneous, such as those having elective hip, knee or other surgery. In contrast, hip-fracture patients are very heterogeneous, ranging from the fit, active (albeit osteoporotic) "young" elderly, to the very frail, bedridden 90-years-plus residents of nursing homes. A clinical pathway developed from evidence-based practices may be the most efficient way to restore the mobility of elderly patients and ensure their discharge back to their pre-admission residence. However, because of the high level of comorbidities in these patients, the potential for variation from the pathway is high.2 Choong and colleagues describe a controlled trial of a clinical pathway for patients with proximal femoral fracture in a major teaching hospital.8 Modest benefits were found for the hospital budget, and clinical outcomes for patients on the pathway appeared no worse than for patients who received standard hospital treatment. Use of the pathway seemed to have little real effect on shortening stay in comparison with the control group; the major difference in stay was found for patients who required review by the Aged Care Assessment Team and were therefore likely to be frailer. The frail elderly have not usually been seen as a target group for clinical pathways, but future studies of this group may show that they benefit from this approach without adverse outcomes on complications or discharge destinations. This study illustrates the problems of assessing the usefulness of clinical pathways, which should be addressed in the design of future studies. The clinical relevance of short reductions in length of hospital stay (1.4 days in this instance) is open to question. Economic aspects need to be documented as part of study design to allow analysis of cost effectiveness. The real effectiveness of the pathway for the community, rather than just the hospital, remains unclear, and future studies need to include strategies to assess that effect. The overall economic benefit to the community should take into account the increased use of community services, use of interim or permanent residential care, and extra costs and stress for families who provide a large proportion of the care after discharge from hospital.3 Clinical pathways have developed primarily in large metropolitan hospitals with resources to research and implement the process, while proximal femoral fractures are treated in a wide range of hospitals with varying levels of funding and allied health support. These pathways may have the potential to improve clinical outcomes and costs in hospitals where the number of femoral fracture patients is too small to warrant an orthogeriatric unit or where there is no access to a designated rehabilitation unit. Ultimately, the generalisability of this approach will become evident as more research in this area is reported. Recent reports in the Journal highlight the difficulties in transforming evidence into practice.12,13 Despite these difficulties, compliance with evidence-based best practice in the management of fractured neck of femur, together with preventive measures such as early management of osteoporosis and falls prevention programs, should help lessen the current and future economic and personal burden of hip fracture in Australia. Cheryl E Swanson Research Scientist, Division of Orthopaedic Surgery Catherine E Yelland Director, Geriatric Assessment and Rehabilitation Unit Gregory A Day Senior Lecturer, Division of Orthopaedic Surgery University of Queensland and Royal Brisbane Hospital Brisbane, QLD Cooper C, Campion G, Melton IJ III. Hip fractures in the elderly: a world-wide projection. Osteoporosis Int 1992; 2: 285-289. March LM, Chamberlain AC, Cameron ID, et al. How best to fix a broken hip. Med J Aust 1999; 170: 489-494. Swanson CE, Day GA, Yelland CE, et al. The management of elderly patients with femoral fractures. A randomized controlled trial of early intervention versus standard care. Med J Aust 1998; 169: 515-518. Dowsey M, Kilgour M, Santamaria N, Choong PFM. A prospective study of clinical pathways in hip and knee arthroplasty. Med J Aust 1999; 170: 59-62. Sanders KM, Nicholson GC, Ugoni AM, et al. Health burden of hip and other fractures in Australia beyond 2000. Med J Aust 1999; 170: 467-470. Farnsworth MG, Kenny P, Shiell A. The costs and effects of early discharge in the management of fractured hip. Age Aging 1994; 23: 190-194. Caplan G, Board N, Paten A, et al. Decreasing lengths of stay: the cost to the community. Aust N Z J Surg 1998; 68: 433-437. Choong PFM, Langford AK, Dowsey MM, Santamaria NM. Clinical pathway for fractured neck of femur: a prospective controlled study. Med J Aust 2000; 172: 423-427. Tallis G, Balla JI. Critical path analysis for the management of fractured neck of femur. Aust J Pub Heath 1995; 19: 155-159. Kitchiner DJ, Bundred PE. Clinical pathways: a practical tool for specifying, evaluating and improving the quality of clinical practice. Med J Aust 1999; 170: 54-55. Dwyer P. Legal implications of clinical practice guidelines. Med J Aust 1998; 169: 292-293. Doust JA, Silagy CA. Applying the results of a systematic review in general practice. Med J Aust 2000; 172: 153-156. Rubin GL, Frommer MS, Vincent NC, et al. Getting new evidence into medicine. Med J Aust 2000; 172: 180-183. Make a comment Choong

Cheryl E Swanson · Catherine E Yelland · Gregory A Day

