Volume 177 Issue 11

Health is one of our major industries, employing more than half a million people — 7.1% of the national work force.1 In the 1999–00 financial year its funding reached $55.7 billion, equivalent to 8.8% of Australia's GDP. The major costs are incurred by the hospital sector ($19.1 billion), medical services ($9.7 billion) and pharmaceuticals ($6.5 billion).2 Conventional wisdom would have it that such an extensive and expensive enterprise as ours is underpinned by a lively culture of research and development informing health policy. But is it? In October this year, the National Health and Medical Research Council (NHMRC) announced that, commencing in 2003, it would support 406 new research projects to the tune of $150 million.3 This welcome announcement was quickly followed by press releases from universities and research institutes proclaiming their success in attracting funds. However, not one of the 406 projects directly involves health policy research and development (R&D).3 Furthermore, of the 16 new NHMRC program grants — larger and longer-term multidisciplinary grants funded with an additional $118 million — only one (with funding of $6.8 million) specifically addresses health policy.4 In short, from 2003, less than three cents of every dollar the NHMRC is investing in new research has been earmarked for policy R&D in an industry that costs the nation nearly $56 billion. So, is health policy R&D in Australia a virtual desert? Before dismissing such a judgement as being too harsh, it might be helpful to revisit health policies that have had a major impact on our health system in the final quarter of the 20th century. Most will acknowledge that these include Medibank (1975) and its progeny, Medicare (1984);5 casemix funding (1993) that accelerated the drive for efficiency and effectiveness in the hospital sector;6,7 the evidence-based medicine movement (early 1990s)8 that, among other things, augmented the growth of evidence-based guidelines;9 and finally the development of an organisational structure for general practice — the Divisions (early 1990s).10 While not wishing to downplay the contributions of many Australians to these health policies, is it not significant that all but one were imported ideas? Medibank came from Canada,11 casemix funding from the United States,12 and evidence-based medicine from North America and the United Kingdom.8,13 Is it not intriguing that during this period of change, our own health bureaucracy apparently remained devoid of productive policy ideas? Why has Australian health policy been a net importer of ideas? Could it be that its culture has not fostered an environment for "think tanks", such as the Institute of Medicine and the Commonwealth Fund in the US, the King's Fund and the Nuffield Trust in the UK, or the Canadian Health Research Foundation, all of which regard health services research and policy as their primary concern? There can be no doubt that coping with the clinical dividends of biomedical and biotechnology research, along with changes in society's expectations, will require innovative approaches to the health system through R&D. This can best be fostered in an environment free of political patronage, that is permeable and receptive to ideas from academia, the health professions and bureaucracies, and the community itself. It will require capacity building, as recently recognised by the belated development of the Joint Health Services Research Program, a cooperative initiative of the NHMRC, the Commonwealth Department of Health and Ageing and the States.14 But, most importantly, it requires a flagship — an independent institute — for vision and leadership. Australia's health policy community recently published a collection of essays, Daring to dream: the future of Australian health care,15 which paid tribute to the many contributions of John Deeble to healthcare in this country. His legacy is wide-ranging, from Medibank and the Australian Health Institute (the progenitor of the Australian Institute of Health and Welfare) to his work in Indigenous health. The essays clearly show that the R&D desert of Australian health policy is dotted with oases. The dream, surely, is to consolidate this enterprise and other ventures, such as the Health Leaders' Network (www.hln.com.au), into a policy flagship. Is it dreaming too much to envisage a John Deeble Institute of Australian Health Policy? Australia is currently blessed with an array of internationally acclaimed medical research institutes. In light of this, the stark absence of an internationally recognised Australian institute for health policy is a damning national disgrace.

Martin B Van Der Weyden MD, FRACP, FRCPA

The virus recognises the similarity of people on the planet. Scientists and policy makers must do the same. Helene Gayle (Director of the CDC's National Center for HIV, STD and TB Prevention) The AIDS epidemic is wreaking havoc and misery around the world and exposing the most awful inequalities and human frailties. In Australia, our population is relatively cocooned from this chaos (Box 1), although the conference heard of the established epidemic in our nearest neighbour to the north, Papua New Guinea, and the worrying emerging epidemic in Indonesia. Worldwide statistics can become numbing, causing human suffering to be ignored. Even for clinicians and researchers in the HIV/AIDS field, the magnitude of the problem is frequently too daunting to either comprehend or tackle in a useful way. However, the realities, and importantly the will, of good, hard-working people in the field were on display at the International AIDS Conference in Barcelona in July 2002. International AIDS conferences are amazing events, bringing the global issues surrounding HIV to the fore. They can be incredibly poignant, wonderfully motivating and equally frustrating all at the same time. Frequently, issues come into stark focus that challenge the status quo. Activists in the field of HIV/AIDS are not shrinking violets. Global access to anti-HIV medicationsWe must corner rich nations with the truth (Jeffrey Sachs, Economist and Advisor to the United Nations Secretary-General) The issue that galvanised many of the participants at Barcelona was the injustice of the lack of access to life-saving, but expensive, antiretroviral drugs in developing nations. In Barcelona, the momentum of providing global access to HIV/AIDS medicines gathered steam. The road to global access is likely to be long and full of pot-holes. The establishment of the Global Fund for AIDS, TB and Malaria provides a major focus for raising the estimated US$13 billion required per year to scale-up preventive approaches and to provide wide access to antiretroviral drugs in resource-poor nations. There was a real sense of holding political leaders accountable to ensure a more equitable future. In the words of Peter Piot, Executive Director of UNAIDS: Let's make the AIDS response truly political — let's bring forward the day when leaders who keep their promises on AIDS are rewarded with our trust, and those who don't, lose their jobs to those who will. Some political leaders were booed from the stage as the audience turned against their meagre or delayed responses to the epidemic. There have been successful pilot and expanding programs of antiretroviral treatment in several developing countries. There is growing unease that a poorly coordinated approach in the developing world will lead to the high levels of resistance to antiretrovirals now present in the developing world, squandering an opportunity to make a very major impact in these countries. Averting the errors made in antiretroviral therapy in the developed nations could potentially lead to more durable responses to antiretroviral therapy. These errors include serial monotherapy, sequential changes in the presence of imperfect HIV suppression, and decisions made to introduce new therapies on the basis of single equivalence studies measuring only short-term surrogate endpoints. The US-based AIDS Clinical Trial Group study, with 384 investigators, reported the first of the long-term strategy studies, in which outcome was based on time to first and second change of therapy in 980 individuals. This provides important information to guide treatment strategies across the globe. Essentially, the length of time to failure of first-line antiretroviral therapy was substantially longer with the initial combination of zidovudine, lamivudine and efavirenz, and the time to the second failure was substantially longer with either first- or second-drug regimens including zidovudine, lamivudine and efavirenz. No benefits of using four antiretrovirals over three were shown.1 For HIV-infected people with anti-retroviral resistance, the conference heard of encouraging efficacy reports of new drugs, such as tenofovir and T-20 (enfurvitide), as well as exciting preclinical information on integrase inhibitors. Unfortunately, the cost of these newer drugs will be prohibitive in developing countries. Not only are the treatment factors (regimen, the timing of commencement, affordable appropriate monitoring, support of adherence) important, but also support for training of healthcare professionals and commitment to ongoing funding for therapy is essential. The World Health Organization (WHO) report entitled Scaling up antiretroviral therapy in resource-limited settings continues to assist this process.2 Providing treatment for HIV is now thought to provide tremendous spin-offs for enhanced prevention. People with access to treatment are more likely to get tested for HIV infection and modify behaviour if found to be positive. Reductions in infectious virus load after treatment are likely to reduce transmission, although this is not yet definitely proven. Increasing use of medications is likely to drive global prices down. The problem of accurately taking all combination anti-retroviral therapy (adherence) continues to be shown to be a major factor affecting long-term success of therapy. To this end, an increasing number of studies of once-daily treatments are being reported. This offers practical options for improved adherence and intermittently delivered therapy (Box 2). No cureHIV treatments are most certainly not a cure. This was soberly brought home by a pioneering researcher in this field, Dr Robert Siliciano, from Johns Hopkins University, describing HIV as "intrinsically incurable". One problem lies with the dastardly ability of HIV to lie dormant in a population of cells called resting memory T cells. These cells are "designed to wait" for a lifetime to ward off previously encountered pathogens. It will prove very difficult to flush the virus out of these cells once it has taken hold. VaccinesThere is hope that a vaccine will eventually be developed that can prevent HIV infection around the world. Although this is one of the "star-wars", "high-tech" approaches to prevention, significant gains have been made in the last two years. There are three important considerations for an effective vaccine against HIV/AIDS — the vaccine must induce (i) T cell responses against virus-infected cells, (ii) neutralising antibodies against free virions, and (iii) mucosal immunity. Vaccines that induce high levels of T cell responses against HIV in animal model systems, although incapable of preventing infection altogether, are able to control viral replication for long periods. To prevent infection altogether, high levels of neutralising antibodies will be required. The induction of broadly reactive neutralising antibodies to HIV has proven very difficult, but there are now hints about potentially successful approaches. The virus is in the mucosal tissue during the first few days of infection. In 3–5 days the virus spreads and virus latency occurs. In 6–9 days the virus has spread systemically. An effective vaccine needs to work at the mucosal site of infection before systemic dissemination occurs. One major obstacle against engineering an effective vaccine is that HIV is capable of escaping both neutralising antibodies and cellular immune responses. Furthermore, there is no definitive HIV marker for protection. There were mixed reports on whether a vaccine could induce immunity across different subtypes of HIV-1 — cross-subtype T cell immune responses exist for T cell-inducing vaccines, but there are no vaccines offering a breadth of neutralising antibodies. The vaccine world is waiting with bated breath for the outcome, due to be released early in 2003, of the world's first efficacy trials in humans of HIV vaccines using envelope protein approaches with alum as the adjuvant. These trials have been conducted efficiently, albeit not without controversy, in 2500 subjects in Thailand and 5000 subjects in the United States and elsewhere. Controversies in these trials have included whether it was justifiable to proceed to human efficacy trials with vaccines that performed poorly in some preclinical studies; the provision of clean injecting equipment to trial participants; and the lack of provision of antiretroviral treatment to subjects who become infected during the trial. Encouraging reductions in risk behaviour have occurred during these efficacy trials; however, a sufficient number of seroconversions have occurred which, when the data are unblinded, should provide a robust analysis of efficacy. One final important point emphasised was that vaccine research should be complementary to, and not in competition with, therapeutic research. Other prevention approachesThe definition of insanity is doing the same thing over and over again and expecting a different result. Rita Brown (arguing for innovative programs to prevent the spread of HIV). In addition to enhanced standard prevention approaches of education, behavioural change, condoms (both male and female versions) and others, further exploration of biomedical approaches to prevention are being evaluated. Male circumcision appears to provide considerable protection from HIV, and observational studies and trials are now under way to evaluate this approach more rigorously in developing countries. Treatment of other sexually transmitted infections is now being evaluated (eg, control of herpes simplex with aciclovir) as a means of preventing HIV acquisition and transmission. Non-occupational postexposure prophylaxis with antiretrovirals is now common in many developed countries, although gathering data on its efficacy has been difficult. The spectre of pre-exposure prophlyaxis with antiretrovirals was also raised. Widespread use of antiretrovirals as pre-exposure prophylaxis has worrying implications for the development of antiretroviral resistance, but, if infection was completely prevented, resistance would not occur. Call for actionA recurring message at the conference was the need for decisive action now. As Helen Gayle said, quoting an African proverb: The best time to plant a tree was 20 years ago; the next best time is now. 1: Global distribution of the AIDS epidemic in 2001 Numbers of people living with HIV at the end of 2001 (and, in parentheses, those newly infected with HIV during 2001) as estimated by UNAIDS and WHO. Data available at: http://www.unaids.org/barcelona/presskit/graphics.html#global.htm (accessed October 2002, no longer available). 2: Once-daily HIV medications to overcome problems of adherence Currently available once-daily antiretroviral medications in Australia/USA Efavirenz Tenofovir Didanosine Ritonavir-boosted amprenavir Antiretroviral medications suggested for future development as once-daily medication Nevirapine Abacavir Other ritonavir-boosted protease inhibitors Atazanavir 3TC FTC T-1249 (fusion inhibitor) Stavudine XR (slow-release version of stavudine) 3: More quotable quotes from the Barcelona AIDS conference Helene Gayle (Director of the CDC's National Center for HIV, STD and TB Prevention, and of the Bill and Melinda Gates Foundation HIV/AIDS and Tuberculosis Program:When will justice come to Athens? Justice will come when those that are not injured are as indignant as those that are (quoting the Greek historian Thucydides). Suniti Solomon, Director, Centre for AIDS Research and Education, India:In Zambia, a widow must cry with only one eye (describing how women whose husbands die of AIDS must keep an eye on their assets, which are often seized by relatives of the deceased). Paul Farmer, Professor of Medical Anthropology, who has established a modern medical centre in a squatter settlement in central Haiti, and introduced antiretroviral treatment:Now my children are not ashamed to be seen with me (quoting a Haitian patient describing the reduction in stigma since starting antiretroviral treatment).

Stephen J Kent MB BS, MD, FRACP · C Jane Dale BSc, PhD · Anne M Mijch MB BS, FRACP

We can no longer ignore human-induced climate changes that are likely to affect our health There is wide agreement among climatologists internationally that human-induced climate change is now under way.1 Global climate change is one of various large-scale, unprecedented environmental perturbations occurring in today's world. These environmental changes reflect the rapid increase in human domination of the biosphere as human numbers increase and as economic activities intensify.2,3 This process has, apparently, now passed certain critical points. Indeed, one recent environmental analysis showed that humankind has been operating in ecological deficit since the 1970s: we now consume and deplete Earth's natural environmental capital faster than it is being replenished and restored.4 These changes — climate change, stratospheric ozone depletion, loss of biodiversity, worldwide land degradation, fresh water depletion, disruption of elemental nitrogen and sulfur cycles, and global dissemination of persistent organic pollutants — have enormous potential consequences for the sustainability of ecological systems, food production, economic activities and the health of human populations. This may have sounded farfetched to "linear optimists" a decade ago. With the passage of each year, and continued global environmental trends, it now seems increasingly plausible. This issue of the Journal, meanwhile, features an ensemble of articles highlighting the current health effects of environmental exposures in five key areas: air,5 food,6 soil,7 water8 and ultraviolet radiation.9 Last year the United Nations Intergovernmental Panel on Climate Change (IPCC), in its Third Assessment Report, documented a coherent pattern of recent changes in various physical and biological systems.1 This included glacier retreat, sea-ice diminution, earlier bird-nesting, earlier flowering, altered timing of insect migration, and so on. While one swallow does not make a summer, the IPCC pointed out that the overall pattern points to the incipient impact of global warming. Where and when, therefore, might we see effects on human health? The answer is complex. First, most health outcomes are multicausal, and inevitably various non-climate causal factors are also changing over time. Second, climate change affects local environments differently, according to characteristics of local geography. Further, the vulnerability of each human population varies as a function of locality, level of material resources, technological assets and type of governance. For example, the small Pacific Island states are likely to feel the effect of climate-induced sea-level rise in the next 20–50 years. The resulting impairment of agriculture and freshwater resources is a particular concern, along with the health consequences of population displacement. Several recent reports have suggested that we may now be seeing some early impacts of climate change on infectious diseases. For example, tickborne (viral) encephalitis in Sweden appears to have increased in response to a succession of warmer winters over the past two decades,10 and there is some, though still inconclusive, evidence of malaria ascending to higher altitudes in the eastern African highlands in association with local warming.11 Meanwhile, the intensification of the El Niño Southern Oscillation (ENSO) over the past quarter-century, a likely consequence of global climate change, has been accompanied by a strengthening interannual association of the ENSO index with rates of diarrhoeal disease in Bangladesh.12 Of course, the health prospects are not all bad. Some impacts would be beneficial. For example, milder winters would reduce the seasonal winter-time mortality peak in temperate countries, and a further increase in temperatures in currently hot regions might impair mosquito survival. Overall, however, scientists have consistently predicted that most effects of climate change on health would be adverse.13 The impacts mostly entail changes in the frequency or severity of familiar health risks — such as the effects of floods, storms and fires; the mortality toll of heatwaves; the range and seasonality of infectious diseases; changes in local agro-ecosystem productivity and its nutritional consequences; the impact on health of changes in fresh water supplies; and the many repercussions of economic dislocation and population displacement. Studies in Australia are beginning to give us a better information base for estimating the impact of changes in climatic means and variability. For example, the dependence of Ross River virus disease on climate variation and its viral repercussions is becoming clearer.14,15 Various other studies have been reported on the climatic influences on Murray Valley encephalitis and on mortality from thermal stress.16 Hall et al (page 614) describe the relationship between temperature and the occurrence of food-poisoning.6 This year, the Federal Government funded its first formal assessment of the effects of climate change on health in Australia over the coming decades (soon to be published). Meanwhile, even as average global surface temperatures gradually rise, it is likely that we will face an increase in climatic variability, including extreme weather events.1 Indeed, many scientists now consider that human health and safety are more endangered by an impending increase in extreme and anomalous weather events than by changed average climatic conditions.17 The human species, because of its social organisation and cultural practices, is better buffered against environmental stressors than many other plant and animal species. Hence, Homo sapiens is likely to be affected less soon and less sensitively than most other species. Not surprisingly, therefore, there is little empirical evidence to date that climate change is already affecting human health. However, invoking the precautionary principle, we can recognise that adverse impacts are both likely and, in many cases, potentially serious. By thinking more ecologically about the large-scale influences on population health and disease, we could apply a more anticipatory approach.3 Society's ultimate objective should not be to generate wealth and increase consumption for its own sake, but to maximise the wellbeing, health and survival of its people. Indeed, the growing recognition of the links between ecological infrastructure, social conditions and health is beginning to highlight population health as a criterion of "sustainable development".18 We and our governments need to move beyond the narrow, short-term vision of the UN World Summit on Sustainable Development, held in Johannesburg in August 2002. The outcome of the Summit was constrained by preoccupations with achieving continuing economic growth, the needs and responsibilities of transnational corporations, and the alleviation of poverty — primarily by the creation, not redistribution, of wealth. Much of the debate was distorted by recriminations between rich and poor countries, and by self-interested US power-play tactics to minimise various international collaborative commitments. There was relatively little recognition of the damage that humankind is now doing to Earth's life-support systems, and its consequences for humans. Considerations of health in relation to ecological sustainability received little attention. One positive, late-breaking development at Johannesburg was the commitment made by Russia and China to comply with the international Kyoto Protocol on greenhouse gas emissions. Indeed, that initiative left Australia looking even more aberrant on this great modern environmental issue than it did before the Summit. The topic of climate change and health will evolve rapidly during this decade. Researchers are increasingly coming to grips with this and related issues. The point of such research is to enrich the information base for farsighted decision-making. As Rene Dubos, the eminent microbiologist, might have said if he were alive today, "Think future, act now."

Anthony J McMichael MB BS PhD · Rosalie E Woodruff BA MPH

We need imaginative city planning which redirects spending on roads to public transport, footpaths and cycleways The classic divisions of environmental health by the vectors food, air and water lend themselves to studies of the causes of disease, but the best approach when looking for environmental health interventions is to focus on the organised areas of human activity that have the greatest impact on the environment — housing, employment, manufacturing and transport. Of all these, transport provides perhaps the greatest potential for health gain, at least in First World countries. The choices we make in transport bear directly on the health of the population. During 2001, an average of 159 597 vehicles crossed the Sydney Harbour Bridge daily in both directions. This compares with an approximate average of 10 900 vehicles crossing the Bridge daily when it was opened in 1932 (Mr Barry Armstrong, Traffic Data Analyst, Traffic Information Group, Traffic and Transport Directorate, NSW Roads and Traffic Authority, August 2002, personal communication). The most familiar risk to health in our car-dominant transport system is road-accident death and injury. In 1999, road accidents resulted in 509 deaths and 12 000 injuries in New Zealand,1 and, in Australia, 1759 deaths1 and an estimated 30 000 injuries requiring hospital treatment.2 About a third of the deaths occurred among children and adults under 25 years of age.1 In fact, these figures reflect recent declines in road accident fatalities in Australia and New Zealand, and one of the public health success stories of the second half of the 20th century. In both countries, fatality rates more than halved between 1970 and 2000. Road accidents are frequently attributed to speeding, carelessness and risk-taking, but changes in the behaviour of road users do not explain the drop in the road toll: more important factors have been better vehicle design (including seat belts), safer roads and fewer vulnerable road users (such as pedestrians, bicyclists and motorcyclists).3 By the standards of most OECD countries, however, our rates of road-accident deaths and injuries are still high. In 1999, road deaths per 100 000 were 13.3 (NZ) and 9.3 (Australia), compared with 9.7 (Canada), 6.6 (Sweden) and 6.0 (Britain).1 Furthermore, current patterns of industrialisation worldwide suggest that road accidents will become more prominent as a cause of death and injury. Already, more people are killed on the roads each year worldwide than die from malaria (2.3% v 1.9% of the global population).4 By 2020 road accidents are predicted to rank third among the causes of global disability-adjusted life-years lost, after cardiovascular disease and depression, and ahead of cancer. Road accidents are nevertheless just the tip of the transport and health iceberg. The effects of vehicle emissions on public health have been considerably under-rated. New data on the relation between exposure to fine airborne particles and mortality suggest that the burden of disease attributable to traffic pollution may be at least as great as that caused by road accidents. In Europe, the number of premature deaths among adults caused by vehicle emissions was estimated to be more than twice the number of deaths from road accidents, albeit with rather fewer years of life lost.5 Using the same approach, in New Zealand we have estimated that about 400 deaths per year can be attributed to traffic pollution.6 By comparison, about 960 deaths per year in Sydney in 1989–1993 have been attributed to exposure to particulate pollution from all sources.7 Not counted in these analyses are the effects of global air pollution as a result of vehicles, roadbuilding and fuel production. The transport sector is a major contributor to climate change. Transport emissions — already responsible for 28% of total greenhouse emissions in New Zealand8 and 16% in Australia9 — are increasing more rapidly in both countries than those from any other sector (see also the article by McMichael and Woodruff [page 590] on climate change and health10). Perhaps the most serious public health implication of our car-dependent societies is the unprecedented level of sedentariness that this lifestyle encourages. In cities, where the majority of Australians and New Zealanders now live, the proportion of trips made by walking, cycling or using public transport has plummeted. In the past 10 years, the proportion of New Zealanders cycling to school and work has fallen by more than 20%.11 In New Zealand and Australian cities, fewer than 5% of workers commute by bicycle, compared with 15%–20% in European cities.12 Fifty years ago, in New Zealand, there were 13 cars per 100 people; now, in both New Zealand and Australia, there are close to two cars for every three people. Some of the consequences of declining physical activity, such as increasing bodyweight and cardiovascular disease risk, are well known. Others, such as the dominating influence of trends in physical activity on the diabetes epidemic, are just becoming apparent.13 The evidence that lack of physical activity is strongly linked with certain cancers (colon and breast cancer, in particular) suggests that motor cars should be included in any up-to-date list of cancer-causing agents.14 A recent assessment of risk factors in Victoria suggested that lack of physical activity was outranked only by tobacco as a cause of ill-health.15 The Mount Victoria Tunnel connects the eastern suburbs of Wellington, NZ, with the city centre. When it was built in 1934, it was used each day by about 4000 vehicles and 2000 pedestrians. In 2001 there were about 34 000 (Health and safety aspects of the Mt Victoria Tunnel. 5th year medical student project. Wellington: Department of Public Health, Wellington School of Medicine and Health Sciences, 2001). Current transport patterns in Australia and New Zealand are firmly entrenched. For almost every aspect of daily life — recreation, socialising, employment — we depend on using a private motor vehicle. As a result it is difficult to avoid trade-offs that make sense at the individual level, but in the broad scheme of things only make the problem worse. We have all heard self-justifying comments such as: "If everyone else goes shopping in a four-wheel-drive then I feel much safer in one too", or "I need to drive the kids to school because the roads are too busy for them to walk". How can we change this? There are plenty of options that would result in benefit to the environment, the economy and human health. Examples include more fuel-efficient vehicles, and a better public transport system. Governments need to promote active transport strategies, such as supervised walking groups of schoolchildren ("walking school buses"), and workplace incentives to reduce car travel, such as public transport vouchers instead of company cars, and changing rooms and showers for cyclists. But major gains will require serious attention to the underlying structural factors that have produced our current high level of car-dependence12 and made walking and cycling more difficult and hazardous. These include removing economic subsidies that hide the true costs of roads and parking facilities, and limiting the urban sprawl that, to a large extent, dictates the use of cars. We need to think more imaginatively about how people can be helped to live close to the facilities they value. This means challenging many of the assumptions on which car-dependent city planning is based (such as the need for segregated land use and low-density housing). To achieve these goals there must be substantial redirection of transport spending from roads to other means of getting around, including public transport, footpaths and cycleways. Examples of positive changes that are now occurring include a less car-dominated National Transport Strategy in New Zealand, and initiatives such as New South Wales/Sydney Action for Transport 2010. We recognise the extreme difficulty of making these changes — there are many powerful reasons why society is car-dependent, including perceived comfort, convenience and security. But the negative health aspects of our present transport system have been under-rated. As Peter Newman, Professor of City Policy at Murdoch University, has pointed out,12 the changes that have to be made require a critical change in mindset, from the privatised world of the motor car and the remote, car-dependent suburb, to the public realm of common spaces, community interests and a global environment that we all share, and on which our public health depends.

Alistair Woodward PhD · Simon Hales PhD · Sarah E Hill MB ChB

While excessive exposure to ultraviolet radiation (UVR) is a significant cause of disease burden in Australia and the Western Pacific region, there are well documented beneficial as well as adverse effects of UVR exposure. Ambient UVR levels do not translate directly to personal UVR dose and thus to biological effect — each person's sun-exposure behaviour and pigmentation also play a role. Exposure in childhood may be more important than exposure in adulthood for both beneficial and adverse effects. Stratospheric ozone depletion increases ambient UVR in the UVB wavelength, possibly the most important wavelength for both beneficial and deleterious health effects. There is ongoing research examining the effects of UVR exposure on immune function, including an examination of the possible role of lack of UVR exposure in the aetiology of multiple sclerosis and type 1 diabetes mellitus.

Robyn M Lucas MB, ChB, MPH · Anne-Louise Ponsonby MB BS, PhD, FAFPHM

There are many contaminated soil sites in Australia. Contamination may be from human activities (eg, smelters, industrial waste dumps, old gasworks) or from naturally occurring sources (eg, surface mineralisation). Concentrations of contaminants may vary markedly across a site. Their distribution may be localised or quite extensive. Common contaminants include lead, arsenic, cadmium, petrol and diesel products, and polycyclic aromatic hydrocarbons. People living on or near a contaminated site will often be concerned about potential effects on their health. Assessing their exposure potential and/or measuring levels of biological markers often allays concerns, but occasionally confirms them (eg, elevated blood lead levels and subtle cognitive effects have been found in some people living near the Port Pirie lead smelter).

Andrew J Langley FAFPHM FAFOM

Urban air pollution levels are associated with increased mortality and cardiorespiratory morbidity. These health effects occur even at exposure levels below those stipulated in current air-quality guidelines, and it is unclear whether a safe threshold exists. Air pollution in Australia and New Zealand comes primarily from motor vehicle emissions, electricity generation from fossil fuels, heavy industry, and home heating using wood and coal. In individual patients a direct link between symptoms and air pollution exposure may be difficult to establish and may not change their clinical management. However, avoiding exposure during periods of peak pollution may be beneficial. Although there is some evidence that urban air pollution in Australia and New Zealand has been decreasing (through reduced car use, improved emission-control technology and use of more energy-efficient devices in the household and in industry), pollution levels are still unsatisfactory. Further reductions may prevent hundreds of cardiorespiratory hospital admissions and deaths each year.

Tord E Kjellstrom MedDr, MEng · Anne Neller BSc, PhD · Rod W Simpson BSc, PhD

The risk of contamination of drinking water supplies with microbial pathogens is minimised by modern approaches to water management, but continues to be the major public health concern. Chemical contaminants usually pose little health risk except at very high levels, but debate continues over the potential adverse health effects of low-level, chronic exposure to compounds such as disinfection byproducts. Recreational water contact can be associated with adverse health outcomes either from microbial infections or exposure to cyanobacterial toxins. Environmental issues such as increasing salinity and global warming are likely to affect the sustainability of our current drinking water supplies and increase the threat of waterborne disease outbreaks. New technologies, use of alternative water sources, such as rainwater tanks, water reuse and restrictions will undoubtedly be part of the solution to our diminishing water resources, but have the potential to introduce new health threats.

