Volume 195 Issue 5

Asbestos manufacturers have never warned homeowners of the risks of renovation On the Australian mainland, there have only been two manufacturers of asbestos cement products used in home construction and renovation: James Hardie and Wunderlich, a subsidiary of CSR. Asbestos products were manufactured from the 1920s up until 1984, when Hardies ceased using asbestos in their building products (Wunderlich had been acquired by James Hardie in June 1977). In 1978, James Hardie boasted that their products were in most homes in Australia. The range of asbestos cement building products (once widely known as “fibro”) that were made in Australia include flat and striated walls, eaves and panels; corrugated panels (used primarily for fencing and roofing); flat sheets covered with crushed or artificial brick; flues for gas heaters; thick sheets for flooring or as tile underlay; and sheets covered with coloured or patterned vinyl used in bathrooms and other wet areas. As the country with the highest rate of mesothelioma in the world,1 Australia has lived through two “waves” of asbestos-related disease — the first from the mining of asbestos and the manufacturing of asbestos products, and the second from asbestos use in industry. In this issue of the Journal, Olsen and colleagues clearly reveal that the “third wave” of the asbestos disease epidemic in Australia comprises non-industrial users of asbestos products,2 and a significant contributor to this cohort are the non-professionals who cut and fixed asbestos cement products in home renovation or maintenance and other do-it-yourself activities, or who demolished asbestos cement products during renovations. Family members present during these activities are also part of this cohort. The most alarming feature of this third wave is its potential to continue to grow for many years to come. Neither James Hardie nor CSR have ever taken any steps to systematically warn people who have asbestos products in their homes — including products that contain the highly dangerous Wittenoom blue asbestos used by both manufacturers — of the potential for fatal consequences in 20–40 years if they demolish those products today. We contend that the manufacturers have a legal duty of care to these people (Box). Claims for compensation and damages for people with asbestos disease because a manufacturer breached a duty of care have been pursued for over 25 years. Many of the legal precedents derived from the early claims against CSR by workers at the Wittenoom mine, and against James Hardie by its employees, have been applied in these product-user claims. Most mesothelioma claims are now successfully resolved out of court without a trial. When this does not occur, the claims primarily involve one or two instances of construction or demolition. The major issues of controversy are (i) the claimant’s ability to prove that the manufacturer could, and should, have taken steps that would (before the time of exposure) have drawn the risk to the user’s attention; and (ii) proving, more probably than not, that the exposure in such limited circumstances was a cause of, or made a contribution to, the mesothelioma manifesting many years later. Almost from the first acceptance in 1960 of mesothelioma as a cancer uniquely related to asbestos, it has been recognised that this cancer could be caused by very low exposures.1 The argument is sometimes put that mesothelioma can occur without asbestos exposure at all, or can be caused by exposure to the very low “background” levels present in most urban environments and some non-urban environments. In reality, in an individual mesothelioma case, all cumulative asbestos exposure — “background”, unrecalled or unrecognised exposure, and specifically recalled exposure — must, on biological mechanistic grounds, be considered to be playing a part in causation.3 With acceptable evidence of specific exposure, no matter how slight, a claimant should succeed, as such exposure would add more than a minimal dose to any background exposure. No threshold for asbestos causation of mesothelioma has been demonstrated.4,5 The article by Olsen et al documents an upward trend in mesothelioma cases in home renovators.2 This trend was appearing in reports of the Australian Mesothelioma Register operated by the National Occupational Health and Safety Commission (NOHSC) up to 2001.6 However, until now, it has not been possible to statistically confirm the trend, because of incomplete coverage of the Register from 2001 onwards. This was a consequence of the drastic cutbacks in the scientific capacity of the NOHSC, and over-stringent privacy legislation preventing comparisons with state cancer registries and the collecting of data on exposure history. We hope that the newly reconstituted Australian Mesothelioma Registry collaboration, administered by the New South Wales Cancer Council, and covering all mesothelioma cases in Australia diagnosed after 1 July 2010, will enable continued monitoring across the whole of Australia of this tragic third wave of the mesothelioma epidemic. While the Western Australian Mesothelioma Register study2 and the new Australia-wide initiative will be of small comfort to those who already have or will develop mesothelioma, these initiatives may assist in maintaining an awareness of the risks of exposure during home maintenance, and of other possibly unrecognised exposures, and hasten regulatory and control activities both nationally and internationally. All asbestos use was banned in Australia in 2003, and it is also banned in 56 other countries. (There are a few very limited, technical exceptions to the ban; eg, for military use where no substitute is available.) However, there are a few countries where it is still being used in building products (eg, India, Thailand, Russia, China and Indonesia). Data from Australian registers serve a very important purpose in sending a global warning of the deadly nature of this substance and the need for a complete global ban on any future use.7 The legal duty of care A manufacturer of an asbestos cement building product owes a legal duty of care to users of the product. The duty obliges the manufacturer to take reasonable care that a person is not at risk of suffering a foreseeable injury from using the product. A foreseeable injury is one of which the manufacturer, knowing the way the product is used, and up to date with the literature concerning injury from use of such a product and any potentially dangerous components or ingredients of that product, is, or ought to be, aware. As asbestos cement building products were used in homes, people who used the new product in the construction or renovation of their homes were owed the duty, as will the people who later demolish and remove the product, as both uses should be contemplated by the product manufacturer. The steps required of the manufacturer to discharge this duty — ceasing manufacture, warning, and recall — will be proportionate to the likelihood, and the potential seriousness, of the injury. If a person is injured because of a breach of the duty of care, they are entitled to compensation commensurate with the loss and harm suffered.

John R C Gordon BJuris, LLB · James Leigh MD, FAFOEM, FAFPHM

Simple strategies can reduce harms from misuse of pharmaceutical opioids Sustained-release opioid drugs have been used increasingly over the past two decades to treat all types of chronic pain, including chronic non-cancer pain.1 Rates of prescribing have increased in developed countries such as Australia, Canada, the United Kingdom and the United States since the beginning of the 21st century.2-4 In the US, aggressive marketing of sustained-release formulations of oxycodone to primary care physicians and directly to patients between 1996 and 20075,6 resulted in a 10-fold increase in their per-capita use, and an alarming increase in the number of deaths from overdose with prescription opioids. In 2007, the number of deaths from oxycodone and other pharmaceutical opioids (11 499) outnumbered overdose deaths from illicit heroin and cocaine combined (around 8000).7 The article by Roxburgh and colleagues in this issue of the Journal8 provides an assessment of harms arising from recent increases in opioid prescribing in Australia.1 Roxburgh and colleagues show that pharmaceutical opioid prescribing has increased, with those for sustained-release forms of oxycodone supplanting those for morphine.8 Most oxycodone prescriptions have been to adults over the age of 50, with the steepest increases in rates of prescribing to patients aged over 70 years.8 These patterns suggest that most prescribing has been for chronic non-malignant pain, the prevalence of which increases steeply with age.1 Increased opioid prescribing has been accompanied by increases in the number of people seeking treatment for dependence on prescribed opioids in Australia. The number of fatal overdoses involving oxycodone has also increased, but, unlike in the US, the number of deaths in Australia from oxycodone reported by Roxburgh and colleagues was much lower (59) than the number of deaths from all other opioids (including heroin; 315) in 2005 (this was the most recent year in which the two could be directly compared). Roxburgh and colleagues report that in 90% of cases, deaths from oxycodone overdose involved either the use of the drug in combination with other opioids, benzodiazepines and alcohol, or the contribution of concomitant medical conditions. Just over half of the deaths (53%) occurred in people who were prescribed oxycodone, probably for the relief of chronic pain. A quarter of all these deaths, and those of a third of people with no history of illicit injecting drug use, were found to be suicides. Fatal overdoses among those with a history of injecting drug use were more likely to involve males, as is true of overdose deaths in this population more generally.9 Injecting drug users were more likely to be using diverted opioids at the time of their death, although a third were prescribed these drugs. There are a number of strategies available to governments to reduce pharmaceutical opioid misuse and the harms arising from it.1 Clinical recommendations are as follows: First, doctors and patients need to be educated about the risks of dependence on, and overdose of, these drugs, especially when higher doses are prescribed. Patients need to be informed by prescribers and pharmacists about the risk of fatal overdose if they use these drugs in combination with other drugs that depress the central nervous system, whether prescribed ones like benzodiazepines, or the more readily available alcohol. Second, clinical guidelines are needed on the place of opioids in the treatment of chronic pain, especially non-cancer pain. There is a need for clearer clinical guidelines for primary health practitioners to ensure that opioids are not used as first-line drugs for chronic pain, but are reserved for use when other forms of treatment have been tried.1,5,10 Third, clinical priority should be given to reducing suicides in patients who experience chronic pain and who are prescribed opioids. Prescribers need to be cautious in prescribing opioids to depressed patients. They should also enquire about suicidal ideation in patients who have chronic pain and who have been prescribed these drugs long term but have incomplete pain relief. Fourth, smaller quantities of these drugs should be prescribed to allow for more regular review of their effectiveness in relieving pain. Compliance with the prescribed medication regimen should be carefully recorded and a clear plan of action should be documented when significant non-compliance is identified. Referral to pain specialists should be considered if pain control is incomplete, and referral to addiction specialists should be considered if dependence on opioids is suspected. Policy recommendations are as follows: Enhanced prescription monitoring systems are needed to reduce both doctor-shopping by patients and imprudent prescribing by doctors. These systems should be computerised, nationally consistent and, ideally, real-time.1,5 It is also critical for doctors and pharmacists to monitor patterns of chronic opioid use in patients whom they see. The pharmaceutical industry needs to ensure that these drugs are marketed to prescribers in responsible ways, and that clinical information for patients advises about the risks of using these drugs in combination with other central nervous system depressants. Governments need to examine ways of increasing access to buprenorphine and methadone treatment for people who use opioids illicitly, and who may be using pharmaceutical opioids to self-treat.1 If Australian policymakers and doctors want to avoid the disastrous US experience with pharmaceutical opioids, these steps should be taken now while the misuse of these drugs is still a manageable problem. Whatever policies are implemented, it is essential that we assess rigorously their impacts on both the quality use of these medicines in relieving chronic pain and on the harms arising from their inappropriate use.