Editorial Virtually viewing the large bowel: the future of colorectal cancer screening? New technologies add to the debate over how best to screen for colorectal cancer MJA 2000; 172: 416-417 Colorectal cancer is a disease ideal for screening: it is common; prognosis is poor if it is detected late but excellent if it is treated early; and there is a premalignant phase (the adenoma) which has a relatively long dwell time during which it can be detected and treated relatively safely. In addition, higher-than-average-risk groups can be identified and targeted. It has been recommended that a colorectal cancer screening program be established in Australia, but, because of uncertainties about the program's feasibility, that this be implemented through a series of pilot studies.1 Nonetheless, for asymptomatic individuals aged over 50 years without a family history of colorectal cancer, the National Health and Medical Research Council favours screening by annual faecal occult blood testing (FOBT), complemented by flexible sigmoidoscopy every five years.2The problem is that all current screening tools are imperfect. FOBT is most widely advocated as the only test shown to reduce mortality from colorectal cancer (by 15%-33%) when used for mass population screening.1 It is also cheap, safe and can be administered by the general practitioner. Accuracy depends on the type of FOBT used and the frequency of testing, but, on an individual basis, FOBT misses between 21% and 63% of cancers and most adenomas, and has a false-positive rate of 2%-13%.3 Flexible sigmoidoscopy is under trial both in Australia and overseas as a tool for population screening. The rationale is that most neoplasms occur within reach of the flexible sigmoidoscope, and that distal adenomas may be predictors of proximal lesions. In this issue of the Journal, Nicholson and colleagues4 show, as have others,5 that, among screened subjects with adenomas, 25% have proximal adenomas only (defined by Nicholson et al as proximal to the splenic flexure). These are beyond the reach of flexible sigmoidoscopy. This study illustrates one of the problems of flexible sigmoidoscopy screening -- accuracy for cancer and polyp detection. However, other important issues must be considered in assessing a screening test, such as acceptability, compliance, availability, safety and cost. Indeed, in the Australian context, initial participation rates in flexible sigmoidoscopy screening have been disappointing (12%),6 although recent data indicate that these rates have increased to around 40% (Associate Professor John Olynyk, Department of Gastroenterology, Fremantle Hospital, Fremantle, WA, personal communication). The findings of Nicholson and colleagues support the need for imaging the whole colon in colorectal neoplasm screening. Methods advocated for this include double-contrast barium enema and colonoscopy. Both have their supporters. However, data on use of these methods for population screening of average-risk individuals are limited, and both have drawbacks that make them unlikely to be widely accepted for mass screening. Setting aside considerations of compliance, double-contrast barium enema is probably not sufficiently accurate without concomitant flexible sigmoidoscopy (which would increase costs and almost certainly decrease compliance), and imposes a significant radiation dose. Total colonoscopy has the advantages of accuracy and ability to combine screening with therapy (polypectomy) but carries a small but significant risk.7 A certain level of competence is required to achieve adequate rates of caecal intubation, and, although it is difficult to determine exact completion rates, outside specialist centres they may be only 80%-90%8,9 or less. Taking into account the need for sedation, consequent bed fees and cost of time off work, colonoscopy is relatively expensive. A recent contender for screening is virtual colonoscopy (computed tomography [CT] colography). After bowel preparation, the colon is insufflated with air or carbon dioxide, and a spiral CT scan performed, preferably in supine and prone positions. Because of the volumetric nature of data acquisition, sagittal and coronal reformatted images can be viewed, as well as the source axial images, and endoluminal images can be reconstructed, simulating an endoscopic view. Navigation using these images can be achieved by manual manoeuvres or "fly-through" techniques that automatically centre on the bowel lumen. While not yet as accurate as colonoscopy for polyp detection, virtual colonoscopy is likely to become significantly more accurate with expected developments in hardware and software. Currently, virtual colonoscopy is more accurate than FOBT and can probably compete with flexible sigmoidoscopy with regard to larger polyps. A study from Boston has reported sensitivities of 91%, 82% and 55% for polyps of diameter 10 mm or more, 6-9 mm, and 5 mm or less, respectively.10 Virtual colonoscopy also has several potential advantages as a screening tool: it is minimally invasive and quick for the patient (the scan takes only a few minutes); no sedation is required; and initial studies have shown that it is highly acceptable to patients.11 Its "high-tech", virtual reality profile makes it potentially attractive to the lay public. While using ionising radiation, dosages are considerably less than for double-contrast barium enema