Volume 190 Issue 12

The risk of bleeding, as well as patient preferences, must be considered when deciding duration of warfarin therapy Venous thromboembolism (VTE) affects about 17 000 Australians each year, usually as deep vein thrombosis (DVT) of the legs or pulmonary embolism (PE).1 The sequelae of VTE include death, post-thrombotic syndrome, chronic pulmonary thromboembolic disease and recurrent VTE. Anticoagulation with an oral vitamin K antagonist (warfarin), overlapped for the first 5–7 days with unfractionated heparin, low-molecular-weight heparin or fondaparinux, prevents thrombus progression and reduces the risk of recurrent VTE and death during the acute phase.2,3 When treatment is continued beyond the acute phase, warfarin reduces the risk of recurrent VTE but increases the risk of bleeding and requires frequent laboratory monitoring, which is inconvenient for patients. Thus, decisions regarding the optimal duration of anticoagulant therapy must balance the increased risk and sequelae of recurrent VTE when warfarin is stopped against the risk of bleeding and the inconvenience of continuing treatment.3 Many randomised controlled trials have evaluated the optimal duration of anticoagulant therapy in patients with VTE, and their results can be summarised as follows: In patients with a first episode of VTE that is provoked by a reversible risk factor, 3 months of anticoagulant therapy halves the risk of recurrence compared with the level of risk achieved with 1 month of therapy.4 The risk of recurrence beyond 3 months is low.4 In patients with isolated provoked or unprovoked calf DVT, 6 weeks of anticoagulant therapy is as effective as 3 months’ therapy.5 In patients with a first episode of unprovoked VTE, 3 months of anticoagulant therapy is as effective as 6 months’ therapy,5,6 but there is a high rate of recurrence (about 10%) during the first year after stopping warfarin; in subsequent years, the recurrence rate decreases to 3%–4% per annum.7,8 Continuing warfarin treatment beyond the acute phase for 1–2 years reduces the risk of recurrence during treatment by as much as 90% compared with no warfarin, but a “catch-up” phenomenon occurs after stopping warfarin, so that after several years the risk of recurrence is similar in patients who are treated for 3 months compared with those treated for 12 months.9 Although the efficacy of long-term treatment with vitamin K antagonists for preventing recurrent VTE is impressive and consistent,7,8,10 pooled data from 10 trials involving 4833 participants provide no evidence that long-term anticoagulant therapy reduces fatal PE.8 Trial data show that continuing warfarin treatment beyond 3 months is associated with an annual risk of major bleeding of 1%–3%,11 and the incidence of major bleeding is likely to be even higher in unselected patients not enrolled in a clinical trial. Long-term warfarin therapy targeting an international normalised ratio (INR) of 1.5–2.0 is less effective for the prevention of recurrent VTE than warfarin therapy targeting an INR of 2.0–3.0; nor does the lower target ratio reduce the risk of bleeding.12 Several new oral anticoagulants (eg, rivaroxaban, apixaban, dabigatran etexilate) that selectively target coagulation factor Xa or factor IIa (thrombin) are in advanced stages of clinical development.13 These agents appear to be attractive alternatives to warfarin for long-term management of patients with VTE because they can be given in fixed daily or twice-daily doses without laboratory monitoring. However, it remains to be seen whether the new oral anticoagulants will provide a more favourable risk–benefit profile than warfarin during long-term treatment. Our recommendations for duration of anticoagulant therapy for VTE (Box) are generally consistent with those of the 2008 American College of Chest Physicians guidelines.14 The risk of bleeding and patient values and preferences must be taken into account when making treatment decisions. Patients with acute DVT or PE or both should receive warfarin for a minimum of 3 months. An exception is patients with isolated calf DVT, for whom 6 weeks of warfarin treatment is adequate. Patients whose first episode of proximal DVT or PE is provoked by a transient risk factor (eg, surgery) can stop treatment after 3 months because they have a relatively low risk of recurrence after warfarin is discontinued. Patients with a persisting reversible risk factor should continue taking warfarin until the risk is no longer present. Compared with those who experience provoked VTE, patients with a first episode of unprovoked proximal DVT or PE have a substantially higher risk of recurrence after warfarin treatment is discontinued, presumably because they have a chronic propensity to thrombus formation. However, there is little point in continuing treatment beyond 3–6 months in these patients unless a decision is made to treat indefinitely, as the benefits of extended treatment are lost when warfarin is discontinued. Long-term or indefinite warfarin therapy seems reasonable for patients with a history of limb- or life-threatening VTE, chronic pulmonary thromboembolism or severe post-thrombotic syndrome, and for patients who prefer to continue anticoagulant treatment. Indefinite treatment also seems reasonable for patients at very high risk of recurrence, such as those with a history of recurrent unprovoked VTE, high-risk thrombophilia (eg, antiphospholipid antibody syndrome, antithrombin deficiency, multiple thrombophilic defects) or active cancer (or those receiving treatment for cancer). Other tests (eg, for residual thrombus detected by compression sonography, or D-dimer) might also identify patients at increased risk of recurrence, but their utility in determining the optimal duration of anticoagulant therapy remains uncertain. Ultimately, the question of which patients will benefit from indefinite anticoagulant therapy requires evaluation in large randomised controlled trials that have sufficient power to show a worthwhile reduction in morbidity or mortality or an improvement in quality of life. Recommended duration of anticoagulant therapy Condition Recommended duration Evidence grade* Provoked VTE (transient risk factor) 3 months 1A Isolated calf DVT 6 weeks† 1B First unprovoked proximal DVT or PE Minimum 3 months Consider long-term‡ 1A 2B Recurrent unprovoked VTE Long-term 1A Cancer-related VTE Minimum 3 months§ Continue during treatment for cancer and while cancer is active 1A 1C VTE with high-risk thrombophilia¶ ** Minimum 3 months; consider long-term 2C Limb- or life-threatening VTE** Minimum 3 months; consider long-term 2C Chronic thromboembolic pulmonary disease Long-term 1C Severe post-thrombotic syndrome** Consider long-term 2C DVT = deep vein thrombosis. PE = pulmonary embolism. VTE = venous thromboembolism. * Based on the grading system used by the American College of Chest Physicians (ACCP) guidelines.13 Strong (Grade 1) recommendations can be applied uniformly to most patients. Weak (Grade 2) suggestions require more judicious application. Level A denotes high-quality evidence; Level B, moderate-quality evidence; and Level C, low-quality evidence. Risk of bleeding, as well as patient values and preferences, must be taken into account. † Unlike the ACCP guidelines, which do not provide a separate recommendation for calf vein thrombosis, we recommend 6 weeks, based on the results of the Durée Optimale du Traitement AntiVitamines K trial.5 There is no evidence to guide the treatment of calf vein thrombosis limited to muscle veins; if anticoagulants are used, we suggest that the duration of use does not exceed 6 weeks (Grade 2, Level C). ‡ Unlike the ACCP guidelines, we do not explicitly recommend long-term treatment after a first episode of unprovoked VTE. Our recommendation attaches a relatively high value to the burden of long-term anticoagulant therapy and a lower value to preventing recurrence beyond the acute phase. § Low-molecular-weight heparin is the preferred treatment. ¶ Includes patients with antiphospholipid antibody syndrome, antithrombin deficiency and multiple thrombophilic defects. ** The ACCP guidelines do not provide guidance for these categories of patients.

Nina C Raju MB BS, FRACP, FRCPA · Jack Hirsh MD, FRCPC, DSc · John W Eikelboom MB BS,MSc, FRCPC