Karin Leder FRACP, MPH, DTHM · Martha I Sinclair PhD · John J McNeil FRACP, PhD, FAFPHM

About four million cases of foodborne infectious disease occur annually in Australia; new foodborne pathogens, such as enterohaemorrhagic Escherichia coli, are emerging. Climate change, combined with changes in how we produce and distribute food and how we behave as consumers, have the potential to affect foodborne disease in the coming century. Foodborne disease outbreaks are now more far-reaching (and sometimes global) due to modern mass food production and widespread food distribution. There are strong seasonal patterns for Salmonella and Campylobacter infection in Australia. Global warming may increase the incidence of infections, such as salmonellosis, and diseases caused by toxins, such as ciguatera.

Gillian V Hall MB BS, PhD · Rennie M D'Souza MB BS, PhD · Martyn D Kirk MAppEpid

The ANU Medical School will have a rural and regional focus, taking advantage of its unique geographic and demographic characteristics After intense public debate and a committee of inquiry lasting eight months, the announcement that the Australian National University (ANU) was to develop Australia's 12th and the world's 896th medical school was made in April 2001 by representatives of the Commonwealth and Australian Capital Territory governments and the Vice Chancellor of the ANU. This event represented the culmination of a process that has evolved over several decades. In the early 1970s the ANU narrowly missed out on a medical school, which went to the University of Newcastle. The 1980s had seen an involvement in the teaching of a small cohort of final-year students from the University of Queensland in Canberra, and in 1993 the University of Sydney began to develop its Canberra Clinical School.1 The Clinical School was successful, especially in its teaching programs, as judged by student satisfaction and assessment scores. This positive experience formed a sound platform on which to develop a fully fledged medical school. But why Canberra? The Commonwealth and some State governments have a track record of supporting the development of medical schools in regional Australia. The medical schools at the University of Tasmania, the University of Newcastle and James Cook University (Qld) are notable examples. Canberra, as well as being the national capital, has grown in recent decades to be an important regional service centre, particularly in the provision of health and education for south-east New South Wales; indeed, the "hole in the doughnut" is a popular colloquial description of the situation, evident on studying a map of the region. In spite of the ACT jurisdictional boundary, Canberra has close links with its surrounding area, which, incidentally, despite appearances to the contrary, includes a number of areas with some of the poorest social indicators in NSW.2 Placing a new medical school in this region, centred on the resource of ANU and building on the already established Canberra Clinical School, will help meet a regional need and will allow the new medical school to meet one aspect of its founding mission: to be rural and community focused. The ANU Medical School (ANUMS) will have links with the ACT Department of Health and Community Care and the Southern Area Health Service of the NSW Health system. Canberra, the "bush capital", is very close to the small population centres of south-eastern NSW. The School intends to take advantage of the diversity of the surrounding area and provide rural experience from very early in the course. For example, we plan a one-day-a-week clinical experience from the first week of the course. We will be able to use close rural locations such as Yass, Queanbeyan, Goulburn and Cooma, all of which are within an hour's travelling distance of Canberra. We plan to give selected students the opportunity to spend one of their clinical years in a rural setting, learning medicine, surgery, obstetrics and gynaecology synchronously while their urban colleagues rotate through traditional blocs. The School will provide a four-year graduate medical program with a thematic structure and a problem-based learning approach. Resources will dictate that our adherence to the problem-based approach will be less during the clinical years than is the case in the University of Sydney's graduate program. However, we intend to push the bounds of certain elements of this type of curriculum further. Taking full advantage of the ANU faculty, the students will have an understanding of international health and the impacts of globalisation, as well as a strong commitment to multiculturalism. At first sight this may seem at odds with a rural and community focus, but the need to develop rural and community medical programs and teaching experiences is indeed global. ANUMS sees itself evolving as a "type A" medical school — one that "prepares its graduates to properly practise in a health system — which it would have contributed to designing — to best serve the priority health needs of society".3 In planning the course in Canberra we intend to avail ourselves of the opportunities afforded by its status as the national capital. Thus, we will approach a number of Commonwealth departments and agencies (eg, the Department of Health and Ageing, Department of Defence, Therapeutic Goods Administration and the Australian Institute of Health and Welfare) to provide input into course planning and teaching. The ANU and the University of Canberra have an understanding to collaborate. This is most likely to occur during the clinical years, when we intend to introduce team training of medical students and other health science students in competency-based clinical skills training. At this stage of the course we intend to introduce combined teaching of medical students from the ANU with other health science students from the University of Canberra. Training together will prepare students for the teamwork of professional life. In this way, the School will have a focus on quality and safety, which are important issues in medicine in Australia in the early 21st century.4 We see this as part of restating the role of medicine as a profession, with a particular emphasis on the obligations that that entails.5 Drawing on the ANU's existing strengths, human rights will become a major focal point of our ethics program. The School faces a challenge in developing a research profile within the ANU, whose medical research organisations (eg, the John Curtin School of Medical Research) are already well established. We will endeavour to complement what already exists and concentrate on community-based and translational research, particularly at the Canberra Hospital. We have agreed from the outset to foster research in our rural clinical school. The long gestation of ANUMS did not lessen the controversy of its birth. We will add 60 places, including 25 rural bonded places, to the medical student population of Australia. ANUMS will be innovative, different and will complement other medical programs, contributing to the rich diversity of medical education that already exists in Australia.6

Paul A Gatenby PhD FRACP FRCPA · Nicholas J Glasgow MD FRNZCGP FRACGP

"Operation Bali Assist" was the name given to the Australian Defence Force (ADF) evacuation of injured Australians and foreign nationals after the Bali terrorist bombing on 12 October 2002. The operation involved the triage, stabilisation and evacuation of 66 critically ill patients from Bali to Darwin over 21 hours. Subsequently, the patients were stabilised in Royal Darwin Hospital (RDH) and then, under direction of Emergency Management Australia (EMA), transferred to various centres in Australia. The Royal Australian Air Force (RAAF) transported 35 patients in four separate missions and the operation involved 50 medical staff. Deployment ADF reservists sent in a Hercules C-130 13 October 2002, 0700 EST: The RAAF was tasked by Headquarters Air Command to send a Hercules C-130 transport aircraft to Bali for medical evacuation of Australians injured in an explosion the previous night. The initial information suggested that up to five patients might be seriously injured, possibly more. The medical team assembled at the RAAF's No. 3 Combat Support Hospital at Richmond Air Force Base, NSW, and prepared equipment to be loaded on the aircraft. This included equipment to transport two intubated and ventilated patients, 20 NATO litters (canvas stretchers in a standard size to fit any aircraft) for other patients, four units of locally sourced blood, and other items essential for an aeromedical evacuation (AME) in a military aircraft. 13 October 2002, 1530 CST: The aircraft arrived in Darwin and the AME team, which included one medical officer, three critical care nurses and three medical assistants, was advised that in Bali there were 15 very seriously injured and 20 seriously injured patients. The team was joined by two Army Reserve specialists (a surgeon and intensivist from RDH), another Air Force medical officer and nurse from RAAF Darwin, and extra equipment to allow the surgeon to perform operations as required. By this stage, a second aircraft was en route to Darwin from Richmond Air Force Base to assist in the evacuation. Phase 1: AME Bali to Darwin, 1930 13 October 2002 to 1400 14 October 2002Denpasar Airport, 13 October 2002, 1930 CST: The first RAAF aircraft arrived in Bali. The initial plan was to assess patients waiting at the airport and load these for the return flight. However, on landing we were informed that five casualties had just left on a private Learjet to Perth and that the most seriously injured people were at Sanglah Hospital (more than 40 minutes away by road). The medical team then split, leaving a medical officer and two medical assistants to prepare an Aeromedical Staging Facility (ASF), while the remainder went to Sanglah Hospital to manage the triage, resuscitation and movement of patients to the ASF. Three satellite phones were distributed to the medical officers to allow communication on the ground and to relay medical information and casualty estimates to Headquarters Air Command in Australia. Denpasar Aeromedical Staging Facility The ASF was situated in the airfield fire section in a hangar housing fire trucks and appliances. This provided shelter, light, electricity, places to hang IV lines, vehicle access, and direct access to the tarmac where RAAF Hercules C-130 aircraft would unload supplies and load patients. What greeted the medical team at Sanglah Hospital was something they will never forget. The hospital was overwhelmed with injured Australians with severe burn, blast and shrapnel wounds. There were two critical patients: one was a man with 80%–90% burns who was being ventilated by an Australian paramedic from Darwin on holiday; the other had extensive burns and had had a laparotomy for shrapnel wounds to the abdomen. Denpasar Airport, 13 October 2002, 2230 CST: The first aircraft had to leave for Darwin because of aircrew duty limits (the crew's duty time had already been extended twice). On board the RAAF Hercules C-130 were 15 patients: two critical and 13 relatively stable. One and a half hours into the flight, one critical patient died, despite aggressive attempts at resuscitation. The others thankfully remained stable and on arrival in Darwin were transferred to RDH. Denpasar Airport, 14 October 2002, 0130: At the ASF in Bali, casualties were pouring in, with up to 30 patients on the hangar floor being stabilised and operated on by medical staff and volunteers. The patients were mostly young, quiet and stoical. There were no complaints or unreasonable demands; on the contrary, most were concerned for their mates. Casualty management at Denpasar Denpasar Airport, 14 October 2002, 0430 CST: The second C-130 departed for Darwin with 22 patients on board (two in intensive care and ventilated, six in a serious condition). Denpasar Airport, 14 October 2002, 0600 CST: A third C-130 arrived with three anaesthetists, extra nursing staff and supplies. It was closely followed by a fourth C-130 carrying an AME team and two anaesthetists. The newly arrived staff were most welcome, and increased the capacity to stabilise patients before flight. Soon after, a fifth C-130 arrived with four more AME members and further supplies. Airway and circulation assessments, femoral lines, venous cutdowns — a gritty but surreal scene on the floor of a concrete fire hangar in tropical heat, ringed by anxious friends, relatives and interested Balinese emergency service personnel. Denpasar Airport, 14 October 2002, 0830 CST: The third aircraft was loaded with 16 patients (most critical patients last on – first off) and departed. The fourth C-130 was not far behind, carrying 11 patients and all remaining medical personnel who had been on the ground since the beginning of the evacuation. Left behind were 11 medical personnel, but no patients. The team resupplied and cleaned the ASF and consulate, and two medical personnel left the airport to check that no injured Australian or foreign national had been left behind in the hospitals or hotels. In the Denpasar Airport civilian terminal, large numbers of tourists evacuated by Qantas were checked for injuries requiring potential AME. Over the next few hours, only two more patients arrived at the ASF (one with three surfboards!). Denpasar Airport, 14 October 2002, 1400 CST: The fifth C-130 departed with all medical personnel, two patients and a small number of uninjured Australians (and three surfboards). Sixty-six patients were evacuated out of Bali in 21 hours using five Hercules C-130 aircraft and 34 Australian permanent and reserve military medical staff. An ASF was established to allow for stabilisation, resuscitation and field surgery to the injured people awaiting transport on military aircraft. Importantly, the medical staff were able to communicate through satellite phone to military headquarters to allow appropriate medical staff and supplies to be brought to the ASF and to coordinate the evacuation. Civilian retrieval companies, including Qantas, complemented the evacuation. Phase 2: AME Darwin to various major burns units, 2400 13 October 2002 to 1700 15 October 2002 Sydney: awaiting the arrival of patients from Darwin. The strategic AME component of Operation Bali Assist began while the first phase was ending. Civilian retrieval organisations (Royal Flying Doctor Service, Medical Emergency Adult Retrieval Service, CareFlight, and Retrieval Team Royal Adelaide Hospital) had flown to Darwin and began to transport ventilated patients to various hospitals throughout the country. This activity continued into the night of Monday. We focus on the ADF activities. Darwin, 14 October 2002, 1300 CST: The initial directive from Air Command was that there would be two strategic AMEs: one to Perth and the other to Brisbane, then Sydney and Melbourne. However, this soon changed, with the news that RDH and EMA had requested four strategic AMEs that evening: to Perth; to Adelaide then Melbourne; to Brisbane; and to Sydney. These were to be conducted in quick succession and would require a high level of logistical and personnel support. Darwin, 14 October 2002, 1600 CST: The first meeting was held with the staff from the RDH to determine the numbers of patients to be transferred to each of the capital cities, the priority of the patients, and how these patients were to be transported. A difficulty at this meeting was that patient priorities were still changing because of ongoing resuscitation and initial surgery. However, it was resolved that only the AME to Perth would transport ventilated patients; the other AME would not do so unless necessary. At the meeting, a rough patient manifest was determined for the AME to Perth. This included 12 patients, with burn surface areas between 5% and 40% and with varying degrees of blast and shrapnel injury. Two of the 12 patients were intubated and ventilated. It was decided that the most efficient means of transferring patients from RDH to the C-130 Hercules was by the RAAF ambulance bus. This bus is capable of carrying patients on NATO stretchers and can allow for transfer of a large number of patients. Volunteer crews from RAAF Darwin were responsible for loading and unloading the bus and aircraft under the direction of medical personnel. Darwin, 15 October 2002, 0150 CST: The first of the AMEs departed Darwin. The six-hour flight to Perth was uneventful until two hours out from Perth, when a ventilated patient suffered a cardiac arrest. Resuscitation efforts by the staff on board were successful. All patients were eventually transferred to Royal Perth Hospital. Darwin, 15 October 2002, 0305 CST: The second AME departed for Adelaide. On this flight were six patients with burn areas ranging from 15% to 50%, two patients with shrapnel injury, and two family members. None of the patients had been previously intubated and ventilated, but there was concern that one patient might have needed ventilatory support during flight. Also on this flight were three members of the Royal Adelaide Hospital retrieval team who had been working for the previous 24 hours. All patients were transferred to their destination medical facilities without incident. Darwin, 15 October 2002, 0530 CST: The third AME (seven patients with various blast, burn and shrapnel injuries) departed for Brisbane. By that stage of the operation, medical supplies and medications were beginning to run low and equipment issues began to appear. A late request from RDH to transfer a ventilated patient was accommodated; however, when reviewed, the patient was deemed to be too unstable for the four-hour mission to Brisbane. The medical staff on this flight consisted of two RAAF Specialist Reserve anaesthetists, one Navy Reserve anaesthetist and one Army Reserve anaesthetist, all proceeding home following the first phase of the operation. Without these Reserve personnel, the mission would not have been conducted. All members of the team remaining in Darwin were beginning to show obvious signs of fatigue by the time the third AME departed. The fourth AME was delayed while patients were prepared, and did not depart Darwin until about 1100 CST on Tuesday. On board the final flight were the bulk of the initial crew from RAAF Base Richmond who had mobilised initially, additional Reserve specialists and a CareFlight member who had been stranded in Darwin. Eight patients with various areas of burns and two family members were transferred on this flight. In all, 35 patients were transferred to the four capital cities over 16 hours on Tuesday, 15 October 2002. Crews that had been pushed to the limits of fatigue, having been working for an average of 34 hours with only broken sleep, undertook this feat and continued to provide optimal care for their patients until the work was completed. The second phase of Operation Bali Assist enabled the load to be shared among burns units across Australia. It ensured that most patients would be treated in their home State and it allowed the RDH the ability to cope with the numbers of injured patients for the time necessary to conduct vital resuscitation before resources became stretched. DiscussionA terrorist act causing large numbers of critically injured Australians in a country where the provision of medical services differs from our own provided unprecedented challenges. This tragedy required a response not previously conducted by Australia. Burns required prompt resuscitation and expert surgical management. It was recognised that the best response for these victims was to bring them safely to Australia and then to specialist burns units around the country. Military and civilian agencies, their planners and operators worked seamlessly to meet this challenge. No single agency could have conducted the whole operation. The tragedy focused the resources of the nation to give the best outcome for injured Australians. The AME had unique problems. There were large numbers of critically injured patients, necessitating large numbers of Specialist Reserve support, significant quantities of oxygen, IV fluids, blood products, drugs (morphine, ketamine, midazolam, muscle relaxants, antibiotics and Tet Tox) and critical care equipment (oxylog, Propaq monitors, etc). In the short response time, these were sourced from ADF facilities in Sydney and Darwin, and local hospitals in Sydney, Darwin and Adelaide. Each C-130 aircraft arriving in Bali brought more supplies, until the surplus allowed some excess fluids to be sent to Sanglah Hospital on our departure from Denpasar. The prompt response and support of ADF Specialist Reserve allowed expert medical care to be projected with this operation. As always, they provided experienced clinical judgement, procedural skills and support to the permanent medical force. The RAAF has identified areas for future improvement to maximise the capability we can project. These mainly focus around critical care equipment update, and training and alliances with civilian critical care services. Operation Bali Assist was successful because of the united and dedicated response of all people involved. So often in tragedy, individuals and organisations exceed normal expectations; this was no different. The ADF, EMA, the Department of Foreign Affairs and Trade, RDH, burns units around Australia and the Australian public were all crucial to the best outcomes for the victims of terrorism in Bali. With this operation comes the responsibility to ensure Australia's capability to react to such tragedies is enhanced. The possibility of future acts of terrorism ensures its maintenance.

Gregory V Hampson MB BS · Steven P Cook MB BS · Steven R Frederiksen MB BS

Several Australian medical practitioners were holidaying in Bali at the time of the nightclub bombing on 12 October 2002. On learning of the disaster, they went to Sanglah Hospital to assist. With the very limited resources of the hospital, they helped in providing emergency treatment, stabilising patients, and preparing Australian patients for evacuation. (MJA 2002; 177: 624-626) Bali is a common holiday destination for Australians — within easy reach, with a wonderful climate, a range of costs to suit all budgets, and friendly Balinese people. So it was that some medical practitioners from Australia happened to be in Bali near Kuta on the evening of 12 October 2002 when bombs exploded in a local nightclub, killing more than 100 people and injuring many more. On Sunday morning, we made our way to Sanglah Hospital to help the injured (Box). The hospital and patientsThere are several hospitals in Bali. The main one is Sanglah Hospital, laid out in extensive grounds with long, open corridor wards fed by a maze of partly covered walkways. Directories are not easy to read or follow. The scene at the hospital was like a movie set gone wrong, with many people milling around the walkways and in the wards. One of us was confronted with a multitude of patients (mostly Australian) with relatively minor injuries — lacerations, shrapnel and other foreign body wounds, and minor burns. These patients were given basic treatment and advised to fly back to Australia as soon as possible. The more seriously injured patients had been admitted to wards. An early decision was made to try and locate the non-Indonesian patients into ward 6, which we called "Australia Ward". This allowed us to focus our resources, but created logistical problems, as the beds were old, heavy and not on wheels. Moving them involved placing a hydraulic hoist arrangement under the bed, manually pumping it up to raise the bed, and then slowly and precariously wheeling the bed to Australia Ward. Almost all ward patients had serious, full-thickness burns (ranging from about 25% to 85%) and many had shrapnel wounds or intra-abdominal injuries. One patient had a torn right brachial artery, one a crushed left foot and right leg (both requiring amputation), another a fractured cervical vertebra and fractured pelvis and intra-abdominal wounds with damaged bowel. Two intensive care units held several ventilated patients with severe injuries, including major burns and abdominal trauma. One of these patients was a young unidentified girl who had a severe head injury and inhalation burns and was on escalating doses of inotropic drugs. She was looked after initially by an Indonesian neurosurgeon. It was evident her death was imminent. A difficult decision was made to transfer her to Australia in the hope that she would survive the trip and die on home soil. Our initial aims were to: resuscitate; treat emergency situations as they developed; stabilise the patients as much as possible; coordinate the evacuation in conjunction with the Australian consulate and the Australian military attaché; triage patients for evacuation (most severe and stable out first); and transport patients to the airport for stretcher flights to Australia as soon as practicable. Ambulance transport was available, with at least nine ambulances ready to shuttle patients — one patient per ambulance. Limited resourcesWard work was very arduous with the limited equipment available. Vital resources such as monitoring equipment, oxygen, large-bore cannulas and central venous lines were in extremely short supply. All patients required intravenous fluids, with several needing central lines, but we could find only four to use. Intravenous cannulas were small-bore and, as the burns commonly involved all limbs, insertion was often not easy. As luck would have it, our wonderful anaesthetic registrar made it look easy. The "rule of nines" was used to estimate the percentage total body surface area (%TBSA) and the Parkland formula (4 mL/kg/%TBSA burn in the first 24 hours) was used to calculate each patient's fluid requirement. The required amounts were written on patients' bed sheets or fluid balance charts and instructions given to the volunteers monitoring individual patients to ensure that each patient received the required fluid. As only 500 mL saline flasks were available, we needed to pump in the fluids. The small-bore cannulas often blocked or slowed. At least 40 urinary catheters were inserted and urinary outputs were monitored closely. Hourly urine volumes were measured, and specific gravity was estimated by the urine's colour. Medical records, including fluid balance charts, were kept as accurately as circumstances allowed. Our aim was to send the charts with the patients on evacuation — we felt communication to our Australian colleagues for ongoing care was very important. Cephalosporin antibiotics were available and given to all patients intravenously. Pain medication was in limited supply; some IV flasks were already made up with pethidine/saline and these were infused, titrating against pain. We split the limited available ampoules of pethidine and tramadol between us and administered and charted them according to pain levels. One of us well remembers an Australian man whose face was totally burnt, who could hardly open his eyes and, like many, could not hear well because of blast injury deafness. When offered pain relief he said, "No thank you doc, but go and see someone who needs it more than me". Unfortunately, despite his return to Australia, he did not survive. His unselfishness will live on. Burns were dressed as much as possible with the limited dressings available. Silver sulfadiazine started to become available late Sunday afternoon, but only in small tubes and limited supply. We had a dressing trolley with small amounts of gauze but no true bandages, and limited "semi-sterile" open bottles of antiseptic. We ran out of disposable gloves — no sterile gloves could be found. The water was not to be trusted for washing. Routine blood tests were not available and we had limited blood for transfusion. Four units were sent to us from the Royal Australian Air Force (RAAF) (2 O Rh– and 2 O Rh+) and yet many patients needed transfusing. We had no cross-matching facilities and were afraid to give Rh+ blood to young women. As time went by, limb swelling and peripheral ischaemia developed in many patients. About 20 escharotomies and fasciotomies were performed using limited equipment (eg, a blade without a handle). In most instances, these were performed without anaesthesia and analgesia because of the severe lack of resources. The patients understood the need for these operations and showed great courage in withstanding the severe pain. StaffWe would like to pay tribute to the few, overworked Australian nursing staff who aided us greatly. We had a smaller room in which we placed two very sick patients — one with more than 80% body burn and intra-abdominal wounds and one with a severed brachial artery which our Indonesian colleagues had repaired with a saphenous vein graft. In this quasi "high dependency unit" was a lovely New Zealand nurse who was very attentive. We are sure there were other medical staff who ably assisted the injured and we apologise that we cannot name them all. We hope that this record does them justice. A strong part of our team were the many volunteers who gave so much of their time and energy. With no training, just goodwill, they stayed for hours beside a fellow human being following our instructions — taking pulses, measuring urine outputs, checking IV fluid rates. Other volunteers spent hours manually fanning patients, as the ward had no air-conditioning. Evacuation The Australian embassy staff were excellent and very active in liaising with the Indonesian authorities, the hospital, the RAAF and the airport authorities. Initially we were told that aircraft would be arriving in the early evening of Sunday, 13 October, but this was delayed by a few hours. The first plane was a private jet, which took five seriously ill patients to Perth. The other planes were RAAF Hercules C-130 aircraft, each capable of transporting 28 stretcher patients and with a medical crew on board. They would transport patients to Darwin, where the patients would be reassessed at the Royal Darwin Hospital and then transferred to burns units around Australia (see page 620). The "walking wounded" from smaller peripheral hospitals and the Sanglah Hospital were evacuated to Sydney and Perth on a Qantas airliner and a privately owned jet. As the time to evacuate patients arrived, we listed the patients in the ward, grading them according to seriousness of injury, stability for travel, and need to get urgent multidisciplinary treatment in a better-equipped environment. As soon as the evacuations cleared Australia Ward, other patients from nearby wards were moved in. Eventually only eight or so Indonesian burns patients remained; these patients were treated no differently from those evacuated, except we were instructed that they were to remain. We found it difficult to leave these patients behind in the ward at this time (about 3:30 am, Monday, 14 October 2002), but we had learned of eight non-Indonesian patients in other hospitals. Leaving the Indonesian patients to Indonesian medical staff, we divided ourselves into three groups with three ambulances each and an Australian Embassy staff member to travel to each hospital and escort the patients to the airport for evacuation. On arrival at the airport we were impressed by the marvellous job the RAAF had done in setting up a triage hospital. The RAAF medical teams continued with the care of patients. We were required to perform two more fasciotomies at the airport, but as the last plane arrived we all headed back to our hotels, weary and drained from the experience. AftermathWe are indebted to our Indonesian colleagues for their care, without which we feel sure that many more lives would have been lost. We have attempted to convey the enormity of the situation, which is hard to appreciate without having been there. It is difficult to imagine an Australian hospital, despite its access to resources, coping with such a dramatic onslaught of casualties with so much carnage. Nevertheless, Bali is an underdeveloped country with matching facilities and this made it all the more difficult to attain the goals we set. It made us all very proud to know that the last of the RAAF aircraft took off from Denpasar Airport within about 30 hours of the explosion, taking the last of the 66 seriously injured patients back to Australia. We had performed as a team, used inner strengths none of us could ever imagine, brought people together and amassed a powerful human spirit that would leave all physically, mentally and emotionally drained. It is important to learn from this Bali bomb disaster, as, although we all pray for the day that all humans can live in peace, we all know that there will remain an element among us intent on repeating such atrocities. As doctors we must always be available to assist the injured. The disaster also brings home to us the powerful message of how fortunate we are to have trained so well in our profession in Australia. Although nothing could have prepared us for this situation, we feel that our Australian medical training was second to none. In the following days we would all suffer the problems of having been so intimately involved in a disaster — feelings that interfere with our daily lives. Physical and mental tiredness, emotional feelings that interfere with eating and sleep. Some of us have had stress reactions; however, experienced counselling has been invaluable as a preventive therapy. We are all now back to a near-normal life. Hannie Rayson, the renowned Australian playwright, wrote on "Courage" for one of us to read at a State memorial service for the victims of the Bali bombing. It epitomises how we, as doctors, felt: In the middle of this outrage, I was delivered an unexpected privilege — I experienced the force of the human spirit. I saw how courageous and selfless men and women can be, when the chasm opens beneath them. Tony Pethick, a general practitioner from Perth, had just returned to his hotel near the Sari Club when there was an initial "pop" noise followed by a much larger explosion. This almost blew him off his feet and shattered all his room's windows. He ran onto the street to see a massive orange mushroom cloud rising nearby and people staggering, running, and screaming. A man was clutching his abdominal viscera, hanging from an abdominal wound; there were lots of people with minor burns. Cars on fire were slewed across the road; in one the driver was slumped over the door, and closer inspection revealed he had been decapitated. After initial "numbness", Tony picked up a seriously burnt person from the roadway, and covered some of the burns with t-shirts from a nearby shop window. He then placed the patient into a small van and took him to a nearby clinic. More than 30 injured people were in the clinic, lying 2–3 per bed or on the floor. There was virtually no equipment. Tony comforted several patients, and they were slowly transferred to Sanglah Hospital. He accompanied one young girl with severe burns who was conscious until she was taken to the operating theatre. Holding her hand, he told her he would see her later. Some hours later, he found out that she had died — he telephoned her mother to explain. After several hours' sleep, he joined the other doctors at Sanglah Hospital. Priya Thalayasingam, an advanced trainee in anaesthetics, and Vijith Vijayasekaran, an advanced trainee in plastic surgery, are a couple from Perth. They arrived in Kuta on Saturday, 12 October, for a week's holiday. That night, as they returned to their hotel, they witnessed an explosion in the distance. At that stage, they were unable to find out what had happened, but early on Sunday morning their parents phoned, and they learned that many Australians had been injured in an explosion at the Sari nightclub. After several attempts, they contacted the Sanglah Hospital and Australian Consulate staff and proceeded to the hospital. John Hogg, a general surgeon from Wollongong, had arrived in Bali with his wife Linda, on the afternoon of the bombing. They were woken early the next morning by a call from their daughter in Australia, telling them of the blast. They immediately took a taxi, asking the driver to take them to the main hospital. John became involved in patient care, while Linda spent the next 20 hours trying to locate the missing, often in the morgue. Graeme Southwick, a plastic surgeon from Melbourne, had been a guest lecturer in Kuta and was spending three days after the conference with his wife at a resort. In the early hours of Sunday morning, his son phoned to say that a bomb had exploded in Kuta. Television reports initially suggested only a few casualties, but soon the full extent of the disaster became apparent. Phone calls to two hospitals on three occasions offering help were rejected. A few hours later a plastic surgeon in Jakarta (who had attended the conference) phoned to request help (agreed to by the Indonesian Minister of Health), and this opened the door to the hospitals. → See also "Operation Bali Assist. The Australian Defence Force response to the Bali bombing"