when low-dosage protocols are used. Using the current scanning protocol in our institution, total effective radiation dose has been calculated to be less than 5 mSv, even when supine and prone scans are performed (compared with about 8 mSv for conventional double-contrast barium enema). In addition, early studies hold out the possibility that magnetic-resonance (MR) virtual colonoscopy may eventually supersede CT virtual colonoscopy, eliminating ionising radiation.12 Lastly, there is the potential to detect incidental extracolonic disease, such as asymptomatic aortic aneurysms and renal carcinoma. Problems currently limiting the application of virtual colonoscopy as a screening tool include its lack of sensitivity for small polyps, particularly those 5 mm or less in diameter.10 Does this matter in the context of a screening program? Probably not: the chances of a 5 mm lesion being malignant are negligible; if screening takes place every five years the dwell time for such a small lesion allows an enlarging lesion to be picked up on subsequent examinations. A further limitation is the need for bowel preparation, which is likely to be a significant factor in reducing participation rates. However, the use of faecal tagging to allow software to differentiate faeces and polyps may eventually minimise, or even eliminate, the need for bowel preparation. In addition, other factors, such as availability, operator experience and cost, need to be evaluated in assessing the potential role of virtual colonoscopy as a screening tool for colorectal cancer. Much of the present cost is related to the time required for image processing and reading of the images by the radiologist, which is as long as 30-45 minutes with current commercially available technology. However, this time will inevitably be reduced significantly by further technological advances, such as faster computer processing and automated polyp detection software. Finally, it would be preferable that images are read promptly so that individuals with abnormalities have the opportunity of proceeding to same-day colonoscopy to avoid the need for a second bowel preparation. So, is virtual colonoscopy a viable option as a screening tool for colorectal cancer in the average-risk individual? There is little doubt that, in its current state of development, it is not ready for widespread use. In addition to the limitations already discussed, the excellent sensitivity data reported by some centres10,13 have not been widely replicated.14 Equally, there is a high probability that, at its rate of evolution, in the not-too-distant future CT (or MR) virtual colonoscopy will become an accepted (or even the accepted) modality for colorectal cancer screening. In the meantime, while waiting for the technology to catch up, feasibility studies of virtual colonoscopy are needed to examine issues such as participation rates, factors affecting recruitment into screening programs, acceptability and cost. Richard M Mendelson Radiologist Geoffrey M Forbes Gastroenterologist, and Clinical Senior Lecturer University of Western Australia, Royal Perth Hospital, WA Disclosure statement: The authors are active in clinical research into virtual colonoscopy and are planning a feasibility study of the technique in colorectal cancer screening. Australian Health Technology Advisory Committee. Colorectal cancer screening. Canberra: AGPS, 1997. National Health and Medical Research Council. Guidelines for the prevention, early detection and management of colorectal cancer. Canberra: NHMRC, 1999. Allison JE, Tekawa IS, Ransom LJ, Adrain AL. A comparison of fecal occult blood tests for colorectal-cancer screening. N Engl J Med 1996; 334: 155-159. Nicholson FB, Korman MG, Stern AI, Hansky J. Distribution of colorectal adenomas: implications for bowel cancer screening. Med J Aust 2000; 172: 428-430. Kadakia SC, Wrobleski CS, Kadakia AS, Meier NJ. Prevalence of proximal colonic polyps in average-risk asymptomatic patients with negative fecal occult blood tests and flexible sigmoidoscopy. Gastrointest Endosc 1996; 44: 112-117. Olynyk JK, Aquilia S, Fletcher DR, Dickinson JA. Flexible sigmoidoscopy screening for colorectal cancer in average-risk subjects: a community-based pilot project. Med J Aust 1996; 165: 74-76. Waye J, Kahn O, Auerbach M. Complications of colonoscopy and flexible sigmoidoscopy. Gastrointest Endosc Clin N Am 1996; 6: 343-377. Thiis-Evensen E, Hoff GS, Sauar J, et al. Flexible sigmoidoscopy or colonoscopy as a screening modality for colorectal adenomas in older age groups? Findings in a cohort of normal population aged 63 to 72 years. Gut 1999; 45: 834-839. Freeman B, Engel JJ, Fine MS, DiVita DP. Colonoscopy to the cecum: How often do we get there? Experience in a community hospital. Am J Gastroenterol 1993; 88: 789. Fenlon HM, Nunes DP, Schroy P, et al. A comparison of virtual and conventional colonoscopy for the detection of colorectal polyps. N Engl J Med 1999; 341: 1496-1503. Forbes GM, Mendelson RM. Patient acceptance of virtual colonoscopy [letter]. Endoscopy 2000; 32: 274. Debatin JF, Luboldt W, Bauerfeind P. Virtual colonoscopy in 1999: computed tomography or magnetic resonance imaging? Endoscopy 1999; 31: 174-179. Kay CL, Kulling D, Hawes RH, et al. Virtual endoscopy -- comparison with colonoscopy in the detection of space-occupying lesions of the colon. Endoscopy 2000; 32: 226-232. Rex DK, Vining D, Kopecky KK. An initial experience with screening for colon polyps using spiral CT with and without CT colography (virtual colonoscopy). Gastrointest Endosc 1999; 50: 309-313. Make a comment