Australia can benefit from lessons learned in the epidemic of C. difficile infection in Europe and North America It is 30 years since Clostridium difficile was shown to be the cause of pseudomembranous colitis and many cases of antibiotic-associated diarrhoea in humans. In the interim, C. difficile has risen from relative obscurity to become a major hospital pathogen. Two factors were particularly important in its emergence during the 1980s. First, increased and inappropriate use of some broad-spectrum antibiotics, particularly cephalosporins, predisposed more patients to infection with C. difficile. Second, contamination of the hospital environment with C. difficile spores was, and remains, a significant problem, as the spore is likely to be the infective particle. The epidemiology of C. difficile infection continues to evolve, and developments overseas in the past decade threaten not only parts of Australia’s vast agricultural sector but also the country’s health care system. Since 2002, rates of C. difficile infection have escalated, with outbreaks of severe infection in North America and Europe caused by an epidemic strain — polymerase chain reaction (PCR) ribotype 027 (also known as North American pulsed-field type 1 [NAP1]). This strain is characterised by the production of greater amounts of toxins A and B and an additional, binary toxin, as well as resistance to fluoroquinolone antimicrobials.1 When this editorial was submitted for publication in January 2009, there was no evidence that this epidemic strain was present in Australia. However, C. difficile PCR ribotype 027 has now been isolated for the first time in Australia, as reported in this issue of the Journal2 (Riley et al). Although the patient most probably acquired the organism while travelling in North America, this case illustrates the ease with which it could be introduced into Australia. Thought to be driving the epidemic in humans in North America and Europe are the overuse of fluoroquinolones and fluoroquinolone resistance, but the ageing population and improved case ascertainment may also be contributing to the dramatic increase in cases. Other factors may also be important, such as the increase in prescription of proton-pump inhibitors, which coincided with the emergence of epidemic C. difficile.3 Several recent observations from overseas have broad relevance for Australia. First, there has been an apparent increase in community-acquired C. difficile infection in the absence of classic risk factors such as antibiotic exposure, leading to suggestions that all patients with community-acquired diarrhoea should be tested for C. difficile.4 Assertions that community-acquired C. difficile infection is a new disease4 are not correct — it has been recognised in Australia for over 15 years but is underdiagnosed.5 Therefore, it is difficult to determine whether this increase is a true increase or rather reflects better case ascertainment. Nonetheless, the suggestion that C. difficile infection should be considered more than just a hospital problem is valid, and general practitioners need to be aware of this change in epidemiology. The prevalence of binary toxin-producing C. difficile in human disease is also increasing, and there is an association between binary toxin-producing isolates and community acquisition.6 Second, it is speculated that C. difficile is part of a zoonosis, and that transmission of infection via spores may be foodborne.7 There is compelling evidence for the former, but none for the latter. C. difficile is known to colonise many animals.8 Indeed, as in humans, it probably colonises the gastrointestinal tracts of most infant animals until weaning. There was alarm at a report that 20% of a small sample (n = 60) of retail beef in Canada contained C. difficile.9 Equally disturbing are reports that many pig herds in the United States are infected with C. difficile. The overall prevalence of C. difficile in piglets from 10 herds in North Carolina was 48%, and ranged from 0 to 97% across the herds. Mortality for piglets with C. difficile infection is 15%, and animals that survive are 10% underweight when they go to market.10 Most animal isolates of C. difficile produce binary toxin, and both pigs and cattle harbour PCR ribotype 078 — a strain that, like ribotype 027, produces increased amounts of toxins A and B, in addition to binary toxin. In the Netherlands, the prevalence of human C. difficile infection with ribotype 078 strains has increased since 2005; these infections were in a younger population and more frequently community-acquired than infections with ribotype 027 strains. In the eastern Netherlands, where more than 90% of the country’s pig farms are located, over 20% of human isolates are now ribotype 078, and human and pig strains of C. difficile are highly genetically related.11 In Australia, little is known about the prevalence of C. difficile in pigs. A small study in 2007 found C. difficile in 10 of 37 samples (27%) from piglets with diarrhoea, but none of the isolates were ribotype 078 (unpublished data). Why is C. difficile infection increasing in pigs in Europe, and what are the implications for Australia? The use of antimicrobials for growth promotion was banned from 2006 in Europe, and even earlier in Denmark, starting in 1995. However, since 2000, the use of therapeutic antimicrobials in production animals has increased in Europe in general, and specifically in Denmark, a big producer of pork. Of real concern is evidence of greater use of cephalosporins in animals. While the number of pigs in Denmark increased by 50% in the past 15 years, the amount of penicillinase-susceptible penicillins used increased by 400%, and cephalosporins by 1000%. Most of this increase was in piglets and sows.12 Although the total amount of cephalosporins used remains small, this is a worrying trend. If the situation is similar in the Netherlands, and anecdotal evidence suggests that it is, then this may be analogous to the situation in humans in the 1980s when there was a dramatic increase in C. difficile in many hospitals, driven by cephalosporin use.13 The overlap between the location of pig farms in the Netherlands and the occurrence of human ribotype 078 infections suggests a common source.11 This is likely to be the environment. The Netherlands has one of the highest population densities in the world. If infection rates in pig farms in the Netherlands are as high as those in the US,10 then it is likely that a large proportion of the Dutch population comes into contact with C. difficile spores every day. Individuals are at risk of infection if they are taking antimicrobials or any other medication that perturbs the gut flora. The good news for Australia is that, with our very low population density, a similar risk to humans is unlikely to develop. However, this is no reason for complacency. Every effort should be made to stop epidemic C. difficile from becoming established in our production animals. Unfortunately, the mere perception of C. difficile infection as a foodborne disease will damage the industry. Even before the first isolation of C. difficile PCR ribotype 027 in a patient in Australia, health care practitioners were becoming justifiably concerned. A proposal for C. difficile to be made notifiable in all states and territories of Australia was approved at the Australian Health Ministers’ Advisory Council meeting in November 2008. Australia’s conservative policies on fluoroquinolone use in humans and animals may offer some protection. However, if cephalosporin use is driving C. difficile infection in animals overseas, then additional efforts to target cephalosporin use in veterinary medicine may be needed in Australia. The solution to these problems continues to lie in surveillance for the emergence of virulent strains of C. difficile, promotion of judicious use of antimicrobials in both human and veterinary medicine, and environmental cleanliness, the latter perhaps easier said than done outside health care facilities.

Thomas V Riley MAppEpid, PhD, FRCPath

Reintroducing the alcopops tax is important, but more comprehensive reform of alcohol taxation and other broader measures are needed To those Australians who believe that alcohol consumption in this country is causing too much damage, and that a public health-focused, evidence-based alcohol policy can make a difference, the defeat of the “alcopops” legislation in the Senate in March this year was a disappointment. However, this is no reason to stop national action to reduce damage from alcohol. The thousands of Australians whose lives are damaged by alcohol, and the hundreds each year whose deaths could be prevented, are too important.1 Concerned organisations need to collaborate and advocate for a comprehensive, evidence-based approach to reducing the alcohol toll. Their ultimate goal should be to move to a more moderate and responsible drinking culture in Australia. The first question is what to do with the more than $400 million raised from the alcopops tax. Our elected representatives are to be congratulated on voting in May to retain it, rather than handing it back to the alcohol industry. Judging by past performance, had it gone to DrinkWise, it would have been spent on soft-sell advertising, which the great body of evidence suggests has no impact on alcohol consumption or consequent harms.2,3 The alcopops revenue should be directed to independent public health agencies to develop evidence-informed interventions that aim to reduce consumption and consequent harms. The Alcohol Education and Rehabilitation Foundation is one such entity, established using tax revenues generated in similar circumstances from beer sales. The national Preventative Health Taskforce has already developed a framework to prevent alcohol-related harms,4 and will soon deliver a final report and recommendations for action, including an overarching National Prevention Agency, which will need funds. With additional funding, the National Health and Medical Research Council (NHMRC) could give special priority to alcohol-related research. Funding of agencies such as VicHealth and Healthway in Western Australia, which were originally supported by tobacco revenues, could also be considered. The Royal Australasian College of Physicians welcomes the federal government’s initiative to reintroduce the alcopops tax legislation in the current sitting of Parliament, but encourages the government to go further. Although there was evidence the alcopops tax was followed by reduced overall alcohol consumption,5 if the government wishes to address the full range of alcohol-related harms — which include much more than binge drinking in young people — it should comprehensively reform alcohol taxation. Controlling price is by far the most effective, and cost-effective, single intervention available to control consumption and consequent harms.2,3,6 A comprehensive reform of alcohol tax is needed, with public health as a principal objective. Specific elements could include: taxing beverages on the basis of their alcohol content — a volumetric system; a minimum price per standard drink; and additional taxation based on evidence of harm associated with particular beverage types. A proportion of alcohol-related tax revenues should be directed towards prevention and treatment of alcohol-related problems. The Australian public will probably support such taxes.7 Taxation policy is crucial but must be part of a broader approach. There is good evidence for the effectiveness of controlling the availability of alcohol by regulating the number, nature and opening hours of alcohol venues.2,3,8 The forthcoming review of the Northern Territory’s Liquor Act provides an opportunity to encourage alcohol legislation to genuinely focus on preventing alcohol-related harms, and not just on regulating the sale of alcohol. The role and practice of alcohol promotion should also be closely examined. Loosening the link between alcohol advertising, sponsorship and sporting organisations may be an important way to encourage Australian drinking culture to evolve in a healthier direction. Some alcohol tax revenues could be directed towards replacing alcohol-industry sponsorship, as was done for tobacco in several states, or buying back alcohol advertising during sports programs, as suggested by the Australian Medical Association.9 Although prevention is essential, many people and their families are already suffering from the effects of alcohol. More treatment programs are urgently needed, particularly in rural and remote areas, where alcohol problems are even more common than in the cities, and for groups with particular needs, such as Aboriginal people, who need tailored programs. Finally, a strong vision and framework would bind all these strategies together. The National Alcohol Strategy10 expires this year, and another is needed: one that more closely follows the evidence of what really works in reducing harm. Much good work to reduce the harms from alcohol has been done in Australia by individuals and organisations such as the Public Health Association of Australia and the Australian Drug Foundation. However, much more is needed, as the level of harm is still unacceptable, especially among young people. We in the health profession need to play a greater advocacy role, in partnership with others within and beyond the health sector, such as the Cancer Councils, and social welfare and community organisations. The Royal Australasian College of Surgeons Trauma Committee, with its experience in road trauma and interpersonal violence, has indicated a strong interest in being involved. We need to be part of, and to help build, active coalitions. We should heed the lessons learned from the fight against tobacco. Although there are important differences between alcohol and tobacco, much is similar in the need to change the culture surrounding their use, and in the large and powerful industries that profit from their sale. Overcoming these obstacles will require an alliance of organisations, with a common understanding of the key issues, goals and ways to achieve them, and persistence in their pursuit. With thousands of lives lost or damaged, and billions of dollars wasted every year,1 this is our challenge and our responsibility.

on behalf of the Royal Australasian College of Physicians Alcohol Advisory Group.*

Objectives: To determine whether redesign of pathology processes, including indicators of sample priority, could reduce patient length of stay (LOS) in an emergency department (ED), and assess the long-term impact of two indicators of sample priority on pathology clinical performance indicators for ED samples.Design, setting and participants: Two observational studies of de-identified data from standard databases were conducted — a single-site pilot trial of patients attending the ED of one hospital compared with historical controls, and a multisite study of 132 521 full blood count (FBC) requests for patients attending seven EDs that utilised either of two pathology process changes (coloured specimen transport bags alone, or coloured specimen bags plus blood tubes with a priority indicator).Main outcome measures: LOS in the ED was measured for the pilot trial, and collected-to-validated times for FBCs that fulfilled computer algorithm validation rules were measured for the multisite study.Results: In the pilot trial, the redesigned pathology process resulted in a 29-minute reduction (15.6%) in the median ED LOS for all patients (P < 0.001) compared with historical controls. In the multisite study, use of coloured specimen bags plus blood tubes with a priority indicator resulted in an 8-minute reduction (20.1%) in mean collected-to-validated times for FBC requests compared with FBC requests that used coloured specimen bags alone (P < 0.001).Conclusions: Our pilot trial revealed a direct relationship between pathology process design and LOS in the ED, suggesting that redesigned pathology processes can significantly reduce LOS in the ED. Our multisite study showed that collecting samples directly into blood tubes with an incorporated priority indicator reduces pathology test turnaround times. These data suggest that LOS in the ED can be significantly reduced by simple changes to pathology processes, such as collecting samples directly into specimen containers with an incorporated priority indicator.

Andrew J Francis MB BS(Hons), FRCPA · Michael J Ray PhD, BAppSc(Medical Technology) · Mary C Marshall BAppSc(Biology), GradDip Professional Communications

Objective: To characterise epidemiological, clinical and laboratory features of children in New South Wales with chronic hepatitis B (HBV) or C (HCV) infections.Design and setting: Retrospective record review of epidemiological, clinical, laboratory, liver biopsy and treatment data for children (aged < 18 years) referred to tertiary referral paediatric and refugee clinics in NSW with chronic HBV or HCV during 2000–2007; and comparison with NSW Health notification data for the same period.Main outcome measures: Numbers and characteristics of referred children with HBV and HCV, and notifications to NSW Health.Results: During 2000–2007, 79 children with chronic HBV and 29 with HCV infection were referred to specialist clinics, while 930 children with HBV and 777 with HCV infection were reported to NSW Health. Most of the referred children with HBV were born overseas, while most with HCV were born in Australia to mothers with a history of intravenous drug use. Of the 79 HBV-infected children, 56 were e-antigen positive. Most HCV-infected children (23/29) had alanine aminotransferase levels ≤ 2 times the upper limit of normal, and more than half of those who had genotype determined had type 2 or 3. Fibrosis was evident in liver biopsies performed for both HBV and HCV.Conclusions: Although advanced liver disease was uncommon in children referred with HBV or HCV infection, a large number of infected children in NSW were not referred for specialist medical care, indicating that opportunities to intervene early in the natural history of these infections, particularly HCV, are being missed.