Graeme J Southwick FRACS, FACS · Anthony J Pethick MB BS · Priya Thalayasingam MB BS · Vijith S Vijayasekaran MB BS · John HW Hogg FRACS, FRCS(Engl)

How a peace-loving suburban Sydney GP, practising primary prevention her way, ended up in solitary confinement I've always believed that it's part of my job description as a doctor for me to be aware of environmental issues and to address them as best as I can. So, I've been a long-time supporter of Greenpeace (www.greenpeace.org) and a member of the Medical Association for Prevention of War (in NSW, called Health Practitioners for Global Responsibility; www.mapw.org.au, mapwATmapw.org.au). And, since 1997, this desk-bound GP has worked as a volunteer "medic/deckhand" on Greenpeace ships, like the Rainbow Warrior, for a couple of months each year. As medic, I ensure that the ship's hospital, which doubles as my sleeping cabin, is ready for emergencies, illness or injury. It's well stocked, with resuscitation equipment, surgical supplies and drugs; we are prepared for anything, from draining a pneumothorax to flying out someone with a spinal injury. For example, I've attended to crew after they were "rained on" with heavy metal tools as they climbed up an oil tanker and treated hypothermia after cold water immersion. I also train crew in first aid, including resuscitation (and working out team approaches in emergencies) and practise primary care and preventive medicine, from mosquitoproofing the ship to discussing outbreaks of worms. When not working as a medic, I am under the charge of the bosun, who assigns me to deckhand jobs — for example, painting the mainmast, restacking the hold or standing watch (which involves working a night shift), with opportunities to improve navigation and radio skills. When the ship is engaged in protest actions, I can either stay aboard as part of the back-up crew or volunteer to be involved as an activist. I've been directly involved in several campaigns. My first was in Central America after Hurricane Mitch swept through in October 1998, where I worked alongside locals, hauling bulk bags of rice and beans, tents and boxes of clothing and medicines into wharfside sheds for later distribution. My most recent expedition, to Sweden, provided a very different experience. ProtestOn 4 June 2002, the Rainbow Warrior and her crew embarked on a protest involving the cargo vessel ms Fagervik, which had dumped a large amount of oil into the Baltic Sea in February 2001. Although evidence suggested that the Fagervik's spill had been deliberate, the local Swedish court had decided to prosecute the ship's owners for an accidental spill (with a small fine) rather than for a deliberate spill (a criminal offence). Greenpeace wanted to protest about the facts that deliberate oil spills are frequent (about 1000–2000 a year in the Baltic) and virtually go unpenalised. We believe that ship owners and industry should bear the full financial liability for the effects of oil discharges, whether or not intent can be proven. Our specific goal was to board the Fagervik en route to the port of Norrköping (about 160 km south of Stockholm). The action took place in the usual non-violent manner that Greenpeace is committed to. We spent the first day of the protest in a rubber Zodiac boat doing action manoeuvres — painting slogans, hanging banners, and getting "climbers" (those who climb up ships' hulls) on board the Fagervik. ArrestIn the early evening on that first day of the protest, I joined a few other protestors on board the Fagervik. As part of the protest, I chained myself to the boat, as did Kristina, a 27-year-old German. The Swedish police boarded the ship that same evening, and at 10 pm Kristina and I were arrested. We were charged with aggravated trespass and taken to the town lockup to be held in solitary confinement. It was an unprecedented reaction to a Greenpeace protest. We had been told, in the routine legal briefing before the campaign, that such a charge, with a two-year prison sentence, was possible but unlikely. More likely was a charge of minor trespass, with release within four days. Under Swedish law, there is no bail; one can be held in custody indefinitely until trial — which, I was told, could be many months off. In solitaryThat night, I was put into a concrete basement cell, 1.5 m by 3 m, that boasted a floor mat to sleep on and a drain hole, which others had clearly used as a toilet. I, too, later resorted to using the hole for the same purpose, as it could take up to an hour after pressing a buzzer before a guard would respond to take me to the actual toilet. The cell walls, floor and mat were encrusted with recent faeces and blood. Later, I found out that my dingy cell was more generally used as the "drunk cell", for those who were drug or alcohol affected when arrested. My watch and warm boat suit and gumboots were confiscated and I was issued cotton pants, a shirt and plastic scuffs to wear. I felt not only isolated but also powerless; contact with Kristina and my personal lawyer was denied me; later we presumed that this was because of a fear of terrorism; that there was a risk of "collusion" between my lawyer and myself (I was allocated a State lawyer). I was also denied direct contact with my family and it was days before I was finally able to make contact with the Australian consulate. The seamen's mission priest and the prison nurse were other eventual, permitted visitors. In the first few hours, I observed my fear and confusion growing. Then, I remembered Victor Frankl's words in his book Man's search for meaning: 1 Everything can be taken from [us] but one thing: the last of the human freedoms — to choose one's own attitude in any given set of circumstances, to choose one's way. I resolved to apply myself to keeping mentally clear and stable. I began by getting a rough idea of the time from my meal deliveries. Then, knowing the link between exercise and wellbeing, I began a workout program that encompassed every exercise I had ever learnt and devised ways of timing half-hour walking periods without a watch. I'd practised yoga and meditation for many years, and drew on that practice to maintain an attitude of acceptance and calm. It became an incredible comfort to me when, each day, the inner reality of the meditation space became stronger as my small, shabby and uncertain external world shrank in importance. Initially, what there was to read was in Swedish. Greenpeace members attempted to send books, music, and clothes, but not much was allowed through. So, I began drawing. One kind guard gave me pencils and paper, and would sharpen them on his shift, saying that he trusted me not to use them as a weapon. By the time I was released, one whole wall of my cell was covered with paper and my own huge mural of Sydney Harbour. The guards would stop by to see my drawings, and indeed they became friendlier during my imprisonment, sometimes offering me a second cup of tea in the day. A guard confided "I like what you do. Tonight I give 500 kronas ($100) to Greenpeace". Many asked whether I really was a doctor and one sought my advice concerning his dying father. Meanwhile, the small fiord township of Norrköping was anticipating a large and complex trial and Greenpeace continued the Fagervik protest for several more days, with a flotilla of small boats and climbers on board (as well as continuing arrests). Greenpeace also mounted a networked international campaign calling for our release. The media took hold of the story, with incredibly supportive coverage of our stance. ReleaseI was working at my wall, well prepared for a long stay, when a guard came into my cell to tell me that I was to be released forthwith. It was 14 June, ten days after our arrest. My reactions ranged from relief to confusion, knowing that a trial and possible further imprisonment lay ahead. The police superintendent came to my cell, shook my hand, and apologised for keeping us in cells intended for overnight use only. The guard on duty farewelled me with a hug, sorry to see us go. I thanked him for the pencils. Kristina and I emerged from the building to be met with banners, flowers and friendly faces I did not know from the Stockholm Greenpeace office. I still had no shoes and one large Swede gave me his sandals. Again, I found myself watching my reactions: ordinary things, like seeing the sky and breathing the air seemed wonderful. I'd been used to solitary silence and was now being interviewed by the mass media. On release, I learnt that during our imprisonment a large export company had announced it would not use the Fagervik or any "dirty" ships (ie, sea-polluters) for transport — I felt a deep sense of effort rewarded. On trialTwo weeks later, four Greenpeace activists, including myself, were found guilty of aggravated trespass and given a two-year suspended sentence. This means that, if we work in any future protest actions in Sweden, we risk getting arrested and having to serve out our sentence. We can understand some of the reasoning behind this sentence — a year ago, Sweden was shaken by violent anti-globalisation demonstrations in Gothenburg. However, we plan an appeal, as it's important to make a distinction between violent protest and the right to non-violent, thoughtful protest about community issues. In the courtroom, I was asked if I regretted my actions. Through a translator, I replied along these lines: I do not regret my actions. What I regret is the harsh reaction by this legal system to a peaceful protest. As a medical doctor in Australia, I see people dying of cancer and babies born with abnormalities. It isn't enough for me to just keep treating sick people — I also feel compelled to speak up about the issues behind some of these illnesses. I understand that pollution in the Baltic Sea is already so high that pregnant women are advised not to eat the fish from it. I believe it is important to encourage governments to enforce restrictions on industrial release of what is unsafe into the water, air and soil. PrivilegedSo, was going to prison worth it? It was a privilege to be able to speak and act for what I believe matters. Environmental issues are not remote from primary care, they are increasingly recognised as an integral part of it.

Elizabeth D Rickman MB BS

The recent pioneering Public Report Card 2002 — Aboriginal and Torres Strait Islander health, entitled No more excuses,1 outlines where we are today and how the health of our Indigenous population compares with that of other similar countries — New Zealand, Canada and the United States. Produced by the Australian Medical Association, it is a "warts-and-all" assessment which is designed to show what is working and where we need to do better. Where do we stand on health?There have certainly been some gains. The health of Indigenous infants has improved dramatically, although from a low baseline, and most of the gains occurred 20–30 years ago.2 The current infant mortality rate for the Aboriginal and Torres Strait Islander population is almost three times that of the general Australian population, twice that of the Maori, and 50% higher than the mortality rate of US Indigenous infants.3 This is some improvement on previous rates, but we can and should do better. Death rates overall for Indigenous people in Australia are still three times as high as for the rest of the population: diabetes death rates are eight times as high, respiratory deaths four times as high and circulatory conditions almost three times as high.4 These are unacceptable statistics for treatable and preventable conditions. On the other hand, there are number of recent good news stories. Programs in the Northern Territory and elsewhere have shown that birthweight, the critical factor in the survival of newborn infants, can be improved.5,6 More dramatically, death rates from pneumonia have dropped by around 40% since 1996 (derived from Australian Bureau of Statistics data). This is important, because this reduction is likely to be due, in part, to recent government initiatives for promoting pneumococcal vaccination. This is a real indication of the kind of rapid and substantial gains that can be achieved through application of knowledge we already have. (Well done, even if long overdue.) Progress in providing access to health services for Aboriginal and Torres Strait Islander communities is much too slow. There is a gross shortage of doctors working in Indigenous health, with an estimated 60% increase required (ie, at least 500 doctors). The number of nurses also needs to increase by 25%, and there are sizeable deficits in all the other health professions.7 There has been some improvement in basic services and facilities to some areas, but too many Aboriginal and Torres Strait Islander communities still lack adequate water, electricity and sewerage services.8,9 In other fields influencing health, there has been some modest improvement in educational benchmarks, but still only a third of Aboriginal and Torres Strait Islander children reach Year 12 at school.10 Most tellingly, however, are the data for the most reliable overall measure of health — median age at death, currently 51 years for the Aboriginal and Torres Strait Islander population. There has been no improvement at all in this measure in the last 10 years.3 In this same period, the median age at death for the total Australian population increased by three years, so that the gap in median age between Indigenous people and the rest of the population has now increased to a staggering 26 years. Median age at death is much higher for the Indigenous populations of New Zealand (59 years), Canada (65 years) and the United States (63 years) and, in contrast to the situation in Australia, has been progressively increasing for the last 25 years,11 and probably for much longer. What about health spending?Spending on Aboriginal and Torres Strait Islander health is increasing, but, incredibly, the Commonwealth Government, through programs under its direct control, still spends less per capita on Indigenous people than it does on the rest of the Australian population — 74c on Indigenous Australians for every $1 spent on the rest of the population! The real increase in spending on Indigenous health between 1995–96 and 1998–99 was 15%.12 This is worthwhile, but nowhere near enough to cater for the higher levels of illness among Indigenous people. There has been a major new initiative, the Primary Health Care Access Program, with three key features: needs-based funding, funds pooling and community control. However, the funding for the program is totally inadequate, and at this stage only selected communities can participate in a program which is needed for Indigenous people throughout Australia.13 The consequences of the funding shortfall are major deficiencies in the crucial prevention and early treatment services required to break the cycle of ill-health. Why do we do so much worse than other countries?What is it about Australia that stops us from achieving the gains seen in the health of the Indigenous populations in other Western democracies, or, for that matter, in developing countries around the world? There is, after all, nothing absolutely unique either about the disease pattern or the history and circumstances of the Australian Indigenous population. Heart disease, respiratory conditions, injuries and diabetes are also the major conditions for the Indigenous populations of other countries. Dispossession, forcible relocation, removing children from their families, and heavy-handed paternalism are certainly not unique to Australia. Nor is Australia incapable of doing well with health and health services. Depending on which measurement you take, Australia is arguably the second- or third-healthiest country in the world, with a proud record in confronting difficult and complex issues such as AIDS and cancers in women.14 Why is the government not doing more?It is symptomatic of our lack of progress that this report card, and its call for action, comes not from the government, but from health professionals. Surely one would hope that some response, some soul searching, some rethinking would be evoked by the fact that over the last 10 years, despite some good news, the overall mortality of the Australian Indigenous population, alone among Western nations, has not improved, is much worse than for the Indigenous populations of New Zealand and North America, and that the gap between the mortality rate of the Indigenous population and that of the rest of the Australian population is becoming wider. But no, there is simply a deafening silence; a case of industrial deafness. Shortfalls in medical services for rural areas have produced major government programs and initiatives, and a massive injection of funds. Where is the response to the huge shortage of doctors and nurses to work in Indigenous health, and the major gaps in the workforce of all the other health professions? For any other section of the population there would be a massive outcry and appropriate remedial action. In fact, for Aboriginal and Torres Strait Islander health, the Commonwealth Government seems to be tied up with a curious logic that requires "good news" from spending less on people with worse health before it will fully rectify the health service deficiencies needed to address the worse health! Australia is locked into a cycle of endless consultation, policy and strategy formulation and measurement. Report after report is produced showing that Indigenous health is poor, improvement patchy at best, and that, overall, the gap between Indigenous and non-Indigenous health is widening. These reports reach the highest levels of Australian public and political life and are simply noted, or evoke defensive bureaucratic responses. We must act on the reports, not just note them. Flat-lining for 10 years is not good enough! Many worthwhile activities are under way, but would any informed observer really claim that current or planned prevention and treatment services, staff provision and training plans, and environmental improvements, will do the job, or are anywhere near sufficient to bring about the Indigenous health gains seen in other countries most like Australia? What do we need to do?We don't need new solutions, new strategies, some magic bullet. We need to implement strategies, like the National Aboriginal Health Strategy,15 that have been around for more than a decade. The Report Card reinforces previous calls for a national program to build up the necessary community-controlled health services for prevention and treatment; for the Primary Health Care Access Program to be given the funds required to provide those services; for a National Training Plan to train the staff, particularly Indigenous staff, required to deliver those services; and for a National Infrastructure Plan to rectify the continuing deficiencies in water supply, sanitation, education and other basic services. Australia spends over $50 billion per annum on health for its total population.16 It isn't that the modest funds required for adequate health services for Aboriginal and Torres Strait Islander people are out of reach, or that the services required are beyond our technical capacity. It is ultimately a commitment to implement the recommendations of the endless reports, and this is what the AMA, in support of Aboriginal and Torres Strait Islander organisations, is urging on the nation. Straws in the wind?Despite the general lack of progress, there are straws in the wind. The appointment of a new Health Minister and a new head of the Commonwealth Department of Health provides a fresh opportunity for dealing with the issues highlighted in the Report Card. Death rates of the NZ Maori and the Indigenous peoples of Canada dropped by 30% in the 1970s.17 Over a 40-year period, the health of the Indigenous populations of the United States improved twice as rapidly as that of the non-Indigenous population.14 Australia can do the same, and that should be our aim. Summary of the AMA Report Card on Aboriginal and Torres Strait Islander health Status Comment Infant mortality rate Indigenous rates are 2 times the total population rate Rapid fall in the 1970s. Rates in Indigenous Australians almost twice as high as those of the NZ Maori and US Indigenous populations Low birthweight Indigenous babies are twice as likely to have low birthweight. Little overall improvement since 1991, but effective programs developed and implemented in the Northern Territory and South Australia Expectation of life The gap between Indigenous and non-Indigenous people is 20 years In North America and New Zealand, the life expectancy gap (Indigenous v non-Indigenous) is 5–7 years Median age of death For Indigenous people this is 25 years less than for non-Indigenous people There has been no improvement in the median age of death in the Indigenous population in Australia in the past 10 years Standardised mortality ratios Indigenous rates are three times those of the total population High rates for diabetes, respiratory, circulatory and other conditions in the Indigenous population Mortality from pneumonia A dramatic decline in Indigenous rates since 1996 Pneumoccocal and influenza vaccines may be contributing to the decline in mortality from pneumonia Health workforce Estimated at least 59% increase in doctors required, and a 25% increase in nurses Required increase related to difficulties in accessing preventive and early treatment services Infrastructure 21 communities lack water, 80 lack electricity and 91 sewerage Some improvement, but significant gaps Education Year 12 retention rates are 36% for Indigenous people v 73% for the total population Some improvement, but significant gaps Health funding 15% real increase in government funding between 1995–96 and 1998–99 Level of health spending is 22% higher for Indigenous people but a needs index of 200% is required Aboriginal Community Controlled Health Services (ACCHS) OATSIH funding of community-controlled services increased by 50% between 1995–96 and 1999–2000 ACCHS with a network of culturally appropriate healthcare services provides a model for Indigenous health services OATSIH = Office for Aboriginal and Torres Strait Islander Health.

Ian T Ring MB BS, FAFPHM · Ngaire Brown B Med, MPHTM

The first, and only, time I questioned my decision to spend seven months working with Médecins Sans Frontières (MSF) in Afghanistan was when I crossed the tarmac of Hobart Airport to board my flight there on 17 February, 1999. My decision to go had been driven partly by a growing frustration with the increasing bureaucratic constraints of general practice and partly by a desire to re-explore the challenges of Third World medicine. My first encounter, many years ago, had been in Bangladesh, where cases seemed to walk straight out of the pages of Bailey and Love's venerable Short practice of surgery. Now, I was headed for a very different country, which, as we all know, has been subject to 20 years of continuous and continuing warfare. About a million Afghans have been killed during this time and at least 700 000 people displaced within the country itself, as well as two to three million refugees to neighbouring Pakistan and elsewhere. Key health indicators place Afghanistan among the most unfortunate countries in the world (Box 1). Life expectancy — at just 45 years of age — and childhood and maternal mortality figures are nearly the worst in the world. The mission where I was to be stationed for the next seven months — in the village of Baharak in the very impoverished northeastern province of Badahkshan (Box 2) — had just reopened; it had been shut down in 1990 after the murder of a French MSF logistician. As I boarded my flight and the plane took to the air, I dismissed any misgivings about my decision and pondered what lay ahead. Based in BaharakAll MSF personnel are given detailed clinical, cultural and security briefings before deployment. These were to prove invaluable. Baharak is in one of the least developed areas of Afghanistan. The village and its environs are devoid of infrastructure — there is neither power nor reticulated water, no communications systems or drivable roads; all this lack is compounded by the further lack of any local governmental administrative structure and the fact that the area is prone to frequent local conflict. Our clinic consisted of a simple wood-and-mud-rendered structure divided into two parts (male and female, Box 3). Given its location, in addition to no power or running water it also operated without any pathology or x-ray service to speak of. So, clinical management was pragmatic — basic, old-fashioned case definition; and treatment in accordance with MSF/World Health Organization (WHO) protocols, facilitated by modern generic drugs and IV fluids held in our pharmacy (Box 4). The problems we dealt with were varied — each day would provide about 300 patients: one or two trauma cases and obstetric emergencies on a background of ever-present infectious disease and malnutrition. On occasion, we would be further challenged with rarer but equally life-threatening presentations of a more exotic nature, such as anthrax, haemorrhagic fever and retinoblastoma (Box 5). Types of traumaGuns and minesGunshot wounds, the result of frequent, ongoing clashes between rival Northern Alliance commanders, and mine injuries, a legacy of the past Soviet occupation (1979–1989), were a daily occurrence (Box 6). Afghanistan is the most heavily mined country in the world, with an estimated 10 million mines sown. As the front lines have shifted over time, so has control of the minefields, and complete confusion now reigns about the size, content and disposition of these fields, which kill or wound seven to 10 people in Afghanistan every day. Baharak was a Soviet garrison during the occupation, and had been particularly heavily mined in an effort to deter mujahidin attacks. Now, these mines accounted for many injuries and deaths we saw, particularly among children attending their animals in the surrounding fields. We generally provided first aid, with wound surgery conducted in the provincial city, Faizabad, three hours away by road. However, when the road to Faizabad was cut for security reasons, we needed to conduct surgery as best as we could manage at Baharak. With no formal surgical training, no x-ray machine, no blood, and only ketamine for anaesthesia, management was restricted to debridement or amputation and was very much a case of "flying by the seat of one's pants". StoningsI had known to expect injuries from land mines, but on only my second day in the clinic I also met with the unexpected. A man was brought to the clinic in extremis. He had been subjected to public stoning for adultery. His condition was incompatible with survival and a solemn reminder of the country's profound cultural standards. There were two other stonings (also for adultery and also fatal) during my time in Baharak. Women and mothersCultural factors, poor maternal nutrition and a lack of trained midwives in Afghanistan contribute to the country's high maternal mortality rate. It is the world's second worst, after Sierra Leone. A mother with anaemia and sepsis related to a five-day-old retained placenta typified the sorts of presentations to be dealt with on a daily basis. We were fortunate to have an English midwife with 20 years' experience in the Third World working with us. Cultural constraints did not allow me to examine female patients; at all times, they were required to be fully covered in their shalwar kameez. As necessary, the midwife would conduct the patient examination, relaying her findings to me from behind a screen. Infectious diseasesThe commonThe leading cause of child mortality was diarrhoeal illness and dysentery, which related to the absence of safe water and poor sanitation. In summer, the incidence of both dysentery and typhoid escalated dramatically; sporadic cases of cholera were also seen (Box 7A). The simple use of oral rehydration salts was lifesaving for many. Malaria accounted for about 35% of all the summer admissions. On our arrival, the tuberculosis program was almost non-existent. Poor compliance and the inappropriate use of drugs of poor quality, that had made their way from Pakistan to the local bazaar, also contributed to the problem. The disproportionate number of extrapulmonary cases confirmed our fears that the more infective active pulmonary cases were either not presenting or being missed (Box 7B). Leishmaniasis is endemic in Afghanistan, but invariably in the cutaneous, self-limiting "oriental sore" form (Box 7C). A few cases of the more serious visceral leishmaniasis, kala-azar, had been documented in the past, and we saw many patients with remittent fever and grossly enlarged spleens who often did not fit the patterns of chronic malaria, brucellosis or myeloproliferative disorders. More than likely, several of these patients were dying of treatable visceral leishmaniasis. The absence of any antimonials usually used to treat kala-azar related to the lack of information on the prevalence of this condition; the absence of any firm epidemiological work on this and other infectious diseases significantly hampers the development of an effective health strategy in Afghanistan. The rareOn occasions, I was confronted by rare but life-threatening conditions. Anthrax, a significant part of the germ warfare repertoire, is endemic in Afghanistan, and usually seen as the relatively benign cutaneous form. The systemic form is anything but benign. One unfortunate patient, who had handled a dead sheep a few days earlier, presented to our mission with the typical black eschar and oedematous swelling over one eye. He developed frighteningly progressive respiratory distress and died some hours later, despite aggressive doses of intravenous antibiotics. For me, pneumonic anthrax is now a case of "once seen, never forgotten". Then, one afternoon, I was asked to review a patient with uncontrollable epistaxis. The two health workers who were attempting to stem the bleeding were heavily contaminated with blood. Of greater concern to me was the fever, haematuria and petechial rash over the patient's body, including his soft palate. An infectious diseases colleague had warned me of the existence of Congo-Crimean haemorrhagic fever (CCHF) in Badahkshan and the serious risk of nosocomial transmission. Everyone was disinfected and the patient barrier-nursed as best we could manage. As always, treatment was fairly pragmatic. If the patient did have CCHF, there was little we could offer. The only treatable cause of such a presentation I could think of was a coagulopathy due to fulminating malaria and typhoid, so the patient was commenced on quinine and chloramphenicol. He survived, but developed paraplegia, presumably from a secondary spinal bleed. On completion of my mission in Afghanistan, I took a sample of the patient's serum back to Geneva (despite some misgivings about the ethical and legal implications of carrying such potentially biosensitive material about the world); immunofluorescence confirmed the presence of IgG antibodies to CCHF. Safe and secure?Security is an important concern for any MSF deployment. Strict SOPs (standard operating procedures) were adhered to, with regular HF (high frequency) radio skids to our head of mission in Tajikistan, the neighbouring country to the north. They had a rear link to Geneva by satellite phone. More often than not, deteriorations in the regional security situation were relayed by these means rather than by locals. Taliban offensiveDuring the July offensive, Taliban forces advanced rapidly on two axes nearby, one towards Faizabad and the other along the Panjshir Valley. At the same time, reports were received of a large group of Taliban gathering at Shah Salim Pass, on the border with Pakistan to the south. All United Nations flights to Faizabad were cancelled, so any rearward evacuation of our missions to Tajikistan was potentially threatened. In our MSF vests, my Swiss physician friend, Philippe, and I felt secure. We both thought we were about to witness a defining moment in Afghan history, but a brilliantly executed counterattack by the Northern Alliance commander Ahmed Shah Massoud thwarted the Taliban advance (Box 8). Northern AllianceWe shared a meal with commander Najmaddin Khan, at that time the second most important commander in the Northern Alliance after Massoud. I remember that he had a nervous tic and that the meal was interrupted frequently by calls on his satellite phone to other alliance commanders. On one occasion Massoud arrived by helicopter to visit Najmaddin; two hours later a Taliban MiG fighter plane bombed Baharak. Taliban intelligence was excellent; fortunately, their aim was not so good. Najmaddin was ambushed and killed in Baharak a month after I left Afghanistan. Massoud was assassinated by suicide bombers (posing as journalists) on 9 September last year — two days before the terrorist attacks in the US. Away from BaharakWakhan CorridorOne of the highlights of my time in Afghanistan was an exploratory mission into Wakhan, the poorest and most remote district of the country, located in the far northeast bordering Tajikistan (to the north), China (to the east) and Pakistan (to the south). If, in shape, the map of Afghanistan is thought of as resembling an irregular leaf hanging from a stem, then the stem would be the Wakhan Corridor. The district has an average altitude of 3000 metres and is subject to harsh climatic conditions. It is also devoid of any infrastructure, and the medical facility at Ishkashem is up to 10 days' travel by donkey from the more remote areas of the district. The first stop of our trip was to pay respects to the local Shah, who seemed a very reasonable man with the best interests of his people at heart. From there we travelled with his opium-addicted uncle, who facilitated our entrez to the villages (Box 9). Afghanistan is currently the world's leading supplier of illicit opium, providing a significant source of revenue for arms for military commanders, or, as one farmer put it, "the West sends us weapons, we send the West our white powder with respect" (Box 10). It soon became apparent that opium addiction was common in Wakhan, primarily as a substitute for non-existent health care. Its analgesic, antitussive and constipating effects provided a panacea for many of the area's endemic diseases. LathyrismOur predeployment briefing had mentioned a suspected case of lathyrism near the village of Khandud. Lathyrism is a neurological disorder, known since the time of Hippocrates. It is associated with the consumption of Lathyrus sativus — known locally as patak (and also known as chickling pea, grass pea and kesan dahl). Although very nutritious and cheap, this legume contains a potent neurotoxin, which eventually causes irreversible spastic paralysis, hyperaesthesia and paraesthesiae (Box 11). As we conducted primary health checks in various villages, we found that many locals complained of muscle stiffness, with examination revealing very obvious lower-limb clonus, consistent with lathyrism. Obviously, the condition was endemic. Most of the locals knew of the association between patak and lathyrism but continued to eat it out of economic necessity. OutbreakAs we progressed further into Wakhan, we had to abandon the vehicle and travel by horse. Many villages hadn't seen a foreigner for more than 20 years, including the village of Daghullaman. There, we investigated a report of an outbreak responsible for many deaths. At one stage, barely enough of the 300 villagers were strong enough to secure adequate water for the others. Active cases had a virulent flu-like illness, many with complicating pneumonia. We treated them empirically with the last of our dwindling supplies of ciprofloxacin, forearmed with the knowledge of a large but similar outbreak that had occurred a few months earlier along the Tajik border, and which WHO tests had implicated as klebsiella infection. Health surveyWe conducted a mid upper arm circumference survey, studying 365 children between 6 months and 5 years of age, confirming that about half of them were nutritionally at risk. Immunisation was non-existent, and measles accounted for a disproportionate number of deaths in childhood — 12 children in one house alone. A measles vaccination program was subsequently implemented in Wakhan by MSF. A spot of sportsOn the return journey from Wakhan, we made the most of an opportunity to take part in some fishing and hunting activities. The fishing was very productive and we followed the usual Afghan tradition of using rapidly expanding bait (Box 12). An ibex hunt was also conducted along traditional Afghan lines — using Kalashnikovs. The meat provided a welcome change from Wakhan bread and yoghurt. FaizabadThe final phase of my time in Afghanistan was spent assisting with the newly established mission in Faizabad (Box 13), aimed at developing the inpatient capability of Faizabad Hospital. This hospital was the only formal surgical facility in a district of 700 000 people, with a grand total of one operating theatre and two trained Afghan surgeons. The challenge of working there was made all the greater by the lack of blood cross-matching reagents, and the amazing situation whereby the more experienced of the two surgeons was only permitted to operate on the most difficult cases. Between times, he was kept in jail for the murder of his brother! What now?What does the future hold for Afghanistan, for MSF and for me? Afghanistan's long and continuous history of conflict is a tribal phenomenon fed by foreign interference, from the time of Soviet occupation to the current flow of arms from neighbouring countries to often rival military commanders throughout the land. I think that, in the current political and diplomatic milieu, the likelihood of a peaceful and united Afghanistan unfortunately seems unlikely. Further, a drought is now in its fourth year and about half of the country remains inaccessible to aid organisations. MSF, from its noble but humble beginnings in 1971, has grown to become the world's largest non-government medical organisation. Its stance of absolute neutrality enables it to meet its charter of providing independent humanitarian medical aid to populations in crisis and, in addition, advocacy; MSF was awarded the 1999 Nobel Prize for Peace. MSF continues to work in Afghanistan, although operations have been classified as a result of the antiterrorist measures taken after September 11, 2001. For me, the common threads of experiencing the Third World as a doctor have been not only the fascination of the medicine, but also the marvellous humility and dignity of the patients and the privilege of working alongside some very special people. 1: Afghanistan: key health indicators1,2 Population: 20.9 million Mortality (under 5 years): 26% Maternal mortality: 1.7% Life expectancy: 45 years Access to safe water (rural): 5% Access to adequate sanitation (rural): 1% Malnutrition (under 5 years): 35% Malaria: 3 million cases annually 3: Female outpatients department in Baharak. 4: Traction, Afghan style. 5: Retinoblastoma. 6: Mine injuries occurred daily. 7: Infectious diseases. A. Cholera, with skin turgor demonstrated. B. Tuberculosis of the spine leading to gross deformity. C. Leishmaniasis, also known as "oriental sore". D. Epistaxis associated with Congo-Crimean haemorrhagic fever (CCHF). 8: Local Baharak commander and troops. 9: Travelling the remote Wakhan Corridor. 10: The panacea opium. 11. Lathyrism associated with patak consumption. Fishing using ammunition for bait. 13: Faizabad street scene.