Wayne D Hall PhD · Michael P Farrell MB, FRCP, FRCPsych

Low infectivity but high mortality: strategies to minimise spread until the vaccine arrives are the key Hendra virus (HeV) infection in humans is an emerging zoonotic disease that has a high mortality rate, but low infectivity. In all cases to date, the infection has been transmitted to humans from bats of the genus Pteropus (flying foxes) via an intermediate equine host. HeV and Nipah virus are the only known members of a new genus, Henipavirus, within the family Paramyxoviridae. HeV was first described after an outbreak of severe respiratory disease in horses that led to the deaths of 14 of 20 infected horses and the death of a horse trainer — one of two humans infected — in Brisbane in 1994.2 There have been seven cases of HeV infection producing pneumonic or encephalitic illnesses in humans. Four of these people died, three soon after exposure and the fourth from fatal encephalitis caused by HeV, which developed 13 months after full recovery from an initial aseptic meningitis.3 Of the three survivors, two made complete recoveries while the third experienced ongoing complications of the initial encephalitis.4,5 Subsequent serological testing for HeV in a large number of human contacts of the first three cases of HeV infection was completely negative.6 Before 2011, there had been 14 events of spillover of HeV infection from flying foxes to horses, and subsequent transmission to humans in five of these events. All events occurred in coastal Queensland except for one in northern New South Wales. Forty-four horses were infected; 34 of these (75%) died and the remaining 10 survived but were later euthanased. Seroepidemiological studies of more than 2000 horses and more than 5000 samples from 46 other animal species in Queensland did not identify HeV infection.7 Spillover events have occurred through most months of the year, but with increased frequency from June to September. The virus can survive under ideal cool and moist environmental conditions (eg, in bat urine at 22°C in the laboratory) for up to 4 days, but is generally thought to survive for only hours. Horses are thought to be infected by ingesting food or water contaminated by urine, saliva or birthing products of infected flying foxes. The virus amplifies within the horse, and humans who are exposed to a large amount of the secretions or blood from an infected horse can become infected. Laboratory studies have shown that horses may excrete virus for up to 72 hours before showing clinical signs.8 All seven humans infected with HeV to date had high levels of exposure to body fluids of infected horses, such as during unprotected autopsy or by direct contact with respiratory secretions or aerosols. Not all people with high-level exposure have contracted the disease or seroconverted. There is no evidence that prolonged close contact with flying foxes engenders a risk of HeV infection in humans.9 A wide range of mammals carry the appropriate receptor enabling them to be infected with HeV experimentally.10 Yet, although HeV infects the endothelium of blood vessels in many species in the laboratory, resulting in systemic vasculitis, outside the laboratory setting, only flying foxes, horses and humans are known to have been infected. One dog is known to have seroconverted without any clinical illness or detection of virus. Flying foxes were identified as the natural host in 1996, and antibodies to HeV have been found in archived samples of flying fox serum dating back to 1982.11 Flying foxes do not develop overt disease. All four species of flying fox in Australia, from as far north as Madang in Papua New Guinea to as far south as Melbourne, have been found to carry the virus.12 HeV is genetically stable, and there is no evidence that the virus has changed significantly since it was first isolated in 1994.8 This year has been a major year for the detection of spillovers of HeV into horses, with 14 events being notified by 17 August. Eight of these occurred in Queensland, with one being the first event notified west of the Great Dividing Range, in Chinchilla. Ten horses had been infected in Queensland and, for the first time, a dog has seroconverted, probably through contact with an infected horse. Six spillover events had occurred in northern NSW, with seven horses becoming infected. No humans have been infected this year to date, although not all of those potentially exposed have reached the end of their incubation periods; no one had a high degree of exposure to infected secretions. The incubation period in humans is 5 to 21 days. The clinical presentation has been variable, with both respiratory and encephalitic symptoms. There has been no transmission of HeV between people, but routine droplet precautions are advised. There is no known effective treatment for Hendra virus infection, and clinical management is based on treating symptoms as they arise. When a person has had high-level exposure to body fluids of infected horses, an experimental human monoclonal antibody (mAb) can be made available for postexposure prophylaxis. Henipavirus mAb has been shown to be effective in preventing infection in ferrets if administered within 12 hours of intrathecal injection of a high dose of HeV.13 However, this product has not yet been trialled for safety or efficacy in humans. It has been administered to three humans. The first person was late into the progression of severe encephalitis and subsequently died. The second two had moderately high-risk exposure, but no evidence of infection, and they did not develop illness or seroconvert. Currently, despite its unknown safety or efficacy, mAb is offered to people who have had high-level exposure to infected horse blood or secretions, after obtaining ethics approval and appropriate consent for each individual. Preventive measures are essential. Horse owners are advised to keep horses away from flowering and fruiting trees, and to remove feed and water troughs from under trees. Vets are advised to wear appropriate personal protective equipment when attending a sick horse or when performing invasive or aerosol-generating procedures on any horse. Horse owners and the public are advised to isolate sick horses from people, horses and other animals. The most promising prospect for controlling HeV outbreaks in humans is the vaccine for horses that is expected to be marketed in 2013.14

Jeannette R Young MB BS, FRACMA, FFPH · Christine E Selvey MB BS, MSc · Rick Symons DSC, PhD, MACVS

The full content of this article is available by downloading the PDF.

The full content of this article is available by downloading the PDF.

Tobacco control advocate Simon Chapman explains how this public health reform will work In past months, Australian news audiences have been exposed to some exotic, presumed-extinct species on their screens and radios. After more than 15 years, the tobacco industry dodo is back and walking among us, attempting to fly. Australia’s pioneering plain packaging legislation has brought it out into public, in a desperate effort to prevent the fall of a domino that promises to cascade globally, ending the industry’s centrepiece of tobacco promotion: the lure of the pack. The University of California’s Stan Glantz once remarked that those who lead the tobacco industry are like cockroaches: “They love the dark and they spread disease.”1 Ever since the magnesium glare unleashed by the public release of its internal documents via the 1998 Tobacco Master Settlement Agreement in the United States, the industry has kept well out of public view, working behind the scenes to shore up its ebbing credibility. The court of public opinion told tobacco companies they were regarded as the most untrustworthy of all industries.2 Media appearances had become progressively humiliating as their spin was rejected. But the truth serum contained in the millions of now-public pages of court-ordered internal documents sealed their public fate. The industry had known tobacco killed, but had lied about it for decades. Their marketing divisions had underlined the vital importance of recruiting youth, and their chemists had been busy working to enhance the addictiveness of nicotine. Australia’s historic plain cigarette packaging legislation is a weapons-grade public health policy that is causing apoplexy in the international industry. It is likely to have little effect on heavily dependent smokers, who tend to be brand-loyal and less image-conscious, but without branding, future generations will grow up never having seen category A carcinogens packaged in attractive packs. Today’s 19-year-olds have never seen local tobacco advertising and youth smoking rates are at an all-time low. Plain packs will turbocharge this trend, making smoking history. Tobacco is a dying market in nations like Australia, which leads the world in comprehensive tobacco control. Australian Institute of Health and Welfare data released in July of this year show only 15.1% of Australians are now smoking daily3 — the lowest percentage ever recorded. From the beginning of the 20th century, when machine-manufactured cigarettes were first marketed, the advertising and packaging industries did all they could to portray cigarettes as a means of signalling personal identity to the young as they took up smoking. A callow youth who wouldn’t be seen dead with an Alpine felt assured by the promise of masculinity in pulling out a packet of Marlboros. Those not wanting the social opprobrium that can come with being showy had the iconic ordinariness of Winfield to clutch as their totem. Those wanting to affect retro stylishness have Peter Stuyvesant or Lucky Strike, and wannabes, any number of haute couture brands — designer carcinogens. But from next year, all cigarette packages will look the same, distinguished only by the brand name in standard typeface. The industry’s re-entry into policy debate has produced some high comedy. In advising government that plain packs will “not work”, it sought a role as a wise public health authority, when of course its fiduciary duty to its shareholders demands that it support policies that maximise use. It has commissioned reports that purport to show that 15.9% (1 in 6) of cigarettes being smoked now are illicit, when the latest Australian Institute of Health and Welfare national survey reports that a mere 1.5% of smokers use illegal tobacco more than half the time.3 Most of all though, its blank-cheque advertising campaigns, imploring the government to desist, say to anyone with half a brain that the industry knows plain packs will “kill their business”, as the cover story of a tobacco trade magazine put it in 2008. That’s precisely the plan. Tobacco kills one in two of its long-term users. The tobacco industry’s current undisguised panic shows that plain packs will hit them very hard. If she were to do nothing else, Minister for Health and Ageing Nicola Roxon has marked her tenure with this legislation, which has just been passed, unopposed, in the lower house of Parliament. It will stand in public health history as a major chapter of how governments put the health of the population before the corporate interests of a pariah industry. Just one disease caused by smoking — lung cancer — was rare before 1930. Over the next 50 years, it rose to become the world’s leading cause of cancer death. In countries like Australia, it is now on the wane. Plain packaging will accelerate its eventual demise as a major cause of death.

Simon Chapman PhD, FASSA

Obstetrician Brian Peat believes salaried doctors are favourably placed to provide best-practice care That any sane nation, having observed that you could provide for the supply of bread by giving bakers a pecuniary interest in baking for you, should go on to give a surgeon a pecuniary interest in cutting off your leg, is enough to make one despair of political humanity. George Bernard Shaw, The doctor’s dilemma (1906)1 A number of studies have consistently shown that fee-for-service payment is associated with an increase in the number of diagnostic tests and procedures performed when compared with payment by salary or capitation.2 It is more difficult to show that this is a bad thing; however, as imperfect tests are applied to populations of lower prevalence for a condition, we would expect more false-positive results. Also, since all procedures carry complications, we would expect there to be more complications.3 Even if salaried doctors, on the other hand, may be at risk of underservicing, this is addressed by peer review and outcome audit. Salaried payments have the advantage of lower administration costs. A substantial cost of the fee-for-service system is in recording individual items and arranging payments. This may be relatively simple when the item of service is a simple consultation, but more difficult when the items are complex. A portion of the cost is also in preventing fraud, rorting of the system and simple overservicing. In private practice, overheads, including rent and clerical staff, are substantial and may be important in giving a competitive edge in the pursuit of patients.4 Overall, the cost of a fee-for-service system looks greater than a salaried workforce; however, this is not necessarily so. It depends on supply and demand. General practitioners are in relatively high supply and receive low fee-for-service payments. Competition means they can only charge a modest patient copayment. Specialists, on the other hand, are in low supply and can generally charge large copayments. Salaried specialists, being currently in low supply, are able to negotiate relatively high salaries with money for holidays, professional development and superannuation. Salaried doctors have no conflict of interest in the doctor–patient relationship, which engenders a patient’s trust, and reduces anxiety for the practitioner. They are in a better position to consider all aspects of the patient’s health, and to appropriately delegate tasks knowing they will not be out of pocket. This is particularly an issue as we see more lifestyle-related, chronic illness that does not fit into the short-consultation model. Fee-for-service items created for the management of chronic illness are an improvement. However, they can still distort best practice if seen merely as dollar amounts requiring expenditure. In a practice where patients with chronic illnesses are treated, a doctor may be required to take on the role of team leader, a difficult role to provide an item of service for; however, it is one well suited to a salary package.5 A list of items of service that are funded by a third-party payer may, in practice, limit the doctor to offering only those options — otherwise, the patient may feel pressured to accept and cover the full cost of the service. If it were possible to provide a fee for service that was linked to an improvement in health, it may be difficult to attribute any improvement to the actions of the doctor. Unfortunately, in many areas of medicine, especially surgical procedures, good evidence from clinical trials that links health interventions to better health is lacking. Without such evidence, doctors may be likely to choose to perform the better-remunerated procedures. How does the method of payment affect relationships between doctors? When I started as a staff specialist I was told by a visiting medical specialist colleague that I was “a coat not a suit”. Nevertheless, I think if we perform our respective roles the relationships should not have problems. However, beware of salaried doctors undercutting doctors paid through fee-for-service arrangements at the local private hospital! Bitter fighting can break out between doctors if one craft group thinks it is getting a worse deal than another. It would be simple to change the current balance of numbers of salaried doctors and those receiving fee-for-service payments. Simply roll back some of the more outrageous subsidies to private practice, such as the thirty per cent health insurance rebate and the safety net, and direct that money to providing more salaried positions. Private hospitals face the difficulty of doctors acting in concert to resist moves by the hospital or the health insurers to lower costs by employing salaried doctors. Perhaps, as the medical workforce increases in number over the next few years, we will see a relative oversupply in some areas break this deadlock. Finally, in talking to our trainees and medical students, I have found there is enthusiasm for a salaried payment system. They do not see medicine as a business in which a craftsperson hawks their wares among the populace for a fee. Rather, they see themselves as providing a social service.