Scott Nightingale BMed(Hons), MClinEpid, FRACP · Michael O Stormon MB BS, FRACP · Andrew S Day MD, FRACP · Murray T Webber BMed, FRACP · Kate A Ward BPhty(Hons), MPH · Edward V O’Loughlin MD, FRACP

Objective: To identify potential weaknesses in the system of managing warfarin therapy.Design, participants and setting: A structured interview-based study of 40 community-dwelling patients taking warfarin and with an international normalised ratio ≥ 6.0 and 36 of their treating doctors (35 general practitioners and 1 specialist), conducted between July and November 2007. Patients all received services from and were recruited sequentially by a large, private metropolitan pathology provider in Melbourne.Main outcome measures: Patients’ demographic, clinical, cognitive and psychosocial characteristics, warfarin knowledge, medication complexity and adherence; and doctors’ experience with, approach to and involvement in warfarin management, and their perception of responsibility for warfarin management and patient education.Results: Interviews revealed multiple difficulties, including cognitive dysfunction, possible depression, and medication non-adherence, in 30 of 40 patients. Of 36 doctors interviewed, 12 were unaware of these difficulties in their patients. Five doctors considered they had sole responsibility for their patients’ anticoagulation, while 15 confirmed a mutual relationship with the pathology service, and 16 deferred total responsibility to the pathology provider. Only 14/36 doctors reported conducting patient education at commencement of warfarin therapy, with the other 22 stating this was the responsibility of the initiating specialist, pathology service or dispensing pharmacist.Conclusions: There is a need for improved role clarification in coordinating warfarin management. We propose exploring the possibility of a Warfarin Suitability Score to assist better recognition of patients in whom treatment may be problematic, along with a model of care using practice nurses with GPs to facilitate optimal patient care.

Judy A Lowthian BAppSci(SpPath), MPH, LMusA · Basia O Diug BBioMedSci(Hons) · Sue M Evans BN, GradDipClinEpi, PhD · Ellen L Maxwell MB BS, FRACP, FRCPA · Alison M Street MB BS, FRACP, FRCPA · Leon Piterman MMed, MEdSt, FRACGP · John J McNeil PhD, FRACP, FAFPHM

Objective: To identify and quantify current deficiencies in primary and secondary stroke prevention, as well as potential gains from optimal employment of thrombolysis.Design, participants and setting: Observational study of 259 consecutive patients admitted to a tertiary hospital stroke unit from 24 January 2006 to 10 January 2007, with retrospective assessment of prestroke risk factors and therapies to determine stroke preventability, based on relative risk reductions from published meta-analyses of preventive therapies.Main outcome measures: Numbers of strokes preventable by optimal risk factor modification and numbers of strokes with preventable disability through optimal thrombolysis; characteristics of patients with preventable strokes; contributions of each risk factor to stroke preventability.Results: 183 patients had a disabling or fatal stroke; 135 patients had at least one suboptimally managed risk factor. On the basis of prespecified stroke preventability weightings, 70 strokes were preventable. The younger the patient, the more likely that the stroke was potentially preventable (relative risk [RR] for age < 60: ≥ 80 years, 3.10; 95% CI, 1.96–4.92). Smoking, inadequate control of hypertension and suboptimal anticoagulation accounted for nearly 90% of preventable strokes. Patients with target systolic blood pressures of 130 mmHg or lower were more likely to have inadequately controlled hypertension (RR, 4.27; 95% CI, 2.58–7.05). By comparison, disability could have been prevented in four strokes through optimal thrombolysis.Conclusions: A significant proportion of stroke remains preventable, especially in younger patients, by optimal modification of risk factors, particularly smoking, blood pressure and anticoagulation. Only a small proportion of patients will benefit from best-practice thrombolysis.

Timothy J Kleinig MB BS(Hons), FRACP, BA · Thomas E Kimber MB BS, PhD, FRACP · Philip D Thompson MB BS, PhD, FRACP

Implementing existing knowledge about cardiac rehabilitation (CR) and heart failure management could markedly reduce mortality after acute coronary syndromes and revascularisation therapy. Contemporary CR and secondary prevention programs are cost-effective, safe and beneficial for patients of all ages, leading to improved survival, fewer revascularisation procedures and reduced rehospitalisation. Despite the proven benefits attributed to these secondary prevention interventions, they are not well attended by patients. Modern programs must be flexible, culturally safe, multifaceted and integrated with the patient’s primary health care provider to achieve optimal and sustainable benefits for most patients.

Tom G Briffa PhD · Leigh Kinsman RN, MSc · Andrew J Maiorana MSc, PhD · Robert Zecchin RN, MN · Julie Redfern BSc, BAppSc(Physio)(Hons), PhD · Patricia M Davidson RN, PhD · Glenn Paull RN, CCUCert, BN(Hons) · Amanda Nagle PhD · A Robert Denniss FRACP, FAHA, FCSANZ

Improved leadership and recognising each others’ humanity are necessary for true health care reform I write this as an envoi immediately before my departure for a senior health position in Canada. Reflecting on my 35-year career in health care in Australia, I am concerned that, despite all the reform — which has been significant over this period, especially in reducing financial barriers to access — our health care sector still has not tackled fundamental challenges. The health system has been adept in responding to technological change, but our track record in responding to sociological change is poorer, and this gives cause for concern for the future. Health care use varies with age, with health care use concentrated in the last few years of life — typically over the age of 75 years. In the next decade or so, those aged over 75 years will be “baby boomers”, replacing those who grew up or lived through the Great Depression and World War II. Baby boomers tend to have very different expectations of clinicians and health care facilities, and to have a greater sense of entitlement. Most will also be regular users of the Internet. So what does this mean? Meekly waiting for care will be a thing of the past. Grateful acceptance of “cattle class” in outpatient departments will also go. “Charity” care by public hospitals officially ended with the introduction of Medicare in 1975, and is not part of the baby boomers’ adult experience. Patronising care, and patients’ acceptance of whatever is on offer, will become a thing of the past. There will be increased expectations of provision of accurate, up-to-date information; frank discussion of choices, attendant risks and likely outcomes; and treatment consistent with contemporary recommendations known to the patient (at worst from the trashy magazines that still adorn waiting rooms, or Internet sites of dubious validity; at best from websites that provide evidence-informed endorsed care paths). These changes are already happening. When things go wrong, there is and will be increasing pursuit of openness about the reasons why. Changes are also occurring in the workforce: the “team” with the medical team leader is under challenge, with expectations of shared leadership and more egalitarian styles. Nurse practitioners, podiatric surgeons and others are encroaching on the previously sacrosanct medical turf. Unfortunately, medical students still seem to be acculturated into the old paradigm — they emulate what they see their superiors do and, in contrast with other students, grow less team-oriented over their course of study.1 For the past 12 months, I have had dual roles: involved in macro system improvement as a member of the National Health and Hospitals Reform Commission (NHHRC), and leading statewide reform (principally focused on hospital-level change) as chief executive officer of Queensland Health’s Centre for Healthcare Improvement. These roles have involved considering the broad architecture of Australia’s health system and the day-to-day reality of provider-level change. The interim report of the NHHRC proposed macro levers of change — changed incentives on hospitals through activity-based funding, and on primary health care through steps towards limited enrolment-based care.2 But these macro changes do not, and can not, change the internal workings of hospitals and other health facilities. Levers for that are in the hands of individual managers and staff, and are not amenable to change with the levers in the hands of the NHHRC. Yet it is internal organisational processes that have such a profound impact on the working lives of health sector employees, and in turn affect patients’ experiences of the care received. It is here that the provider-level reforms, such as those initiated by Queensland Health, are so important in setting a context for the interaction between the patient and the clinician (Box). The changes in Queensland Health were made possible by political commitment to respond to two external reviews of the health system stimulated by the events in Bundaberg.6 The government responded quickly to these inquiries with a significant injection of funds and a reform agenda. Queensland, of course, is not the only state subject to either adverse safety issues or external inquiries.7,8 Unfortunately, the recent Garling Inquiry9 does not appear to have stimulated the same fundamental reform in New South Wales that Queensland embraced. The macro changes proposed by the NHHRC would lead to improved rationality of Australia’s health care system, and position us better for the technological, demographic and epidemiological challenges that confront us. Organisational changes, such as those being implemented in Queensland, help to create a better environment for the day-to-day workings of the system. But neither will guarantee the fundamental patient-centred reforms needed to respond to the sociological changes described above. Nor will they ensure that the micro environment of care, the interactions between clinicians and patients, between doctors and other health workers, will change. Of course, no health care system can guarantee perfect care and perfect outcomes for individual patients. It is inevitable that some health professionals will have a “bad hair day” — the result of activities the night before, work pressure, momentary distraction in thinking about issues at home or behaviour of their work colleagues. Even the best intentioned health professional can make a mistake. But it is these micro interactions that determine the patient experience, and tomorrow’s patients will expect more from their encounters and will be less tolerant of practices of the past. So what is to be done? Recognising the humanity of our patients and coworkers would be a start; as work interactions involve two people who are human, and equal in political and moral terms. So no pedestal, despite the information differential and the “sick role” that clinicians have traditionally expected of those they treat and care for. Improved leadership is also essential. Tolerance of temper tantrums is becoming a thing of the past. Dealing with aberrant behaviours is not enough. Leaders need to emphasise the importance of good communication between all partners in care, and provide the necessary training and time for this. Training for leaders is a sine qua non, as are systems to support leaders in the challenges they face. I expect Canada faces similar challenges, and I trust we can all learn from each other in transforming patient care. Provider-level change in Queensland Health, 2006–2009 Changing culture through the largest leadership development program in Australia (not only in the health sector), with more than 5000 managers and supervisors (just over half of whom were clinicians) participating in 2-day workshops to improve leadership skills; A reinvigorated clinical governance system to improve reporting of clinical incidents and near misses,3 to improve investigation of serious adverse events and to improve monitoring of performance to identify deviation from the state average;4 and An emphasis on the alignment of clinical governance with line management accountability.5

Stephen J Duckett PhD, DSc, FASSA

A key challenge for the Australian health care system is ensuring that the numbers, distribution and skill set of the health care workforce are adequate to meet the emerging health needs of an ageing population with increasingly high expectations of health care. Professional and government responses have given priority to increasing the overall numbers of practising clinicians by investment in additional training places. Another approach is to enhance productivity of the existing workforce by activating strategies of professional enablement that remove constraints imposed on clinicians by inefficient work practices and inappropriate training programs, maladaptive organisational attributes, misdirected financial and non-financial incentives, and adverse sociopolitical influences.