Robert A Simpson AM, RFD, MB BS, FACRRM

An ophthalmologist remembers his time spent at a mission hospital in Pakistan After September 11, 2001, TV bulletins about attempts to destroy al-Qaeda and the Taliban featured footage of Quetta, a city in Pakistan on the fabled North West Frontier, just south of Afghanistan's Kandahar (see Map in Simpson). The news recalled memories of the weeks I'd spent there, 42 years previously. More came flooding back as I leafed through the pages of my photo album. From Karachi to QuettaAlmost naked, I sweated on a Karachi hotel bed, the ceiling fan spinning above me. What had I let myself in for? Disconsolate, missing my wife and new firstborn son who were already back home in Australia, I could well understand why Somerset Maugham's expatriate Englishmen took to drink in the equatorial Empire. It was the northern spring of 1959, and I was overnighting in Karachi, then Pakistan's capital, en route to Quetta, near the border with Afghanistan. After three and a half years away from Australasia gaining specialist ophthalmic training in England and the USA, I'd allowed an American colleague to entice me to detour on my way home — for a 10-week stint at Quetta's Church Missionary Society Hospital. I hadn't thought of arranging professional indemnity insurance (!), and I'm not even sure travel insurance would have covered all the potential risks. The next morning, I boarded my train to the north. In addition to my ticket, I'd purchased, on advice, my personal air conditioner — a 30kg block of ice in a tin tub placed under my seat for the 24-hour trip. As we journeyed through the Desert of Sind, on the strategic railway built by the British in 1895, stories of the British Raj, India's frontier, the Khyber Pass, the Bengal Lancers and Gunga Din ran through my head. The last remnants of my ice block were melting away as the train chugged up the final slope of the Bolan Pass to enter the Quetta plateau. Missionaries among the militaryThe city of Quetta is a hill-station, about 1700 metres above sea level, in a valley ringed by snowy mountains rising to about 2500 metres. In spring, the valley floor is lush and productive, but the overgrazed hillsides are always bare. The city was rebuilt after being destroyed by earthquake in 1935. Low-rise to the eye, Quetta was, to me, reminiscent of an Australian country town. The population was about 30 000 in winter, doubling in summer. Quetta has long-standing military connections, beginning with its name — derived from "kuwetta", meaning "fort". In the centre of town, on a hillock, is the famed Red Fort antedating British rule. The British arrived in about 1876, encountering tribal groups of Brahuis and Baluchis, as well as the Pathans, the Pashtun nomads. Fearing Russian encroachment via Afghanistan, the British military commanders of the day considered the chain of missionary hospitals positioned along the frontier, including the one at Quetta, to be the equivalent of several battalions. These missions, in effect, garrisoned the border with Afghanistan, supplementing the forts along the thousand miles from Iran to China. During the Second World War, although not an active theatre of war, this garrison town was the second-largest military establishment in the British Empire, after Aldershot. Quetta's military cemetery holds the graves of soldiers from all over the old Empire, from many cultures and religions. In 1959, Quetta still retained the Commonwealth Staff College founded at the height of Empire in 1907. Security was still a concern and became evident to me in a personal way. One day, when I'd cycled out of town to photograph the scenic city and surrounds, two policemen pounced on me and confiscated my camera film — India and Pakistan were already battling over Kashmir and there had been recent bomber activity at the Indo-Pakistan border. Western medical outpostQuetta's mission hospital was originally established in 1886, and had been rebuilt after the earthquake. In the courtyard there were small cottages forming the caravanserai where patients were nursed by relatives who also took care of food and cooking. Throughout the day, electric amplifiers and loudspeakers alerted us to the call of the muezzin, reminding our Christian medical island of the dominant culture that lapped against the walls of the hospital compound. Purdah (seclusion) and veiling were still upheld in Quetta despite its cosmopolitan community. The hospital had a segregated women's section, the zenana wards. The hospital served the city and the region, catering particularly to the trans-border nomadic Pathans who moved down through the Bolan Pass to the southern plains during the winter, returning to the hills of Afghanistan during the summer. Accordingly, these tribal nomads had two opportunities each year to benefit from Western medicine. Cataracts and neglected chronic diseases were common presentations, as was diarrhoea. I myself suffered diarrhoea on several occasions and progressively lost weight during my stay. Faecal tests positive for blood and/or amoebae sentenced one to amoebicides; negatives dictated sulfas, to which my bugs responded. The diarrhoea was surely related to the town's contaminated water supply. Irrigation water from the city's reservoirs flowed through the streets alongside the footpaths. Using removable paddles, the waterman selectively diverted the flow into separate open channels for individual sections of the town on given days. Not surprisingly, the water reaching our vegetable gardens in the hospital compound was murky. This public health issue didn't seem to agitate either the city authorities or, in general, the Western doctors! In winter, the hospital ran an outreach clinic at Shikarpur, 200 miles to the south. Many such clinics, known as "cataract camps", were held on the Indian subcontinent under missionary auspices, foreshadowing the Fred Hollows Foundation. Cataract surgery and other proceduresEvery operation began with a Christian prayer. For the anxious patient, this was extra premedication. Local anaesthesia was used for cataract operations — patients' eyelids were kept open during the procedure with a pair of locally made fork retractors, handheld by the assistant, one of the male nurses trained in the hospital's own program. Graefe section with conjunctival flap was standard, progressing to intracapsular extraction. I carried out over 100 cataract procedures in my 10 weeks, and many plastic operations on eyelids and tear ducts. I treated one patient with retinal detachment. I also assisted at numerous general surgical procedures and outpatient clinics. The hospital's surgeons — Pakistani Christians as well as English — were skilled in all aspects of surgery (ophthalmology included). I saw many cases of advanced cancers of the head and neck such as I'd never before witnessed that were managed with massive excisions and repairs. Radiotherapy was available in the form of radium needles. When two of those valued needles were mislaid, many of the hospital staff devoted the day to search for them — they turned up when an American geologist scanned the rubbish tip with his Geiger counter! A social summerThe social atmosphere throughout my stay was memorable. I was made to feel one of the family by the hospital's director, Dr Ronnie Holland, son of a previous director, Sir Henry Holland, who had been knighted for heroism in the 1935 earthquake. His wife, Joan, was a remarkable woman who, while pregnant, had survived near-fatal polio, being kept alive with manual resuscitation until an iron lung could be procured and repaired. She now worked from her wheelchair, as nurse-anaesthetist. Sunday was a real day of rest, commencing with chapel and then a relaxing picnic lunch on the English lawn of the hospital gardens, next to a rich and varied orchard. It was here that I became partial to green tea. At the Hollands' table, I met intriguing characters from many cultures. They included the indigenous Bishop of Karachi, Chandhu Ray — an amiable man with whom to exchange philosophies; Parsee merchants, who were the first to tell me that their dead were disposed of on special towers, for the vultures; and American scientists working for United Nations agricultural or prospecting agencies. Among other social engagements were invitations to dinner with Australian army officers at the Staff College. When it came time for the Hollands to open the hospital's summer cottage in the hill-station of Ziarat, 70 miles east, and elevated some 900 metres above Quetta, I accompanied them. We set off for the weekend through a narrow defile to a higher plateau before climbing the dusty hills on one side of the broad valley. As I swallowed the dust and, terrified, looked over the rim of the snaky alpine tracks, I was told that Alexander the Great had passed along the valley below after conquering Swat, in the border regions near China. At various points in our passage, we came across clusters of flags on poles like those marking golf holes, but twice as tall — markers of nomad graves. At 630 metres above sea level, juniper trees suddenly appeared on the valley walls, creating a new demarcation line between the bare slopes below and the trees, which only thrived above this height. The mountain air was laden with the scent of thyme, as well as juniper. ReflectionsAt the end of my adventure, returning to my hotel in Karachi, I was surprised to find that Bishop Ray had left a message for me. He invited me to lunch with him, and then came to the airport to see me off. His touching courtesy prompted me to ponder the situation of the Christian minority and its missionary doctors, whose lives I had shared. My missionary friends were not confounded by their inability to care for everyone, everywhere in the region. They were realists, content to do all they could to meet local needs. To them, their calling didn't involve self-sacrifice (although a young English nurse did die suddenly during my visit). Perhaps the missionary urge, previously a preserve of the Christian medical missionaries, can be best illustrated by paraphrasing Sir Henry Holland: Our aim is to care for the whole person, body, mind and spirit. Our healing is like a sermon in the ward. It's not bait to lure the people. It's delivered in dedication to our calling, undaunted by dangers and difficulties. Today, the North West Frontier is an even more dangerous place than it was in 1959. Opposition to the presence, and even to the work, of medical missionaries has intensified. I reflected on what the hospital and I had provided for each other. I'd assisted slightly with the patient load. Quetta gave me the benefits of concentrated experience with advanced, neglected, untreated disease; further medical and surgical insight; and the privilege of working with admirable colleagues dedicated to the impressive people native to this frontier. I'd learnt much more in Quetta than surgery alone.

Ivan Cher FRACS

An elective term in Malawi inspired students to make a difference in medical aid. When, at the end of 2000, medical students Greg Fox and Greg Moloney travelled from the University of New South Wales (UNSW) to Blantyre, Malawi, Africa, to complete an elective term at Queen Elizabeth Central Hospital, they witnessed a health system drastically hampered by a shortage of medical resources. On return to Australia, they resolved to "give back" to those in the developing world who had taught and welcomed them so generously. With the support of other UNSW medical students, the Medical Students' Aid Project (MSAP) was born. Our non-profit, student-run, volunteer organisation is the first of its kind in Australia. Our primary goal is to deliver targeted medical aid to hospitals in developing countries. Working in the children's ward we realised what a huge difference some basic items such as cannulas, needles and emergency equipment would make to the doctors' ability to care for sick children. The health problems facing these countries are not simple, but we believe that many individual contributions can together make a difference — Greg Fox (left) and Greg Moloney MSAP co-founders. IdealsMSAP tries to ensure that all aid is appropriate and beneficial to our partner hospitals. We do so by delivering only aid that is specifically requested by recipient hospitals. At the beginning of each year, our partner hospitals submit a prioritised wishlist for medical aid, which we use to direct our efforts in fundraising and equipment seeking. MSAP student volunteers visit partner hospitals each year as part of their final-year elective term. Their visits are timed to coincide with the arrival of aid, to ensure it is used appropriately. The hospital wishlists are refined through first-hand feedback during these visits. Forming long-term, sustainable partnerships with the partner hospitals enhances MSAP's effectiveness. Donating to the same hospitals each year ensures that lessons learned from previous years can be used to better meet our goals in the future. Partner hospitals share a number of qualities: they have a need for aid that may be met by MSAP; they provide valuable experience of medical practice in the developing world; and they are in locations that will continue to attract medical students in the future. In return for our efforts, our visits to partner hospitals enrich us with a vivid cultural and educational experience, the memories of which we carry back to share with fellow students and the wider community. Partner hospitalsThe MSAP partner hospitals in 2001 were in Malawi (Box 1), Samoa (Box 2), Tonga (Box 3) and India (the Lady Willingdon Hospital in Manali). Korle-bu Hospital, in Accra, Ghana, has been included in 2002 and has already received a paediatric cystoscope (worth over $5000), and diathermy and laparoscopic equipment. Smaller donations of equipment and medication will also be made to Gizo Hospital in the Western Province of the Solomon Islands and Hospital Santa Barbara in Sucre, Bolivia. "As a MSAP volunteer, I have become aware of the stark contrast between the First World ideals of sterile operating theatres and universal vaccination and the developing world reality of overcrowded clinics and inadequate resources. It is satisfying to have made a small contribution towards bringing the two worlds closer. MSAP has been an important part of my medical education." — Asif Saber, MSAP member How MSAP worksMSAP is entirely student administered and receives generous support from the UNSW Faculty of Medicine and the UNSW Foundation. All MSAP members volunteer their time and the university covers our administration costs. About 20 medical students were involved in 2001 and 2002. Our current patron, Dr Gaye Casper (Senior Conjoint Lecturer, School of Women's and Children's Health, UNSW), provides moral support and practical advice to the students. MSAP collects tax-deductible monetary donations from private and corporate sources. Monetary donations are used to purchase equipment and to fund transportation. Donations of basic and specialised medical equipment are received primarily from Area Health Services in New South Wales. Other sources include private donors, such as retired doctors, medical companies and volunteer organisations such as Global Medical Support (which sends medical supplies to countries in need). MSAP purchases subsidised and in-date medication through Overseas Pharmaceutical Aid for Life (OPAL) (http://www.opal.org.au), a South Australian company that supplies pharmaceuticals to developing countries in accordance with WHO Guidelines for Drug Donations (http://whqlibdoc.who.int/hq/1999/WHO_EDM_PAR_99.4.pdf, link updated Nov 2005). OPAL puts together medication packages, organises customs documentation and arranges commercial delivery or delivery by MSAP volunteers. All equipment collected by MSAP is stored free-of-charge at a Waverley Council depot in Sydney. Towards the end of the year we organise "packing days" to sort equipment onto pallets for shipment to each hospital. Five pallets of equipment were sent overseas in 2001 and in 2002 we expect to deliver five more. "Throughout Australia, large quantities of medical equipment — such as superseded anaesthetic equipment, ECG machines and glucometers — lie in storage and are desperately needed in developing countries" — Peter Fox, MSAP volunteer So far, medical equipment has been transported by commercial shipping lines at MSAP's expense. Members have also carried small quantities of equipment with them when visiting partner hospitals. Free transportation to Tonga in 2002 has been negotiated through the Tongan Consulate General in Australia and the Pacific Forum Line. In two years MSAP has delivered over $100 000 worth of medical aid. The community role of MSAPMSAP is active in international health education for other medical students through lectures, "Developing World Health" night and contributions to student publications. MSAP also contributes to wider UNSW campus activities, for example through our involvement with Anti-Poverty Week. Our annual "MSAP Benefit Night" increases awareness of our cause, raises funds and gives us a chance to thank donors for their generosity. Updates, our newsletter, communicates activities and news to followers. The futureIn just two years, we have received enormous support from the medical profession and the broader community. With ongoing assistance we will continue to expand as an organisation and maintain our capacity to deliver medical aid to the developing world. MSAP has inspired considerable interest among medical students from other Australian universities, who are eager to establish similar ventures. We hope to share our experiences and encourage others to adopt an active role in developing world health. 1: Queen Elizabeth Central Hospital, Blantyre, Malawi MSAP donations 2001: Equipment with a paediatric focus (eg, cephalosporin antibiotics, high-kilojoule powder, paediatric nasogastric tubes and textbooks). 2002: Medications worth $2500 (mainly antibiotics), urine dipsticks, psychiatry textbooks. No pallets sent this year (too expensive). We spent two months studying paediatrics at this tertiary referral hospital towards the end of 2001. The cases we saw were sometimes novel, sometimes gratifying and sometimes heartbreaking. HIV is having a devastating effect in Africa, while conditions such as meningitis, malaria, tuberculosis and malnutrition, readily treatable in Australia, are moving beyond the capacity of the systems attempting to cope with them. One afternoon we basked in a golden sunset by the serene lake shore as fishermen in dugout canoes repaired their nets and infants cavorted in the waters. We'd just finished a long afternoon's clinic where one young man with advanced AIDS sought treatment for painful, widespread shingles; a stooped old lady who had lost all her family wanted relief for her chronic back pain; and a younger widow needed to go to hospital immediately for a renal infection but couldn't afford the dollar to get her there. At least we could help her. Through MSAP, I know that we have made a small but undeniable difference to the patients we met, who first became real and then became our friends. Rebecca Blake, Toby Winton-Brown Women and children fetching water from the village pump. 2: Tupua Tamasese Meaole Hospital, Apia, Samoa MSAP donations 2001: Syringes, gloves, defibrillator, textbooks. 2002: New ECG machine, 1 pallet of equipment (nebuliser, glucometers, ophthalmoscope/otoscope, stethoscopes, anaesthetic equipment, sutures, catheters, stoma-related products). At the end of 2001, I had the privilege of spending two months working in the emergency department of this tertiary referral hospital. Hundreds of patients would queue each day with complaints that would be easy to address in Australia but impossible to treat locally given the lack of basic medications. I will always remember the young patient who sat, seemingly forever, on the surgical ward awaiting an amputation, as his leg infection could not otherwise be treated. The most rewarding part of my time in Samoa was being able to give something back to the community through the MSAP donations. It was overwhelming to see how grateful the people were for these basic medications and equipment. Cath Tacon MSAP volunteer Cath Tacon handing supplies to Dr Satu Viali. 3: Vaiola Hospital, Nuku'alofa, Tonga MSAP donations 2001: Syringes, bandages, sutures, surgical forceps, operating microscope, hysteroscopy and laparoscopy equipment. 2002: Three pallets with similar supplies to those sent in 2001; medications worth $2000 (mainly cephalosporin antibiotics); cardiotocography machine. Throughout 2001, members of MSAP put an enormous amount of energy into collecting and transporting equipment for the Polynesian kingdom of Tonga. Being our inaugural year we had no way of knowing exactly what to expect or how our donation would be received, but my anxieties were allayed the moment I stepped off the plane by the warm welcome I received. The arrival of medical equipment at Vaiola Hospital, a tertiary referral hospital, was greeted with great excitement and thanks. One of the antibiotics was used almost immediately to treat a man with several resistant infections. The equipment "handing over" ceremony was reported by the local newspaper and even made the Tongan Nightly News! Sarah Woodgate MSAP supplies outside Vaiola Hospital, Tonga.

Angus G Ritchie · Adrian T Fung · Peter N Fox · Kathryn E Roberts · John S Vedelago · Rebecca C Blake · Asif A Saber · Jess M Glass · Linda K Martin

More patients than beds. Dr Lion, Dr Kimborarith and Dr Thaly doing ward rounds on the verandah of the Takeo Eye Hospital. Bombed in secret for years by the United States during the Vietnam War, overrun by Pol Pot and his murderous Khmer Rouge, invaded by Vietnam in 1978, blighted by landmines, and lurching through periods of famine, post-colonial political crisis, and intermittent civil war, Cambodia has suffered terribly. Its people are among the poorest in Asia. Aid work commenced by the Maryknoll organisation in 1993 has expanded and been handed over to another Catholic charity, Caritas, supported by funding from Germany and Australia. The centrepiece of the project is an eye hospital in Takeo, 80 km south of the capital, Phnom Penh. Here, services are provided to the poor and local doctors and nurses are trained in the basics of ophthalmology. This is the story of my short time working at Takeo Eye Hospital around Christmas 2001: a day in the life of a volunteer. You can tell that French colonialists were in Cambodia; the bread is excellent and a breakfast favourite at the Café Chisor where I start the day. I hail a prowling motorscooter, because taxis do not exist, and negotiate a price to the Takeo Eye Hospital on the outskirts of this small town. As we bounce and weave along the dilapidated dirt tracks that pass for roads, I notice some causes of the eye trauma that will present to hospital today. Workers threshing rice by hand or angle-grinding in metal shops have no eye protection. Despite the dust and insects, none of the "moto" riders wear goggles, let alone a helmet. The hospital is run by a Dutch ophthalmologist, Dr Franz Lion, and staffed by his three trainees, Dr Eng Kimborarith, Dr Sok Chenda and Dr Poch Thaly, who have come from various distant provinces, leaving their families behind, to attend the 18-month Basic Eye Doctor course. In the high humidity and with a lack of basic hygiene, many injuries from foreign bodies result in corneal ulcers. Pathology services are virtually non-existent and mixed infections are the norm anyway, so ulcers are treated with a combination of antifungals, antibiotics and antivirals. Our day begins with a ward round before 8 am, but the nurses start much earlier, removing dressings and ensuring that the patients' relatives are out of the wards. There are two rooms, each with about 20 wooden platforms making the 40 hospital beds. These are rarely sufficient, and today we have an additional 20 patients who have spent the night on the verandah. Our procession enters each area in turn, led by Dr Lion and his cheery salutation of "Sua s'dei" (an informal "hello"). The patients return the greeting and offer the traditional hands-together gesture of Buddhist greeting. One elderly lady just claps. Brief examinations are undertaken and results of the previous day's surgery are revealed. Patients with corneal ulcers are quarantined in their own ward and it too is full. Carers, who spent the night on the floor beside their relatives, are cooking breakfasts over the fires in the communal kitchen area outside the wards. Other nurses are already assessing new patients, some of whom have travelled great distances and have queued since dawn. To ensure the afternoon's surgery will start on time, nurses will only accept new patients until mid-morning. We join them in the outpatients area; a large room with four small desks, slit-lamps and a few tables for simple procedures. The verandahs are used for assessments of visual acuity, visual fields, eye movements and other basics. A toddler is brought in by her father with a lacerated cornea. Like many locals, he traps wild birds and keeps them at home before slaughter or sale. She has been pecked in the eye and, incredibly, is the third such young patient this week. The injury occurred about a week ago and precious time (and money) has been wasted on "traditional healers" in the interim. She will be properly assessed under anaesthesia this afternoon. A stork tethered outside a Cambodian business. Trapping wild birds for food or sale is common. In my time at Takeo Eye Hospital, I saw three children with eye injuries from being pecked by trapped birds. Another child is screaming inconsolably. He is found to have a small rice grain in the upper conjunctival fornix. I imagine that in future he will not stand so close as his parents bash rice sheaves against the threshing boards. I'm obtaining valuable experience with the slit-lamp in reviewing some of the long-term ulcer patients, but their progress is sometimes discouraging. Every surgery list includes eviscerations of eyes that cannot be saved. One of my patients today is a 10-year-old girl with the classic Khmer smile that the guide books always mention. I've never found out how she lost her left eye; I'm just worried about the persistent ulcer on the right that has her vision down to "count fingers at two metres". Uveitis is a common and painful condition in this community, but in the harvest season only very serious ailments will cause an adult to leave their fields. Advanced cases of uveitis with bizarrely misshapen irides due to lens adhesions are frequent. A steady stream of elderly patients present with glaucoma and cataracts. Lunch is an event I've been enjoying with the local doctors for a few weeks now. One of the cleaners is given funds and goes to the market daily. She returns to prepare delicious traditional meals; like the spicy soup, curried fish, and pickled vegetables which we eat noisily and with gusto, as is the custom. I'm told this feast is only "simple food". It costs me two dollars but that is the daily wage in Cambodia. Everyone who survived the Khmer Rouge has a story, and now that I know them better the trainees are talking about some of these events. Dr Thaly's family were separated to work on different communes for almost the entire four years of Pol Pot's regime. All educated people were considered counter-revolutionaries. Dr Thaly confirms that people were killed simply because they did not have the calloused hands of a peasant, as depicted in The Killing Fields. One doctor in a nearby town survived by passing himself off as mentally handicapped, feigning a twitch and a stammer for four years, and is now unable to cease these behaviours. The afternoons are dedicated to surgery. The operating theatre is airconditioned, but a wardsman armed with a flyswatter watches for intruding insects. Equipment is basic; fragments of razor blades serve as scalpels and haemostasis is achieved with a probe heated in a candle. Adult patients are given a face block and walk in and out of the surgery. Children are anaesthetised with ketamine, and vital functions are monitored by a stethoscope. The eye of our bird-peck girl collapses as the wound is explored and another evisceration is performed. But there are many successful outcomes: tarsal plate rotations for trachoma, trabeculectomy for glaucoma (drugs are unaffordable), lid elevations for ptosis, corrections for strabismus, pterygia removed, and sight restored for many patients by cataract extractions. Last year, this hospital performed 3100 operations. Surgery at Takeo Eye Hospital: barefooted patients and doctors in thongs. In the late afternoon, Dr Lion enthusiastically summons us for a tutorial. Afterwards, I stay back to do some study, but mostly chat, with the trainees. Later, as I'm walking home two nurses on a moto stop and offer a lift. As three is only half the maximum number that I've seen on a Cambodian motorscooter, I feel quite secure. The best place for dinner is back at Café Chisor. This was set up by Dr Lion's wife as a non-profit enterprise to provide employment and training for local women. The food is traditional, wonderful and very affordable, but I have been startled by a scorpion and a snake during meals here, much to the amusement of local patrons. Very few westerners visit Takeo and young Khmers are desperate to learn English, so I am quite popular. I've started giving impromptu lessons to relatives of the cafe's staff and they return the favour in kind. We often end up just laughing at each other. As I return to my room, extinguish the candle (the electricity has failed again) and carefully slither under the mosquito net, I'm very grateful to have learned from the inspirational Dr Lion and other staff, and to have been of some assistance to the needy patients of Takeo Eye Hospital. I hope that this project will one day mean that there are enough Cambodian eye doctors to go around.