Brian B Peat MB BS, FRANZCOG

Urologist and AMA Victoria past president Douglas Travis believes fee-for-service encourages productivity and transparency From the perspective of doctors, patients and funders, fee-for-service is the best method of remuneration because it provides the best transparency, accountability and incentive for everyone. As a patient, you pay for what you get, and, as a doctor, you get paid for what you do. There are a number of claims for and against the fee-for-service model. I am focusing here on the specific issue of the best method of remuneration for a doctor’s efforts, and do not intend to address the separate issues of public versus private medicine, or free services versus out-of-pocket services. The first claim is that payment on a fee-for-service basis encourages overservicing.1 Theoretically, this could be true, but it is a small-volume threat. The reality is that the overwhelming majority of doctors are flat out doing the necessary work for their patients. They simply don’t have time to overservice. In fact, salaried remuneration encourages underservicing. While many salaried doctors do work excessive hours to cope with ever-expanding workloads, it is the human condition to watch the clock and not put in the maximum effort when you are paid by the hour. This risk outweighs the risk of overservicing under fee-for-service arrangements. In addition, the transparency of fee-for-service makes employers more accountable to doctors, reducing the potential for exploitation of doctors’ goodwill in both the public and private systems at all pay grades. Fee-for-service is also said to result in people being unable to afford medical care. However, the method of remuneration of doctors does not determine the cost of a service to the patient. For example, general practitioners who bulk bill are paid on a fee-for-service basis, but their patients have no out-of-pocket expenses. Conversely, private radiology and pathology companies often pay salaries to doctors, but patients pay out-of-pocket expenses. It is the quantum of remuneration to doctors, not the method, and the level of rebates from third parties that influence the end cost to patients. There are concerns that fee-for-service encourages doctors to try to provide more services in a given period of time, with resulting compromises to the quality of services provided. This is a theoretical problem, as proven by decades of high-quality fee-for-service work in Australia. Doctors have been and can be trusted to provide quality work in a fee-for-service environment. Fee-for-service is said to cause doctors to work excessive hours to their detriment. I contend that many salaried full-time doctors, in both the public and private systems, work excessive hours to their detriment, motivated by work addiction or greed. Work addiction and greed are difficult issues, which in themselves are the problem — not the method of remuneration. Another misconception is that, because fee-for-service is tied directly to patient services, there is no incentive for doctors to maintain continuing medical education (CME) or other quality improvement (QI) activities. However, QI can be incorporated into fee-for-service remuneration2 — for example, practice incentive payments are, in reality, fee-for-service payments related to QI. In any case, regulators are stepping into the quality field — CME is mandatory in order to maintain registration, and practice accreditation is spreading through all forms of medicine. Even if, in the past, fee-for-service meant you could theoretically ignore QI and CME, that era has gone. The area for which fee-for-service is not an appropriate funding model is research and teaching. Research work should be salaried. Likewise, remuneration for teaching should be time based, or if a doctor wishes to do it for nothing, so much the better. The fee-for-service model should have no impact on teaching and research. It might be argued that governments and other employers are ideologically opposed to fee-for-service, but what they are opposed to is uncapped, uncontrolled expenses, and to paying doctors remuneration deemed to be “excessive”. Most public-system fee-for-service schemes that have been stopped were uncapped and consequently led to budget blowouts, and were discontinued for that reason. In fact, governments are rushing headlong into fee-for-service remuneration at the macroscopic level in health, as shown in the establishment of the Independent Hospital Pricing Authority;3 it is just that it is called “activity-based funding”. Block funding (the equivalent of a “salary” model of funding) is on the way out because fee-for-service is better for all parties. In summary, I believe that fee-for-service remuneration encourages productivity, is more transparent and provides better accountability for all parties than a salary-based method of remuneration.

Douglas G Travis MB BS, FRACS(Urol)

People power and social networking tools for patients In 2004, Ben and Jamie Heywood launched a social networking site called PatientsLikeMe (PLM) (http://www.patientslikeme.com). They were motivated by their younger brother Stephen’s tragic journey with amyotrophic lateral sclerosis (ALS) and the desire to connect and share information with other ALS sufferers. Members of the PLM community create a profile to record and track their health over time, including quality of life, symptom control, and treatments and their efficacy and side effects. Members can also connect through online discussion, and the site has over 110 000 members with a counter on the homepage rising every few minutes. From April 2011, the site has opened up to all health conditions, after initially focusing on a few neurological disorders, such as ALS, multiple sclerosis and Parkinson disease. The savvy developers have produced an appealing Web 2.0 interface and the site links to other online platforms such as Facebook, Twitter, YouTube, blogs and free podcasts on iTunes. PLM’s stated aim is to help patients answer the question, “Given my status, what is the best outcome I can hope to achieve and how do I get there?”.1 The therapeutic effect of online communities is mixed2,3 and often not sustained, as are the effects of patients recording and monitoring their own health.4 PLM member postings declare the value of diarising their symptoms and treatments and also cite the importance of feeling that they are helping others by sharing their stories. Patients can print off a summary of their profile, called the Doctor Visit Sheet, to share with their doctor, providing a modern version of the patient diary. Members can opt to have their profile shared with other community members or to be publicly available. Some post video clips of their stories via YouTube, and many use the discussion forum facility, which has a code of conduct restricting industry and others from directly contacting patients. Members can delete previously entered information so that it is no longer visible to other community members, but PLM keeps the data indefinitely. Removing a profile requires contacting PLM staff and cannot easily be done independently by the member. PLM also promotes itself as a research tool, and this is where the site becomes more controversial. Patient profiles form a huge database of symptoms and treatment effects that can be accessed by researchers from academia and industry for a fee. PLM promotes this as a way to access patient data and “bypass around restrictive privacy rules that tie scientists in red tape”5 since data sharing is part of the user agreement for PLM community members. PLM openly declares itself as a for-profit company and was named by CNN Money in 2007 as one of the “top ten start-up companies most likely to upend existing industries — and spawn entrepreneurial opportunities”.5 Industry can buy access to particular PLM data, can deliver surveys through the site, can access PLM “leaders” (online expert patients) or pay for particular features to be added to the site for particular conditions. There are strong similarities here with Facebook, which has been criticised for profiting from companies accessing personal profile data for marketing and other purposes. Although PLM started out using Web 2.0 technology to find potentially effective treatments for rare conditions such as ALS through online data sharing, it now faces the challenge of balancing such goals with profit-driven ones. Used responsibly, PLM could be a revolutionary tool for medical research, particularly if the methodological limitations of its data are openly acknowledged. There is huge potential to identify case series for rare conditions and to develop hypotheses for effective treatments, which should be more rigorously assessed. One of the greatest strengths of the site is the wealth of patient-relevant outcome data, which may better inform researchers designing clinical trials. The large longitudinal datasets of chronic disease treatments can also provide adverse event data that may not occur in clinical trials due to limited follow-up periods and underpowering for unforeseen rare events. PLM monitors the site for serious adverse events and reports them to the United States Food and Drug Administration if appropriate. There are also rich data on non-pharmacological treatments used by patients and their perceived effects. The site can also link people to the clinical trials register to look for trials that they may wish to join. Although the PLM dataset is large and expanding, its degree of representativeness needs to be borne in mind. PLM claims to have 10% of all newly diagnosed ALS sufferers in the US on its site. Generalisability is an issue that PLM faces together with other researchers, as the opt-in requirements imposed by privacy legislation can significantly change sample characteristics.6 Like Facebook, PLM keeps extending the capabilities of its site, and members can invite their care team to view their profile. Is this a step towards online health care on social networks? There’s no doubt that social networking platforms for patients are potentially powerful tools for patient empowerment and for improving the efficiency of hypothesis development, patient-centred designs for clinical trials, and identifying potential serious adverse events of treatment. However, a number of questions arise. Should these platforms be left to the jurisdiction of private enterprise or should the non-profit or government sector address this need? Is there a need to regulate aspects of social network sites for patient protection or should people simply be better informed about the benefits and risks of social network sites?

Lyndal J Trevena MB BS(Hons), MPhilPH, PhD

21-Hydroxylase deficiency (21-OHD) is the most common cause of congenital adrenal hyperplasia, with an incidence of 1 : 14 000 live births and equal prevalence among males and females. Newborns with the most severe “salt-wasting” form of 21-OHD are susceptible to salt-wasting crises in the first few weeks of life. This is associated with morbidity and mortality. 21-OHD newborn screening (NBS) is currently performed in many countries. Despite several prominent medical societies recommending 21-OHD NBS, no state in Australia currently screens for this condition. We report a case that illustrates the need to reconsider including 21-OHD in NBS. 21-OHD NBS can be reliable, sensitive and effective in reducing morbidity and mortality.

Joyce Y Wu MB BS, MAACB, FRCPA · Sudeep MB BS, FRACP, DCH · David M Cowley MB ChB, FRCPA, FHGSA · Mark Harris MB BS, FRACP, MD · Ivan N McGown BSc, MIT, MHGSA · Andrew M Cotterill MB BS, FRACP, MD

To the Editor: I endorse the viewpoint expressed by Jenkins and colleagues.1 They refer to the dearth of hospital medical generalists, at a time of increasing numbers of elderly patients with multiple comorbidities. Nowhere is this lack of appropriate clinical skill to match demand so apparent as in our regional centres. More often than not, junior doctors are responsible for older patients, and are required to manage disparate inputs from several medical and/or surgical subspecialists. Particularly for surgical patients with medical comorbidities, the junior resident medical officer (generally supervised by a visiting surgeon) is an inappropriate medical “case manager”. There is a desperate need in our regional centres to train and employ hospital-based generalists. At the same time, there is a need to move away from the visiting medical officer (VMO) fee-for-service model, designed around the needs of private practitioners, and move towards a hospital-based specialist model, in which specialists are available, accessible and part of the fabric of our hospitals. While the VMO model has been useful, it is no longer appropriate as a basis for default clinical care arrangements. Only by moving towards a hospital-based generalist model, as suggested by Jenkins et al, will we see an improvement in hospital culture, junior doctor supervision and training, and, most importantly, medical governance for best patient care in our regional hospitals.