Ian A Scott FRACP, MHA, MEd

Early diagnosis and treatment of rheumatoid arthritis (RA) is necessary to prevent joint damage and long-term disability. High rates of false-negative and false-positive results of the rheumatoid factor (RF) test make it generally unhelpful in the early diagnosis of RA. A new clinical test for RA — the anti-citrullinated peptide antibody (ACPA) test — is now widely available in Australia. Owing to its high specificity (95%), a positive ACPA test result usually confirms a diagnosis of RA in a patient with undifferentiated inflammatory arthritis. The superior specificity of the ACPA test provides an argument for it to replace the RF test in the primary care setting. Performing both tests adds little to the use of the ACPA test alone. An early diagnostic opinion from a rheumatologist is still recommended, as the ACPA and RF tests frequently return negative results in early RA.

Simon M Chatfield MB BS, FRACP · Ian P Wicks MB BS, PhD, FRACP · Allan D Sturgess PhD, FRACP, FRCPA · Lynden J Roberts MB BS, PhD, FRACP

Health care-associated infections (HAIs) are a major clinical and economic problem in Australian hospitals, and a significant proportion are preventable. HAIs are the result of complex environmental, microbiological, pathological, behavioural and organisational factors, and prevention requires a multifaceted (“bundled”) approach, including appropriate policies, educational programs for health care workers, and adequate resources to implement them effectively. Failure to protect patients from avoidable harm, including HAIs, has significant ethical implications; it often reflects both organisational systems failure and non-compliance of health care workers with evidence-based policies, including hand hygiene. If implemented with appropriate safeguards, infection control “bundles” that include sanctions for poor compliance with hand hygiene and other infection control policies, will achieve sustained improvements where previous approaches have failed.

Gwendolyn L Gilbert MD, FRACP, MBioethics · Paul Y Cheung BSc(Hons), MAppLing, PhD · Ian B Kerridge BA, BMed(Hons), MPhil(Cantab)

Falling numbers of deceased organ donors and longer kidney transplant waiting lists have increased the emphasis on live kidney donation to meet demand for kidney transplantation. Several new strategies have been introduced to expand live donation beyond the classic direct donation. These include: altruistic donation; paired kidney exchange (PKE); and altruistic donor chains programs. Using incompatible donor–recipient pairs and altruistic donors, the Western Australian PKE program achieved nine successful kidney transplantations between October 2007 and November 2008. If PKE were performed routinely in Australia, the rate of kidney transplants could increase by 7%–10%.

Paolo Ferrari MD, FRACP, FASN · Claudia Woodroffe BAppSc · Frank T Christiansen MD, FRCPA

I am a sports physician. Until recently, the only clots of any interest for me were sportspeople who missed easy goals, dropped catches or couldn’t hit a ball. Clinically, my only interest in thrombosis was in the differential diagnosis of calf tears. All that changed one morning 18 months ago. I was sitting at the kitchen table reading the paper, having just finished breakfast. Suddenly, I felt horrible, the worst feeling I had ever had, but one that is difficult to put into words. I remember calling out to my son in the adjoining room that I felt terrible. That was the last thing I remembered for a while. My son came into the room to find me slumped on the floor, not breathing. He tried unsuccessfully to lift me up and then called my wife who was in another part of the house. Together they were able to sit me up and, after a minute or two, I apparently made some choking sounds and commenced breathing again. A few minutes later, I regained consciousness, blissfully unaware that anything had happened. The ambulance arrived soon after and I was taken to hospital, where I was diagnosed, after a ventilation–perfusion lung scan, with a pulmonary embolus (PE). I had not had any calf swelling or pain and an ultrasound failed to demonstrate any calf thrombus. My only risk factor was that I had returned from a week-long trip to China 3 days previously. I do a lot of flying. I have been looking after national sporting teams for 25 years and have attended numerous world championships, Olympic, Commonwealth and university games, as well as doing many other tours. In all my flights with teams, the recent trip with the Socceroos to China was my first in business class. So much for “economy class syndrome”! I was placed on the usual regimen of short-term subcutaneous enoxaparin sodium therapy and oral warfarin, and my progress was quite uneventful. I was seen by a consultant haematologist, who suggested that I keep taking warfarin for 6 months, then stop taking it and have further blood tests to determine whether I have any risk factors. He also suggested that I subsequently use subcutaneous enoxaparin whenever I flew. As I knew very little about deep vein thrombosis or PE, I decided I would do some reading. I ascertained that my recommended treatment regimen of 6 months of oral warfarin and subsequent use of subcutaneous enoxaparin when travelling was almost universally recommended. Yet I felt uneasy. I felt very reassured while I was taking warfarin, particularly as all the literature says it is virtually impossible to have a recurrence of venous thromboembolism (VTE) while taking warfarin. The prospect of discontinuing warfarin did make me feel uneasy. The general consensus among medical people with whom I discussed my condition was that, as there was a “roughly similar chance” of having a haemorrhage while taking warfarin and having a recurrence of PE while not taking it, there was probably no point in staying on the drug. Interestingly, they always seemed to qualify their advice with the words “but of course it is up to you”. I was not totally convinced by that argument, for two reasons. Firstly, I had never had a haemorrhage, but I certainly had had a PE, and a near-fatal one at that. It’s amazing how such an experience concentrates the mind. If the risks were indeed 50:50 then I figured I would err on the side of preventing the PE rather than worrying about a haemorrhage. My second reason was more objectively based. When I looked further at the literature, I began to doubt the mantra that the chances of a warfarin-induced haemorrhage and a recurrence of VTE in the absence of warfarin were similar. The three major studies in this area1-3 all showed a significant risk of recurrence of VTE in the first year after cessation of oral anticoagulant therapy — in the order of 10%, rising to about 15% after the second year. Readers, I don’t know about you, but a 15% chance of having a potentially fatal event in the next 2 years is not a prospect I relish. I would much rather take the 1%–3% risk of a haemorrhage. Quite apart from playing the percentages, there is also the matter of peace of mind. I would feel extremely anxious about my health if I were not taking anticoagulants, and I would certainly not fly. This would involve giving up an important and enjoyable aspect of my job, including, I hope, accompanying the Socceroos to South Africa for the next World Cup, not to mention the prospect of overseas holidays and visits to children working and studying overseas. Clive Kearon, Chair of the American College of Chest Physicians (ACCP) evidence-based clinical practice guidelines on antithrombotic therapy for venous thromboembolic disease, stated recently that a general recommendation of 3–6 months of anticoagulant therapy is no longer appropriate.4 He quoted the 2008 ACCP guidelines, which strongly recommend that . . . in the absence of risk factors for bleeding, which include being older than 75 years . . . patients with a first episode of proximal deep venous thrombosis or pulmonary embolism remain on indefinite anticoagulant therapy, provided that good anticoagulant monitoring is achievable and indefinite treatment is consistent with patient preferences. I will certainly be following those guidelines and I strongly suggest that clinicians who are still giving out the “warfarin for 6 months” mantra reconsider their position in light of the clinical evidence and the potential to improve patients’ quality of life by reducing anxiety.