Leo J Ryan LLB(Hons), BSc

We report a 44-year-old Western Australian man who suffered a cardiac arrest several hours after a bite by a brown snake. He was successfully resuscitated after bolus administration of undiluted brown snake antivenom. We suggest that an initial bolus dose of at least five ampoules (5000 units) of undiluted brown snake antivenom should be given as primary therapy for cardiac arrest following brown snake envenomation in Western Australia. (MJA 2002; 177: 646-649) Brown snakes are the leading cause of both snakebites and snakebite fatalities in Australia.1,2 The characteristic feature of significant envenomation by brown snakes is defibrination coagulopathy caused by potent procoagulants in the venom. However, the cause of cardiac arrest after this envenomation is unclear. One hypothesis, derived from animal models, is that early massive thrombosis results in collapse, cardiac arrest and death. The brief thrombotic phase of envenomation occurs before the development of defibrination. It is hypothesised that coronary vessels become temporarily occluded, resulting in hypotension, collapse and cardiac arrest.3,4 We report a patient who was successfully resuscitated after cardiac arrest following brown snake envenomation. The clinical and laboratory evidence appears to support the above hypothesis. Western brown snake (Pseudonaja nuchalis). Illustration copyright Dr Julian White, Head of Toxinology, Women's and Children's Hospital, North Adelaide, SA (Clinical toxinology resources <www.toxinology.com>) Clinical recordA 44-year-old man found a snake (later identified as Pseudonaja nuchalis, also known as a gwardar) in his house in Toodyay (85 km east of Perth). He attempted to catch it and was bitten on the middle finger of the left hand. He was alone and placed a single compression bandage on his left upper limb extending from the fingers to the elbow. He then drove to his general practitioner, a journey of 15 km, taking about 10 minutes. The GP observed no symptoms or signs of envenomation and referred the patient to Royal Perth Hospital by ambulance. In transit, several minutes from Swan District Hospital, the patient complained of feeling unwell with chest tightness, and rapidly became unresponsive. It was decided to seek medical attention at Swan District Hospital. 02:15 hours after the bite: On arrival at the hospital, the patient was in a tonic–clonic state and unresponsive. Electrocardiography (ECG) revealed a narrow complex rhythm with no cardiac output (ie, pulseless electrical activity). Standard advanced life support measures were commenced, including cardiopulmonary resuscitation, intubation, and administration of two 0.5 mg doses of adrenalin and one litre of normal saline. In addition, undiluted snake antivenom was given as an intravenous bolus, comprising one ampoule of polyvalent antivenom and two ampoules each of brown snake antivenom (2000 units) and tiger snake antivenom (6000 units). The situation was discussed with the on-call toxicologist at the local poisons information centre. Once further antivenom supplies were obtained, another ampoule of polyvalent antivenom and three ampoules of brown snake antivenom (3000 units) were administered. Spontaneous circulation resumed within one minute of administration of these three ampoules. Total cardiopulmonary resuscitation time was 11 minutes. When the patient's condition was stabilised, he was transferred to Royal Perth Hospital. En route, the first signs of coagulopathy appeared, with bleeding lips and gingivae (Box 1). Results of laboratory investigations are shown in Box 2. 03:10 hours after the bite: On arrival at Royal Perth Hospital, the patient's heart rate was 105 bpm, blood pressure was 135/60 mm Hg, and pupils were equal at 4 mm diameter and briskly reactive. Examination revealed bleeding gingivae and nose, suffusion petechiae around the eyes, oozing from venepuncture sites, and rosé-coloured urine. ECG findings are shown in Box 3. Initial management involved reinforcing the compression bandage and extending it to include the whole of the left upper limb, and infusion of 10 ampoules of brown snake antivenom in 100 mL 0.9% saline over 15 minutes. Following this infusion, no further oozing of blood was noted. The compression bandage was then removed. The patient's clinical condition remained stable. Cranial computed tomography revealed no evidence of intracranial haemorrhage, nor early evidence of arterial thrombosis or ischaemia. 05:00 hours after the bite: The patient was transferred to the intensive care unit, where his condition remained stable. Repeat coagulation studies at 05:53 hours after the bite revealed a plasma fibrinogen level still below 0.3 g/L (Box 2). A further five ampoules of brown snake antivenom were infused. 11:38 hours after the bite: Coagulation studies demonstrated the return of measurable clotting activity, with a fibrinogen titre < 0.3 g/L, but an international normalised ratio (INR) of 2.7, and an activated partial thromboplastin time (APTT) of 64.4 s. No further antivenom was given. 14:49 hours after the bite: Repeat coagulation studies revealed a rising fibrinogen titre of 0.5 g/L, INR of 1.8, and an APTT of 44.7 s. The patient was subsequently extubated, neurologically normal. No additional blood products, such as fresh frozen plasma or cryoprecipitate, were administered at any stage. In view of the high antivenom load given to the patient and the consequent risk of serum sickness, the patient was commenced on a five-day course of oral prednisone (50 mg/day). Day 2: The patient was transferred to the cardiology unit for investigation of the chest pain, collapse and subsequent rise in plasma troponin I level. He had no risk factors or previous history of cardiac disease, and experienced no further episodes of chest pain. An angiogram four days after envenomation revealed normal left ventricular function and normal coronary arteries. There were no abnormal neurological findings, and he was discharged after the angiogram. At follow-up a month later: The patient was well but reported a mild flu-like illness with rash and sore joints between days 17 and 21 after envenomation. DiscussionDeaths after brown snake envenomation tend to be either early (within hours) or delayed (days after the bite). Early deaths have been thought to result from a primary cardiotoxic effect, anaphylaxis, or early massive thrombosis.3,4 Delayed deaths appear to result from secondary complications, such as intracranial haemorrhage.5,6 Our patient described chest tightness immediately before his sudden collapse, and the post-resuscitation ECG was non-specific, possibly consistent with diffuse myocardial ischaemia. These changes could be associated with short-lived coronary vessel occlusion by thrombi generated by venom procoagulants.3,4 The rise in serum troponin I level was consistent with the effects of cardiopulmonary resuscitation, but could also represent ischaemic injury to the myocardium.7 An in-vitro study showed that the venoms of three Pseudonaja spp. have strong coagulant activity.8 There is strong prothrombin activator activity (Factor Xa-like) converting prothrombin to thrombin, with no dependence on Factor V and little dependence on calcium and phospholipid. Intravenous injection of venom in dogs showed the potential for early thrombosis, resulting in hypotension, cardiac arrest and death.3,4 There have been previous reports of survival of patients in extremis after brown snake envenomation. In 1975, Sutherland described a 42-year-old woman who suddenly collapsed about 20 minutes after envenomation. She was said to be pulseless, but her condition improved within 30 seconds of receiving antivenom.9 In another report, a 52-year-old man became unconscious within 15 minutes of a bite by Pseudonaja textilis. He received 1000 units of brown snake antivenom intravenously 30 minutes after the bite, and his condition stabilised.10 However, in neither case did the patient require external cardiac compression or advanced life support measures, such as intubation and adrenalin. We believe that the more severe nature of our patient's condition makes this case notable. Antivenom dosing is controversial and to some extent arbitrary. However, as a result of this case, we propose that cardiac arrest due to massive brown snake envenomation in Western Australia should be treated with an initial minimum bolus of at least five ampoules (5000 units) of undiluted brown snake antivenom. This contrasts with the usual slow infusion of diluted antivenom. Even higher doses of antivenom may be required. A study in dogs found that the dose required to prevent cardiovascular depression and coagulopathy induced by P. textilis was 25 times the current recommended dose for clinical use.11 Other authors have also stated that the necessary dose of antivenom may be greater than current recommendations.5 In addition, the venom of the western brown snake (P. nuchalis, or gwardar) may be more potent than that of the eastern brown snake (P. textilis),12 while antivenom raised against P. textilis may be less effective in neutralising the venom components of Western Australia's P. nuchalis.13 It should be noted that antivenom is an increasingly scarce resource, and that stocks in many hospitals are limited. Some clinicians might have considered administering adjuvant therapies, such as fresh frozen plasma, to our patient. However, our approach was consistent with the guidelines of the antivenom manufacturer, which state that fresh frozen plasma "is usually not needed and is contraindicated until all circulating venom has been neutralised with adequate antivenom, except if there is severe, life threatening haemorrhage".14 Our patient had acceptable INR and APTT readings within two hours of the last antivenom dose, and his fibrinogen level had returned to levels associated with haemostasis within five hours. He remained clinically stable, with no evidence of active haemorrhage.15 During the initial resuscitation, we chose a smaller than standard dose of adrenalin (0.5 mg v 1 mg) to avoid further increasing the risk of intracranial haemorrhage.6 As the cardiac arrest was witnessed, with only a short interval before resuscitation began, and as the cause was known, it was decided that a lower dose would provide the optimum balance between benefit and risk. Our patient also illustrates the need to emphasise the public health message for the community — early application of appropriate first aid is effective in brown snake envenomation.16 Correct first aid comprises pressure immobilisation bandaging of the entire limb, keeping the patient still, splinting the limb and seeking medical attention. In many fatal cases, there has been a failure to apply correct first aid.17 Despite the development of antivenom, pressure immobilisation bandages and venom detection kits, brown snake envenomation still causes deaths, so consultation with an expert is always appropriate. 1: Coagulopathy after brown snake envenomation The first signs of coagulopathy were bleeding lips and gingivae, which became apparent three hours after the snakebite. 2: Results of laboratory investigations in a 44-year-old man with brown snake envenomation Hours after bite Platelets (x 109/L) INR APTT (s) Plasma fibrinogen (g/L) Fibrinogen degradation products (μg/mL) Serum creatinine (μmol/L) ALT (U/L) Creatine kinase (U/L) Troponin I (μg/L) Reference range 150–400 0.9–1.3 29.5–40.5 2.1–4.0 < 0.4 60–105 < 41 < 190 < 0.10 02:15 33 > 10 > 180 < 0.3 > 20 108 113 143 < 0.4 Treatment with 2 ampoules of polyvalent, 5 of brown snake and 2 of tiger snake antivenom 03:40 111 > 10 > 180 < 0.3 > 20 131 201 164 < 0.4 Treatment with 10 ampoules of brown snake antivenom* 05:53 214 > 10 > 180 < 0.3 > 20 133 277 259 2.8 Treatment with 5 ampoules of brown snake antivenom (infusion completed at 09:30) 09:34 161 > 10 > 180 < 0.3 > 20 127 243 366 10.4 11:38 167 2.7 64.4 < 0.3 131 238 14:49 148 1.8 44.7 0.5 > 20 134 223 462 6.8 20 133 1.3 38.4 1 > 20 123 197 518 4.8 45 129 1.1 30.6 2.7 119 148 381 93 151 1 31.4 3 98 77 INR = international normalised ratio. APTT = activated partial thromboplastin time. ALT = alanine transaminase. * Results of Venom Detection Kit testing of the bite site taken at 03:24 hours after the bite were strongly positive for brown snake venom. 3: Electrocardiogram after brown snake envenomation Electrocardiogram 03:10 hours after the snakebite revealed sinus tachycardia, with a mild intraventricular conduction disturbance with a (pre-existing) right bundle branch block pattern (A), and mild generalised ST-segment depression (B).

Michelle A Johnston FACEM · Daniel M Fatovich FACEM · Andrew D Haig FACEM · Frank F S Daly FACEM

To the Editor: Box jellyfish envenomation, particularly from Chironex fleckeri, is an important cause of morbidity and mortality across coastal areas of northern Australia.1 The distribution of C. fleckeri extends from Broome (18°S) on the Western Australian coast, across the Northern Territory coast and down the east coast of Queensland, at least as far as Gladstone (26°S). Another multitentacled box jellyfish (chirodropid) has been found in north Queensland in the Cairns to Townsville region.2 Smaller than C. fleckeri, this box jellyfish has been called Chiropsalmus quadrigatus. It has not caused documented fatalities in Australia,1 and is likely to be a different species to C. quadrigatus, which has caused many fatalities in the Philippines and Japan.1 The Australian species has therefore more recently been referred to as Chiropsalmus sp. C. fleckeri and Chiropsalmus sp. are both present in tropical waters during the summer months, although C. fleckeri stings have very rarely occurred in each of the months outside the official "stinger season" (October 1 – June 1 for the Northern Territory).3 Over the past 10 years, there have been reports of box jellyfish being present off the beaches of the Gove Peninsula on the northeast tip of Arnhem Land, Northern Territory, during the middle of the year (ie, outside the stinger season). We first obtained samples netted on 2 June 1991 at the Gove mining town of Nhulunbuy (12°S), and in that year the same species was present throughout June and July. Preliminary analysis at the Museum and Art Gallery of the Northern Territory confirmed the jellyfish to be a multitentacled box jellyfish, similar to the Queensland Chiropsalmus sp. The same jellyfish species was netted at Nhulunbuy in June 1992 and September 1993, but not in 1994. Between 5 May and 6 October 2002, hundreds of Gove chirodropids were netted on weekends at the Nhulunbuy town beach by the local surf life-saving club. They were not present every weekend, but on some days hundreds were present in shallow water, precluding swimming and normal club activities. Contact with the tentacles of the jellyfish during netting caused only mild pain, redness and itching, which usually resolved within two hours. There have been no systemic symptoms suggestive of the Irukandji syndrome. The appearance of the Gove chirodropid in large numbers during the cooler mid-year months is unprecedented for Australian chirodropids and has implications for public health warnings. To date the Gove chirodropid has not been found during the summer months, when C. fleckeri is present in the same location. The distribution, ecology and taxonomy of this jellyfish remain to be elucidated. 1: The Gove chirodropid compared with Chironex fleckeri The Gove chirodropid (right) swarms in shallow water and is consistently 5–10 cm in diameter across the bell. This is smaller than Chironex fleckeri (left), which can have a bell diameter of up to 22 cm. The Gove chirodropid is quite fragile and tentacles quickly break off when it is netted, but there are often about five tentacles extending from each pedalium. 2: Comparison of nematocysts Nematocysts (original magnification x 400) from the tentacles of the Gove chirodropid are cigar shaped (right) and therefore similar to those of C. fleckeri (left).

Bart Currie · Melita McKinnon · Bernie Whelan · Philip Alderslade

Puffer fish poisoning has been documented rarely in Australia. It results from ingesting tetrodoxtoxin found in the liver, ovaries, intestines and skin of the fish. Over a recent 16-month period, 11 cases of puffer fish poisoning were reported to the NSW Poisons Information Centre. Symptoms of poisoning may include paralysis, respiratory failure, numbness, paraesthesia, nausea and ataxia. Health professionals should be aware of the condition so as to institute early and appropriate management. (MJA 2002; 177: 650-653) Tetrodotoxin (TTX) is present in high concentrations in the liver, ovaries, intestines and skin of puffer fish (Box 1).1 Although TTX poisoning caused by ingestion of the fish is common in some parts of the world, it occurs only sporadically in Australia, with only 16 published cases reported over the past 200 years.2-7 (This figure does not include the 11 cases described here.) One of the earliest descriptions of puffer fish poisoning in this region can be found in Captain James Cook's journal from his second voyage in 1774 (see Time Capsule, page 653).3 The majority of reported cases have occurred in southeastern Asia,1,8-10 particularly Japan, where puffer fish is considered a delicacy.1,11 Although improved legislation governing marketing and preparation of the fish has reduced the incidence of puffer fish poisoning in Japan, it remains the most common cause of fatal food poisoning, as there are still some unlicensed cooks and untrained workers involved in preparing the fish.1,11 Before 1950, all reported cases in Australia were fatal,5 and in Japan up to 100 deaths a year were reported.11 We describe 11 patients with puffer fish poisoning, four of whom underwent comprehensive neurophysiological testing. Clinical findingsFor the period 1 January 2001 to 13 April 2002, records of 149 453 calls to the NSW Poisons Information Centre were searched for instances of puffer fish poisoning. The Centre covers New South Wales and Tasmania 24 hours a day and the rest of Australia overnight. Of 195 calls coded as food or fish poisoning, there were five calls regarding puffer fish. Two were minor cases involving people who had been squirted with fluid from puffer fish. The three remaining calls were from hospitals: a total of 11 affected people (described here) were involved. Patient 1A 33-year-old woman presented to a semi-rural hospital with nausea and vomiting, perioral paraesthesia, dysarthria, ataxia and hyperventilation after ingesting seven puffer fish several hours earlier (see Box 1). Her vital signs were stable and the FEV1 (forced expiratory volume in one second) was 2.2 litres (normal range, 3.3–4.0 L). However, an hour after presentation she became more dysarthric and developed limb paresis with hyporeflexia. In view of progressive lethargy, dyspnoea and a fall in FEV1 to 1.5 L, she was intubated and ventilated, then transferred to the intensive care unit of a metropolitan teaching hospital. On arrival, the patient was haemodynamically stable but her pupils were dilated and non-reactive to light. Investigations, including a lumbar puncture and cranial computed tomography scan, were normal. With a presumptive diagnosis of tetrodotoxin poisoning, the patient was managed with supportive care. Over the next two days, her condition improved, deep tendon and pupillary reflexes returned, and she was extubated on Day 2. The other symptoms gradually resolved, and she was discharged on Day 5 after full neurological recovery. Patient 2A 40-year-old man presented to a metropolitan teaching hospital (see Box 2). He stated that he had eaten 10 small toadfish eight hours earlier, together with drinking a significant quantity of alcohol. Following ingestion of the toadfish he had collapsed a number of times and felt tingling of his hands and feet and around his mouth. With each collapse, he experienced generalised weakness, but did not lose consciousness. He had no relevant past medical history. On examination he was afebrile, with a pulse rate of 110 beats/minute, blood pressure of 140/80 mmHg, respiratory rate of 16 breaths/minute and oxygen saturation of 96%. A neurological examination was entirely normal. After uneventful overnight observation, he was discharged. Patients 3–11Seven adults and two children ate a soup made from about 30 puffer fish, gutted with heads intact and boiled in fresh water. The cook referred to the fish as puffer fish, and one of us (J U) identified one of the fish as a puffer fish. All nine patients had been previously well, not taking medication, and with no known allergies. The patients' clinical features are shown in Box 2. One child was completely asymptomatic, and the other had mild symptoms of perioral numbness and dysaesthesia of the extremities for five hours. Both were discharged from the emergency department. Most of the seven adults presented to hospital with nausea, perioral and lingual numbness, dysaesthesia of the extremities, dizziness and gait ataxia. Several patients had vomiting and one was experiencing respiratory distress. Neurological examination revealed marked ataxia in all seven patients and limb weakness in two patients (more marked in the upper than lower limbs). One patient had decreased sensation in the hands and feet. Most symptoms resolved over 48 hours, but slight weakness and ataxia of the lower limbs remained. These resolved completely over the following week. Neurophysiological investigation was undertaken in four of the adult patients (see Box 3) within 24 hours of ingestion. DiscussionAlthough puffer fish poisoning is rare in Australia, our report highlights the seriousness of TTX poisoning and its potential to be life-threatening.11 However, early recognition of the condition and supportive care in a modern intensive care unit should ensure a safe outcome. The clinical effects of TTX poisoning have been graded by the severity of neurological and cardiovascular involvement (Box 2).11 In this series, one patient had Grade 3 poisoning, and most others Grade 2 poisoning. Most of the patients exhibited typical neurological features, including perioral numbness and/or paraesthesia, distal limb numbness/paraesthesia and ataxia — symptoms similar to those seen in previous case series.1-10 Gastrointestinal features were also typical, with nausea, occasional vomiting, but no diarrhoea. Cardiovascular effects (not present in this series) occur only in the most severe (Grade 4) cases. The onset of symptoms in TTX poisoning is usually rapid, but is dependent on the severity of poisoning. In the moderately severe cases in this series, symptoms had all occurred within 90 minutes. In reported fatal cases and severe poisoning, symptoms have almost always developed within 1–2 hours.10 The majority of moderate to severe cases in this series resolved within five days, consistent with previous reports,3,6 although this also depends on the severity. In minor cases the duration of symptoms may only be a few hours. The relatively mild symptoms experienced by patients 3–11 probably reflect the relatively low dose of TTX ingested. TTX is present in high concentrations in the viscera of puffer fish, particularly the liver and intestines (Box 4). These organs were removed before cooking the fish soup, and the amount of TTX was subsequently diluted by adding fresh water to the soup and possibly by subsequent boiling. With higher levels of TTX, paralysis and respiratory failure are inevitable, although consciousness is not lost except in extreme cases (Box 2). Of interest, such a process has been implicated in the phenomenon of "zombification" in Haiti.22,23 Nerve conduction studies revealed clear abnormalities. Nerves in the patients tested were of high threshold, and exhibited slow conduction and reduced-amplitude compound potentials, indicating that some axons were unable to conduct at all. This effect was greater in sensory than motor axons, correlating well with the greater prominence of sensory symptoms (dysaesthesiae and numbness) relative to motor symptoms (weakness) in these patients. Voltage-dependent Na+ channels underlie action potential generation and are the chief determinants of membrane excitability in human nerves.24,25 Tetrodotoxin blocks Na+ channels at very low concentrations, affecting action potential generation and impulse conduction. It is important that health professionals are aware of TTX poisoning because of the potential for severe and life-threatening effects. All but the mildest cases (Grade 1) should be admitted to hospital for observation until the peak of the clinical effects has passed. After 24 hours it is extremely unlikely that life-threatening effects will occur in patients who have not already developed severe effects. Early diagnosis by recognition of the combination of clinical effects in people ingesting puffer fish is essential to management. 1: The common toadfish (Tetractenos hamiltoni) The fish pictured here is approximately 10 cm in length. Photo courtesy of Erik Schlogl. 2: Description of 11 patients presenting with puffer fish poisoning Patient Sex, age Onset (minutes) Gastrointestinal features Neurological features Duration of symptoms Severity grade* 1 F, 33 NR Nausea, vomiting Perioral paraesthesia, dysarthria, ataxia, limb weakness, hyporeflexia and ophthalmoplegia. Decreased FEV1, with respiratory failure. 5 days 3 2 M, 40 60 Nil Perioral and extremity paraesthesia, dizziness. 18 hours 2 3 F, 5 NA Nil Nil. NA NA 4 F, 12 NR Nil Perioral and extremity paraesthesia. < 6 hours 2 5† M, 33 30 Nausea, vomiting Perioral and lingual numbness, dysaesthesia of extremities, dizziness and gait ataxia. 5 days 2 6† F, 47 NR Nausea, vomiting Perioral and extremity paraesthesia, dizziness and gait ataxia. 5 days 2 7 M, 39 60 Vomiting Perioral and lingual numbness, dysaesthesia of extremities, dizziness and gait ataxia. Mildly reduced power in upper and lower limbs. 5 days 2 8† M, 41 60 Nil Perioral numbness, dysaesthesia of extremities, dizziness and gait ataxia. Decreased sensation in hands and feet ("glove-and-stocking" distribution). 5 days 2 9 F, 35 60 Vomiting; simultaneous incomplete miscarriage Perioral and lingual numbness, dysaesthesia of extremities, slight dizziness and gait ataxia. Normal power and sensation. Respiratory distress. 5 days 2 10† M, 47 30 Nausea Perioral and lingual numbness, dysaesthesia of extremities, dizziness and gait ataxia. Mildly reduced power in upper and lower limbs. 5 days 2 11 M, 50 90 Nausea Perioral numbness, dizziness and gait ataxia. Normal power and sensation. 5 days 2 NA = not applicable. NR = not recorded. * Clinical grading system for tetrodotoxin poisoning based on symptoms and signs present (after Fukuda and Tani12): Grade 1: perioral numbness and paraesthesia, with or without gastrointestinal symptoms (mainly nausea). Grade 2: numbness of tongue, face and other areas (distal); early motor paralysis and incoordination; slurred speech; normal reflexes. Grade 3: generalised flaccid paralysis, respiratory failure (dyspnoea), aphonia and fixed/dilated pupils; patient still conscious. Grade 4: severe respiratory failure and hypoxia; hypotension, bradycardia and cardiac dysrhythmias; unconsciousness may occur. † Neurophysiological testing was done on these patients (see Box 3). 3: Neurophysiological investigation of patients with puffer fish poisoning Neurophysiological investigation* was performed in four adult patients (numbered 5, 6, 8 and 10 in Box 2) within 24 hours of puffer fish ingestion. None of the patients studied had a history of medical conditions known to affect nerve function, and none were taking any regular prescribed medication. Results of motor (Figures A1–A3) and sensory (Figures B1–B3) nerve conduction studies of the median nerve in patients with puffer fish poisoning and control subjects are compared. (Results are expressed as mean ± standard error of the mean and compared using an unpaired two-tailed t-test.) Stimulus–response curves showed that the stimulus current (threshold) required to generate compound muscle action potentials (CMAPs) and sensory nerve action potentials (SNAPs) was significantly higher in patients with puffer fish poisoning than control subjects, suggesting an overall reduction in axonal membrane excitability (Figures A1, B1).13 Compound potentials were smaller in amplitude (Figures A2, B2) and of longer latency (Figures A3, B3) in affected patients compared with controls. These parameters are dependent on Na+ channel function and suggest reduction both in the number of conducting axons and in the conduction velocity of those axons still available for impulse transmission. Overall, these findings indicate a reduction in Na+ conductance in the nerves of affected patients, consistent with direct blockade of axonal Na+ channels by tetrodotoxin. *Method: Motor and sensory nerve conduction studies of the median nerve were performed using surface electrodes. Results were compared with established normative data using previously described standard techniques.14,15 The median nerve was stimulated at the wrist, with the evoked orthodromic compound muscle action potential (CMAP) recorded from thenar muscles and antidromic sensory nerve action potential (SNAP) recorded using ring electrodes around the index finger. Latency was measured to peak response. Skin temperature was recorded at the site of stimulation in each patient throughout the study, and individual measurements were compensated for temperature using the relationship found in normal subjects.16,17 4: Puffer fish poisoning Tetrodotoxin (TTX) is present in high concentrations in the liver of puffer fish, with progressively decreasing amounts in the ovaries, intestines and skin.1 TTX poisoning can occur from ingestion of a wide range of bony fish from families in the order Tetraodontiformes, most importantly the family Tetraodontidae (puffer fish).11 While none of our cases were confirmed by expert identification of the fish, the description by the patients suggested puffer fish (sometimes called "toadfish" in Australia), and the clinical features were consistent with TTX poisoning. Although ciguatera is also caused by ingestion of fish, the clinical effects differ, and tropical reef fish are mainly implicated.18 The fish ingested by patients 2–11 were from the Georges River, in southern Sydney. While 35 species from the family Tetraodontidae occur in New South Wales, the species in the cases described here were most likely Tetractenos hamiltoni (common toadfish), T. glaber (smooth toadfish), or Torquigener pleurogramma (weeping or banded toadfish), all of which are common and have been recorded in the Georges River and Botany Bay (Doug Hoese and Mark McGrouther, Fish Section, Australian Museum, personal communication). The common toadfish is a sandy to whitish colour, with small brown spots over most of the back and upper sides. The lower sides often have brown bars and blotches (Box 1). It occurs from southern New South Wales to northern Queensland in shallow coastal waters and estuaries. The smooth toadfish looks similar to the common toadfish, but has larger spots and distinct body spines. With other species of puffer fish found in tropical waters, the potential for TTX poisoning exists in many coastal regions of Australia. The in-vitro effects of TTX are well characterised. It is a selective blocker of voltage-sensitive sodium channels and prevents conduction in motor and sensory nerves by blocking sodium channels at the nodes of Ranvier.11,19 Less is known about the in-vivo effects in humans. Nerve conduction studies have been limited,20,21 and demonstrate effects on muscle and sensory action potential amplitudes.20

Geoffrey K Isbister BSc, MB BS, FACEM · Julie Son MB BS · Josef Ujma MB BS · Brendon Smith DipRACOG, DA, FACEM · D G Milder MB BS, MD, FRACP · Frank Wang BSc(Med), MB BS · Catriona J Maclean MB BS · Cindy S-Y Lin MEngSc, PhD · Matthew C Kiernan PhD, FRACP · Corrine R Balit BPharm

Objective: To determine the effect of temperature on lethality of venom from Chironex fleckeri (the potentially fatal box jellyfish).Design: Venom extracted from nematocysts of mature Chironex fleckeri specimens was exposed to temperatures between 4°C and 58°C for periods of two, five or 20 minutes, and then injected into freshwater crayfish (Cherax quadricarinatus) to assess lethality.Main outcome measure: Venom lethality, assessed as time to cardiac standstill in crayfish after intramuscular injection.Results: Venom lethality was significantly affected by both temperature (F7,34 = 21915; P < 0.0001) and time of exposure (F2,34 = 9907; P < 0.0001). No significant loss of lethality was seen after exposure to temperatures ≤ 39°C, even after 20 minutes' exposure. At temperatures ≥ 43°C, venom lost its lethality more rapidly the longer the exposure time. Venom was non-lethal after exposure to 48°C for 20 minutes, 53°C for five minutes, and 58°C for two minutes.Conclusion: Exposure to heat dramatically reduces the lethality of extracted C. fleckeri venom. Although heat application may be of limited use in treating C. fleckeri envenoming because of the speed of symptom onset, its use in other box-jellyfish envenomings, such as Irukandji syndrome, requires investigation.