Joanna R Sutherland

To the Editor: I commend Jenkins and colleagues for an engaging article on the future of general medicine in Australia.1 It mirrors a debate that is occurring in many acute-care hospitals, particularly in the context of a nationwide shortage of acute-care beds and increasing numbers of older patients presenting with chronic and multisystem disease.2 Currently, emergency physicians see the majority of acutely unwell patients who present to Australasian hospitals, particularly large urban centres, which is of great benefit to these patients.3-5 Thus, creating a new specialty of acute-care physicians to look after these undifferentiated patients seems like unnecessary duplication of service. Indeed, this duplication is one of the main issues in the journey of patients through the acute-care hospital system, particularly in tertiary institutions. After presentation to an acute-care hospital, patients often experience multiple consultations in multiple venues before admission to a home medical ward. They are often seen by a junior emergency doctor, then a senior emergency doctor, then a registrar from a subspecialty, and finally by the general medical registrar — and only then are they “admitted” and the often lengthy wait for a hospital bed commences. This journey could be dramatically improved by a single emergency department consultation with a senior emergency doctor (registrar or above), with stabilisation and immediately necessary investigations being done at that stage. After this, the patient could be either discharged to the community or admitted directly to a home medical ward where they can be seen by the home inpatient team. This would abolish much of the duplication that currently occurs and ultimately make the hospital visit safer for the patient and more cost-effective for the hospital.

Alan E O’Connor

To the Editor: Kelly and colleagues are to be applauded for their call for a no-fault compensation scheme.1 If only such a scheme had been available in the early 1960s, when my sister (who has approved this letter) developed encephalitis secondary to a vaccinia inoculation. Then she, and our parents, would have been spared decades of struggling with the sequelae of this acquired brain injury in a “fault averse” system. The few who have been seriously harmed should not be forgotten by the millions who have benefited.

Mark R Nelson

To the Editor: This year marks 10 years of successful operation of the Sydney Medically Supervised Injecting Centre — Australia’s only supervised injecting facility (SIF). It is one of 90 such facilities globally, with SIFs operating in eight different countries for up to 25 years. Legislation to lift the trial status of the Sydney centre was passed in the lead-up to the recent New South Wales state election, nearly a decade after the centre opened. Despite not having explicitly supported the centre while in opposition, at the Centre’s 10-year anniversary event on 6 May 2011, the newly elected Liberal–National coalition government signalled its willingness to contribute to bipartisan support of the centre. While the Sydney SIF has survived this transition into institutional “adulthood”, operation of the only other SIF in the English-speaking world, located in Vancouver, Canada, remains a politically sensitive issue. Indeed, the Supreme Court of Canada is currently deciding whether the right to establish and operate a SIF lies with the provincial or the federal government. The Australian and Canadian SIFs have much in common: both have a history of politicisation, both were established under trial conditions, and both have been subject to rigorous independent scientific evaluations. They have each contributed much to the large body of evidence showing the benefits provided by SIFs to individual drug users and to surrounding communities. Specifically, SIFs have been shown to reduce numbers of deaths from drug overdose,1 reduce numbers of ambulance call-outs2 and hospital admissions, improve client outcomes,3 enhance referral to drug treatment programs,4 improve public order (eg, by reducing injecting drug use and syringe disposal in public locations),5 and be cost efficient.6 No adverse consequences have been associated with their operation. There is widespread support for SIFs. This includes many Australasian specialist medical colleges as well as the Australian Medical Association and many scientific and research institutions. The majority of the Australian population also support SIFs, as shown in the recent National Drug Strategy Household Survey.7 Yet despite this, and the continually accumulating evidence showing the public health benefits of SIFs, the idea of establishing new facilities remains politically charged in the Australian context. In Melbourne, a local council recently urged the Victorian state government to consider establishing a SIF in an area with entrenched, street-based drug use. However, this was swiftly rejected, and calls for SIFs in other Australian states have been similarly refused by state governments. Indeed, the current legislation in NSW precludes the operation of any additional SIFs. But for the Sydney SIF, it appears that the repeated political hurdles which characterised its first decade of operation have finally diminished. In this single instance at least, the scientific evidence on SIFs has prevailed. Editor’s note: Ironically, after this letter was accepted for publication, the New South Wales Christian Democrat Fred Nile (Member of the Legislative Council) gave notice of intention to submit a Bill to close down the operation of the Sydney Medically Supervised Injecting Centre. No further details are available at time of going to press.

Marianne E Jauncey · Ingrid A van Beek · Allison M Salmon · Lisa Maher

To the Editor: A report in the Weekend Australian earlier this year described an increase in oxycodone-associated deaths, in parallel with an increase in prescriptions for the drug, sometimes known as “hillbilly heroin”.1 These increases are likely to reflect a change in doctors’ prescribing behaviour. Strong opioids were traditionally prescribed for cancer pain, often in the terminally ill, but since the 1980s they have been increasingly used for treating chronic non-cancer pain, despite an absence of new evidence of effectiveness or of whether opioids provide net benefit or harm to patients in this setting.2 Cancer patients are likely to die from their illness before the opioids have a chance to injure them, but patients with chronic non-cancer pain are not, and this is where oxycodone-associated deaths are more likely to occur. A contemporary view is that chronic non-cancer pain should be regarded as “a disease entity”,3 but equating a symptom with disease means that the patient becomes the sole arbiter of whether he or she is ill. The prescribing doctor has no means by which to objectively determine treatment outcomes. The notion of chronic non-cancer pain as a disease entity is based on neuropathological changes described as “central sensitisation”, which may result from nerve damage or from persistent peripheral nociceptive input.3 The concept is not intellectually challenging where there is objective evidence of either nerve damage or injury to somatic or visceral structures. Now, however, when medically inexplicable pain follows injury that may be so subtle as to be unassociated with any discernible abnormality, central sensitisation is invoked as the explanation du jour, without a critical assessment based on anatomical and physiological principles. Prescribing opioids in this setting may have inadvertently contributed to the reported increase in oxycodone-associated deaths. Guidelines exist for prescribing oral controlled-release opioid analgesics for chronic non-cancer pain.4-6 They advocate a signed patient–doctor agreement covering, among other things: the necessity for a single prescriber; a recommendation for all drug dispensing to be from the same pharmacy; no replacement for lost, stolen or destroyed prescriptions; and a requirement for consent for random urine and blood screens. However, these are just guidelines, not mandated, and there are no Australian data on compliance with them. Based on international data,7 the guidelines are likely to be more honoured in the breach than the observance. I advocate that a signed patient–doctor agreement should be mandatory in Australia before the prescription and dispensing of opioids for chronic non-cancer pain. This should be sighted by Pharmaceutical Benefits Scheme authorities before such dispensing is authorised, and a copy should be held by the dispensing pharmacy. A review of prescription guidelines for opioid analgesics in chronic non-cancer pain might reduce the epidemic of prescription drug misuse4 and mortality.

Mark S Awerbuch

To the Editor: In his thought-provoking editorial in the May issue of the Journal,1 Tait made reference to an apparent recent improvement in the life expectancies of Indigenous Australians by citing a 2010 Australian Bureau of Statistics (ABS) report entitled The health and welfare of Australia’s Aboriginal and Torres Strait Islander peoples, Oct 2010.2 In this report, the life expectancy for Indigenous Australians was quoted as 67.2 years for males and 72.9 years for females, compared with 78.7 and 82.6 years for non-Indigenous males and females, leaving a “gap” of 11.5 years and 9.7 years, respectively. These figures are from 2005–2007 (which includes the 2006 Census year), and are quoted again in this year’s update report from the Australian Institute of Health and Welfare.3 At first glance, they appear to be a startling improvement on the figures from 1996–2001, which quote (as late as 2005) Indigenous life expectancies of 59.4 and 64.8 years for males and females respectively, representing a “gap” of about 17 years for both.4 Unfortunately, the apparent improvement represents not a miraculous leap forward in Indigenous health care and outcomes, but rather a change in the methodology used to calculate life expectancies around the time of the 2006 Census. The essence of the change was from an indirect to a direct demographic method of compiling life-expectancy estimates, which entailed correcting Indigenous death registration data before calculating death rates. The ABS anticipated the potential for confusion (not to mention premature celebration), and so included warnings that comparisons should not be made between published estimates of Indigenous life expectancies on their website and in subsequent reports, as well as producing a discussion paper outlining and justifying the changes.5 The October 2010 ABS report explicitly stated that: “Differences should not be interpreted as measuring changes in Aboriginal and Torres Strait Islander life expectancy over time”.2 As with any statistical analysis, the underlying issue is the quality of the data. As we continue to work to narrow the “true” Indigenous life-expectancy gap, we need to be mindful of the importance of accurate record-keeping, including the identification of Indigenous status, if future analysis of mortality statistics is to stand up to scrutiny.

Lachlan J McIver

To the Editor: Since publishing its first national report on mortality data from 2009,1 the Australian and New Zealand Audit of Surgical Mortality (ANZASM) has provided coverage of surgical mortality in participating hospitals across Australia. In their recent article promoting the role of clinical-quality registries in improving the quality of health care in Australia, Evans and colleagues2 describe the importance of national registries, particularly in high-cost areas of medicine. Evans et al present the proposed national quality indicators from a 2009 Australian Institute of Health and Welfare report3 and categorise them as current national indicators, indicators requiring data development and those for which a suitable data source has not been identified or substantial development is required to operationalise the indicator. Indicator 36, “Independent peer review of surgical deaths”, is categorised as the third type. The rationale for this indicator stated that the template of the Scottish Audit of Surgical Mortality had been adapted for use in Australia by some states and territories. The report recommended that data from these sources be reported nationally, ensuring that methods of collecting the data would become standardised across the participating states and territories. We wish to highlight that this is now the case. The ANZASM is an independent, peer review audit process overseen by the Royal Australasian College of Surgeons (RACS) and funded by state and territory health departments. The audit is designed to identify and monitor improvements in the quality of surgical care through the collection and analysis of patient mortality data. It aims to improve the the delivery of safe, efficient and effective surgical care by identifying, improving and preventing system and process errors. The database is standardised across all sites. In January 2010, to ensure complete participation by RACS Fellows in this activity in all states and territories across Australia, participation was deemed a mandatory continuing professional development activity (Category 1, surgical audit and peer review). Feedback is provided to individual surgeons on their cases, and overall results are summarised in a de-identified manner as case-note reviews and annual reports that discuss system issues arising on a state and national basis. These issues are analysed further, and recommendations for quality improvement in surgery are disseminated by the ANZASM to the broader surgical community and the respective regional departments of health through its annual reports, case-note-review booklets and, more recently, through workshops and seminars.