Peter D Brukner OAM, MB BS, FACSP

We report the first isolation in Australia of a hypervirulent epidemic strain of Clostridium difficile, PCR ribotype 027. It was isolated from a 43-year-old woman with a permanent ileostomy, who appears to have been infected while travelling in the United States. The isolate was positive for toxin A, toxin B and binary toxin, and resistant to fluoroquinolone antimicrobials, and had characteristic deletions in the tcdC gene. All diagnostic laboratories and health care facilities in Australia should now be on high alert for this organism. Clinical recordA 43-year-old woman was admitted to a Perth hospital at the end of October 2008. She had been diagnosed with ulcerative colitis 8 years previously and, in 2002, underwent proctocolectomy and permanent ileostomy. Since then, she had experienced a number of stoma problems requiring surgical repair or local revision. On this occasion, computed tomography (CT) showed a parastomal small-bowel herniation, with a normal appearance on ileoscopy. The herniation was repaired with intraperitoneal mesh. After the operation, the patient developed small-bowel ileus and was placed on total parenteral nutrition. She then developed a central-line infection, with both Serratia marcescens and Staphylococcus epidermidis isolated from a central venous catheter tip, for which she was treated with intravenous cefepime and vancomycin (each, 1 g 12-hourly) for 10 days. A subsequent ileoscopy did not show any mucosal abnormality. Culture and faecal cytotoxin testing of the stoma fluid for Clostridium difficile was negative before her discharge from hospital at the end of November 2008. The patient subsequently travelled to the United States and, while in New York City on Christmas Day, became unwell with high ileostomy output, cramping abdominal pain and vomiting. Despite progressively worsening symptoms, she travelled to Hawaii via Vancouver, Canada. On arrival in Hawaii, she required hospitalisation and was admitted to an intensive care unit in Honolulu on 6 January 2009 with a diagnosis of complicated C. difficile infection with generalised sepsis and acute renal failure. An ileoscopy showed diffuse inflammation and ulceration of the ileal mucosa. She recovered slowly after treatment with oral vancomycin (250 mg 6-hourly), and was discharged after 14 days. On her arrival back in Australia, the symptoms recurred. An ileoscopy on 4 February 2009 showed a single inflamed ulcerated area close to the stoma, and biopsy specimens of this area were reported as consistent with pseudomembranous enteritis and C. difficile infection (Box 1). Culture of the ileostomy fluid again resulted in the isolation of toxigenic C. difficile. The isolate was determined to be positive for toxin A (tcdA), toxin B (tcdB), and binary toxin (CDT) by polymerase chain reaction (PCR) testing for toxin genes (tcdA, including the repetitive region, tcdB, and both the cdtA and cdtB binary toxin genes).1,2 The antimicrobial susceptibility profile of the isolate on E-strip testing (AB bioMérieux) indicated fluoroquinolone resistance: penicillin, susceptible (S) (minimum inhibitory concentration [MIC], 0.75 mg/L); clindamycin, S (MIC, 2 mg/L); metronidazole, S (MIC, 0.38 mg/L); levofloxacin, resistant (R) (MIC, > 32 mg/L); moxifloxacin, R (MIC, 16 mg/L); and vancomycin, S (MIC, 0.38 mg/L). The tcdC gene (which encodes a negative regulator in toxin production) was sequenced and found to contain an 18-base-pair deletion, as well as a single nucleotide deletion at position 117,3 characteristic of the epidemic C. difficile strain, PCR ribotype 027. On the basis of these findings, the patient’s isolate was PCR ribotyped,4 which confirmed it to be C. difficile PCR ribotype 027 (Box 2). Because of the severity of the patient’s initial illness, she was treated with a further 14-day course of oral vancomycin (250 mg 6-hourly). Her condition improved, and she has remained well since, with two negative cultures for C. difficile since cessation of vancomycin. DiscussionA hypervirulent, epidemic strain of C. difficile, PCR ribotype 027, has been responsible for outbreaks of severe disease in North America and Europe. This organism is characterised by production of increased quantities of toxins A and B, plus an additional, binary toxin (actin-specific ADP-ribosyltransferase), and fluoroquinolone resistance. Overuse of fluoroquinolones is probably driving epidemic spread of this strain in North America and Europe, and attributable mortality in people aged over 60 years who are infected has been over 10%. There has been concern in Australia because of the lack of suitable surveillance systems to detect the entry of epidemic C. difficile into this country;5 this is the first report of such an occurrence. This case is unusual because infection apparently occurred while the patient was travelling. Travel-associated C. difficile infection is extremely rare and, to our knowledge, acquisition of C. difficile during travel has never been proven. However, C. difficile is known to cause diarrhoea in travellers, as a result of antibiotics given either as prophylaxis before the journey, or as treatment for traveller’s diarrhoea afterwards. Indeed, in 1995, we reported three cases of laboratory-proven C. difficile infection following doxycycline administration for malaria prophylaxis.6 All three patients apparently acquired the organism outside Australia, although this could not be proven as no cultures for C. difficile were performed before travel. Six cases of C. difficile infection were recently reported in Spain in travellers who took antibiotics to treat an acute diarrhoeal episode and subsequently presented with prolonged or recurrent gastrointestinal symptoms, including diarrhoea.7 Interestingly, the first isolation of C. difficile PCR ribotype 027 in Austria was from a British tourist who was admitted to a hospital in Tyrol with a 5-day history of nausea, watery diarrhoea and lower abdominal pain. She was reportedly taking antibiotics prescribed by her physician to treat bronchitis, and the authors believed she acquired the strain in Great Britain before travel.8 We believe our patient most likely acquired C. difficile infection in New York City. According to the US Centers for Disease Control and Prevention, C. difficile PCR ribotype 027 has now been detected in 40 US states, including New York.9 It is less likely that she was infected while passing through Canada, even though PCR ribotype 027 is thought to be endemic in the western part of that country.10 In either case, as she had not been in contact with the health care system at that stage of the trip, community acquisition is most likely. Recent reports suggest that community acquisition of C. difficile is increasing worldwide.11 The lesions associated with C. difficile infection in humans are generally restricted to the colon, but pseudomembrane formation has been described in patients with an ileostomy.12 Our patient may have been at risk of C. difficile infection for two reasons. First, in ulcerative colitis, the intestine is known to be more readily colonised by C. difficile, and much of this colonisation occurs in the community rather than the health care setting.13 To what extent that risk is modified by colectomy is not known. The upper gastrointestinal tract microflora in patients with an ileostomy is similar to that of the colon 1 to 3 weeks after the ileostomy.14 Second, our patient had completed a course of antibiotics about 1 month earlier, and the “normal” microflora may not yet have re-established enough to provide any protection. We were fortunate that this patient was seen at an institution that routinely cultures for C. difficile. Currently, most laboratories in Australia do not culture for C. difficile, instead relying on either enzyme immunoassays or PCR tests. As molecular typing is required to identify C. difficile PCR ribotype 027, at a minimum, all patients with severe, suspected C. difficile infection should have specimens cultured, and any isolates should be sent to a laboratory with expertise in identifying epidemic strains. General practioners and diagnostic laboratories need to be reminded that patients presenting with community-acquired or travel-related diarrhoea may have C. difficile infection. Periodic targeted surveillance with molecular typing of C. difficile isolates should be funded by government, as suggested previously,5 until more rapid molecular diagnostic tests to identify epidemic strains are developed. We were also fortunate that the patient was seen as an outpatient on her return to Australia, and did not require hospital admission, minimising the possibility of contamination and spread of epidemic C. difficile within the hospital setting. However, this case exemplifies the ease with which this organism could be introduced into Australia. The conservative policies on fluoroquinolone use in this country may afford some protection against the establishment of epidemic C. difficile. Ciprofloxacin and moxifloxacin are the only fluoroquinolones available in Australia; levofloxacin, gatifloxacin and others are not. Nonetheless, all diagnostic laboratories and health care facilities in Australia should now be on high alert for the epidemic strain of C. difficile. 1 Ileal biopsy specimen from the patient, February 2009 Mucosa adjacent to the ulcer showed acute inflammation, with neutrophils invading the surface mucosa (stain, haematoxylin and eosin; original magnification, × 400). 2 PCR ribotyping of the Clostridium difficile strain isolated from the patient in February 2009 Polymerase chain reaction (PCR) amplification of ribosomal RNA intergenic spacer regions results in specific banding patterns (ribotypes), which can be used to genetically fingerprint strains of Clostridium difficile. Ribotyping showed the similarity between the patient’s isolate (lane 4) and the epidemic 027 strain (lane 3). Key to lanes: L = molecular weight ladder 1 = reference strain, VPI 10463 2 = ribotype 014 (the most common ribotype in Australia [unpublished data]) 3 = ribotype 027 (epidemic strain) 4 = patient’s isolate.

Thomas V Riley MAppEpid, PhD, FRCPath · Sarah Thean BSc(Hons) · Graham Hool MB BS, FRACS · Clayton L Golledge MB BS(Hons), DTMH, FRCPA

Clinical record An 8-year-old Indigenous Australian boy was transferred from a regional hospital to a metropolitan paediatric hospital, with fevers, 2 weeks of left hip and thigh pain, and a left thigh abscess that had begun to discharge. Two weeks earlier, he had fallen while rollerblading and had sustained a superficial wound on the left thigh. He complained of ongoing left hip and groin pain and presented on several occasions to his general practitioner, who diagnosed a soft tissue injury. On arrival, the patient was in septic shock. Outside-taken radiographs (Figure, A) and magnetic resonance imaging (MRI) (Figure, B) showed extensive osteomyelitis and bony destruction, focused at the left ischium. The necrotic ischium, pubis and hamstrings were debrided and large purulent collections were drained from the thigh; swabs were taken for microbiological culture. The initial debridement did not involve the exploration of the internal aspect of the pelvis. During a second debridement, 48 hours later, the pus had a faeculent odour and colour. Bowel involvement was not detected at this stage. During the third debridement, 5 days after the initial surgical treatment, faeculent fluid drained freely from the wound and further exploration revealed a retroperitoneal sigmoid colon perforation. The general surgical team created a colostomy and the wound was packed with gentamicin antibiotic beads and covered with a vacuum dressing. Two strains of Escherichia coli, mixed anaerobes, Candida species and non-multiresistant, methicillin-resistant Staphylococcus aureus were cultured from the samples taken during the initial debridement. The patient was treated with oral clindamycin and rifampicin. After almost 9 weeks in hospital, he was discharged with a prescription for these antibiotics to be taken for 1 year. The patient’s colostomy was reversed at 6 months with no complications. One year after discharge, the boy had a 3 cm leg length discrepancy and reduced range of motion of his left hip. An MRI scan 1 year after discharge showed regeneration of the ischium and pubis, avascular necrosis of the left femoral head and formation of a left hip pseudoarthrosis (Figure, C). Despite radiographic changes, at follow-up he was surprisingly active, could walk over 1 km without pain, participated in sport (including soccer), and rarely needed analgesics. A: Outside-taken plain anterior–posterior pelvis radiograph showing left hip subluxation, bony changes in the ischium, ilium and pubis, and distended small bowel. B: MRI at initial presentation showing large medial thigh collection (large arrow), left hip subluxation and oedema in the soft tissue, and fluid collection in the retroperitoneum (small arrow). C: MRI of the pelvis 1 year after discharge showing partial resorption of the left acetabulum and confirming avascular necrosis of the left femoral head (arrow). Pelvic osteomyelitis is a rare occurrence, with reported rates of 1%–11% of all cases of acute haematogenous osteomyelitis (AHO) occurring between the ages of 7 and 14 years.1 In a review of the medical records of 220 children with AHO, 19 children had pelvic osteomyelitis.2 A review of cases of AHO at our institution showed infection of the pelvis in 8% of 102 patients with AHO and a male : female ratio of 2.1 : 1.3 Pelvic osteomyelitis has been described in three entities — gluteal, lumbar and abdominal.4 Although these designations can be useful for determining the spread of infection, they have no prognostic value.4,5 Acute pelvic osteomyelitis is often not initially recognised. It can be difficult to detect due to its variable clinical signs and differential diagnoses.1 In one study, the time span between initial symptoms and the diagnosis ranged from 1 to 8 days.2 Difficulty diagnosing the condition may result in a delay of appropriate treatment.1,6,7 In our patient, plain radiographs (which are usually normal for the first 7–10 days8) and magnetic resonance imaging (MRI) scans showed extensive bony and soft tissue destruction of the left hemipelvis, hip and thigh. Is it plausible that these changes occurred within 2 weeks, considering the patient’s history? As we were unable to find supporting reports in the literature, this matter was discussed within various hospital departments. Concerns were raised that the time frame was too short to cause this level of destruction. It was proposed that the mixed flora that were cultured could cause a high level of destruction within 14 days. Although plausible, there was no direct evidence to support this theory. When during the course of the infection did the bowel perforation occur? In the literature, we found two case reports of a bowel perforation associated with pelvic osteomyelitis. Both occurred in adult patients, and bony infection was secondary to Crohn disease in both cases.9,10 On arrival at our hospital, our patient’s radiographs showed dilated loops of bowel and no signs of free gas. The MRI scan showed oedema and signs of inflammation of the soft tissue at the perineum, surrounding the rectum, urethra, bladder and sigmoid colon. Free fluid was seen within the pelvis; however, there was no obvious pelvic collection. Enteric flora were cultured from the initial intra-operative swabs. These factors indicate that the bowel perforation was probably present on arrival, possibly as a sealed perforation, which was only detected 5 days after the initial debridement. Although we were unable to ascertain the cause of the bowel perforation, we believe that its association with pelvic osteomyelitis was significant. We recommend that sophisticated imaging studies be performed at an early stage. MRI is the most sensitive test for osteomyelitis of the pelvis and spine, with a reported sensitivity of 97%–100% and specificity of 73%–92%.11 Staphylococcus aureus is the most common causative organism in AHO, accounting for 76% of cases, with an increased emergence of community-acquired methicillin-resistant Staphylococcus aureus (MRSA) accounting for 9% of these.3 Aggressive community-acquired MRSA, which was isolated from the initial swabs, was thought to be the causative organism of this patient’s pelvic osteomyelitis. We believe that the late diagnosis and the bowel perforation contributed to the extraordinary tissue destruction described in this article. We believe that the extent of the patient’s recovery, including the partial repair of bony destruction, was remarkable. Most cases of pelvic osteomyelitis reported in the literature were treated adequately with antibiotics alone; surgical intervention was rarely required.1,5 Complications, including recurrence and permanent sequelae, were uncommon, with rates reported between zero and 7%.1,5 Increasing rates of community-acquired MRSA require clinicians to consider whether a change to more efficacious antibiotic therapy is necessary if the patient is not responding to flucloxacillin alone. Unusual circumstances that delay the diagnosis can always occur, particularly in rural communities, where access to sophisticated imaging is limited. Lessons from practice Negligible accidents can form the starting point of life-threatening osteomyelitis, particularly in the pelvic region. To avoid major complications, it is important to repeat physical examinations within a short time period (ie, daily). If any doubt arises regarding a correct diagnosis, check for inflammatory parameters and refer the patient to a major hospital for sophisticated imaging and commencement of appropriate treatment. Consider magnetic resonance imaging early, as this is the most sensitive method for detecting (pelvic) osteomyelitis.