Teresa J Carrette MSc · Jamie E Seymour PhD · Paul Cullen FACEM · Peter L Peiera FACEM · Mark Little FACEM, MPHTM

Left to right: Professor John Tyrer with three of his "disciples" — Mervyn Eadie, myself and Bryan Emmerson — taken in 1999 when I retired as Director of QIMR. As I reflect on my professional career, the one word that repeatedly springs to mind is "mentorship". I have been fortunate in having had truly remarkable mentors at several key points in my career. Family firstThe first was my father, who, while not university educated, was an intelligent man who ran the family printing business. His professional contacts convinced him of the importance of a sound education for his only son, and when I declared an interest in Medicine and Law he suggested that the two in combination would be very useful. I chose Medicine — in part, because I was intrigued by our family illnesses and surmised that an insight into them would be of benefit to the whole family. This, of course, proved correct. Throughout my school and university years, my mother suffered from post-encephalitic parkinsonism. This placed a great burden on my younger sister, who undertook the family's domestic responsibilities when still in high school. My father died during my fourth year of medical studies and my mother soon after my graduation. Local heroesMy next influential mentor was Frank Garlick, a perspicacious surgeon at the Royal Brisbane Hospital (RBH). It was he who, in 1956, detected a spark of enthusiasm for inquiry and research in a young medical student and so encouraged me to pursue my then interest in malignant melanoma. My dissertation (published in Trephine, the annual magazine of The University of Queensland's Medical Students Society) won the prize for the best research project by an undergraduate student at the university's medical school, and this experience kindled my life-long interest in medical research. After Garlick came John Tyrer, who had not long been appointed to the first full-time chair of medicine at The University of Queensland based at the RBH. Tyrer steadily built a strong department of medicine, having had the foresight to create several "temporary clinical lectureships". These positions were filled by aspiring medical registrars who had successfully negotiated the hurdle of membership of the Royal Australasian College of Physicians, and provided them with the opportunity to combine clinical responsibilities with research — usually towards an MD thesis. It is interesting to reflect on the number of people who spent their formative years being nurtured in such positions who subsequently went on to become academic leaders in Australia. They include Bryan Emmerson (rheumatologist, professor of medicine and head of the department, based at the Princess Alexandra Hospital, Brisbane, 1985–1994) and Mervyn Eadie (neurologist, professor of medicine and head of department at Royal Brisbane Hospital, 1994–1997), to name but two. I greatly lament the fact that, during the 1980s, these positions were abolished progressively as increasing financial constraints affected the university. It was as a temporary clinical lecturer that I found myself fascinated when I realised that four young women with haemochromatosis were from the same family. The literature at that time indicated that the disease was rare in women, especially premenopausal women, and that it was usually due to excess alcohol consumption. These women were all teetotallers, firing up my interest in challenging the existing dogma. Encouraged by Tyrer and his deputy, Martin Lloyd, I undertook a systematic study of iron metabolism in families of patients with haemochromatosis and families of patients with alcoholic cirrhosis.1 This, together with some rather tedious animal studies in iron-loaded rabbits, eventually led to a successful MD thesis and several publications, one of which occasioned an editorial in The Lancet.2 But, more importantly, these achievements provided me an opportunity to work with the doyenne of liver disease, Professor (later Dame) Sheila Sherlock — again following overtures made by John Tyrer on my behalf. International influenceMuch has been written about Sheila Sherlock and her enduring influence on aspiring hepatologists from many countries, including the many obituaries published following her death last year.3,4 In 1965, I was just one of some 20 research fellows — from countries far and wide, including the USA, South Africa and Asia — working in her unit, located in wooden huts up on the roof of the Royal Free Hospital in Gray's Inn Road, London. Sheila took a sincere personal interest in each of us and our careers. Given my published work in haemochromatosis and iron metabolism, Sheila resolved that I should "broaden horizons". She suggested I tackle the topical subject of bilirubin metabolism and Gilbert's syndrome with Barbara Billing, who had recently joined the unit as its only basic scientist. It was an enjoyable and productive association that added new information on haemolysis and Gilbert's syndrome, which Sheila quickly put into clinical perspective.5 Barbara Billing herself was also an excellent mentor and taught me a great deal about laboratory research. Like other fellows in the unit, I was not only exposed to the whole repertoire of liver disease, but also Sheila Sherlock's brilliant clinical acumen and lucid thought processes. Sherlock made a particular effort to train her fellows to present their work at meetings clearly without notes, and set an example by always rehearsing her own major lectures and speeches with staff members and research fellows. Her clarity of communication was legendary. She would convert an amateurish first draft into a manuscript promptly accepted by the New England Journal of Medicine — without revision! She exposed us to "the big names". I felt privileged to be sent to Caroli's unit in Paris to lecture on our work (Caroli, the famous French hepatologist, is noted for Caroli's disease, a congenital cystic dilatation of the intrahepatic bile ducts and associated disorders). Most of her fellows had similar experiences. My subsequent international training, some years later, was equally important but different and complementary. In 1972–1973, Kurt Isselbacher — at that time chief of gastroenterology at Massachusetts General Hospital (MGH) and Harvard Medical School — introduced me to North American academic medicine and laboratory science. Kurt was yet another active mentor, involving me in giving lectures to Harvard medical students, presenting medical grand rounds at MGH, and a harrowing experience as discussant at one of the weekly clinicopathological conferences, published, as usual, in the New England Journal of Medicine.6 The case was one of cholestasis and cholangitis in a man with alpha-1-antitrypsin deficiency. He also recruited me as a contributor to Harrison's Textbook of Medicine, a unique opportunity. I have continued to contribute to each subsequent edition of the book as author of the chapter on haemochromatosis.7 In 1978, a sabbatical at the Rigshospitalet in Copenhagen with Niels Tygstrup — renowned for his extensive work on quantitative tests of liver function — broadened my horizons once again. His unit had strong expertise and interest in basic immunology as it applied to the liver, adding a further dimension to my perspective of international hepatology. Back in AustraliaIn 1966, I had been fortunate in securing a senior lectureship in the department of medicine at The University of Queensland and the Royal Brisbane Hospital. The next vacancy did not occur until eight years later! The department had been progressively strengthened by Tyrer, and was arguably the most productive department in the biological sciences and medicine faculties at the university. With my two inspired colleagues, June Halliday and Graham Cooksley, I established the first academic liver unit in Australia, which, over the years, attracted numerous scholars, both science-based and medical, each adding stimulus and challenge. These scholars included, among others: Geoff Farrell, head of the Storr Liver Unit in Sydney; Mark Bassett, gastroenterologist and associate professor, the Canberra Hospital and Clinical School; Keith Tolman, head of gastroenterology at Utah Medical School, Salt Lake City; and Paul Adams, an international authority on haemochromatosis, from Ontario, Canada. Our research focus was, of course, on haemochromatosis and iron metabolism, with our original research contributions opening doors to both the International Association for the Study of the Liver and the biennial meetings on iron metabolism. Fortunately, these international meetings were held in alternate years. Graham Cooksley later extended our research repertoire to include the immunology of liver disease and then viral hepatitis. Our combination of two physician scientists with a full-time NHMRC-funded basic scientist proved a successful formula. We were awarded an NHMRC program grant (iron metabolism and liver disease) in 1982 that was renewed at every subsequent quinquennial review until it was incorporated into the block grant for the Queensland Institute of Medical Research in 1998 (see below). During this period, I was privileged to be elected President of the International Association for the Study of the Liver. We hosted the World Congress of Iron Metabolism twice: in 1989, in Brisbane, and in 2001, in Cairns; we also hosted the Biennial Scientific Meeting of the International Association for the Study of the Liver in 1990 on the Gold Coast. The Queensland Institute of Medical ResearchLeft to right: Graham Cooksley, myself, June Halliday and John Tyrer — in 1982, at the announcement of the NHMRC Program Grant. In 1988, I undertook my last sabbatical at the Queensland Institute of Medical Research (QIMR). This experience allowed me to become acquainted with the Institute's staff and science and successfully apply, in 1989, to become its Director. The 10 years that followed are now history, but I still find it interesting to reflect on the developments that occurred at QIMR during that time. My predecessor, Chev Kidson, had made significant advances by linking the Institute with The University of Queensland (rather than the State health department) by recruiting some high quality staff, and by securing funding from the Queensland government for a new purpose-built 11-storey institute — the Bancroft Centre. The Centre was opened by the then State Premier, Wayne Goss, in 1991. This new facility allowed a fivefold expansion of the Institute, achieved smoothly over the next five years. Queenslanders were recruited back from overseas, including Graham Kay, who established QIMR's transgenic facilities. Others came from the southern Australian States, notably Anne Kelso and Andrew Boyd among those recruited from the Walter and Eliza Hall Institute, with the assistance and strong support of Sir Gustav Nossal. The Liver Unit — myself, June Halliday and Graham Cooksley and some 25 staff — moved en bloc into the Bancroft Centre (Graham as Director of the Clinical Research Centre of the Royal Brisbane Hospital Foundation, which was also situated in the building). It soon became apparent that the expanding Institute would benefit from independent peer review. In 1994, with the strong support of Judy Whitworth, then chair of the research committee of the National Health and Medical Research Council (NHMRC), I was able to put together a formidable review committee. Chaired by Keith Peters, chairman of the department of medicine at Cambridge University, UK, and including Peter Doherty (then professor of immunology at St Jude's Hospital for Children, Memphis, Tennessee), Bob Williamson (then professor of biochemistry, St Mary's Hospital, London), the committee included three Australians. Professors Fiona Stanley (the Institute for Child Health, Western Australia), Richard Smallwood (professor of medicine, the Austin and Repatriation Hospital, Melbourne) and Ashley Dunn (the Ludwig Institute, Melbourne) were all nominated by the NHMRC. A week-long in-depth review by this committee made a huge impact on the strategy and further research directions adopted by the Institute. I also believe that this committee influenced the NHMRC with respect to block funding. Its last term of reference, clearly the most challenging, was to address whether QIMR should apply for block funding. After deliberation, the committee concluded that, "in the Australian context", QIMR should indeed apply to the NHMRC for block funding. However, it was also clear that the largely international committee saw significant disadvantages in block funding. Keith Peters conveyed these sentiments, at the time, to Judy Whitworth. Interestingly, since 1998, NMHRC block funding has been progressively abolished and the program and project funding system restructured. As a result, total NHMRC funding to the QIMR (including program grants, project grants and fellowships) has increased from $6.0 million in 1998 to $7.82 million in 2002 — an increase of about 30%. The "White Knight"By 1996, the "new" Bancroft Centre was fully occupied and we dreamed of new ways to expand the Institute. All were futile until, in 1998, the fortuitous juxtaposition of two "once-in-a-lifetime" events enabled us to realise our dream. Firstly, we were approached, anonymously, by a US organisation — which we later found out was Atlantic Philanthropies in New York — after they had conducted an independent assessment of the Institute. After protracted discussion with their Dublin-based consultant, two visits by him, and submission of a detailed business plan, we were advised that their board would support our "dream", with a donation of $20 million, conditional on our raising the remaining $35 million required within six months! Of course, this proved a difficult challenge, but with the bipartisan support of the Queensland government ($20 million), the assistance of the Leukaemia Foundation ($5 million) and the QIMR Trust ($10 million) the target was achieved. The second fortuitous event was the concomitant rebuilding of the Royal Brisbane Hospital and the Royal Women's Hospital, which released space for a new building close to the Bancroft Centre. State authorities graciously provided the space to QIMR and the new 10-storey Comprehensive Cancer Research Centre was completed in 2001. Soon afterwards, Mr Clive Berghofer (a Queensland grazier and real estate developer) generously donated $5 million for the naming rights for 10 years — a rare occurrence in Australian science! A special feature of the development has been the inclusion of a clinical trials centre occupied and administered by QPharm, a newly established independent company that conducts phase I clinical trials of new compounds. State authorities have also granted QIMR the former Queensland Radium Institute (QRI) building, available from 2004, which lies between the old and new QIMR buildings. Thus, when fully developed, the new QIMR will occupy three buildings and have a total staff of over a thousand. A new eraThe new Queensland Institute of Medical Research (QIMR) (left), incorporating the Bancroft Centre, and the Clive Berghofer Comprehensive Cancer Research Centre, with the former Queensland Radium Institute building in between. From 2004, QIMR will comprise all three buildings. In 2002, on retiring from the QIMR, I was invited to become the Director of Research at the redeveloped Royal Brisbane and Royal Women's Hospital — in some respects, a position more challenging than Director of QIMR! While I continue to enjoy some clinical practice and teaching, the challenge to stimulate research in the hospital environment is formidable. For decades, the RBH has been the flagship of Queensland's hospital health and medical research effort, but financial stringencies of recent years have indeed taken their toll. While Australian medical research institutes have increased in size and number over the past 10 years, university departments, and particularly our teaching hospitals, have found it increasingly difficult to fund research. Moreover, with ever-increasing clinical demands, less time for research and uncertain career paths, I believe young graduates are now discouraged from embarking on clinical research or a career in research or academia. Although this is, to some extent, a global problem, it is so particularly in Australia, where, for example, in contrast to Canada and the USA, there is a very significant difference between stipends for research fellows as opposed to those in clinical posts. I sincerely hope that current efforts by the NHMRC and others to boost clinical research, such as with the introduction of NHMRC practitioner fellowships and the NHMRC Centres of Clinical Excellence Program, will be successful. Thus, I am delighted that the potential gap between basic and clinical research has been bridged at QIMR. The Institute's present Director, Michael Good (with an international reputation in the immunology of infectious diseases), and Deputy Director, Adèle Green (an internationally acclaimed epidemiologist), are both medically qualified scientists; as well, several of the research staff have clinical appointments at the Royal Brisbane Hospital. The Institute's research portfolio now spans the full spectrum, from fundamental molecular research to clinical translational research and clinical trials and, more recently, a research program in Indigenous health. ConstanciesNone of my contributions would have been possible without the devotion and enduring support over 42 years of my wife, Margaret (née Ingram), herself a University of Queensland graduate in education. Margaret has not only raised and nurtured five children, fostering their university education (in medicine, education, psychology, environmental science and music), but has also taken them around the world during my extensive years of training and study leave. Also, it should be apparent that I feel and have always felt passionately about two themes — the importance of mentorship in medicine and biomedical science, and bridging basic science and clinical medicine (from the bench to the bedside and back) to produce clinically relevant research. It is because young researchers were inspired by their mentors that clinical science, and indeed clinical medicine, have become what they are today, and this needs to continue. The importance of this practice has been enunciated well by Dean William Welch, of Johns Hopkins fame, who wrote: Let us not forget that a university or a medical college may have large endowments, palatial buildings, modern laboratories, and still the breath of life may not be in it. The vitalising principle is in the men (and women) — both teachers and students — who work within its walls. Without this element of life, this bond between teacher and taught, these things are but outward pomp and show. But let these greater opportunities receive the breath of life from the inspiration of great teachers and they then become the mighty instrument of higher education and scientific progress.8

Lawrie W Powell AC, FTSE, MD, PhD, FRACP, FRCP, FRCPT

Disobedience, in the eyes of anyone who had read history, is man’s original virtue. It is through disobedience that progress has been made — Oscar Wilde, 1881 The invitation to contribute this piece to the Journal was disconcerting. I told the Editor I felt previous contributors to the Power of One series were all distinguished retirees. What was he trying to tell me? I have just turned 51, but it seems some believe I have been around forever and should write a retrospective piece. Sinking smokingRecently, I was leaked a staff training CD-ROM from British American Tobacco (Australia). Five senior executives sat in front of the camera blubbing about the inexorable fall in smoking rates and how, as the plug had been pulled, this could only get worse. As the remaining water drained from the pool, they tried to inspire their staff by talking up hopes of snatching profit from brands that smokers were inspired to believe were at the luxury end of the market. Luxurious carcinogens! It was desperate stuff, but heartening all the same. In the early 1960s, nearly 60% of men and 30% of women in Australia smoked.1 Today, daily smoking by adults has fallen to under 20% for the first time,2 and shows no signs of having bottomed out. In NSW, lung cancer in men has been falling for 18 years and female lung cancer has stopped rising.3 National death rates from coronary heart disease fell by 59% in men and 55% in women between 1980–2000, in large part because of changes in risk factors like smoking.4 Along with vaccine uptake, the fall in the road toll and arresting the HIV/AIDS epidemic, the fall in the smoking rate is one of the major public health achievements of the past 40 years. Innocents sometimes introduce me as "the person" who is responsible for the revolution in the way smoking is now regarded. This nonsense derives from their youth, mixed with thoughts of David and Goliath — as if a single individual could ever be said to be responsible for turning around something as complex as community and political perceptions of smoking. The metaphor of being pecked to death by ducks provides a more apposite description of the way things work in public health. Strategic pecks that irritate and distract gradually build to a point where those under attack — in this case, the tobacco industry — develop a debilitating siege mentality. While the public appetite for dragon-slayer mythology demands there should be individuals who stand over public health carcasses, many, often unsung, people have oxygenated the huge changes achieved in smoking in Australia. MOP UP and BUGA UPA BUGA UP refacing, circa 1983. Today, smokers huddle in doorways and excuse themselves from meetings. To smoke with equanimity is increasingly to wear a badge of immaturity, low education or resigned addiction. Thirty years ago, it was very different. The tobacco industry had infected smokers with the thought that they had a monopoly on all that was interesting, convivial and sensual. Epidemiological revelations rather ruined all that; but it was advocacy that ensured the translation and transition of epidemiologists' conclusions into policy and law reform. In the late 1970s, I was bored witless in my first job as a community health educator, employed by the NSW Health Commission. While I gave interminable Rotary Club talks to half-sozzled businessmen about the "drug problem", tobacco advertising adorned every conceivable public space. Drug pushers were very publicly jailed while tobacco industry executives were quietly knighted. So, in 1978, with a few colleagues, I formed MOP UP — Movement Opposed to the Promotion of Unhealthy Products. We put out a precocious press release and in the next week were covered by the Sydney Morning Herald as "the latest pebble in the shoe of sin industries".5 We engineered the removal of Paul Hogan from the Winfield advertising campaign;6 "MOP UP's slingshot cuts down the advertising ogre" read one headline. MOP UP re-energised the debate about tobacco advertising that Nigel Gray (then head of the Anti-Cancer Council of Victoria) and Cotter Harvey (founder of the Australian Council on Smoking and Health) had started in the 1960s. At our first meeting — held in the lecture theatre of the Sydney morgue in Camperdown — someone stood up and declared, impatiently, that our political letter-writing plans were pathetic and that, if we had guts, we would take more direct action. BUGA UP, the graffiti movement, was born and over the next eight years revolutionised ordinary people's understanding of the politics of tobacco control.7 My modest involvement was to take ongoing responsibility for the billboard on a shopfront directly opposite the entrance to News Ltd, but my admiration for the dozens of courageous people who risked much over a decade of civil disobedience is boundless. We held a 20-year reunion in October this year. (For a powerpoint collection of BUGA UP's 'greatest hits' see http://tc.bmjjournals.com/cgi/content/full/11/3/DC1). Truth in advertising: the German brand West shows a smoking Olympic athlete "lighting the fire" of a stick-figure woman in front of Australia's Uluru, about the time of the 2000 Sydney Olympics. When I first started in tobacco control, people at parties would occasionally give me wide berth as a probable teetotal morals crusader who would soon move to turn the music down and pluck sweets from children's mouths. MOP UP, and especially BUGA UP, changed all that. Understanding that the tobacco industry is a pariah of the corporate world rapidly became a litmus test for a whole set of values about the abhorrence of putting profit above all else. Today, one never hears a tobacco industry executive in the media. As my colleague Stan Glantz, professor of medicine at the University of California, San Francisco, has said: "They are like cockroaches; they spread disease and don't like to be seen in the light." No respectable politician would now ever risk public association with these executives, and this change in business community status has facilitated the incremental adoption of a legislative program that puts Australia in the forefront of nations trying to reduce tobacco's health toll. Getting the message outThose heady days and my first degree in media sociology gave me a taste for the nature of news values. They blooded me for a career where I have tried to translate epidemiologists' conclusions into discourses that gel with community concerns, and then needed to truncate them into soundbite-length summations if they were to have any hope of making the news. I have always had enormous respect for the power of the news media to influence the way that communities think about issues. My honours thesis on imagery in advertising for psychotropic drugs in medical journals was tabled into the Senate Hansard by Peter Baume in 1979.8 That lit a fire within me: there were ways in which academic work could climb out of its (mostly) cosseted sanctuary and thus get to influence political debates. A luxurious Sunday for me is an undistracted day of writing. Since 1976, I have published over 370 original articles, editorials, letters and commentaries in peer-reviewed journals and another 105 in throwaways. I have written 10 books and large reports. A few of these have become citation classics in my field,9-11 but if I was to nominate my most influential writing without hesitation I would name some of my 93 newspaper opinion pieces, my 130 letters to newspapers or some of my extended radio and TV interviews during critical periods of advocacy for change, like the tumultuous period of advocacy required after the Port Arthur gun massacre in 1996. Years of watching my citation rate splutter upward and 11 years of editing an international journal (Tobacco Control) have taught me that scholarship, for all its importance, exists in intellectual backwaters and rarely influences practice, public or political opinion. Colleagues boast of a paper being cited a few hundred times or of speaking to 5000 people at an international conference. In my opinion, a gloves-off opinion piece in a morning newspaper, followed by a round of interviews on breakfast radio, on the day that a vital public health political decision is to be made will be read, and often discussed, by incomparably more people than a journal's readership. Outside agentAdvocacy, by its nature, involves contested debates — there are always losers when change occurs; so often, they are determined to resist change, and angry when it happens. Public health advocacy often requires pushing governments to act and being critical of inaction. This can brand advocates as troublemakers, with all that can go along with that. I have known David Hill, now the director of the Anti-Cancer Council of Victoria, since 1978 and count him as a close friend. A few years ago, when I was feeling a little disconsolate at being plainly excluded from some key national committees appointed by a minister for health whom I had occasionally criticised, David counselled me to consider that every cause needs different people to work "inside and outside the political tent". He said that those on the inside greatly appreciated that someone with my judgement and determination was outside helping keep policy agendas alive that would otherwise be at risk of neglect, being largely off-limits to those working on government committees. Magnificent mentorsMayer mailI count three mentors in my life. Henry Mayer (1919–1991), Professor of Political Theory at the University of Sydney, invited me to lunch after reading an analysis I wrote of the use of sexually seductive imagery in a doctor-directed advertisement for a bronchodilator.12 Henry was a Renaissance man who read everything from impenetrable European psychoanalytic theory to debates about radio bandwidths. From that day on, seldom a week passed in the next decade when a bulging packet of eclectic pages torn from his astonishing reading habits did not arrive in the mail. "Read this", he'd have scribbled. To this day, I am compelled to open my mail and email before anything else, so exciting were the contents of the material he often sent me. I found out later that Henry was in the same habit with dozens of other people he favoured. My imagination owes him an enormous debt. Godfather GrayNigel Gray, then head of the Anti Cancer Council of Victoria, invited me to go with him to Papua New Guinea in 1983 to help convince the government to ban tobacco advertising. It did, although the law remains poorly enforced. Nigel quickly burst any preconceptions I had about senior, venerable figures in medicine being aloof, arrogant and irrelevant. Besides being great fun, Nigel has an appetite for energetic people who, like him, were prepared to stay for the long haul, always searching for opportunities to reignite concern about tobacco industry actions or complacency in government. He taught me that public health's successes tend to creep along almost imperceptibly and about the importance of setting 10–20-year windows on achievement. He remains the godfather of tobacco control advocacy for many of us.13 "Fearless" LeederStephen Leeder, then head of Community Medicine at Westmead Hospital, asked me to work with him in 1986 and has been a major influence ever since. While he has written some of the most articulate public health policy analyses, and cuts the mustard with most powerbrokers, it is his incandescent humanity that sets him apart for me as one of Australia's most inspirational figures in public health. Affectionately known to many of us as "Fearless" Leeder, Steve's writing and speeches drip with his values. Working with Steve for 16 years has exposed me not just to his intellect, but to his unerring encouragement of others. Whenever I have had moments of doubt about writing what I think and upsetting someone powerful, he has seldom hesitated to say simply, "You must say this . . . if you won't, who will?". He's been a wonderful role model. Citizen ChapmanWinner of the Lung Slayer Award. This portrait, of a 34-year-old man with emphysema, was a rejected entry in the 1984 John Player Portrait Award, National Portrait Gallery, London. An alternative exhibition was held on the footpath outside the gallery (that's me holding the painting). Most days I pinch myself in disbelief that I get paid to do what I would gladly do for nothing as a citizen. My 20 years (1982–2002) as a director and chair of the Australian Consumers' Association (Choice magazine) count as an experience I value enormously. I have swapped tactics with some of the most tenacious exponents of rat-cunning advocacy that you could ever hope to meet. Today, I have seven researchers working with me on a critical history of the tobacco industry as revealed through their internal documents (see http://tobacco.health.usyd.edu.au/). Each day, I see their growing incredulity at what they are discovering and the way this translates into passion about carrying on this work, using scholarship as an instrument of shame that drives policy change. The other day we found an item that read "Australia is a laboratory for the global anti-smoking network. Both anti-smoking policies and the individuals who promote them are exported from Australia and stimulate anti-smoking activities worldwide."14 It's been a huge privilege to be a part of that.

Simon Chapman PhD

Background: In 1941, a Sydney ophthalmologist, Norman McAlister Gregg, correctly identified the link between congenital cataracts in infants and maternal rubella early in pregnancy. Fifty of Gregg's subjects with congenital rubella, born in 1939–1944, were reviewed in 1967 and again in 1991. We reviewed this cohort in 2000–2001, 60 years after their intrauterine infection.Methods: The subjects underwent full clinical assessment, plus pathology tests, an ophthalmological and cardiological review (including electrocardiography and echocardiography) and HLA histocompatibility testing.Results: Since they were first seen in 1967, 10 have died (cardiovascular causes [4], malignant disease [4], AIDS [1], and hepatitis C-related cirrhosis [1]). All surviving men came for review (19) and 13 women (eight women declined). Echocardiography showed mild aortic valve sclerosis in 68%. The prevalence of diabetes (22%), thyroid disorders (19%), early menopause (73%) and osteoporosis (12.5%) was increased compared with the Australian population; 41% had undetectable levels of rubella antibodies. The frequency of HLA-A1 (44%) and HLA-B8 (34%) antigens was increased, and the haplotype HLA-A1, B8, DR3, said to be highly associated with many autoimmune conditions, was present in 25%.Conclusions: This cohort of people with congenital rubella has illuminated our understanding of viral teratogenesis.