Guy J Maddern · Julian A Smith · Wendy Babidge · Gordon S Guy

To the Editor: The research by Rosenwax and colleagues1 and Lowthian and colleagues2 published in the Journal highlights the need for increased capacity in end-of-life care within primary care to reduce the inappropriate use of acute health care services at the end of life. Providing high-quality care for people diagnosed with advanced chronic conditions is among the most complex challenges for general practitioners.3 GPs and other primary care providers are able to provide appropriate palliative and end-of-life care when they are well supported by relevant specialists.3 For patients to be well cared for in the community, it is also necessary for informal carers to have the strength, the will and the skill to provide such care, as well as timely access to support and medical care. The recent National Health and Hospitals Reform Commission’s report4 and the Australian Government’s National Primary Health Care Strategy5 both recognise the need to build “the capacity and competence of primary health care services”4 to support their dying patients. These documents make recommendations that begin to address the current difficulties of caring for these patients in the community. Of significance are recommendations for increased support for carers; improved shared-care arrangements; and better access to specialist palliative care, support and funding for advance care planning and improved access to primary health care professionals.4 This includes a commitment to address workforce shortages and improving out-of-hours access to medical care.5 Such recommendations are positive and will be helpful when they are fully realised. However, issues within primary care — both at the community and individual general practice levels — also need to be addressed. People for whom a palliative approach is appropriate need to be systematically and proactively identified in a timely way. Needs assessment and care planning should be undertaken to ensure that problems and preferences for care are identified and mechanisms are put in place to support such care. To promote optimal end-of-life care, a coordinated, multidisciplinary approach is as important in the community as it is in the hospital setting. Good communication and collaboration between primary care providers, the patient’s specialists and specialist palliative care providers are imperative. Also essential is an ongoing dialogue with the patient and family to enable a clear understanding of the goals of treatment and to proactively plan for likely adverse events. Routinely planning for likely scenarios will potentially reduce the use of acute services and encourage the provision of care in more appropriate environments.

Claire E Johnson · Geoffrey K Mitchell

To the Editor: The finding of Wilkinson and colleagues1 that the Undergraduate Medicine and Health Sciences Admission Test (UMAT) score and medical school performance are only weakly correlated came as no surprise. Another shortcoming of the UMAT process has been its inability to recognise the effects that failure in the test can have upon applicants. The Selection Committee for the School of Medicine at the University of Notre Dame in Fremantle rejected the UMAT from the outset. We considered its content to be arbitrary, and that there was no evidence to suggest that it could predict a medical student’s performance, let alone a medical practitioner’s sensitivity and empathy. My concern with the need for fairness and sensitivity in the selection process evolved from my experience of being approached by applicants to other medical schools who were distressed by their failure to pass the UMAT hurdle. What upset them most was that the UMAT literature claimed that one could not study for the test as it tested “aptitude”. Rejected applicants therefore felt that they intrinsically lacked the necessary personal characteristics to be a good doctor. The truth was that they had not performed as well as others in an idiosyncratic test, which included tests of “spatial orientation” and other arcane matters. At the University of Notre Dame, we recognise the great disappointment that unsuccessful applicants feel and counsel those who contact us. We reassure them that they can try again the next year, and are likely to have a better chance of success then. We never imply that they are not suitable to be a doctor. Medical educators can only expect students to possess fairness, empathy and understanding of the suffering of others if we demonstrate the same qualities to them. In the case of the UMAT — an experiment that has dominated medical student selection in Australia for more than a decade — those qualities have been lacking. I believe that the UMAT has left a scar on many unsuccessful applicants and on the perception of the Australian selection process that was used in many universities over those years. Let us remember that doctors’ responsibility to be caring, sensitive and humane extends beyond the consulting room.

Barry N J Walters

To the Editor: The Hyperglycemia and Adverse Pregnancy Outcomes (HAPO) study, a large, blinded, multinational study, showed an increased risk of adverse maternal and neonatal outcomes in relation to maternal glycaemia, at glucose levels below the current Australian criteria for diagnosing gestational diabetes mellitus (GDM).1 The International Association of Diabetes and Pregnancy Study Groups (IADPSG), an international consensus group, has proposed new criteria for the diagnosis of GDM.2 As a result, these new criteria have been adopted by the American Diabetes Association, which predicts a significant increase in the prevalence of GDM.3 The new criteria were discussed at the Australasian Diabetes in Pregnancy Society annual scientific meeting in 2010. Moses and colleagues accurately outline the increased prevalence of GDM if IADPSG criteria are adopted in Australia.4 An increased prevalence has implications for resource allocation, and the anticipated increase in workload can be managed by appropriate planning and exploration of alternative models of care. We surveyed attitudes to the management of GDM among general practitioners already involved in antenatal shared care programs in the Liverpool and Fairfield areas of Sydney (GDM is not currently part of the shared care program in this urban area, which has a high prevalence of diabetes). Around 120 GPs are enrolled in the antenatal shared care program in the Liverpool and Fairfield areas. Forty-six of these GPs attended an educational meeting at which the survey was distributed, and of the 46 (who all completed the survey), only seven believed that GDM can always be managed in the antenatal shared care program. Seventeen felt that, due to lack of time or lack of access to appropriate resources, GDM cannot be managed at all by GPs as part of shared antenatal care; eight of these 17 indicated that they never initiated insulin for patients with type 2 diabetes. Only two indicated that no up-skilling was required for them to manage GDM. These attitudes may be limited to GPs in urban practices. Whether the involvement of GPs in the management of GDM is appropriate is unclear, and the provision of supporting resources requires further review. Additionally, as determined by Moses and colleagues,4 the predicted increase would come from older women who are possibly more likely to have other comorbidities that make them less suitable for shared care.

Barbara Depczynski · Vincent W Wong · Hamish D Russell · Nicole Opie

To the Editor: Contrast induced nephropathy (CIN) is one of the most important and frequent complications of invasive coronary procedures.1 We have previously reported a multicentre randomised trial comparing use of iso-osmolar and low osmolar contrast agents (iopromide and iodixanol, respectively) in patients with pre-existing renal impairment.2 The overall proportion of patients developing CIN by Day 7 was around 25%, and there was no statistical difference between the different contrast media. There have been few prospective randomised controlled trials to determine the late effects on renal function and outcomes in relation to dialysis and mortality in patients who developed CIN after invasive coronary procedures. We report here on the long-term follow-up of patients enrolled in our initial study. Of the original cohort of 191 patients, 21 were excluded because of lack of follow-up information. We divided patients into two groups based on whether or not they had initially developed CIN, defined as an absolute increase in the serum creatinine concentration of at least 44 μmol/L or by a relative increase of at least 25% from the baseline value on Day 2 or 7 after exposure to the contrast media. The primary end point was persistent renal impairment, which we defined by these same criteria for serum creatinine, and alternatively, by an absolute reduction in estimated glomerular filtration rate (eGFR) of at least 10 mL/min/1.73 m2 (accounting for the coefficient of variation of creatinine and also the age-related decline in GFR3-5). The secondary end point was a composite of death and need for dialysis. Median length of follow-up was 43 months (interquartile range, 31–48 months). Latest serum creatinine results were available from physicians, hospital records or private laboratories for 157 patients. Significantly higher proportions of patients who had CIN at baseline showed evidence of persistent renal impairment compared with patients who did not have CIN at baseline, based on both serum creatinine results (20/40 v 31/117; P = 0.006) and eGFR (22/40 v 28/117; P < 0.001). Mortality was determined for all 170 patients by direct contact or from the national death registry. A significantly higher proportion of patients who had CIN at baseline (2/41) compared with those who did not have CIN (3/129) needed dialysis (P = 0.60). Twelve patients who had CIN at baseline had outcomes of death, dialysis or both, compared with 32 in the other group (P = 0.57). Multivariate analysis showed CIN at Day 2 or 7 was an independent predictor of persistent renal impairment (odds ratio, 3.31 [95% CI, 1.39–7.86]; P = 0.007). Age, diabetes mellitus, sex, hypertension, body mass index, contrast type and baseline eGFR were not predictive. This long-term follow-up showed that CIN after invasive coronary procedures is associated with increased risk of persistent renal dysfunction in patients with pre-existing renal dysfunction. Physicians should be alert to this complication.

Akash Dhawan · Devang Parikh · Ibrahim Shugman · John French · Hisham Hallani · Clyne Fernandes · Craig P Juergens

Objective: To determine trends in incidence of malignant mesothelioma (MM) caused by exposure to asbestos during home maintenance and renovation.Design, setting and participants: Using the Western Australian Mesothelioma Register, we reviewed all cases of MM diagnosed in WA from 1960 to the end of 2008, and determined the primary source of exposure to asbestos. Categories of exposure were collapsed into seven groups: asbestos miners and millers from Wittenoom; all other asbestos workers; residents from Wittenoom; home maintenance/renovators; other people exposed but not through their occupation; and people with unknown asbestos exposure; or no known asbestos exposure. Latency periods and age at diagnosis for each group were calculated and compared.Results: In WA, 1631 people (1408 men, 223 women) were diagnosed with MM between 1960 and 2008. Since 1981, there have been 87 cases (55 in men) of MM attributed to asbestos exposure during home maintenance and renovation, and an increasing trend in such cases, in both men and women. In the last 4 years of the study (2005–2008), home renovators accounted for 8.4% of all men and 35.7% of all women diagnosed with MM. After controlling for sex and both year and age at diagnosis, the latency period for people exposed to asbestos during home renovation was significantly shorter than that for all other exposure groups, but the shorter follow-up and difficulty recalling when exposure first occurred in this group may partly explain this.Conclusions: MM after exposure to asbestos during home renovation is an increasing problem in WA, and these cases seem to have a shorter latency period than other types of exposure. MM cases related to renovation will probably continue to increase because of the many homes that have contained, and still contain, asbestos building products.

Nola J Olsen BAppSc, RGN · Peter J Franklin BSc(Hons), PostGradDipEnvSci, PhD · Alison Reid RGN, MSc, PhD · Nicholas H de Klerk BSc, MSc, PhD · Timothy J Threlfall MB BS, MPH, PhD · Keith Shilkin FRCPA, FCRPath, FHKCPath · Bill Musk FRACP, MSc, MD

Objective: To determine the prevalence of multiresistant organism (MRO) colonisation of reusable venesection tourniquets.Design and setting: A prospective study in a tertiary hospital to collect and analyse reusable venesection tourniquets for the presence of MROs — methicillin-resistant Staphylococcus aureus (MRSA), vancomycin-resistant enterococci (VRE), and extended-spectrum β-lactamase and metallo-β-lactamase-producing Enterobacteriaceae — using a sensitive enrichment method. Tourniquets were collected and tested during a 10-week period between September and November 2010.Main outcome measure: Prevalence of MRO colonisation of tourniquets.Results: The overall colonisation rate of 100 tourniquets randomly collected from general wards, ambulatory care areas and critical care areas was 78%. MROs were isolated from 25 tourniquets collected from a variety of hospital locations, including general wards, the intensive care unit, burns unit and anaesthetic bay. MRSA was isolated from 14 tourniquets and VRE from 19; both MRSA and VRE were isolated from nine tourniquets. There were no microorganisms isolated from 22 tourniquets.Conclusion: Reusable tourniquets can be colonised with MROs and may be a potential source of transmission of MROs to hospitalised patients.