Craig D Hughes BSc, BM BS · Matthias W Axt BM BS, FRACS

To the Editor: The federal government is to be applauded for its decision to re-introduce the “alcopops” tax Bill to Parliament and to try to retain the $300 million raised so far for expenditure on services, programs and research to reduce alcohol-related harm in Australia. The alcopops tax was paid by consumers in the form of higher retail prices, which will fall dramatically if the government again fails to pass legislation to retain the tax. If it transpires that the government cannot retain the revenue already raised, it should be given to an independent public health body (such as the National Health and Medical Research Council [NHMRC]) and not to DrinkWise via distillers and distributors, as has been suggested.1 DrinkWise is a “putatively independent body that was originally funded by the alcohol industry”;2 six of the 11 current members of its board are senior alcohol industry figures. The alcohol industry profits from drinking that contributes significant harm to individuals and communities,2 and it can be relied upon to oppose policies that are known to reduce alcohol consumption across the population.3,4 DrinkWise and similar industry-backed organisations around the world promote industry-friendly programs that do not have an evidence base or are ineffective (such as education campaigns or tepid television advertising),5 while lobbying against the adoption of effective evidence-based interventions, such as higher taxes on alcohol, as these would affect profits.2-4 The Chief Executive of DrinkWise, Chris Watters, recently revealed the organisation’s position on the alcopops tax, reportedly asserting that it did not recommend “fiddling with alcohol tax” because it was “old thinking” and that “the facts just don’t stand up”, and noting that DrinkWise funds many educational programs across the country.6 There is a clear consensus among public health experts worldwide that increasing the price of alcoholic beverages is one of the most powerful and cost-effective strategies that governments have at their disposal to reduce unhealthy alcohol use.7-10 Other effective strategies include drink-driving legislation, random breath testing, increasing the minimum legal age for drinking or purchasing alcohol, restrictions on trading hours and numbers of licensed premises, and better enforcement of existing liquor laws. In contrast, comprehensive reviews of the evidence show that, by themselves, alcohol education programs are ineffective.11,12 Alcohol industry-sponsored agencies have adopted similar public relations strategies to those used by the tobacco industry.3 These strategies distract attention from their concurrent lobbying against the adoption of policies that would actually make a difference. The laudable policy action taken thus far by the government in its attempt to implement the alcopops tax would be enhanced by supporting an independent body, such as the NHMRC, that has transparent funding strategies and criteria, based on an independent peer-review system, to distribute funding for alcohol-related research. We, along with the more than 50 other scientists and health experts listed at <http://www.webcitation.org/5gbwQWf9J> who endorse and are signatories to this letter,13 will not seek or accept funding from DrinkWise. We call on other researchers and community agencies to consider their positions.

Peter G Miller · Kypros Kypri · Tanya N Chikritzhs · Steven J Skov · George Rubin

In reply: I write in response to the letter from Miller and colleagues, recently published online.1 Their letter is an attempt to influence non-government senators as the Australian Government reintroduces the Bill to increase the tax on some alcoholic beverages. There must have been a better way to do this than by besmirching the good work of DrinkWise and its directors. DrinkWise Australia is not an industry-dominated body. It has a balanced board of six members from the alcohol industry and six distinguished community members. Miller and colleagues should know that, in criticising DrinkWise, they also attack the reputations of board members Professor Ross Kalucy, Chair of Psychiatry at Flinders University; Noel Turnbull, Adjunct Professor in Communications at the Royal Melbourne Institute of Technology; Neil Comrie, former Chief Commissioner of Victoria Police; and Terry Slater, who led the Australian Government’s public health programs before heading up the National Food Authority and the Therapeutic Goods Administration. The sixth community representative position on the board is currently vacant and has been offered to the federal health department. DrinkWise does not advocate for or lobby government in respect of alcohol taxation policy for a very sensible reason — alcohol industry leaders advocating for or agreeing on matters affecting price could constitute a breach of the Trade Practices Act 1974 (Cwlth). DrinkWise programs are strictly evidence-based, drawing on specifically funded high-level independent research executed by leading academics at universities including Griffith, Macquarie, Monash, Deakin, Flinders, and the Hunter New England Institute. Moreover, the DrinkWise “Kids Absorb Your Drinking” advertising campaign was developed through qualitative, quantitative and ethnographic research, as well as the findings of an extensive literature review by child heath experts and academics.2-9 Campaign tracking results show that 28% of adults surveyed in March 2009 reported having reduced the amount of alcohol they drink in front of their children in the previous 12 months. When parents who had seen the DrinkWise advertising were asked about its impact on their drinking behaviour, 39% said they were more self-conscious of how they drink in front of their children, 18% had changed their drinking patterns, and 14% had actually cut down how much alcohol they consume when their children are around.10 DrinkWise Australia: receives funding from the federal government and the alcohol industry for the development of both its evidence base and its programs; has no associations with any international alcohol or tobacco lobby groups; undertakes research through Australian universities to develop the evidence base for its interventions; does not interfere with specification of the research hypotheses, research design and techniques, or publication of results; ensures that the research it funds is undertaken in accordance with the universities’ protocols for conducting independent research; and grants the researchers it funds a “non-exclusive, royalty-free, perpetual license to use, reproduce, adapt and publish Project IP [intellectual property] for research, education, academic and consulting purposes”.11 I was particularly surprised that the letter’s authors would trivialise the importance of education in successful drug intervention programs and instead advocate for increased reliance on supply-side strategies. DrinkWise delivers interventions in a variety of settings, not only through the Kids Absorb Your Drinking campaign, but also through practical tools such as a website (http://www.drinkwise.com.au), information materials and discussion forums, as well as working at the grassroots level with groups such as local government, school organisations, community newspapers, Sports Challenge Australia and the Good Sports program. Educational programs informed by scientific literature, that are implemented and evaluated effectively and not used as a standalone intervention strategy, can work.12 We at DrinkWise hope that anyone with a strong commitment to public health will be able to work with us and not against us. This will ensure that we will be able to continue to run evidence-based initiatives to reduce alcohol-related harm in Australia.

Trish M Worth

To the Editor: Skov puts the case for an alcohol taxation policy in Australia.1 Few people, if any, in public health would disagree that alcohol is a serious public health issue in Australia, and few would doubt that higher prices will reduce consumption. But why tax the consumers directly? Why not tax the providers? I propose a tax on the advertising budget of alcoholic beverage producers. Further, this tax should be weighted according to the alcoholic content of the products they sell. Yes, this would mean higher prices for drinkers, but set in this way the incentive mechanism is to get sales and consumption down, firstly by reducing advertising, and secondly by lowering the amount of alcohol in what is sold. It has been estimated that more than a quarter of a billion dollars are spent each year on advertising alcoholic beverages in Australia.2 An average 200% tax, graded by alcoholic content of products, would mean a lot of money for the government! It might well make up for the estimated loss from the defeated “alcopops” tax of $1.6 billion over 4 years.3 Indeed, we should hope that it would not bring in half a billion dollars a year, as both advertising budgets and average alcohol content fall. An advertising tax would almost certainly make much greater inroads into reducing alcohol consumption than would the alcopops tax. It would raise the price for consumers, but to a lesser extent for lower alcohol-content beverages. It would severely discourage advertising, especially of high alcohol-content drinks, and would encourage manufacturers to produce beverages that are lower in alcohol. Any increase in cost to the consumer through taxation risks being regressive and might make the poor even poorer if they continue to drink, with a consequent impact on their health. This needs to be watched. But using the revenues raised to devise a targeted counselling program for those who do want to reduce their consumption (and for those who perhaps cannot do so without help) cannot be beyond the wit of Treasury and the health department.