Jill M Forrest MD BS · Fiona M Turnbull MB, ChB · Gary F Sholler MB BS, FRACP · Richard E Hawker MB BS, FRACP · Frank J Martin FRANZCO, FRACS · Margaret A Burgess MD, FRACP · Trevor T Doran MSc, PhD

The death of a friend solved a centuries-old, oft-fatal mystery My doctrine is produced in order to banish the terror from lying-in hospitals, to preserve the wife to the husband, and the mother to the child... — Ignaz Semmelweis, 1861 Today, a very large proportion of women giving birth receive antibiotics, potent and sometimes in combination, during their accouchement. Routine prophylaxis is widely accepted for caesarean sections, which account for 20%–25% of deliveries.1 Of course, any pregnant woman presenting with an obvious infection will automatically receive an antibiotic. Further, so will most pregnant women with membranes ruptured for any length of time, either before or after labour begins, and any woman in labour with a raised temperature. There is also a more relaxed approach to many former midwifery routines — for example, the abandoning of masks and gowns and the admission of several support people to the delivery scene — which could diminish both younger obstetricians' and midwives' appreciation of the potentially deadly risk of puerperal infection. However, until relatively recently in developed countries, and still in many developing countries, puerperal sepsis was and is a killer.2 Fatal feverImmediately postnatally, the placental site is a large open wound — easily invaded by ascending bacteria. For thousands of years, it was recognised that puerperal women were at risk of a fever that could be fatal. The Hippocratic writings contain references to childbed fever, as do some Hindu texts dating back to 1500 bc.3 Moreover, the potential for birth attendants to initiate such infections seems to have been comprehended by some of the ancient writers, including the Greek physician Soranus, and the Hindus, since advice on hygiene for birth attendants was offered.3,4 Triptych showing the Hôtel Dieu in Paris, about ad 1500. The comparatively well patients (on the right) were separated from the very ill (on the left). Note there were always two patients to a bed. Nevertheless, in ancient and medieval times, mortality from puerperal sepsis was apparently relatively low, as women generally gave birth at home. Peculiar to the puerperium?The 17th century saw the establishment of "lying-in" hospitals in many European cities. While these institutions were, in some ways, an advance — in particular, by relieving obstructed labour with forceps or intrauterine manipulation — the crowding of patients, frequent vaginal examinations and the use of contaminated instruments, dressings and bedlinen spread infection in an era when there was no knowledge of antisepsis. The first recorded epidemic of puerperal fever occurred at the Hôtel Dieu in Paris in 1646. Subsequently, maternity hospitals all over Europe and North America reported intermittent outbreaks, and even between epidemics the death rate from sepsis reached one woman in four or five of those giving birth.5 Numerous bizarre theories as to the cause of childbed fever were expounded — among them that it was due to a "miasma", or the labouring woman's disturbed state of mind, or mechanical pressure from the distended uterus. Certainly, childbed fever was universally regarded as a condition peculiar to women in labour.6 Sepsis suspectedContagion as the basis for childbed fever was first suspected by a number of British physicians in the late 18th and early 19th centuries.7 The name of Thomas Watson, Professor of Medicine at King's College Hospital, London, is not well known, but in 1842 he wrote: "Wherever puerperal fever is rife, or when a practitioner has attended any one instance of it, he should use most diligent ablution." Watson recommended handwashing with chlorine solution and changes of clothing for obstetric attendants — everything, he said, "to prevent the practitioner becoming a vehicle of contagion and death between one patient and another." Unfortunately, Watson's advice seems to have been largely ignored by obstetric practitioners of the time — the contagion theory is completely absent from contemporary obstetric texts.7 Oliver Wendell Holmes Across the Atlantic, in Boston, Dr Oliver Wendell Holmes — pathologist, physician and president of the Boston Society for Medical Improvement — developed an interest in the condition after two related cases were presented to his society. A physician and a medical student both died of septicaemia after performing an autopsy on a woman who died of puerperal fever. Holmes read the existing literature, and became convinced that the condition was highly contagious, and that doctors, nurses and midwives were the active agents of its spread. He began to speak and write on the subject, and in 1843 published his classic essay The Contagiousness of Puerperal Fever.8-10 The essay contains eight rules for the obstetrician, which included not only handwashing and changes of clothing, but also the avoidance of autopsies if obstetric cases were being managed. Holmes' conclusions were ridiculed by many of his prominent contemporaries. For example, Charles Meigs, a well-known obstetrician, was incensed at the suggestion he may himself be transmitting disease. "Doctors," he said, "are gentlemen, and gentlemen's hands are clean."10 Connection comprehendedMeanwhile, in Vienna, Dr Ignaz Semmelweis, a native of Hungary, was beginning a life-long obsession with finding the cause of, and preventing, puerperal fever. However, knowing no English, and far from North America, Semmelweis was unaware of the work of Holmes. Ignaz Semmelweis In 1844, Semmelweis was appointed assistant lecturer in the First Obstetric Division of the Vienna Lying-In Hospital, the division in which medical students received their training. He was appalled by the division's high mortality rate from puerperal fever — 16% of all women giving birth in the years 1841–1843. In contrast, in the Second Division, where midwives or midwifery students did the deliveries, the mortality rate from the fever was much lower, at about 2%. Semmelweis also noted that puerperal sepsis was rare in women who gave birth before arriving at the hospital.6,11 Over the next few years, Semmelweis studied and rejected numerous hypotheses. He did note that medical students and doctors from the First Division performed autopsies each morning on women who had died in the hospital the previous day and that midwives were not required to perform such autopsies. However, he did not immediately appreciate the connection between the two observations.6,11 In March 1847, Jakob Kolletschka — professor of forensic pathology, colleague and friend of Semmelweis — died of septicaemia after sustaining an accidental wound to the hand during an autopsy. On reading the report of Kolletschka's autopsy, Semmelweis was struck by the similarity of the pathological findings to those of women who had died of puerperal fever. He later wrote: "Suddenly a thought crossed my mind: childbed fever and the death of Professor Kolletschka were one and the same. His sepsis and childbed fever must originate from the same source . . . the fingers and hands of students and doctors, soiled by recent dissections, carry those death-dealing cadavers' poisons into the genital organs of women in childbirth . . .".6,11,12 Semmelweis began experimenting with various cleansing agents and, from May 1847, ordered that all doctors and students working in the First Division wash their hands in chlorinated lime solution before starting ward work, and later before each vaginal examination. The results were extraordinary — the mortality rate from puerperal fever in the division fell from 18% in May 1847 to less than 3% in June–November of the same year.11 Doctrine dismissedLike Holmes, Semmelweis found that his conclusions did not receive immediate acclaim from his colleagues and superiors. Indeed, he was treated with scepticism and ridicule by many in the Viennese and wider European medical establishments, including his own professor, Johann Klein. In 1849, Semmelweis' contract with the Lying-In Hospital was not renewed and he returned to Hungary, joining the University of Pest. He presented his findings to the Medical Society of Vienna in 1850. They were not well received, other opponents at that time including the famous pathologist Rudolph Virchow and the prominent obstetrician Friedrich Scanzoni. Semmelweis did not publish his observations until 1861; again, they were greeted dismissively. Embittered, Semmelweis wrote a series of "open letters" to his former professors, accusing them — rightly, as it turned out — of being "medical Neros" and "murderers".11,12 Sadly, his last years were affected by depression and mental disturbance. In July 1865, he was committed to a psychiatric institution in Vienna, and died there two weeks later — ironically, probably from septicaemia following a cut to a finger.3,6 Acceptance of antisepsisParadoxically, within a few years of his death, Semmelweis' doctrine began to be accepted by the wider medical community. In 1874, Billroth demonstrated streptococci in pus from wound infections, and in 1879 Louis Pasteur identified the haemolytic streptococcus in the blood of a woman with puerperal sepsis.3 Joseph Lister, learning of Pasteur's work and germ theory, began to apply antiseptic principles to the practice of surgery, with a dramatic fall in postoperative deaths from infection. As with Semmelweis', Lister's ideas were also greeted with scepticism and it took nearly 30 years for "Listerism" to be universally accepted by medical practitioners.13 By the end of the 19th century, the need for obstetric asepsis was well appreciated. An authoritative text of 1905 gives detailed instructions for the personal hygiene of physicians and nurses attending confinements and instructions on the performance of internal examinations. The importance of "inculcating in the student the principles of obstetrical cleanliness, mechanical and chemical" is emphasised. The need for meticulous antiseptic care during operative vaginal deliveries and manipulations — more frequent then than now — is reiterated.14 Australian medical practitioners were apparently quick to follow the lead of their overseas colleagues in the application of hygienic measures in obstetrics, and of self-regulation when puerperal fever occurred in their practices. Most stopped attending midwifery cases for a time after one or two deaths among their patients.15 Surprisingly though, despite the new understanding of the importance of antisepsis, puerperal sepsis still occurred frequently in developed countries in which figures were kept. It appears the principles of antisepsis were not universally applied. In England and Wales, in the period 1870 to 1890, the maternal death rate in hospital births was around 1 : 20, of which about 40% were due to infection. In the United States, in the 1890s, 20 000 women a year died in childbirth.14,16,17 In New South Wales, in 1894–1896, among confinements of married women, both at home and in hospital, the government statistician found a death rate of 1 : 148, and he commented on the negligence of medical men in filling the certificates required by law. Up to that point, causes of death had been supposedly accurately recorded for more than 40 years, but, in fact, the puerperal nature of fatal infections in women was frequently omitted.14,15 Globally, the most common and most feared infecting organism at the time was the Group A haemolytic streptococcus, whose virulence appears to have diminished in recent years, possibly due to improved socioeconomic conditions and the use of antibiotics. Normally found on the skin, in the nose and throat, and in the vagina, as well as in skin lesions, the streptococcus was introduced into the genital tract during examinations and deliveries. Lacerations, blood loss and exhaustion from prolonged labour increased the possibility of postpartum infection. Staphylococci, gonococci, coliforms and other bowel flora, as well as anaerobes, were less likely culprits, but have assumed greater importance in recent years, as have Group B streptococci.3,7,15 Debating deliveriesIn Australia overall, as elsewhere overseas, the maternal mortality rate (MMR) actually remained steady from 1900 until the late 1930s (5.95 per 1000 women delivered in 1903; 5.13 in 1933). Among developed nations, the United States had the highest MMR and the Netherlands and Scandinavia the lowest, although there were some individual hospitals with remarkably low rates, including the Rotunda in Dublin, Ireland, and Crown Street Women's Hospital in Sydney, Australia.15,17 Causes of the continuing fatal role of puerperal sepsis were widely debated. The medical profession tended to blame untrained midwives, and moved towards their training and registration, which was achieved by the 1930s. Some attributed the rates of sepsis to high levels of interference in labour and delivery, especially forceps deliveries. In Australia, the "lodge" system of practice — whereby families purchased medical services through lodge or friendly society membership — was held to blame. Busy general practitioners contracted under this system were allegedly likely to try to conduct confinements hurriedly.15-17 There were moves both to increase instruction in obstetrics for general practitioners and to encourage specialist obstetricians to do deliveries.15 Antibiotic arsenalAfter 1935, the situation improved rapidly in developed countries. Early that year "a startling therapeutic success" was announced by Domagk in Germany — the prevention of septicaemia in mice experimentally infected with streptococci after the administration of prontosil, a sulfonamide dye.18 In June 1936, Colebrook and Kenny, in a landmark paper, reported their success in treating established puerperal sepsis in women using prontosil — the death rate in apparently similar cases dropped from around 27% to 8%. Colebrook and Kenny wrote (cautiously): ". . . the very low death rate, taken together with the spectacular remission of fever and symptoms observed in so many of the cases, does suggest that the drug has exerted a beneficial effect".18 History was to prove them correct, and in 1939 Domagk was awarded the Nobel Prize in Medicine and Physiology for his work. Prontosil and other sulfonamides were followed by penicillin, to which streptococci causing puerperal sepsis still remain sensitive, and the arsenal of antibiotics used for all other forms of postpartum fever today.3,19 Today, in Australia, deaths from puerperal sepsis are extraordinarily rare (the MMR is currently about 0.1 per 1000 births).2 However, infection and fever are not rare, and the microbes causing them are omnipresent. In caring for pregnant women, especially the many who have some intervention in labour or delivery, we would be wise to reflect that it is only the use of increasingly complex antibiotic regimens which prevents a return to "the terror of the lying-in hospitals".

Caroline M De Costa FRANZCOG, FRCOG

Christmas Eve, a couple of years ago. I was on call for the birth suite until 8 am the next, Christmas, morning but was hoping to be able to stay at home with my family. At 6 pm, I did a festive round with the registrar on duty. Good — only three women in the suite, and two delivered, both delighted with themselves for getting it over before Christmas Day. In the corner room, one woman in early labour — Grace, aged 34. Elderly for a first baby, especially for an Aboriginal woman, the registrar observes. I say hello to Grace, but don't examine her — that's why the midwives and junior staff are here. Surprisingly, no partner or family is with her. Then I realise that I have seen Grace about our town. She is one of the "park people". Virtually homeless, living mostly outdoors, drifting back and forth between town and some of the more remote communities of the region, the park people are frequently subjected to the ire of some of the town's better-heeled residents. Recently, these residents have demanded more stringent "move-on" laws, to keep the park people out of the sight of the tourists and restaurant patrons along the town's seashore. So far, the State's Anti-Discrimination Commissioner has successfully opposed such laws, but for the park people — rather like those people back in Bethlehem whose birth experience we are celebrating tonight — it seems there is no room at the inn. In her time, like other park people, Grace has had many visits to the hospital's emergency department. At every admission, the same comments appeared: "poor historian"; "C2H5OH"; "lacerations"; "bruises". She'd been sutured many times, with the new and old stab wounds noted. A large scar on her throat and another on her left breast were recorded. Unfortunately, no-one noted the scar on her lower abdomen. Longitudinal and midline. A laparotomy scar. Grace hasn't attended any formal antenatal clinics, but thankfully, during one of her visits to casualty a while back, someone did do an ultrasound scan, so we know she is labouring close to term. Routine antenatal blood tests are being done now. She is in established labour, progressing, and all appears well. I leave it to the registrar to check the results, wish everyone a Merry Christmas, and go home. Two hours later, I am rung by an agitated registrar and, on the strength of what I am told, go back to the birth suite. In conversation with one of the midwives on duty, an elderly Aboriginal woman, visiting another patient, remarked of Grace: "Long time since that girl had a baby!". "Oh no," replied the midwife, "this is her first". "No," the woman was firm. "Had the baby when she was 13. A caesarean. At . . . " — and she named a former mission station some hundreds of kilometres away. The midwife hastened to question Grace. Did she ever have a baby before? It was difficult for her to answer; she is indeed a poor historian. For a start, she has no teeth. Those that weren't knocked out in fights have rotted away. Also, chronic middle ear disease since childhood has made her rather deaf. But she does know that, yes, she did have a baby. A girl. Nobody in the hospital had ever asked her before; she didn't know it was important. Did she have a caesarean? Grace is unsure. It was a long time ago. Did the baby come out through that scar on her tummy? Yes, maybe. It was a long time ago. Where is her daughter now? Grace does not know. Obstetric dilemma: is the abdominal scar longitudinal because Grace had a classical caesar, in which case, because of the risk of uterine rupture, caesarean section should be repeated forthwith? Or — and more likely — was the longitudinal incision merely the route to a standard lower-segment operation, allowing Grace the possibility of a successful vaginal birth this time? For the moment, all seems well. Grace is contracting regularly, has accepted pethidine, and is making progress in labour. She now lies in a clean hospital bed, surprised to be — for perhaps the first time in her life — the centre of concerned attention. We try ringing the hospital near the former mission for more information. It's 9.30 pm on Christmas Eve! We're told: "You want records from more than 20 years ago? You must be joking! Ring back next week." An hour later, a further complication arises. Grace's blood has shown unusual antibodies and it will take some hours to find and crossmatch blood if we need it. We decide to ask for the crossmatch and hope that she delivers vaginally soon and that she won't need surgery or blood. Regularly, anxiously, we watch Grace's vital signs and the fetal monitor. Another two hours later, we have blood, Grace's cervix is 8 cm dilated and the fetal heartbeat has been fine. And then, she begins to bleed. Torrentially. Everyone swings into action. After all, this is what we do best. Acute care. Three wise men appear — anaesthetist, paediatrician and theatre porter — bringing not frankincense, myrrh and a manger but ropivacaine, oxygen and a trolley. In five minutes, Grace is on the operating table; another five, and a spinal block is in place. Soon, a rapid repeat caesarean section is under way. The old scar — in fact, a classical — has ruptured and is bleeding profusely, but it's repairable and the baby is alive. On the stroke of midnight, a baby boy arrives. He is small and scrawny, covered in meconium. But when he gives a feeble cry, Grace smiles and reaches out one arm for him (a blood transfusion is running into the other) and she names him, appropriately, Joseph Christopher. Joseph spends that night and the next in the special care unit. He starts to breastfeed. Grace is eating three meals a day, including turkey and plum pudding. But it's Christmas time, the hospital is short of staff and many beds are closed, so even at this inn Grace cannot stay too long. On Day 5 post-op, Grace and Joseph are discharged "home". As Grace has no home, a place is found for her in a hostel, with domiciliary visits planned. On the first visit, the domiciliary midwife finds things are OK; the next day, Grace and her baby have gone. A few days later — in fact, on New Year's Day — Grace presents to the emergency department again, this time with Joseph. He isn't feeding well and is bringing up feeds; and, he has a fever. But we can deal with all that. It's another acute problem, not one of those complicated social issues that, in hospital practice, just have to be put into the "too-hard" basket. The paediatric registrar arrives, Joseph is admitted and a drip is put up. And so the cycle of disadvantage starts all over again — unto a new generation.

Caroline M De Costa FRANZCOG, FRCOG

On changing careers midstream An identical plea for help marked both the beginning and the end of my career as a general practitioner, and I think that the particulars of these two events reflect the great changes that took place during my decade or so spent as a GP. In 1959, I returned to Australia from England and began working as an assistant in a general practice in the eastern suburbs of Sydney. In the middle of the night, in the middle of winter, I received a phone call from a man who politely identified his mother as a patient of my boss. He asked me to come to the house, and said, "Mother can't breathe, doctor"; he surmised that mother might have a bad cold. I took down the name and address, and got dressed, cursing myself for agreeing, without closer inquiry, to see someone who might have nothing worse than coryza at that hour. The patient's home was not far away, but it was a bitterly cold night, with a howling westerly wind blowing; in those days, cars did not come with a heater as standard equipment! When I reached the house, the son (much older than me) took me to his mother, a very elderly woman who was, at once, seen to be in extremis as a result of acute left ventricular failure. A quick history was taken from the son, the standard remedies of the day given — intravenous theophylline, morphine, and digoxin, as I recall — and an explanation of the condition and its bleak prognosis given to the son. The patient died soon after. The son thanked me for attending promptly and for doing what I could. I felt ashamed for my unspoken resentment at the time of agreeing to make this house call, but I also felt a sense of great relief that I had attended. The old aphorism "to cure sometimes, to relieve often, to comfort always" came to mind. I left the practice at the end of that year to join a group practice — still in the eastern suburbs — where I remained for the next 11 years. During that time, my initial indifference to the psychiatric aspects of illness was gradually replaced by a growing realisation of the importance of emotional factors in medical practice. Eventually, I decided to undertake specialist training in psychiatry, and it was agreed that I would leave the practice at the end of 1970. I was on call for the practice on a weekend late in 1970 —perhaps my last weekend on call. The Sunday evening was warm and still. Towards midnight, there was a phone call, and a woman asked me to make an urgent house call, saying, "Mother can't breathe, doctor!". My mind went back to the incident of years before, and I simply took the address without getting any medical details and got there as soon as I could. I found that, this time, Mother was a middle-aged woman with a head cold, who could not breathe through her nose. Respiration through the mouth was unimpeded and examination of the respiratory and cardiovascular systems was otherwise normal. I wrote a prescription for ephedrine nose drops. Both mother and daughter protested that the chemist shops would not be open until the next morning. I suggested that the medical "urgency" of the situation would justify waiting until then. A pensioner medical service voucher was signed, and I left with gritted teeth and, no doubt, seriously high blood pressure. When the red mist settled, I was able to reflect that this might have been a suitable valediction to general practice, an appropriate omega to the alpha of the earlier incident. The two incidents encapsulated some of the reasons for my ever-increasing dissatisfaction with general practice. I had seen the role of the GP move from that of front-line treating doctor — as my training, experience and inclination had taught me to be — towards that of gatekeeper or signpost-man. I had given some thousands of general anaesthetics as a GP, but could see that the days of the GP-anaesthetist were limited, and, in any case, I had decided that I preferred to be dealing with patients who were conscious and inclined to talk. "Blood tests" and medical imaging were insidiously displacing clinical skills as the primary methods of diagnosis. It took a long time, 20 or 30 years, but ultimately I came to be almost glad that I had experienced that second house call. Changing horses in midstream is something to avoid, so it is said, but these two episodes seemed to me to help justify changing my career when in darker moments I had doubted the wisdom of doing so.

Andrew R Robertson MB BS, FRANZCP

For theatre staff, the most precious drug in Buka. When the theatre drug safe has nothing in it bar a packet of tea, you know you are in an unusual operating theatre. When I volunteered for a fortnight in October 2001 with AusAID in Bougainville, which lies between the Papua New Guinea mainland and the Solomon Islands, I knew I'd have to resurrect my Third World anaesthesia skills. One can come to terms with halothane anaesthetics and a single syringe — the real test is the tea in the drug safe. For the record, that packet of tea made the best "cuppa" I'd had in a long time. You put several spoonfuls of tea into a strainer and run hot water from the urn through the strainer until your cup has the desired strength. Two tablespoons lasted all day. It worked — thus passing the acid test of all Third World medicine. Faced with a 13-month-old little boy up for three hours of bilateral talipes surgery, I racked my brains: what was the best way to gas him? First World anaesthesia was precluded by the absence of any endotracheal tubes smaller than 5 mm. Anyway, the ventilator didn't work. So I gave the kiddie a knockout premed and snuck up on him with the halothane. Just a few seconds before his Mum and I fell asleep the kid succumbed and I stuck in a laryngeal mask. He breathed himself to sleep for three hours and the surgeon had no complaints. It's a bit like the old air force adage, "Any landing you walk away from is a good landing". Over the years, I've done lots of tours of "good works" — from trips with the Flying Obstetric Service out of Roma, Queensland (about 500 km west of Brisbane), to those with the Forward Surgical Troop with INTERFET in East Timor in 1999. Nothing has given me the satisfaction of "a job well done" as much as this AusAID tour, and I recommend it to others unreservedly. Our orthopaedic team left Buka knowing there were half a dozen kids walking around the place who couldn't otherwise have done so. How does that compare with the list of arthroscopies that is my usual bread-and-butter? Back of BukaThe Bougainvilleans are trying desperately to put behind them the '89 to '99 "crisis" — their term — when a move to secession left a potentially well-off country devastated by war and pollution (eg, from heavy metal run-off from abandoned mines). Conversations with the intelligentsia left me with the distinct feeling that their support lay with the Bougainville Revolutionary Army (BRA), although they would never admit it, and any conversation on the topic is conducted sotto voce. I was one of a four-man team of orthopaedic specialists who, since the peace treaty of 1999 and supported by AusAID in partnership with the Royal Australasian College of Surgeons, have made an annual trek to Bougainville. Airfares and accommodation organised for us, we arrived without a hitch on Buka, the northernmost of the two main islands of Bougainville. First, we had to separate the "VIPs" from the deserving cases. The surgeon had been here before — indeed, his father was a much-respected "expat" from the days before the crisis — and knew that the first patients to be seen in outpatients would be the important people in the village. The trick is to admit that they need surgery but put them off until the real work is done. We did this very effectively, finishing our 25 cases of the visit with three arthroscopies of knees (the postmaster, the bank manager, and the police chief). Interestingly, from a professional point of view, these last three patients had more postoperative pain than that experienced by all the (far more serious) cases put together. Education is obviously related to pain perception. We were accommodated in a hotel at the opposite end of the village from the hospital. Getting from one to the other involved a long and sweaty walk each morning and evening, sometimes in the dark. A throwaway remark, by a fellow guest and expat, put things in perspective. When we asked whether the locals would harm us, he replied that they would rob us, but they wouldn't kill us or rape us (one of our team was a theatre sister) and, if they did, the village would be pretty cheesed off about it and would probably exercise payback on the perpetrators. When AusAID teams weren't in Buka anaesthesia was reduced to its true role in the spectrum of medicine and was provided, perfectly adequately, by two "technical officers", who, as far as I could see, had been trained in the "recipe technique" (eg, "give two inches of the big syringe and about half of the little syringe"). They provided a service that would be envied in many Australian public hospitals: they never argued with the surgeon, and nine times out of ten the patient went to sleep on demand and woke up afterwards. I discovered — the hard way — that a speedy recovery phase was in your own interest, as you recovered your own patients. If you weren't careful, then, when everyone else was drinking tea, you were still applying jaw support. Our team of four knitted together quite quickly. Sister Mary-Lou — whose name, along with those of all the others in this story, has been changed . . . to protect me! — had never done anything like this before. She worked her feet off for 10 days but gave away her Third World inexperience by expressing disappointment when she found out that the only chemist's shop for a thousand miles did not stock self-tanning lotion, this amidst the second-blackest people on earth after Ugandans. She also let it slip, at the end of the trip, that probably nothing we used was truly sterile, as all the bundles were coming out of the steriliser still wet. If she'd told us this at the beginning, we would probably have gone home, but after two weeks we'd adopted a Bukanian attitude to sterility (ie, near enough is good enough). After all, if one can be "a little bit pregnant" then there's nothing wrong with "nearly sterile". A senior orthopaedic registrar joined us for part of the trip; an excellent fellow who worked very hard, saw things he'd only read about, and was imbued with the concept of pro bono work. The resident doctors, nurses and other staff at the hospital were extremely hospitable to us, and my expressed interest in fly-fishing was rewarded with a social outing in one of the locally built "banana boats" — twenty-three feet of unbreakable fibreglass, with a seriously large outboard. However, as these men fished for the table rather than sport, I felt they found my efforts with a fly rod and "feathers-for-bait" amusing and inconsequential but were too polite to say so. Out and about in ArawaWe spent the weekend in Arawa, the old provincial capital; getting there involved a painful 4-hour trip over dirt roads and tracks in a 4WD "troop carrier". Arawa is now a burnt-out shell after the BRA razed it to the ground in 1989. However, a new hospital has arisen from the ashes thanks to Australian aid and, at the time of our visit, had been open for only six weeks. It had a staff of two: an Australian doctor, only four years out, and a nurse from New Zealand. The doctor was away in the highlands seeing patients, but had already done a laparotomy for stab wounds and a caesar. I read, with morbid fascination, his guide to anaesthesia that was pinned to the wall of the theatre. It enumerates a Plan A, then a Plan B (both simply lists drug doses and techniques for giving a very basic anaesthetic). For Plan C, it simply says: "There is no Plan C". We shared accommodation (with hot showers) with several Kiwi policemen, who were there under an NZAid plan to set up an impartial police force. One of them, a young sergeant, described all the expats in Bougainville as either "mercenaries or misfits". Mature consideration revealed that, on social contact thus far, he was probably correct. However, we couldn't decide which group we fell into — one term was as pejorative as the other. Interestingly, several of the locals we met changed their attitude towards us when they clarified that we were not paid for our efforts and were not affiliated to any religious organisation (unless the RACS considers itself as such?). Tom, the Buka hospital carpenter, had accompanied us to Arawa. He had offered his services as a guide and general factotum, having said that his family came from this area and that he would like to visit them. Over the weekend, it became clear that our friend and ever-helpful guide was actually persona non grata in the area over a past relationship involving the daughter of a prominent local leader. Notwithstanding this social drama, Tom felt himself truly to be part of the team, joining the ward round of all the local "orthopaedic" patients rounded up for us to see during our visit. I might add, as a mere anaesthetist, that I thought his contribution to management was at least as sensible as the experts', and probably took more note of local exigencies. I've always maintained that orthopods were just carpenters with chrome-plated tools. The most threatening few moments of my trip actually happened in Arawa rather than Buka, when the "Team Leader" (his words, not mine) Dr Bones sent me off to find beer to sustain us over our weekend there. Tom established that it wasn't available legally. But, he had an address. We set off in the ambulance with Sister Mary-Lou riding shotgun and soon found ourselves in a back street with unnumbered houses. Tom disappeared, coming back with the going price (remarkably reasonable in the circumstances). Then it was my turn to enter the house, without Tom but with 60 kina and a tachycardia. It did cross my mind that the speech of the locals involved in the transaction sounded unusually Australian, but at the time I was more involved in getting out with a case of local beer and both legs working. Back in Buka, I learnt that these locals were the sons of a Buka nurse who had given up everything to educate her boys in Australia. I was quite proud to think that an Aussie education had given these lads an honourable profession. If you have a few weeks on your hands and can't stand the prospect of spending it on the links or the harbour, give a thought to volunteering your services to AusAid. It will not only broaden your horizons but also "reset your thermostat" as far as the truly important things in life are concerned. Now that I've retired from the black art of anaesthesia, these trips are the only thing I miss about "my old life".

Douglas N Gow

As the United States' unsettling rise to hegemony illustrates, the world becomes a more dangerous place when the balance of power is altered. What is true for geopolitics is true for medicine. I have a simple proposal for restoring the balance of power between the junior medical staff and their consultants and registrars. It relies on the well-proven theory of deterrence. It is the intern's equivalent of a submarine filled with nuclear missiles cruising off the coastal shelf of the registrar's continent. The system works this way. At the welcome and orientation to the hospital for the new interns, the last presentation is by a well-respected intern from the previous year. Ten shiny laminated cards are handed to the shiny new interns and they are instructed in their use. They are admonished to hoard these resources, to use them sparingly and effectively. A few weeks later the morning ward round is drawing to a close. Twenty-five patients have been seen, and seven consultations, two MRIs, a bone scan and a partridge in a pear tree have been generated for the unfortunate but uncomplaining intern. However, at last a line is crossed. A patient who had surgery the night before is rolling around in bed complaining about pain in his knee. He has a urinary catheter because he suffers from prostatism and has produced 20 mL of urine an hour from his generously sized ex-meat packer frame. One can easily see from the foot of the bed that he is as dry as a chip. The two drains appearing from under his bandages are full. The orthopaedic registrar looks at the pulse oximeter and notes a mild tachycardia. The terrible words are uttered: "We'd better get a cardiology consult . . ." (at least his expression is hangdog). This is the time to act. The intern pulls out his wallet and deals the "Get your own damn consult!" card. The registrar accepts it with consternation. He is compelled by the laws of decency and tradition to proceed. Dutifully, he calls the cardiology registrar between cases. He is greeted with the derision such an unnecessary consultation deserves. A hefty dose of humble pie is consumed. A couple of weeks later the temptation arises for another dodgy consultation; this time, some minor basal atelectasis. Noting the oxygen saturation of 94%, the registrar turns to his intern and starts to open his mouth. The intern reaches for his wallet; the mouth is shut; the submarine descends from launch depth and the balance of power is restored.

Richard D Lawson

Background: In 1889, Brown-Séquard, aged 72, reported dramatic rejuvenating effects after self-administering testicular extracts of dogs and guinea-pigs. His report resulted in widespread use of testicular extracts throughout Europe and North America for several decades. More recently, the male ageing process has been attributed to partial androgen deficiency, or "andropause", and testosterone treatment is claimed to improve well-being in middle-aged and elderly men.Design: We prepared extracts from five dog testes using Brown-Séquard's methods and assayed testosterone concentrations.Results: Testosterone concentrations were four orders of magnitude less than that required for a biological effect.Conclusions: Our study illustrates the marked placebo response that can be evoked by androgen treatment. It cautions against the empirical use of testosterone treatment for older men, unless a diagnosis of hypogonadism has been substantiated.