Angie N Pinto MB BS, BSc, MPHTM · Thuy Phan BSc · Gabriela Sala BSc · Elaine Y L Cheong FRACP, FRCPA · Steven Siarakas BSc, PhD · Thomas Gottlieb FRACP, FRCPA

Objective: To document trends in: (i) prescribing of morphine and oxycodone; (ii) hospital separations for overdose; (iii) presentations for treatment of problems associated with these drugs; and (iv) oxycodone-related mortality data in Australia.Design and setting: Cross-sectional study analysing prescriptions for morphine and oxycodone based on figures adjusted using Australian Bureau of Statistics estimated resident population and prospectively collected data from: (i) the National Hospital Morbidity Database on hospital separations primarily attributed to poisoning with opioids other than heroin (“other opioids”); (ii) the Alcohol and Other Drug Treatment National Minimum Data Set for treatment episodes where morphine or oxycodone were the primary or other drugs of concern; (iii) the National Coronial Information System on deaths where oxycodone was the underlying cause of death or a contributory factor.Main outcome measures: Population-adjusted numbers of (i) prescriptions for morphine and oxycodone by 10-year age group, (ii) hospital separations for “other opioid” poisoning, and (iii) treatment episodes related to morphine or oxycodone; and (iv) number of oxycodone-related deaths.Results: Prescriptions for morphine declined, while those for oxycodone increased. Prescriptions for both were highest among older Australians. Hospital separations for “other opioid” poisoning doubled between the financial years 2005–06 and 2006–07. Treatment episodes for morphine remained stable, while those for oxycodone increased. There were 465 oxycodone-related deaths recorded during 2001–2009.Conclusions: Oxycodone prescriptions in Australia have increased, particularly among older Australians. The increase may, in part, reflect appropriate prescribing for pain among an ageing population. However we are unable to differentiate non-medical use from appropriate prescribing from this data. In comparison to heroin, the morbidity and mortality associated with oxycodone is relatively low in Australia. There is a continued need for comprehensive training of general practitioners in assessing patients with chronic non-malignant pain and prescribing of opioids for these patients, to minimise the potential for harms associated with use of these medications.

Amanda Roxburgh MCrim, MPsych(Clin), MAPS · Raimondo Bruno BSc(Hons), PhD, MAPS · Briony Larance BSc(Psych)(Hons) · Lucy Burns MPH, GradDipHealthPolicy, PhD

Bitôt spots on the temporal limbus of the left eye. Clinical record A 52-year-old man presented to the ophthalmology clinic with a 3-day history of tunnel vision and night blindness (nyctalopia). He reported recently needing to wear a headlamp to see adequately in dim lighting, notably while walking to work early in the morning. The patient had a history of hypertension, hypercholesterol-aemia and osteoporosis. Twice in the previous 2 years, he had seen a neurologist for symptoms of lower limb paraesthesiae. At that time, peripheral nerve conduction studies gave normal results, and a clinical diagnosis of peripheral neuropathy secondary to vitamin B12 deficiency was made. Supplement-ation with vitamin B12 and folate was initiated. He also described a 3-hour episode of tunnel vision 2 years before presentation. Examination revealed an otherwise well man with a body mass index of 27 kg/m2 (ie, in the overweight range). His best corrected visual acuity was 6/18 in the right eye and 6/9 in the left eye. Anterior segment examination revealed Bitôt spots, and no staining of the cornea with fluorescein (Figure). Pupillary examination revealed a relative afferent pupillary defect of the right eye, grade 1/4, indicating optic nerve dysfunction. Ocular motility and intraocular pressures were normal. Fundoscopy showed normal peripheral retinal pigment epithelium, and normal discs and maculae. Humphrey visual field 30-2 testing showed peripheral field constriction. Results of the Farnsworth–Munsell D-15 hue test for colour vision were normal. Dark-adapted electroretinography (ERG) revealed bilaterally decreased amplit-udes, consistent with diminished rod function. The results of computed tomography and magnetic resonance imaging of the brain and orbits, using contrast, were normal. Investigations revealed a markedly reduced vitamin A level (0.1 μmol/L [reference range, 1.4–4.0 μmol/L]). Results of a full blood count, electrolyte levels, and liver and thyroid function tests were normal. Vitamin B12 and folate levels were high, consistent with supplementation. Normal results of a malabsorption screen, including levels of fat-soluble vitamins D, E and K, were obtained, and test results for parietal cell and intrinsic factor antibodies were negative. Test results for antiendomysial antibodies were also negative, as were those for IgA and IgG antigliadin antibodies, thus excluding coeliac disease. A diagnosis of xerophthalmia (dryness of the conjunctiva and cornea) was made on the basis of the symptoms of nyctalopia and tunnel vision, as well as the findings of bilateral Bitôt spots, hypovitaminosis A, and diminished rod function on ERG. A dietary history revealed that the patient had suffered from self-diagnosed food intolerance for most of his life. Since childhood, his diet had consisted exclusively of potatoes, white bread (but he refused to eat butter and margarine) and cola. He described nausea and vomiting after eating any other foods. The patient underwent multidisciplinary evaluation by a neurologist, gastroenterologist, psychiatrist, dietitian and psychologist. Dietary supplements were prescribed and cognitive behaviour therapy was initiated. The patient was treated with 100 000 IU of vitamin A daily, given orally for 3 days, followed by 50 000 IU for 14 days. Humphrey visual field results and visual acuity improved within 3 days of commencing treatment. After a month, visual acuity had improved to 6/6 in both eyes, and the Bitôt spots had completely resolved. The relative afferent pupillary defect was no longer present, and Humphrey visual field and ERG results had returned to normal. Vitamin A deficiency is a systemic illness which can increase an individual’s risk of blindness, severe infections and mortality.1 It is rare in developed countries like Australia.2 Vitamin A deficiency and xerophthalmia in developed countries are reported in patients with malabsorption syndromes or liver disease, in those who have had major gastrointestinal surgery, in people with alcoholism, and in those with anorexia nervosa and other psychiatric disorders.3-6 This case is unique because our patient did not have any of these risk factors. This case also highlights the importance of clinicians regularly taking a thorough dietary history, especially in the context of other indications of nutritional insufficiencies, such as osteoporosis and previous vitamin B12 deficiency. Vitamin A is a fat-soluble vitamin found as retinol in dairy products and as provitamin A carotenoids in some fruits and green leafy vegetables.1,7-9 The first clinical evidence of vitamin A deficiency often occurs in the visual system and produces xerophthalmia. The ocular changes of xerophthalmia generally occur in a predictable pattern, as described by the World Health Organization.1 The first stage of xerophthalmia is nyctalopia, the result of defective regeneration of retinal rhodopsin.3,7-9 This responds rapidly to vitamin A therapy, and patients often report regaining their scotopic vision (vision under low-light conditions) within 24–48 hours after the initiation of treatment.1,3,7,9 The second stage of xerophthalmia is conjunctival xerosis, or drying, in which loss of goblet cells and squamous metaplasia of the conjunctiva occur.1,3,7,8 Bitôt spots are bilateral triangular patches of keratinised epithelium at the temporal limbus and nasal limbus of the eye.1,3,7 Colonisation of these patches by saprophytic bacilli, including Corynebacterium xerosis, results in a foamy appearance.1,3,8 Conjunctival xerosis and Bitôt spots respond to vitamin A therapy in 1–5 days.1,3 Corneal xerosis occurs primarily because of instability of the tear film as goblet cells are lost, with subsequent keratinising metaplasia of the ocular surface.1,8 Corneal xerosis usually responds to vitamin A therapy in 1–2 weeks.1,9 If left untreated, corneal drying can result in ulceration, with subsequent scarring and keratomalacia.2,3,7,8 Keratomalacia is a rapidly progressive and irreversible liquefactive necrosis of the cornea that can ultimately lead to perforation and spontaneous loss of intraocular contents.1,3,9 Lessons from practice Vitamin A deficiency is rare in developed countries like Australia. Visual symptoms can often be the first manifestation of a systemic illness, such as vitamin A deficiency. A thorough nutritional screen, including a dietary history, is essential, especially in the context of any other nutritional deficiency. Early diagnosis and treatment of vitamin A deficiency can be curative, preserving vision and life. Uncommonly, in vitamin A deficiency, the xerophthalmic fundus exhibits yellow and white dots peripherally, sometimes associated with a corresponding scotoma (area of diminished vision).1,7-10 These changes respond well to treatment, often returning to normal within 2–4 months.1,8,9 The diagnosis of vitamin A deficiency is made by a directed history and clinical findings, and confirmed by the presence of a low serum vitamin A level, and an abnormal electroretinography result.3,9 In our case, the diagnosis was made accordingly, and all the pathological findings resolved with vitamin A therapy. Vitamin A deficiency is usually treated by administering 200 000 IU of vitamin A orally on two successive days, followed by an additional dose 1–4 weeks later.1 Administration of intramuscular vitamin A is reserved for patients with malabsorption, or those who are unable to tolerate medications orally.1 Ocular vitamin A has not been shown to be beneficial because of the systemic nature of vitamin A deficiency.7 In summary, we present a unique case of vitamin A deficiency and xerophthalmia in an unlikely candidate for malnutrition. Hypovitaminosis A can have potentially devastating visual and systemic effects. To prevent this happening, it is important to maintain a high degree of suspicion, especially in the context of other nutritional deficiencies.

Esra Sanli MB BS, BMedSc · Edwin C Figueira MB BS, MSc, MS(Ophth) · Gaurav Bhardwaj MB BS · Stephanie L Watson MB BS, FRANZCO, PhD · Ian C Francis FRACS, FASOPRS, PhD

A 35-year-old man sent us this self-portrait, taken with a digital camera, showing significant asymmetric flushing on the left side of his face after jogging. The episode resolved spontaneously after 30 minutes of rest. Harlequin syndrome consists of flushing limited to one side of the face due to sympathetic disturbance on the contralateral side.1 Although most cases are benign, imaging and neurological examination should be performed in patients with this condition to rule out serious structural lesions of the sympathetic pathway, such as mediastinal neurinoma, spinal invasion by lung cancer and brainstem infarction.