Richard M Mendelson · Geoffrey M Forbes

Editorials Open invitation from the International Poverty and Health Network to all healthcare professionals Help reduce the burden of ill-health due to poverty MJA 2000; 172: 356-357 The International Poverty and Health Network (IPHN) was created in December 1997, following a series of conferences organised by the World Health Organization with the aim of integrating health into plans to eradicate poverty. The network's formation was a response to the evidence of the persistent and growing burden of human suffering due to poverty. We invite others to join the endeavour. Around 1.3 billion people live in absolute, grinding poverty, on less than $1 per day.1 This is despite the overall substantial growth of the world economy, which doubled over the 25 years before 1998 to reach $24 trillion. Of the 4.4 billion people in developing countries, nearly three-fifths lack access to sanitation, a third do not have clean water, about a fifth lack access to healthcare of any kind, and a fifth do not have enough dietary energy and protein. Economic disparities both within and between countries have grown. In about 100 countries, incomes are lower in real terms than they were a decade ago.2 By 1995, the richest fifth of the world's population had 82 times the income of the poorest fifth. The world's 225 richest people have combined wealth equivalent to the annual income of the poorest 2.5 billion people in the world (nearly half of the world's population).1 At the same time, the world is facing a growing scarcity of renewable resources from deforestation, soil erosion, water depletion, declining fish stocks, and lost biodiversity. The impact of these problems will be felt most by poor populations. Despite overall dramatic increases in life expectancy over the last century, healthcare professionals should be concerned about growing inequalities in health and wealth.3 The precipitous decline in life expectancy in Eastern Europe, particularly in Russia, is a graphic example of how health may deteriorate as societies face sudden social and economic change accompanied by growing poverty. Even among prosperous nations, there are many examples of growing socioeconomic inequalities in health over the past 20 years.4 Health inequalities in Britain have recently been declared the worst ever.5 In Australia, socioeconomic inequalities in health are also significant. For the period 1985-1987, death rates were consistently highest for those living in the most socioeconomically disadvantaged areas.6 This pattern was evident for both males and females and in each of the three age groups studied (0-14 years, 15-24 years, and 25-64 years) and was observed for all-cause mortality and selected causes of mortality. Despite overall declines in mortality rates between 1985-1987 and 1995-1997 for most conditions, the differentials observed in the earlier period were still evident a decade later. For example, during 1995-1997, infants and children living in the most disadvantaged areas experienced the highest mortality rates for perinatal conditions and sudden infant death syndrome, and for injury and poisoning. Similarly, men and women aged 25-64 years residing in the most disadvantaged areas experienced the highest death rates for all-cause mortality, for specific causes such as circulatory, respiratory and digestive system diseases, and for selected causes such as coronary heart disease and stroke, motor vehicle accidents and pneumonia/bronchitis. Although deaths of Indigenous Australians contribute substantially to the higher death rates in the most disadvantaged areas, they are unlikely to be the sole cause of these differentials, particularly in the cities. Rates of premature death (deaths before age 65) are consistently highest for those living in the most socioeconomically disadvantaged areas of the capital cities and other major urban centres (population 100 000 or more) (Box).7 This pattern is evident in both 1985-1989 and 1992-1995 and for all-cause mortality and selected causes of mortality. Death rates for males and females, as well as for most major causes, increase for each quintile of socioeconomic status of area (from the lowest rates in the highest socioeconomic status areas to the highest rates in the lowest socioeconomic status areas). Disturbingly, the gap between the rates in the most well-off and in the most disadvantaged areas has also increased. Internationally, in the 20th century, development has usually been equated with economic growth, but the link between economic prosperity and health, a key component of human development, is not automatic. A recent World Bank study showed that income improvement contributed only about a fifth of the decline in mortality between 1960 and 1990.8 Education of women and the generation and use of new knowledge were more significant factors. Recent work in Canada and elsewhere shows that the early years of child development are also important contributors to health inequalities.9 The International Poverty and Health Network is a worldwide network of people and organisations from health, business, non-government organisations