Andrea J Cussons MB BS · John P Walsh FRACP, PhD · Chotoo I Bhagat MD, FRCPA · Stephen J Fletcher MSc, Dip CB

On the Ides of March 2002, the "Magistrate 2" (M2) virus decimated my computer's hard drive. In one cruel fraction of a second, hundreds of files — not all backed up — representing countless hours of toil, were irreparably destroyed. My immediate sentiments were intense anger, directed at the faceless, malevolent inventor of M2, and despair over my loss. Unbeknown to me at the time, while it was neutering my computer M2 was simultaneously forwarding virus-laden Word files from my hard drive to persons listed in my email address book. Addressees included many parents and teachers of my children's preschool. Further, as luck had it, most of the transmitted files were publications arising from one of my areas of research, namely the use of electroconvulsive therapy (ECT) in children and adolescents. Thus, when they next checked their inbox, parents and teachers unexpectedly received one or more papers on the history of ECT in young people, an epidemiological study on ECT use in children and adolescents in New South Wales, studies on the opinions of teenage patients and parents regarding the treatment and, last but not least, a "user's guide" to how ECT should be administered to the young. Preschool parents and teachers had been oblivious to this particular interest of mine. Though I had nothing to be ashamed of — indeed, ECT can be a life-saving treatment for young people — it is still not an interest one advertises widely, nor mentions in the course of small talk at school meetings or social gatherings. Now, it is probably OK by parents of preschoolers for one of their number to be a child psychiatrist. Indeed, this sometimes comes in handy for the mums and dads ("Has Sarah got ADHD?"; "Is it normal for Trevor to be hitting his baby brother over the head with a cricket bat?", etc). It is, however, clearly another matter if the parent happens to be an expert on the use of "shock treatment" in kids. "Not nice, Dr Walter!", I imagined them saying when the secret was out, "Surely not Garry!". And yet there might have been cause for them to be grateful because, from that time on, classroom behaviour seemed to improve, particularly whenever I was around — dropping off or collecting kids, attending class concerts, etc. Was it possible that the children had been warned about the consequences of not behaving well at school, that they had been told what "Dr Volta" might do? Of course, the kids need not have worried. It was not as though I carried an ECT machine or set of electrodes on me. Must have been the spark(le) in my eyes.

Garry Walter PhD, FRANZCP

Objective: To describe the effect of physicians' dress on patient confidence and trust.Design: A prospective crossover trial involving physicians dressed in "respectable" versus "retro" attire.Setting: A general medicine ward at a tertiary hospital.Participants: 12 male general physicians and 1680 patients.Main outcome measures: Patient trust and confidence as measured by a questionnaire mailed after hospital discharge.Results: Formal attire was correlated with higher patient confidence and trust. Nose rings were particularly deleterious to patients' reported trust and confidence. A minimum threshold of two items of formal attire (dress pants, dress shirt, tie, or white coat) were necessary to inspire a reasonable amount of confidence; this is the NND (number needed to dress).Conclusions: We highlight the need for more research into the effects of physician dress, and coin the term "evidence-based dressing".

Balakrishnan R Nair FRACP, FRCP · Stephen R Mears DipIM · Karen I Hitchcock BA · John R Attia MD, MSc, PhD, FRCP(C)

The Olympic Games should be the pinnacle of sporting achievement, a showcase of the highest athleticism that can be reached by men and women. However, at present, it is estimated that only about 50% of sportspeople take advantage of the performance-enhancing medications developed through the wonders of modern science. This pharmacological nihilism is disappointing. If our best unmedicated athletes can achieve similar performances to those whose performances are pharmacologically enhanced, then how much better might they do with the benefit of modern medical science? What is needed is a level playing field. A fertilised one. We propose that, in future, no athlete should be allowed to compete in the Olympic Games without making maximum use of the miracles of modern medicaments and designer drugs. The Games could then be renamed the Pharmacological Olympic Games. The sponsorship possibilities are infinite. Rules of performanceAll performing athletes will be required to have drug tests at the start and end of competition. Those refusing to provide samples of blood and urine will not be allowed to compete. Any athlete whose samples test negative for performance-enhancing drugs will be sent home in disgrace. Performance-enhancing drugsThe accepted reference work for the sporting pharmacopoeia is MIMS-Sportif. Track and fieldHomoeopathic principles have always dictated that one treats a fever with hot medicines, and a cold with cold ones. Obviously, one can only expect to improve speed with speed. Amphetamines are de rigueur for the ambitious track-and-field athlete. The walkers, however, may prefer to take Slow K. A wide range of uppers is available for the high jump and the high hurdles, and long-acting uppers for the long jump. Cyclists should avoid catching herpes at all costs, because acyclovir can seriously impair their performance. Anti-inflammatories, such as the non-steroidal anti-inflammatory drugs, can help cure a slipped discus. In the poolDivers may benefit from downers, while antibiotics can help any divers suffering from diverticulitis. A new range of stroke medication is available for swimmers. Water polo players will benefit from the new water polio vaccine. The regattaThe COX-2 inhibitors have proved popular among rowers, particularly the coxless pairs. Soccer, tennis, handball, volleyballTestosterone is the drug of choice to improve ball control. Demonstration sportsDemonstration sports are sports favoured by the host country that may become a regular fixture in future Olympics. A demonstration sport with exciting pharmacoathletic possibilities is the dramatic Irish sport of hurling, which can be spectacularly enhanced by the judicious use of ipecacuanha. New developments on the horizonWeight-lifters have found that the new SSRI antidepressants have given them a real lift. Beach volleyball has received a boost from Sandoz, who are adding to Sandoglobulin and Sandomigran with a new drug, Sandobikini. ConclusionThe Pharmacological Olympic Games will showcase the best of what medicine and sport have to offer when the aggressive therapeutics of the heroic physician are harmoniously combined with the ruthless competitiveness of the world-class athlete. Let the Games begin!

David Isaacs · Dominic Fitzgerald

The sun filtered in as he cradled his chin in the palm of his long-serving hand, as he relived the days of his work in the haze way outback in our Great Southern Land. It seems too much to ask, but he's stuck to his task for the span of five decades or so; but his heart it is yearning, his stomach is churning, and he feels it's now high time to go. Ten years have passed by since he first wondered why there was no-one to answer his call — his practice for sale, but there lies a tale — he's just waited and waited, that's all. Will anyone follow his work on the morrow? Have our med schools dried up like Lake Eyre? For each greying carthorse, let's renew the workforce and steer our old docs from despair!

Andrew Beattie

A healthy young man, upon placing the palm of his hand on a wooden floor, experienced an immediate severe burning sensation. A small black shiny beetle was found lying partially crushed. The initial burning pain in the palm subsided, but a dull discomfort persisted for several hours. Examination revealed two areas of dark yellow-brown discoloration, resembling the colour of iodine, on the palm (Box 1). These measured about 1 × 2 cm, with a surrounding halo of mild erythema. The affected skin had normal texture, markings, and sensation, and no blistering or vesication was seen. The patient remained systemically well throughout the episode. No evidence of external biting, stinging or defensive apparatus was found on inspection. The skin changes lasted 3–4 days, and resolved completely. The beetle was identified as a species of bombardier beetle by Daniel Bickel of the Australian Museum, Sydney. Bombardier beetles belong to the large Carabidae family of active predatory ground beetles, and comprise the subfamily Brachininae, with some 500 species. One species, Pherosophus verticalis, is widespread in Australia (Box 2). Chemicals are used defensively by many ground beetles, usually discharged as a fine spray when threatened. At least nine diverse groups of noxious chemicals have been found in these insects, including acids, phenols, hydrocarbons and quinones.1 When threatened, bombardier beetles emit a defensive spray of heated benzoquinones from the tip of the abdomen.2 The quinones are produced explosively at the moment of ejection. This involves a two-chamber system — an inner reservoir chamber stores a solution of hydroquinones and hydrogen peroxide, and a separate reaction chamber contains oxidative enzymes (catalase and peroxidase).3 Mixing of the reaction components leads to catalytic events, with a rapid build-up of pressure from liberated oxygen, and explosive discharge of oxidised benzoquinones (Box 2). This can be accompanied by an audible "pop". The temperature of the emitted reaction mixture has been measured at 100°C.3 This boiling spray can be directed in all directions by a revolvable turret arrangement on the abdominal tip, and effectively deters both vertebrate and invertebrate predators.4 Australia is rich in beetles, with about 20 000 native species recorded.5 Despite this diversity of forms, beetles are rarely directly harmful to humans.6 1: The affected areas of the patient's hand 2: The bombardier beetle and its chemical weapon 1: Pherosophus verticalis, the Australian bombardier beetle. 2: A schematic diagram of the internal defensive gland. The secretory apparatus (A) produces an aqueous solution of hydroquinones and hydrogen peroxide, which is stored in the reservoir (B). When threatened, the beetle releases fluid from the reservoir into the reaction chamber (C), which contains a mixture of catalases and peroxidases. These enzymes catalyse an explosive reaction. The boiling mixture discharges in a spray through the abdominal tip. Reproduced with permission from NSW Agriculture.

Paul G Chee BMed(Hons), BMedSc · Scott M Dunkley FRACP, FRCPA

To the Editor: Over the past 20 years, the prevalence of obesity in the Australian population has more than doubled — from 8.1% in 1981 to 20.5% in 2000.1,2 The rapid and widespread nature of the obesity epidemic suggests that environmental change is a major contributing factor. The patterns and types of foods consumed by Australians have changed markedly within a single generation. One major area of change is the availability and consumption of "fast" foods.3 A key feature of fast-food marketing is the use of "upsizing", a strategy designed to provide the consumer with a "value-for-money" addition to their meal. Upsizing is commonly employed within the context of "meal deals": complete meal options comprising the major food item (burger or chicken product) and, for a small extra cost, larger serving sizes of items such as hot chips and soft drink. Recent data from a US survey have shown that upsizing provides disproportionate increases in energy content relative to purchase cost.4 However, no published data have demonstrated the impact of point-of-sale fast-food upsizing on total energy, fat and sugar availability for Australian fast-food meal-deal options. On 28 July 2002, we purchased major meal deals and the advertised upsizing portions from the four major fast-food chains present in most large Australian cities: McDonald's, KFC, Red Rooster and Hungry Jack's. In order to assess six portions of each meal deal, we purchased two from each of three outlets. The weight and volume of chips and soft drink (non-diet variety) were measured, and nutrients were analysed using the AusNut and AusFoods Australian food databases.5 A summary of our findings is presented in the Box. On average, a 12% increase in purchase cost increased energy availability by 23%, with a 25% increase in fat (10.3 g) and a 38% increase in sugars (18.8 g). The upsizing meal option providing the greatest energy gain was the "fillet burger combo" from KFC (50% increase in energy for a 16% increase in cost). Large meal deals provided on average 5733 kJ (35.4% energy from fat and 21.4% energy from sugar). Based on data from the 1995 National Nutrition Survey, these single meal deals constitute 52% and 77% of the average daily energy intake of male and female Australians, respectively.6 Upsizing is a marketing strategy aimed at increasing the purchase cost of the items by providing the consumer with an added incentive or greater value. Using this strategy, upsizing meal deals double the energy gain relative to the additional cost. Importantly, upsizing also increases fat and sugar intake. With the growing disease burden of overweight and obesity on the Australian healthcare system, the public needs to be aware of the passive increase in energy consumption that can occur in pursuit of "value-for-money" eating options. Excess consumption of sugar and fat from fast-food meal choices adds mainly "empty calories" to the diet, with little nutritional gain and with a real risk of expanding the nation's waistline. Percentage increase in cost, energy content, fat and sugars for various upsizing meal options from four major fast-food outlets Percentage increase Cost Energy content Fat Sugars McDonald's Big Mac McValue meal (medium)* 10.1% 17.8% 16.2% 34.1% Big Mac McValue meal (large)* 20.2% 39.5% 33.1% 80.7% KFC Fillet burger combo (large)† 16.1% 50.3% 56.4% 52.7% Red Rooster Chicken roll combo (large)† 16.6% 27.5% 22.0% 39.7% Hungry Jack's Whopper value meal (large)† 9.2% 15.7% 14.4% 30.2% * % Increase relative to "small" size. † % Increase relative to "regular" size.

David Cameron-Smith · Shane A Bilsborough · Timothy C Crowe

To the Editor: "Chop-chop" tobacco is illicit tobacco that has been grown and clandestinely distributed by farmers and wholesalers and sold on without government intervention or taxation. There is no quality control over this illicit substance, which may be adulterated or "bulked up". It is sold illegally "under the counter" by weight for rolled cigarettes by unscrupulous tobacconists and grocers. This type of tobacco, which has been roughly chopped up (hence "chop-chop"), is very cheap compared with legally produced manufactured cigarettes. The prevalence of the use of chop-chop in the smoking community is unknown. However, the Australian Taxation Office (ATO) has a keen interest in the distribution of this substance, and estimates that many millions of dollars are lost in revenue from the illegal sale of chop-chop. Arrests and fines initiated by the ATO have so far occurred primarily in Queensland and Victoria. Results of analysis of chop-chop vary from batch to batch, but samples have been shown to contain nicotine (Professor G Starmer, Department of Pharmacology, and Mr B Tattam, Mass Spectrometry Unit, Department of Pharmacy, University of Sydney, personal communication). It may also be fumigated with bleach and may be bulked up to add weight (M Rushton, ATO, personal communication). Although most people smoke it because it is cheap, many have misguided beliefs, for which there is no evidence, that it is "better" than other forms of tobacco. Results of a survey of 44 consecutive patients attending the Smokers' Clinics of the Central Sydney Area Health Service 43% currently using "chop-chop" 84% smoke it because it is cheaper 58% believe it is better for you 74% believe it has no additives 16% believe it has no nicotine 63% know it is not legal A retrospective survey was carried out to assess the prevalence of and attitudes towards illicit tobacco smoking among patients attending the Smokers' Clinics of the Central Sydney Area Health Service (approved by the CSAHS Ethics Committee, June 2002). Patients were routinely asked the type of tobacco they smoked and their beliefs regarding this type of tobacco. The results are shown in the Box. Many of the patients attending the Smokers' Clinics (dedicated exclusively to patients who smoke and have chronic obstructive pulmonary disease [COPD]) smoke this type of illegal tobacco. Several patients volunteered that smoking chop-chop precipitated an acute exacerbation of their COPD. Four patients have recently presented to a hospital emergency department for exacerbation of COPD after smoking chop-chop. Although smokers are loath to volunteer their use of this illegal tobacco, smokers and clinicians should be warned that smoking chop-chop does not constitute a positive health move, is not less harmful, and may be quite dangerous. Quitting smoking altogether is the best health move.

Renee Bittoun

To the Editor: These two cases, which occurred many years ago, illustrate a useful clinical sign in the diagnosis of tetanus. An elderly man was admitted to hospital after crushing his finger in a stable door. He commented in passing that when he whistled across the park to his wife that morning, she had not heard him. However, she had heard him the previous two mornings. He was a professional whistler on the radio and, when asked, still appeared to produce a good strong whistle. As it is the high pitch that carries long distances, I pondered the causes of selective pitch loss. I suspected the "risus sardonicus" of tetanus. He was subsequently confirmed to have tetanus and survived. Years later, a middle-aged woman with right hypochondral pain and presumed cholelithiasis presented to a country hospital for a cholecystogram. I chatted to her about her bandaged hand — she said that she had cut it on a jam tin in her house, but that her general practitioner was treating it, and all her vaccinations were up-to-date. Some hours later she complained that her abdominal pain was worse and had moved. I believed that the pain was probably related to movement of gallstones, but was more interested in her hand wound, of which she was dismissive. I asked her to whistle. It was a good whistle, but she commented, "It's not my whistle, I whistle the cows into the bales." Recalling my previous patient with the altered whistle, I diagnosed tetanus and arranged her urgent transfer to a consultant at Sydney Hospital (Sir Kenneth Noad). Indeed, she did have tetanus, and developed laryngeal spasm requiring emergency tracheotomy and 2.5 weeks in a respirator. Sir Kenneth later thanked me for saving the patient's life. The alteration of a person's whistle in tetanus can be explained as an early effect of the increased tone in facial muscles, which causes the classic risus sardonicus. As tetanus toxin must travel from peripheral nerve terminals to the nerve-cell body in the brainstem or spinal cord to exert its effects, muscles of the jaw, face and head, with their shorter axonal pathways, are often involved before those of the trunk and extremities.1

Eric R Dunn

To the Editor: In general, it is unwise for the medical practitioner to stray from those fields in which he or she is trained. To illustrate this point, I report the case of an anaesthetist (me) caring for a patient undergoing general anaesthesia for open repair of a fractured ankle. The operation was nearly over. The ankle had been repaired and the theatre nurse left the scene to assemble the materials needed for a leg cast. The patient was breathing spontaneously via a laryngeal mask airway. Before wound closure, the orthopaedic surgeon requested intraoperative radiography. A large X-ray machine was wheeled into the theatre, and the radiographer positioned it over the patient, took several images and then left to process the films. The surgeon wanted to resume surgery immediately, but who was going to remove the unattended x-ray machine, still poised directly over the operative field? I volunteered. I hit a button on the panel. It manifested as the command for "reverse": accordingly, the machine backed itself into the wall of the operating theatre, trapping me in between. At the same instant, a loud noise — consistent with partial upper airway obstruction — emanated from the anaesthetised patient. I had to free myself from my captor. Immediately. My release strategy incorporated pressing most of the buttons on the x-ray machine in a random manner. As all were imprinted with unrecognisable symbols, this seemed a reasonable, and eventually effective (if not a recommended), method for determining the "forward" function. I quickly returned to the patient's head and managed the airway problem. Thankfully, the patient's oxygen saturation did not decrease and the remainder of the anaesthetic was uneventful (the x-ray machine having been escorted out of the theatre by the radiographer on his welcome return). Although I had been willing and, in fact, keen to expedite the surgical procedure, I suggest that doctors avoid the lure of driving foreign vehicles (they can be savage beasts).

Richard H Riley

The Clinical Toxinology Resources website is now available at www.toxinology.com. It is a vast and growing searchable database, including 6000 images, designed to meet the needs of anyone seeking information on venomous and poisonous organisms throughout the world. Coverage is currently most complete for venomous snakes (over 800 species records); important spiders, scorpions and marine organisms are detailed, and new records are being added weekly. In the next few months, nearly 2500 poisonous plant records will be added, along with records of poisonous mushrooms. There is also a list of antivenoms and antivenom producers worldwide. The recently updated CSL antivenom handbook is available in its entirety; further toxinology resource documents will be added in the future. Access to the site is at two levels: a free general level or a more detailed subscription-based level aimed at health professionals. Subscribers can also log new cases using a secure system. The site was developed by the Toxinology Department of the Women's and Children's Hospital, Adelaide, and the Department of Paediatrics at the University of Adelaide, with the assistance of a small grant and the goodwill and time of a number of experts from Australia and overseas. Subscriptions will be used to help meet the considerable costs of maintaining and extending the site. MJA readers are cordially invited to visit the site and to consider supporting this endeavour by subscribing.

Julian White

To the Editor: In 1995 and 1998 I was fortunate enough to have extended leave of several weeks. On both occasions, when I averaged out the weight of mail, excluding newspapers, waiting for me on my return, it came to about 7 kg per month. I wanted to determine the volume of communication I received in 2002, but: a substantial amount of my mail is now electronic; I no longer have extended holidays; mail cannot be now left unopened and unattended. It is opened by a trusted colleague, scanned into our patients' medical records and the originals left out for me to see on my return; being away would lead to a decrease in the mail I received; weighing individual mail articles would be a tedious test of sanity. So, I logged my mail for four weeks from 13 July until 9 July 2002. I have included neither mail addressed to me at home (which is now minimal and consists mainly of household bills and private correspondence) nor newspapers. A summary is shown in the Box; I have the individual log if anyone is interested. So, how to measure the communication load of a general practitioner? I have weighed it and counted it, but it was not practical to determine how long it took to read. This is because reading it necessitates acting on it, whether this means writing a reply, incorporating it into a patient's history or recalling a patient to order further tests. This communication load on GPs is significant and is a further indication of the complexity of our discipline. The weight of this load has significance for those wishing to communicate with GPs. Anything longer than a page runs a risk of joining the rapidly enlarging pile next to the GP's desk of material that must be read at the first opportunity. Anything else is condemned to the round filing receptacle under the desk. Correspondence received in four weeks 814 emails (62 individually addressed; 752 undirected from various mail groups). 451 individual pathology results downloaded by computer. 181 letters (147 individually addressed; 76 standard-sized letters, undirected, from various organisations; 58 oversized letters, undirected, from various organisations). 8 journals (4 subscribed; 4 unsubscribed). 8 broadsheets. 8 items of other mail, including books and packages of documents, weighing a total of about 3 kg. 112 faxes. Grand total: 1574 individual pieces of communication per month

Christopher D Hogan

One of my poppy plants always sets its buds in pairs, with a stem formation reminiscent of some human anatomy. If its seedlings set true, I may have a new botanical variety: Papaver orchidiformis, var. vasa deferentia.

Alan Moskwa

The only real firefighter in this group was the person taking the photograph, which shows emergency physicians and anaesthetists undertaking breathing apparatus training at the NSW Fire Brigade's "Hot Cell" training centre. Most aren't watching the fire, but one has just noticed it spalling along the ceiling above them.

Antony Nocera

Torsion of the vermiform appendix was first reported by Payne1 in 1918 and remains something of a curiosity, with only 19 further cases reported, 12 in paediatric patients.2,3 Anatomical variations (eg, long mesoappendix), appendiceal tumours and strenuous physical exercise such as calisthenics were suggested to predispose to torsion.4,5 Reported clinical presentations were indistinguishable from acute appendicitis.4 Our patient, a 44-year-old woman, suddenly developed severe abdominal pain while walking, which was unrelieved by narcotic analgesics. Abdominal palpation revealed acute tenderness suprapubically and in the right iliac fossa. Surgical exploration via the standard McBurney incision revealed a dilated gangrenous appendix twisted 360 degrees anticlockwise at its base, as shown in the operative photograph. Histopathological examination of the appendix revealed a cystadenoma close to its distal end. The patient made an uncomplicated recovery after appendicectomy. First report "On Monday, March 13, 1916, while travelling in a train, [the patient] was seized with sudden pain in the epigastrium after lunch. She vomited several times, but the pain continued and was of a colicky nature. At midnight the pain suddenly shifted to the right iliac fossa and became continuous. The following day a doctor was called in; he ordered enemata, and three were given, with very copious results. On the 15th I saw the patient and operated the same evening. On opening the abdomen through the right rectus incision, the appendix was found pointing downwards and slightly outwards in the right iliac fossa. It was quite free except for a slight recent adhesion from the extreme tip to the iliac fossa. On examination it was found to be twisted, and it took three complete turns to unravel it . . . The appendix distal to the narrowing caused by the twisting was gangrenous, and the meso-appendix dark and swollen. The appendix was removed, and the abdomen drained through the original incision. The temperature and pulse became normal on the third day, and the patient made an uneventful recovery. Remarks. — The appendix was 21/2 in. long and contained faecal material. It seems most probable that the previous attacks were due to a 'constipated appendix,' and that the torsion resulted from irregular peristaltic movements on the part of the appendix itself." — Br J Surg 1918; 6: 327

Amy L Moten · Randal S Williams

The Macarthur Ambulatory Care Service has developed a successful program for delivery of intravenous antibiotics at home to provide an alternative to hospitalisation. Although most patients are housebound, some have returned to their usual occupation during treatment, without adverse outcomes. This 57-year-old poultry farmer, referred by a respiratory physician for treatment of community-acquired lobar pneumonia, was receiving intravenous ceftriaxone 1 g daily. For his final dose, the nurse was directed across the farmyard to a large shed, where he was feeding his chickens.

Nicholas P Collins MB BS, FRACGP · Bradley Warner BHlth, RN · Stephen F Wilson FRACGP, FAFRM

One of my most amusing cases concerned two young fellows who had spent a day on the town doing some considerable celebrating. To prepare for more of the same that night one of them decided to clean his teeth. In the course of this procedure he managed to swallow his toothbrush. I was unbelieving when first I heard this story, but, despite his inebriation, the patient was obviously distressed, so oesophagoscopy was indicated. A toothbrush was removed from the upper oesophagus. My relieved patient, hearing my name, said he was used to consulting Dr Beer regularly, and thought that more beer was sure to help him.

Neville Beer

This cheerful "Kilroy was here" image is a CT scan showing the grossly swollen scrotum of a young man after a motor bike accident.

Bit Lock Wong

An abdominal ultrasound of a patient with right iliac fossa pain revealed the culprit, smiling cheekily.

Khimseng Tew

When the patient presented with colicky abdominal pain we smelt something fishy. Abdominal ultrasound confirmed the diagnosis.

Nishantha S Karunaratne

Fetus in feto is a known phenomenon; could this be one? Or neural tissue in a dermoid cyst? Whatever, the patient appears well endowed, with the CT scan showing a spare brain and spinal cord in the thigh muscles.

Rodney H Strahan

This photograph was taken in Udaipur, Rajasthan, India, in 1988. It had occurred to me to submit it to the MJA some years ago, but I wanted first to be sure of the epidemiological validity of this omnibus statement.

Edward Brentnall

Fairfield Hospital, now sadly closed, once described as "an infectious disease training nirvana, where physicians danced naked along the banks of the Yarra", used to attract many returned overseas travellers with fever. Among the tens of thousands of blood smears screened by its excellent malarial scientists, occasionally a gem such as this "Australia antigen" was found. Note that Tasmania is represented by a platelet, rather than as part of the monocyte, surely reflecting the ambivalent status of our island State.

Robert Baird · Bronwyn Munro

Having recently succumbed to the Open Plan Office, the MJA team have grown used to knowing just that little bit more about each other. After a couple of weeks spent in silence with the occasional stifled exclamation, furtive internal office emails and hasty retreats from the building to allow hushed conversations on mobile phones, we grew to like the new arrangements. Personally, I think it's important that we fully experience each other's childcare disasters, partners' nicknames, banking problems, travel plans and favourite humming tunes. So much so that I frequently function as a relay station for those hearing-impaired among us who miss things. But, how to have a secret ballot in the new environment... Competition was, as ever, fierce. Four distinct categories emerged (snapshots, X-rays, "research" and stories) but only two prizes could be awarded. The 21 finalist entries were displayed in a prominent place and the voting began. As often happens in these situations, a solution to the privacy problem presented itself via a complicated "decoy" arrangement, with people loudly declaring their preferences then voting quite to the contrary, so that when the votes were counted and clear winners emerged everybody had to act surprised. All of this year's entries are well worth a read, but DeCosta's "Saving Grace" (page 673) will hold you from beginning to end. It wins first prize in the written category (two bottles of Australian wine to be consumed after Dr DeCosta's next "nightmare" delivery). In the visual category, despite enjoying the usual smorgasbord of bizarre and ribald images, we chose Brentnall's long-hoarded photographic gem, "Cholera Travels" (page 675). Dr Brentnall will be able to show the rest of his travel snaps to a few friends over his two bottles of fine Australian wine. Our great thanks to everyone who entered this year's competition. We know there are more stories and pictures out there and look forward to benefiting from your creativity in the future. Check out this year's batch for inspiration and note our new (open plan) address for early submission for next year's competition.

Ruth Armstrong

Major incident medical management and support. The practical approach. Advanced life support. 2nd edition. Hodgetts TJ, Mackway-Jones K, editors. London: BMJ Books, 2002 (xv + 222 pp). ISBN 0 7279 1391 3. Bushfires, bus and train crashes, and multiple shootings happen in Australia and this is why the Major Incident Medical Management and Support (MIMMS) course was started in about 1995. The course has flourished since then, and now, with terrorism and biological threats very real after September 11 and recent events in Bali, this concise and comprehensive second edition is timely. This volume aims to teach all doctors (from GPs to emergency care specialists) a practical approach to a situation where they are at the scene of a disaster where the number of injured exceed the available resources. It sets out a structured approach and outlines the roles of the various services involved. The clinician will find that this approach is clearly explained. Aided by tables and diagrams, the reader is shown how to assess the scene, communicate appropriately with the services, use an accepted quick triage sieve (in the field using respiratory rate and capillary return), deal with the dead, and do practical procedures from airway management to femoral nerve blocks. Various topics, from media interaction to chemical and radiological incidents, are covered, although biological agents seem to have been forgotten. The great strength of this work is that it is relevant and very practical. It is supplied in a loose-leaf folder so that it can be updated, and there are spaces to record specific local details. In spite of a respected Australian contributor it does have a British flavour, but the principles are universal. In our fast-moving and troubled society, no doctor, whether a rural GP or a city doctor, can be sure he or she will escape being caught up in a major incident. Having medically responded to several of Australia’s major disasters I have done the MIMMS course, and I always take this excellent manual with me. Both are to be recommended most highly. Gordian W O FuldeDirector, Emergency Medicine St Vincent’s Hospital, Sydney, NSW

Gordian W O Fulde