Gavin H Mooney

To the Editor: I write in response to the article by Skov on alcohol taxation policy,1 and in the context of the recent defeat of the “alcopops” tax legislation, which is soon to be reintroduced to the Australian Senate. Our democratic political system has held us in relatively good stead, with a reliable system of checks and balances. However, the rejection of the alcopops legislation arguably represents a failure of democracy and a retrograde step for public health, defeating the first Australian public health-centred alcohol tax policy. For this, Senator Fielding and the Opposition should be held accountable. Yes, the tax is not all encompassing, and expansion to broader initiatives, as proposed by Senator Fielding, is not without merit. However, health experts supported the alcopops tax initiative as an important first step, as outlined in Skov’s evidence-based article.1 Skov highlighted the key issues, including that alcohol-related harm is at unacceptable levels, that action is overdue, and that good evidence from Australia and internationally supports taxation and pricing as being among the most effective measures to reduce alcohol consumption and harm.1,2 Overall, the positives of this initiative clearly outweigh the negatives, and defeating it was arguably naïve and ill informed. Historically, both policy and funding are crucial to public health successes. Following awareness of the problem, change must start somewhere, before broadening over time to deliver health benefits (eg, smoking, seatbelts, speeding — all crucial and effective public health campaigns). The most important aspect of the alcopops tax initiative is likely to be that it is a start and a successful avenue to raise revenue. Extension to a full alcohol content-based tax, education, incentives and regulations will come — but much more belatedly now. The defeat of the alcopops tax legislation has threatened this opportunity to significantly contribute to the fight against alcohol misuse. While opposition is by definition the trademark of Opposition parties, bipartisanship should prevail when community benefits are clear. Perhaps more concerning is that a single politician holding the balance of power can disregard history, expert opinion and popular support, and defeat important public health-centred legislation. The manipulation of our political system with the rejection of the alcopops tax legislation was profoundly disappointing. This initiative should not be defeated again. Our politicians should take heed of history, evidence, expert opinion and public sentiment and vote in the nation’s interest to support the alcopops tax legislation on its return to the Senate.

Helena J Teede

There is nothing a government hates more than to be well informed; for it makes the process of arriving at decisions much more complicated and difficult. — John Maynard Keynes, 1938. To the Editor: I would like to contribute to the debate raised by Skov’s timely article1 on the recently defeated “alcopops” tax legislation — the Excise Tariff Amendment (2009 Measures No. 1) Bill 2009.2 Senator Fielding’s requirement for a ban on alcohol industry advertising during sporting events as a condition for his support of the alcopops tax legislation is rational, visionary and affordable from the additional tax raised. Many of the high-profile individual and public health incidents related to alcohol misuse have been among athletes sponsored by the alcohol industry, and around sporting arenas. As the positive outcome of banning tobacco industry sponsorship of sporting events has demonstrated, such bans have at least as strong an impact as would the increased tax on alcopops on reducing exposure of young people to alcohol.3 It is estimated that the alcohol industry contributes up to 23% ($288 million) of the $1.25 billion in annual sports sponsorship in Australia.4 If the government had agreed to Senator Fielding’s prerequisite amendment, and had also fully taken over sports sponsorship responsibilities, it would have achieved two important public health objectives — a reduction in binge drinking and banning of sports sponsorship by the alcohol industry — and would still have had at least $100 million left to address alcohol-related issues; assuming of course that the real objective of the alcopops tax policy was to prevent alcohol-related harm among youths. Had the government agreed to simultaneously ban alcohol industry advertising in sport and maintain the new alcopops tax structure, it would then be on a moral high ground to implement other important alcohol-related public health measures that require no more than strong political will, such as mandated warnings on alcoholic products at the point of sale. In this respect, the French National Cancer Institute’s recent report that alcohol-related colorectal, breast, oesophageal and liver cancer risks increase from one glass per day, and that the consumption of alcoholic beverages of any type is not advised for anyone,5 is instructive.

Niyi Awofeso

To the Editor: A 70-year-old woman presented to the emergency department with intense pain, erythema, oedema and haemorrhagic bullae of the right lower leg. Twenty-four hours earlier, she had fallen into warm seawater on the south coast of New South Wales, sustaining a penetrating wound by an unknown object. She reported developing excruciating pain and the noted leg changes within hours of the injury. She had a history of systemic lupus erythematosus (SLE), managed long-term with 7.5 mg oral prednisone daily. Soon after presentation, she rapidly developed septic shock, becoming hypotensive, tachycardic, hypoxic and confused. She was experiencing rigors and required inotropic support. On examination, there was marked cellulitis of the right lower leg with purpura and bullae. No crepitus was detectable in the tissues. There was no clinical or laboratory evidence of disseminated intravascular coagulation. Broad-spectrum empirical antibiotic treatment with intravenous gentamicin, cephazolin and metronidazole was commenced, and urgent, extensive surgical debridement of the lower limb was performed (Box). Wound culture swabs and tissue samples were sent for microbiological and histopathological examination. On Day 2, blood cultures taken at initial presentation were positive for Vibrio vulnificus, as were tissue swabs. Based on susceptibility testing, antibiotic therapy was reduced to a single agent, intravenous ciprofloxacin 400 mg twice daily. The patient’s postoperative clinical recovery was slow, but her SLE did not flare up, and on Day 23 she was transferred to a tertiary referral centre for lower-limb skin grafting. Cellulitis is a common presentation to emergency departments, and common organisms are usually implicated. However, in some cases, the presence of more unusual pathogens, such as V. vulnificus, should be considered. V. vulnificus is a virulent halophilic (salt-loving) gram-negative bacterium associated with seawater temperatures (usual range, 18°–24°C). It has two distinct clinical presentations.1,2 The first, well recognised, is septicaemia after ingestion of raw or undercooked seafood, such as oysters, causing acute gastrointestinal disease. The second, not always considered, is necrotising wound infections, as in this case. Open wounds can be directly inoculated with V. vulnificus from seawater containing the organism. “Vulnificus” is a Latin term meaning “inflicting wounds”. Hippocrates described perhaps the first recorded case of a fisherman with pain in the foot, fever, delirium and blistering skin.3 Patients with primary wound infections caused by V. vulnificus develop painful, rapidly progressing cellulitis. More unusually, our patient developed fulminant sepsis from an open wound infection. Patients who are immunocompromised, especially those with alcoholic liver disease, hepatitis B or hepatitis C, have a higher risk of infection with V. vulnificus, as well as patients, like ours, who take long-term steroid therapy.2 Management requires timely recognition, antibiotic therapy and prompt surgical review. Cellulitis of right lower leg caused by infection with Vibrio vulnificus

Tamara C Preda · Veronica A Preda · Allan P Mekisic

To the Editor: A 27-year-old man who had recently emigrated from Sudan was admitted to our department with a 7-hour history of constant peri-umbilical pain. Physical examination revealed inconstant voluntary guarding of the lower abdomen. Full blood and electrolyte examinations were unremarkable. Urinalysis showed protein and traces of blood. A condition requiring surgery was considered unlikely and further investigations were undertaken. Significant bladder calcification was noted from an abdominal x-ray. A computed tomography scan confirmed this finding (Box), and also revealed circumferential distal ureteric calcification, appendiceal thickening with appendicolith, and adjacent fat stranding. Repeat abdominal examination demonstrated right iliac fossa tenderness with a positive Rovsing sign. Acute appendicitis was diagnosed and an inflamed, thickened, retrocaecal appendix was removed laparoscopically. The patient was discharged 2 days later, but did not attend his post-operative review. Histological examination of the appendix demonstrated transmural neutrophil infiltration, without eosinophils. Within the lumen there were numerous oval-shaped helminth ova, some with terminal spines, consistent with acute appendicitis caused by schistosomiasis. The patient did not have a general practitioner, therefore a referral to an infectious diseases clinic was made. He was thereafter lost to follow-up. Infection by schistosomes leads to chronic granulomatous inflammation in many body systems, including the gastrointestinal tract. Adult worms are not usually harmful to the host — eggs provoke a Th2-mediated immune response.1 Three major species of Schistosoma cause schistosomiasis in humans, of which two are endemic in sub-Saharan Africa — Schistosoma mansoni and Schistosoma haematobium. S. haematobium migrates against portal venous flow to the vesical venous plexus, causing urinary tract calcification through chronic inflammation and fibrosis. This species has also been described as a cause of appendicitis.2 Examinations of appendices removed from patients with acute appendicitis in endemic areas have demonstrated schistosomiasis in 2.3%–4.2% of samples, with 2.7% having histological evidence of acute schistosomal appendicitis in one study.3,4 Schistosomiasis can be diagnosed by histological analysis, or urine and stool microscopy. Serological testing cannot be used to differentiate past and present infection, however positive serological results are the basis for treatment of patients in endemic areas. After diagnosis, praziquantel should be prescribed. It is assumed that our patient did not receive praziquantel. He thus risks significant morbidity and mortality from possible gastrointestinal, hepatic, urinary, pulmonary and neurological complications related to chronic schistosomal infection. Surgeons and pathologists should be aware of the atypical pathology of acute schistosomal appendicitis. The number of immigrants arriving in Australia from endemic areas has increased markedly in recent years and further presentations may occur. Non-contrast computed tomography scan of a 27-year-old man with schistosomal appendicitis Calcification of the bladder (black arrow) and distal ureters (white arrows) is evident.

Jordan K Webb · Graeme Thompson

To the Editor: A 4-year-old girl presented with a flyblown scalp to a district aid post outside Madang, Papua New Guinea (PNG). Coincidentally, we were present at the aid post in our capacity as students and lecturers in the tropical paediatrics module of the James Cook University Masters in Public Health and Tropical Medicine course. The child was otherwise healthy, and her scalp had been normal until about 2 days previously, when her mother noticed two developing “sores”. These had deteriorated into circular, foul-smelling ulcers about 1.5 cm in diameter and 2 cm apart on the crown of her head (Box, A), in which live maggots could be seen squirming. The child’s mother had extracted some maggots with a pair of toothpicks (Box, B), and about 10 more were removed at the aid post with tweezers. When no further movement was apparent in the wounds, they were covered with petroleum jelly to suffocate any “stragglers”. No dead larvae were seen the following morning, and the wounds healed rapidly. We believe the most likely culprit was Chrysomya bezziana, or Old World screw-worm fly, although we were unable to preserve a larva for formal identification (by “curing” in very hot water and transporting in 70% ethanol). Old World screw-worm fly is an obligate myiasis-producing fly endemic in PNG. Its larvae are found only in living vertebrate tissues. The child’s mother had not noticed a prior lesion, and we assumed entry was through a graze on the scalp. Although screw-worm fly is endemic throughout tropical and subtropical regions of Asia and Africa, it is not found in Australia. If it became established here, it could devastate the livestock industry, particularly by striking the umbilical region of newborn calves and infesting their abdominal contents.1 The fly is known to be able to travel 100 km,2 further than the distance between the islands of Torres Strait, but has not yet migrated from PNG to Australia. It could also be introduced in livestock vessels returning from Asia or the Middle East; the Australian Quarantine and Inspection Service has strict regulations to prevent this, with all returning vessels thoroughly cleaned before reaching Australian waters. This is justified as it has been documented that sheep shipped from Australia arrived in Bahrain with fly infestation. Presumably, flies were attracted to the ship as it passed the coast of Oman or the United Arab Emirates.3 Infestation is self-promoting, as ovipositing females are particularly attracted to the odour of an existing myiasis, resulting in expansion of the lesion. In our patient, the application of petroleum jelly to the lesions fortuitously covered the odour, reducing the likelihood of reinfestation. Ivermectin is useful in treating affected animals,4 as well as humans5 when the larvae cannot be physically extracted. Scalp of a child with fly infestation A: Circular ulcers on the child’s scalp. B: Removal of larvae with toothpicks.