Agustín Toll · Alberto Gálvez-Ruiz

Desley and Les Carbon are preparing for a much-anticipated road trip from their home in Perth up the Western Australian coast to Exmouth. “I’ve just purchased a couple of large fishing rods”, says Mr Carbon. “My wife loves fishing but she’s allergic to fish — so if she catches any I’ll eat them!” The couple in their 60s are looking forward to a few weeks of relaxation after what’s been a difficult 18 months. Early last year, Mrs Carbon began experiencing recurrent flu-like symptoms, with a hacking cough and difficulty breathing. Multiple courses of antibiotics did little to relieve the symptoms. Her asthma worsened, and she was diagnosed with pneumonia. She had a litre of fluid drained from her lungs, but continued to experience chest pain. “I saw a specialist and said ‘why do I still have pain, when all the fluid’s gone?’” She had various chest x-rays and a CT scan, but nothing showed up. In April, after a PET scan followed by a biopsy, Mrs Carbon was diagnosed with pleural mesothelioma. “The first question I asked was, ‘How long have I got?’ The doctor said 12 months. But I hope I will get a bit longer than that.” **** Mesothelioma is a rare and fatal cancer of the pleura or peritoneum, almost always caused by exposure to asbestos. As Nola Olsen and colleagues write in this issue of the Journal, asbestos was mined and used widely as a building material for decades in Australia. Until the 1960s, 25% of all new homes used asbestos cement cladding. The legacy of this era is that Australia now has the highest mesothelioma rate in the world.1 Historically, mesothelioma was mainly an occupational cancer, but Mrs Carbon is one of a growing number of people with the disease who were exposed to asbestos at home, particularly during renovations or home maintenance. Olsen and coauthors find that although the number of cases associated with occupational asbestos exposure has plateaued, those related to domestic exposure continue to rise. “Malignant mesothelioma cases associated with home maintenance and renovation have increased markedly over the past 10 years and remain on an upward trend”, they write. This group of mesothelioma cases has been called the “third wave”, and it is not known when this wave will peak. The first wave affected workers involved in mining, milling and manufacturing asbestos products, while the second wave comprised workers who used asbestos products in industry, such as builders and plumbers. Margaret Kent, practice group leader in asbestos litigation at Slater & Gordon lawyers, has been obtaining compensation for people with asbestos diseases for the past 15 years. Like Olsen and colleagues, she has noted a “gradual and very discernible” trend in the nature of asbestos exposure among people seeking compensation for mesothelioma. “The decrease in occupationally exposed people and the increase in non-occupationally exposed people have been very obvious. Once upon a time most people who called us would be occupationally exposed but that’s not the case any more.” Clients have included people who developed mesothelioma after washing the clothes of their husband or father who worked in the asbestos industry, people living near a business that used asbestos, or painters who’ve sanded back asbestos-laced walls. Although most of Slater & Gordon’s clients are over 60 years of age, some are in their 30s and 40s. The youngest that Ms Kent has worked with was only 22 years old and may have been exposed as a toddler. **** As an indication of how ubiquitous asbestos is in Australia, Mrs Carbon has identified six occasions when she may have inhaled asbestos fibres, starting from when she was a young girl watching her uncle build extra bedrooms on to their farmhouse. “I used to help my uncle hold the big asbestos sheets while he was cutting them. We would play with the bits that fell off.” At age 25, and newly married, she lived in a house in Albany, WA. When Cyclone Alby tore the asbestos-laden roof off the house in April 1978, she and her husband lifted the pieces of broken roof to be cleared away. The newlyweds renovated their house, including sanding down the eaves, which also contained asbestos. “We used a steel wire brush, and sometimes we used sandpaper. There was lots of dust going everywhere.” Mrs Carbon knew other people with mesothelioma at the time of her diagnosis, but she was shocked to be diagnosed herself. “I had thought it could be cancer, but I never for one minute thought that it was mesothelioma.” **** Ms Kent from Slater & Gordon says there is still a public perception that mesothelioma is an occupational disease. She says most people exposed to asbestos during home renovation had no idea of the dangers and receive a “particularly bad and huge shock when they discover they have an asbestos-related illness”. She is concerned that there is a lot of misinformation in the community about the nature of asbestos and the potential risks of home renovation. “It worries me. We’re a great renovating country and the estimate is that one in three houses has some asbestos in it. Increasingly, people don’t know what it looks like, and they don’t understand that it’s very hazardous, potentially even in small quantities.” She adds that do-it-yourself TV shows have a role to play in increasing awareness of the risks of home renovation. “If they show pictures of people hacking with sledgehammers into asbestos sheeting, then it’s incredibly irresponsible, but if an explanation of the hazards is given, and some attempt to demonstrate doing it properly — then that could be a good thing.” Ms Kent’s concerns are shared by Unions NSW, which passed a unanimous resolution last month, calling on home renovation TV shows to include on-air warnings about the dangers of asbestos. Network Ten’s TV program The Renovators did not respond to the Journal’s request for a comment. Mrs Carbon agrees that there needs to be greater awareness of the risks of home renovation. “You have to be very careful; it only takes one fibre. You really have to wear masks, but we didn’t. We didn’t know anything about it.” **** Mrs Gladys (Joyce) Hyde, aged 78, was similarly surprised when she was diagnosed with mesothelioma 18 months ago, particularly given that she had never worked with asbestos or handled it during home renovation. Her asbestos exposure was indirect and probably occurred when she was living with her family in south-west Melbourne. They were next door to an agricultural company that conducted substantial building work in the late 1970s and early 80s. No one warned the family of possible risks and she had no idea her health was potentially in danger. “We didn’t think about it at all.” She was admitted to hospital 18 months ago because she was having difficulty breathing. “I could barely get to the bathroom to have a shower, it was that bad.” She ended up having five litres of fluid drained. “When they found the mesothelioma, it was a shock.” Professor Bill Musk, a Perth-based respiratory physician, says patients with mesothelioma typically present to their GP with chest pain or breathlessness. “The GP then does a chest x-ray and finds something on it, particularly pleural effusion.” A cell sample to confirm the diagnosis is usually obtained by aspirating the pleural effusion, but false negative results are common. A closed biopsy, a video-assisted thoracoscopic biopsy, or occasionally an open biopsy, can also confirm the diagnosis of mesothelioma. **** Mesothelioma is an unpredictable disease. Once diagnosed, the median survival is 9 to 12 months, but it is difficult to give an accurate prognosis. “Occasionally, a patient survives 10 to 15 years”, says Professor Musk. And although the cancer is almost always linked to asbestos exposure, it’s impossible to predict who, of those exposed, will develop the cancer. Mr Carbon has luckily not developed the disease, despite having sanded back the same eaves with his wife in Albany in the late 1970s. He also had a career as a ship’s master, which involved putting asbestos lagging on exhaust pipes, and later breaking it off when it became hard and brittle. “It was the most dangerous thing we could do to it, but I’ve never experienced any problems”, he said. Mrs Hyde is also acutely aware of the unpredictability of mesothelioma. “My oncologist said that a man could work with asbestos all of his life and never get it, but his wife could wash his clothes and get it. His view was it’s just the luck of the draw.” **** At the urging of her grandson, Mrs Hyde approached the law firm Slater & Gordon to seek compensation. Slater & Gordon’s defendants have included everyone from asbestos manufacturers, James Hardie and Wunderlich (a subsidiary of CSR), to state and federal government bodies. Legal claims focus on proving that there was a failure to warn of the dangers or of the need to take precautions, or to provide ways of minimising the asbestos dust. “It ranges from failure to put a warning on the product to failing to inform the public of the known dangers”, says Ms Kent. As lawyer John Gordon writes in this issue of the Journal , neither James Hardie nor CSR have ever taken any steps to systematically warn people of the dangers of asbestos products in their homes, or “of the potential for fatal consequences in 20 to 40 years if they demolish those products today”. **** Both Mrs Hyde and Mrs Carbon have had chemotherapy. “I’m waiting for 4 weeks to see if the cancer has shrunk. I’m a bit in limbo at the present”, says Mrs Hyde. A grandmother of 10, she is enjoying time with her family. Twice a week she helps with reading lessons at the school where her daughter works. “That’s been fabulous”, she says. She used to be a keen lawn and tenpin bowler, but the cancer and treatment have tired her out. “I was always reasonably active, and then to get something like this and it mucks everything up. It is hard but I’ve got a good family. You just have to keep on going.” Mr and Mrs Carbon are also pushing on. With the oversized fishing rods packed in their motorhome, they’re taking their minds off the diagnosis for a few weeks. “When I was first told it was mesothelioma I thought, ‘how am I going to get this out of my mind? I was thinking about it all day’”, Mrs Carbon says. Mr Carbon says the couple are only now coming to realise the full impact of the diagnosis. “But we’re boxing on and trying to enjoy life, making the most of every minute.”

Sophie McNamara

Rowan Nicks was born in New Zealand on 24 February 1913. He studied medicine at the University of Otago in Dunedin and, on graduation in 1937, worked as an intern at Auckland City Hospital. After his internship, he moved to the United Kingdom to further his surgical studies, working as a demonstrator in anatomy at Middlesex Hospital, London. Rowan served as a Surgeon Lieutenant in the Royal Navy during the Second World War. In 1945, he was appointed Officer of the Order of the British Empire and became a Fellow of the Royal College of Surgeons. After the war, he turned his attention to cardiothoracic surgery, and worked at Royal Brompton Hospital, London. In 1947, he returned to New Zealand to pioneer cardiothoracic surgery at Greenlane Hospital in Auckland. In 1956, Rowan was appointed Staff Specialist in Cardiothoracic Surgery at Royal Prince Alfred Hospital in Sydney. He was involved in the beginning of open-heart surgery in New South Wales in 1957 and played a leading role in the design and development of the first automatic cardiac pacemaker. After the death of his wife Mary in 1969, Rowan travelled widely, visiting hospitals in Africa and India in particular. This was the beginning of his second career as a significant philanthropist. After his official retirement in 1973, Rowan continued to travel and work in hospitals in East Africa, India and Malaysia, as well as in remote Aboriginal communities in Australia. Rowan established a series of scholarships and fellowships for young surgeons from Africa, India, Asia, the United Kingdom and Ireland, and the Western Pacific region. In 2005, he established the Rowan Nicks Russell Drysdale Fellowship in Australian Indigenous Health and Welfare. Throughout his life, Rowan had a sustaining love of nature and gardening. In his later years, he developed his interest in chamber music, symphony and opera. Rowan died on 26 May 2011, and is survived by his extended family in Australia and New Zealand.