and government who seek to influence policy to protect and improve the health of the world's poor, particularly the poorest in all countries. The network urges that a balance must be struck between social development and growth in income; between the human and financial dimensions of poverty; and between redistribution and market reforms. Our aspiration is to achieve a balance between biomedical and social approaches; between population-based health development and a response to individuals; between prevention of disease, promotion of health, and treatment; and between physical and mental health. Over the next few years supporters of the network will strive to reduce the burden of ill-health due to poverty by: engaging in strategic discussions with the International Monetary Fund, the World Bank, the World Health Organization and national governments to ensure that health is put at the centre of development. We urge health impact assessments of all policies; promoting action for health locally, regionally and nationally by working with sectors such as education, business, agriculture and transport; building the evidence base on effective interventions that reduce inequalities in health and on how improved health can reduce poverty; facilitating exchange among healthcare professionals in North and South about effective ways of working; ensuring that education programs for healthcare professionals include information on the impact of socioeconomic inequalities on health and what they can do to reduce these inequalities; encouraging healthcare professionals to work with local communities to improve the health of the poorest; and monitoring trends in health inequalities and using the data to influence policy. We invite others to join us in this endeavour. Why not you? Iona Heath General Practitioner, and Chair Intercollegiate Forum on Poverty and Health, Royal College of General Practitioners, London, UK Andy Haines Professor, Department of Primary Care and Population Sciences Royal Free and University College Medical School, London, UK John Glover Director, Public Health Information Development Unit, University of Adelaide, SA Diana Hetzel Senior Researcher, Public Health Information Development Unit, University of Adelaide, SA For more information, please contact the International Poverty and Health Network (IPHN). Tel: +44 207 539 1570. Fax: +44 207 539 1580. (Roger Drew) Email: drew.rAThealthlink.org.uk United Nations Development Programme. Human Development Report 1998. New York: Oxford University Press, 1998. United Nations Development Programme. Human Development Report 1996-97. New York: Oxford University Press, 1997. McCally M, Haines A, Fein O, et al. Poverty and ill health: physicians can and should make a difference. Ann Intern Med 1998; 129: 726-733. Whitehead M, Diderichsen F. International evidence on social inequalities in health. In: Drever F, Whitehead M, editors. Health inequalities. Office of National Statistics, London: The Stationery Office, 1996. Yamey G. Study shows growing inequalities in health in Britain. BMJ 1999; 319: 1453. Turrell G, Mathers CD. Socioeconomic health inequalities in Australia. Med J Aust 2000. In press. Glover J, Harris K, Tennant S. A social health atlas of Australia. Adelaide: Public Health Information Development Unit, University of Adelaide. In press. Wang J, Jamison D, Bos E, et al. Measuring country performance on health: selected indicators for 115 countries. Washington DC: World Bank, 1999. Mustard JF. Early years of development are important contributors to health inequalities [letter]. BMJ 1999; 319: 319. Make a comment Association between death rates and socioeconomic disadvantage* in major urban centres in Australia There is clear evidence in Australia of an association at the small-area level between high premature death rates and socioeconomic disadvantage, both for deaths from all causes (Figure) and from most selected causes. These associations are generally evident not only between the most advantaged (Quintile 1) and disadvantaged (Quintile 5) areas, but also at each of the intervening levels. The following figures are limited to comparisons for the capital cities and other major urban centres (population 100000 or more). Similar data are being collated for non-metropolitan areas. For male residents aged 15-64 years, the differential in death rates between Quintile 1 and Quintile 5 increased, from 1.53 times higher in the most disadvantaged areas in 1985-1989 to 1.76 times higher in 1992-1995. The increase for females was from 1.30 times higher in 1985-1989 to 1.40 times higher in 1992-1995. In the 15-64 years age group, increases in the differential in death rates for selected causes of death between the most well-off and the most disadvantaged areas were: all cancers: increased from 1.14 to 1.28 times higher; lung cancer: increased from 1.53 to 1.93 times higher; circulatory system diseases: increased from 1.55 to 1.94 times higher (despite an overall decline in death rates of 40%); respiratory system diseases: increased from 1.79 to 2.41 times higher; and accidents, poisonings and violence: increased from 1.42 to 1.53 times higher. *Socioeconomic disadvantage is measured by the Index of Relative Socio-Economic Disadvantage, Australian Bureau of Statistics, 1991 Census. Back to text

Iona Heath · Andy Haines · John Glover · Diana Hetzel