John Masterton · and Brian Morgan

I was raised by my mother with my two older sisters and attended the local state schools, where I did it all — sport, music, even public speaking competitions. I’m not really that different, although I do remember clearly being told by some of the other kids, “You’re not like other black people”. I find that comments like this are made more commonly than they should be. They are generally unsettling and, ultimately, amusing for a number of reasons. What is it about me that was different to “those other black people” that I would stand out? My education is unexceptional in modern Australia: 12 years of school followed by an undergraduate degree in medical science. I have recently completed the Master of Applied Epidemiology through the Australian National University, which has started me on a career in health research. Why should anyone regard this as “different”? Many times when I was starting out in research I felt a deep sense of obligation to work in Aboriginal and Torres Strait Islander (hereafter respectfully referred to as Indigenous) health. I thought my career would only ever be in Indigenous health or involve Indigenous “issues”, and my growing expertise would only ever be appreciated in that arena. I do feel compelled to be somewhere at the forefront of Indigenous health research trying to rectify the history of colonisation that, let’s face it, is always the crux of our peoples’ issues. Over the past few years I have been involved mainly in cancer research projects. Cancer provides a typical example of the inequity experienced by Indigenous peoples. Compared with non-Indigenous Australians, our cancer incidence rate is similar, if not lower, for all cancers combined,1-3 and yet our mortality rate is estimated to be 50% higher for many cancers.4 Our cancer patients have more comorbid disease;5 their cancer is more advanced when diagnosed3,5,6 and they are less likely to take up and complete treatment.5 These factors contribute to their poorer survival, but they do not fully explain the disparity. This disparity is almost absurd in our modern times but, sadly, is our country’s reality. The most profound moment of my career so far took place in a small remote community. I had the privilege of conducting an interview with an Indigenous cancer patient who was receiving palliative care. I had an almost out-of-body experience as I sat intently listening to this person share her cancer journey. As a researcher and as an Indigenous person I was powerfully moved by her story, her family history and the circumstance of what she and her family were facing. She told me she had to leave her community, on her own, to go to two different cities for chemotherapy and radiotherapy when she was first diagnosed. The doctor at the local hospital in their community “didn’t do that much” even when the patient “knew it came back”. When the doctor did do something, he said, “Don’t like the look of that”. The most heartrending part of our interview was hearing firsthand about the stigmas within that community — “There is no community support, people are scared to visit”. To me, this person embodied the documented literature describing the many barriers that are experienced by Indigenous people in response to their dire health issues: living remotely, having to travel for treatment, and enduring social and even cultural isolation. Until that time, I had thought my obligation towards Indigenous health came from outside pressure and expectations; after that interview, I knew that these feelings were deeply personal. In recent years, our governments have given much greater attention to improving Indigenous health. I believe now is the time to reflect on how we conduct research with Indigenous people, to adapt with changing times and to maximise the application and benefits of research findings across the continuum of health. We can take no more chances with the health of our Indigenous peoples. The right methods, the best practice and the leading researchers and health professionals must be involved in rectifying the health and livelihood of our first nations. We know that the interconnection between health and its social determinants — housing, education, opportunity for employment, socioeconomic status and the like — is central to health improvement. The interconnected web of social habits and social status reflects the health of all people. As a society we seem slow to be shocked by the disparity in health issues, even life expectancy, for Indigenous peoples, and much quicker to blame individuals for not taking responsibility for their own health. While this can be true, it’s not central to the reasons why Indigenous peoples’ health is so poor. We seem to “forget” that there are many social problems that exist that stem from years of oppression, including fear of having to access mainstream health services, low socioeconomic status, disease from poor housing conditions and overcrowding, and lower levels of education that lead to lower rates of employment. We need to reconsider our approach to research to properly account for these factors and not just describe them as a fact that will remain unchanged. Indigenous health research remains Westernised — the “one disease at a time” approach. I believe that, until we move towards the holistic health approach with which Indigenous people identify, we will lessen the impact of current research by underselling the outcomes to government, thereby failing to secure future funding, making research findings non-transferable to policy and practice. This is where the next generation of researchers can take us, to enforce the inclusion of those social determinants and look holistically at research. I don’t know the “ideal” way of performing such research, but I believe there is a tangible method that we can find. In a perfect world, I see great health research being performed with good policy and practice outcomes that directly influence change in other social determinants, such as education. In essence, everything fundamental to my opportunity and progression contributes to “not being like other black people”. Some still consider my opportunity and success in education rare, or against the norm. Statements like this are not only made by non-Indigenous people. In fact, I find the most unsettling and upsetting comments are made by other Indigenous people. It saddens me when I hear them dismiss or denigrate the value of education. As more Indigenous people achieve a level of education equal to other young Australians, these attitudes will change, as they must if all Indigenous Australians are to overcome educational, economic and social disadvantage. We will then no longer be seen as different, but as skilled and educated people who bring a wealth of knowledge and inner culture that only an Indigenous person can have. Our skills will be valued and respected and our contribution will not be considered tokenistic. The achievement of education for Indigenous people and their employment in health-related roles is essential to improving health among the Indigenous population. My primary reason and motivation for working in Indigenous health is because it is the greatest area of need in Australia — it’s morally the right thing to do, regardless of what my cultural heritage is. However, when I reflect on my inner driving force to work in Indigenous health, I believe it comes from an inner obligation of personal connection and contribution. This obligation is not something I have always felt at peace with. I have never wanted to be boxed into thinking that I could or would only work on Indigenous issues, as I am made to feel when I hear other people comment that only Indigenous people should conduct Indigenous research. In some situations, this is very true, appropriate and culturally safe, but in other ways this is a perfect example of resistance to change. We have a long way to go, and I believe that it is a step in the right direction for as many people as possible to come on board and offer their skills. We have a lot to learn, but we also have a lot to teach. I’m sure any other Torres Strait Islander or Aboriginal person can relate to the sense of pride inspired by our community occasions — not pride in oneself, but in our community. What an incredible journey our people have had and are still on; after the years of oppression we can still come together and be proud of what we have achieved together. The list of health problems is long for our Indigenous peoples. They can appear overwhelming and sometimes disheartening to someone working in the health field. However, if any population is resilient enough to overcome these health issues, it certainly is the Indigenous population of Australia. Now we need to use that same sense of community pride and dedication to drive improvements in better health outcomes. I often think about the woman I interviewed a little while ago. Her story alone is a motivator for working in Indigenous health; from diagnosis, to treatment, to palliation, there are improvements to be made. Indigenous health needs commitment. It needs focus and continuous drive. So, where can I be the most useful and make the biggest contribution for Indigenous health? I don’t know the answer yet, but I feel privileged to be part of it. And I will have a story to tell.

Lisa J Whop BMedSc, MAppEpid

DiPHD Diagnostic imaging pathways, an iPad application. University of Western Australia and DIP Team. UWA, 2011 ($25.99). DiPHD is a clinical decision support tool in the form of an iPad application, developed by the University of WA in collaboration with the Royal Perth Hospital. For this review, I loaded the DiPHD app (search the iTunes App Store for “Diagnostic Imaging”) onto an iPad 2 (64 GB wi-fi and 3G). I then ran a comparison on the same iPad against the WA Department of Health website Diagnostic Imaging Pathways (http://www.imagingpathways.health.wa.gov.au/includes), from which the app was developed. With a broadband wi-fi connection, the app was noticeably quicker. The app does not include the Image Gallery or the Normal Anatomy from the website, but it does contain the important “Diagnostic Imaging Pathways” section. It is a valuable resource that my hospital has already adopted as its guideline for imaging pathways. It is difficult to think of an acute clinical condition that is not included. The app content is almost the same as the website, with some slight changes in layout that make it easier to access. The layout is also a little different in that you are presented with an anatomical diagram with pointers to the various conditions. The diagram itself does not serve any real purpose and, in some body areas, appears as a picture next to a list of clinical conditions. Like other pathways, these are also open to some debate. For example, “suspected testicular torsion” is directed to urgent surgery, even though many emergency departments have ultrasound capability to exclude torsion. Medical apps for the iPhone and iPad have become the clear leader for bedside clinical information, and the DiPHD is well constructed and accessible. My advice to potential users is to look at the WA Department of Health website first and decide if Imaging Pathways on an iPad is going to be more useful in your clinical practice. In an office-based practice, would you access an iPad, when the same information is available on your desktop computer? Or, as a clinician or junior doctor seeking information at the bedside, does this app fill a niche? Its utility will depend on your clinical practice.

Robert P Dowsett

Many firsts are unremarkable, but some have a lifelong impact. London, October 1993: I took my first steps as an advanced trainee in gastroenterology at King’s College Hospital Institute of Liver Studies . . . and by the end of only my second day, I had become the “experienced” liver registrar and was deemed “ready” to take over the care of an eight-bed liver intensive care unit (ICU). As 5 pm approached, a sense of anxiety settled on me. I had spent 6 months as a mostly overwhelmed ICU resident at a large London teaching hospital, but I was hardly an expert in intensive care, let alone liver intensive care. With extreme ease, the liver ICU day-registrar conducted the handover and provided me with all I needed to know for my first night, scribbled onto a small piece of paper. I was then alone, albeit with six patients, the highly experienced nurses and a very capable gastroenterology senior registrar at home should I need her. By 5:35 pm, I had received my first telephone referral. As the resident — from Cornwall, some 300 kilometres away — described the referral, the number of boxes ticked that fulfilled super-urgent listing for liver transplantation was ominous. Clearly, the patient needed to come and would be my first of many acute liver failure admissions that year. Within the next 2 hours, two expected admissions arrived. The first patient, admitted for routine elective orthotopic liver transplantation for amyloidosis, seemed to have utterly resistant hypotension due to his autonomic neuropathy, despite copious amounts of noradrenaline. The other patient, transferred from a private institution, had multiple organ failure secondary to end-stage liver disease, and highly resistant hyperkalaemia despite continuous dialysis and medical therapy. The next little excitement was that the apparently “stable” patient with acute liver failure from paracetamol poisoning was now becoming much less stable. The liver transplant surgeon decided to take her to the operating theatre to render her anhepatic — a procedure, I was informed, that would ensure haemodynamic stability while waiting for her imminent liver transplant. Reassured, I relaxed when I saw her being wheeled out of the liver ICU. The relief was short-lived, as the next event was an expected death. Then, a frighteningly short time later, the anhepatic patient was wheeled back into the liver ICU. Despite the surgeon’s earlier reassurance, this patient was more haemodynamically unstable than when I had last seen her. At this point, she had a cardiac arrest, and as I turned to resuscitate her, a second patient arrested. Thankful for the experienced nurses, but still wishing I had four hands, I had to manage both patients at the same time. After a bout of frenetic activity, I ceased active treatment on the patient who had a hopeless prognosis — a decision that, on reflection, was appropriate but probably a little beyond my years of experience. I called the consultant surgeon to ask, with some trepidation, if he would consider bringing forward his patient’s planned liver transplant. When she was taken to the operating theatre less than an hour later, I felt hugely relieved. As the night raced into the early hours of the morning, the patient from Cornwall arrived and, with the aid of my crumpled piece of paper and the superb handover from the poor resident who had struggled with her during the 5-hour road ambulance trip, her condition stabilised. With the wintery, watery sun came the realisation that it had been an extraordinary night in an extraordinary place. The memory of it would never dull. In spite of my feeling of terror during that night, I switched discipline allegiance and commenced training in intensive care — only this time, I had to move countries to allow me to do so . . .

Imogen A Mitchell