John S Whitehall · Richard Speare · Heidi E Best · Philippa J Price · Deborah J Mills

To the Editor: A recent review of medical textbooks found that the topic of intravenous fluid therapy is poorly covered.1 Hence, the recent article by Hilton and colleagues provides interesting hypothetical examples of the risk of hypovolaemia and hypervolaemia, as well as imbalances in fluid tonicity, in patients receiving intravenous fluid therapy.2 In particular, the authors recommend the use of intravenous 0.9% saline, as it is reportedly isotonic and hence avoids potential imbalances in serum sodium concentration. However, Hilton and colleagues discuss only tonicity as the determining factor when selecting the type of fluid to give patients. They do not mention that 0.9% saline, also known as “normal” saline, distorts fluid, electrolyte and acid–base balance, despite being isotonic. In healthy subjects, 25% more volume is retained 6 hours after infusion of 2 L of 0.9% saline compared with 2 L of Hartmann’s solution.3 Infusion of 0.9% saline also results in hyperchloraemia, which decreases glomerular filtration rate, and is not seen with infusion of Hartmann’s solution.3 Certainly, the most important side effect of 0.9% saline infusion is metabolic acidosis, caused (according to the Stewart approach) by a reduction in the strong ion difference.4 Using the Stewart approach once again, Hartmann’s solution is “balanced”, ensuring the eradication of infusion-related metabolic acidosis.4 Although tonicity is important in considering the appropriate intravenous fluid therapy, it should not take precedence in the choice of therapy. Such an approach ignores the volume, electrolyte and acid–base disturbances induced by 0.9% saline infusions.

Alexander D Franke

In reply: Franke presents some well known problems associated with intravenous administration of large volumes of 0.9% NaCl, particularly its relatively slow elimination (as compared with Hartmann’s solution), and hyperchloraemic acidosis.1 In isolation, we do not dispute these facts. However, 0.9% NaCl is not unique in having problems — no intravenous fluid therapy is without risk, especially when given in excessive volume, or when the composition is inappropriate for the patient’s needs. It is also important to distinguish maintenance therapy from resuscitation. For postoperative maintenance therapy, we advocate a conservative approach with initial use of minimal volumes of isotonic fluids, to decrease the risk of common complications such as postoperative fluid retention, impaired respiratory function, and prolonged bowel dysmotility. We encourage close monitoring of volume and electrolyte status, and do not exclude the later use of hypotonic fluids.2 Disorders of volume and tonicity (hypo- or hypernatraemia) are the most common serious problems associated with intravenous fluid therapy. The approach we recommend follows the priorities of the kidney: restoration of volume, restoration of tonicity, and restoration of acid–base balance, in that order. If the patient’s requirements for fluid volume and tonicity are met, and tissue perfusion and gas exchange restored, then significant morbidity or death is unlikely to be a direct consequence of isolated 0.9% NaCl-induced hyperchloraemic acidosis.

Carlos D Scheinkestel · Andrew K Hilton · Vincent A Pellegrino

To the Editor: We agree with Smith and Gray that the uptake of telemedicine is slow despite the availability of hardware in many facilities.1 Not every field in medicine is amenable to videoconferencing consultations. Specialties in which the physical examination needs to be performed by the specialist, such as cardiology, are not suitable. However, decisions in medical oncology are based on history, pathology and imaging studies, making the specialty well suited to telemedicine. If physical examination is needed, it can be performed by a proxy examiner. Towns with high patient loads are probably not suited, but towns with fewer patients would be ideal for this method. For the past 2 years, Townsville Hospital’s Department of Medical Oncology has managed cancer patients in Mount Isa (800 km — a 2-hour flight or 10-hour drive — from Townsville, one way) using weekly videolinked clinics. The team comprises a medical oncologist in Townsville, and a senior medical officer (SMO), a chemotherapy nurse, patients and families in Mount Isa. Except for the initial period of familiarisation, running the clinics has been smooth. Forty patients have been managed in Mount Isa in over 200 consultations. Consultations have included new cases, ward consultations and reviews. Four patients were considered for palliation only and were managed in Mount Isa without being transferred to Townsville, which was particularly helpful for those at terminal stages. In 2008, we conducted a survey to assess the level of patient satisfaction and assessed the safety of chemotherapy delivery. We found that all 25 patients who participated in the survey were satisfied with the service, with scores of more than 80% on a five-point Likert scale (ie, “agree” or “strongly agree”).2 Ninety-two per cent of patients would rather “see” the specialist via videoconference than travel to Townsville. All three SMOs and both nurses felt they were able to communicate more effectively with and receive support from the specialists. Thirty-two patients received active chemotherapy between 2006 and 2008. Rate of occurrence of severe side effects among patients in Mount Isa was similar to that of patients treated in Townsville (< 5%). Four patients were admitted for complications, but there were no treatment-related deaths. We believe that this technology is safe and appreciated by patients. The technology can be adopted by medical oncologists to manage patients in rural areas, where travel by specialists and patients is not cost- or time-effective. The major advantages are that the patients have the opportunity to be treated closer to home, and doctors receive specialist support on a weekly basis.

Sabe S Sabesan · Pieter Nel · Suresh C Varma

To the Editor: Climate change has an adverse impact on health.1 Procurement, waste production, transport, and energy and water consumption (ie, the ecological “footprint”) all contribute to climate change. If the principle underpinning the work of all health professionals is “do no harm”, addressing the harmful effects of the health care industry on the natural environment must become a priority. We argue that one way to rapidly achieve this would be to mandate more sustainable practices as part of hospital accreditation. The United Kingdom has specifically targeted its health system to reduce its large ecological footprint,2 but in Australia, progress towards environmental sustainability within health care is uncertain and unmonitored. The contribution by health care to Australia’s national carbon emissions is unclear, but we do know that, for example, Victoria’s public hospitals consume 60% of the total energy used by the state’s government departments,3 so we have the opportunity to make a major impact. There are excellent examples of hospital energy- and water-saving projects with financial recovery within 10 years.2,4 The Environment Protection Authorities of several Australian states are now mandating that heavy users of energy and water (including larger hospitals) have Environment and Resource Efficiency Plans to reduce their footprints,5 but action from hospitals has been unclear. Progress has typically been made on an ad-hoc basis by hospitals acting in isolation, although the Institute of Hospital Engineering, Australia is facilitating a more systematic approach.4 The Australian Council on Healthcare Standards (ACHS), through its Evaluation and Quality Improvement Program (EQuIP)6 accredits Australian hospitals against mandatory and preferred criteria. However, EQuIP does not currently include mandatory criteria that address issues such as energy, water and waste auditing, energy efficiency and the presence of a hospital environmental committee. The accreditation process offers an opportunity to encourage hospitals to prioritise these issues. The ACHS has awarded hospitals in the past for “environmental excellence”, but without a solid framework from the ACHS, the goal of all of our hospitals pursuing sustainability seems unlikely. In 2009, it is out of step with Australia’s shift to a low-carbon future that there are no requirements that hospitals achieve more sustainable use of energy, water and transport, and improve procurement and waste reduction. The introduction of broad environmental standards as part of the accreditation process could be a vehicle for achieving rapid improvements in sustainability across the hospital sector and shift our health system to one that “does no harm”.

Forbes McGain · Grant A Blashki · Kevin P Moon · Fiona M Armstrong

Mojon’s manual of medicine. A cartoon book for daily clinical life. Mojon D. Berlin: Springer, 2009 (xii + 128 pp, $42.45). ISBN 978 3 540 68559 3. And now for something completely different . . . Daniel Mojon, a Swiss professor of ophthalmology, started his “other” career as a cartoonist while attending (boring) medical school lectures. According to a preliminary page of his unique manual of medicine — which is really a cartoon book for daily clinical life — he was most probably infected with a very rare strain of Streptococcus cartoonaurius during a microbiological laboratory course. The Manual has over 100 black-and-white cartoons divided among 13 chapters, which cover 10 medical specialties as well as congresses, the financial aspects of medicine and research. Some are based on what some might call “sick” jokes, which can be readily appreciated by most of us — particularly those who are not, themselves, the butt. For example, with respect to choice of career: “I became a pathologist because I kept turning up late to emergencies . . .” and “With your superficial character I would become a dermatologist”. Most could be considered more than a little sarcastic and a few, like the one depicted here, are simply delightful. After graduation, Mojon’s cartooning career apparently persisted only because he kept being confronted with uninteresting meetings and conferences. In fact, he has become so well known that colleagues in need of sleep avoid sitting close to him due to the loud laughter of neighbouring attendees — perhaps something to keep in mind if you are thinking of taking this book along with you to a meeting or two.

Ann T Gregory

Incorrect name of author: In the Supplement article “Are common childhood or adolescent infections risk factors for schizophrenia and other psychotic disorders?” in the 16 February 2009 issue of the Journal (Med J Aust 2009; 190 [4 Suppl]: S17-S21), an incorrect author name was printed. The third author’s name was provided as Catherine H Stewart. It should have been Claire H Stewart.

Ian B Hickie · Richard Banati · Claire H Stewart · Andrew R Lloyd

Headache heartache Migraine is associated with poorer workplace productivity and decreased quality of life, and the impact of the condition is greatest in the productive period between 25 and 55 years of age. According to a US review of relevant literature, prophylactic triptan therapy appears to be associated with a significant improvement in worker productivity. The authors of the systematic review suggest that in order to produce relevant and useful findings, further research into the impact of migraine should attempt to identify individuals with undiagnosed migraine and include data on presenteeism (employees coming to work in spite of illness) as well as absenteeism. They also comment that as migraine is an episodic, chronic condition, data should be collected in units of time, preferably with the aid of employee diaries to assist in correct recall. Mayo Clin Proc 2009; 84: 436-445 Gene for CF severity The considerable contribution of lung disease to the morbidity and mortality of cystic fibrosis has been targeted by an international group of researchers, who have aimed to clarify the role of neutrophils in the chronic inflammation and airway destruction that characterise the condition. Cystic fibrosis, caused by mutations in the CFTR gene, shows clinical variations in severity, apparently independent of the CFTR genotype. By performing a genome-wide single nucleotide polymorphism scan, scientists were able to identify a gene, IFRD1, which appears to modify disease severity. The gene encodes a protein that regulates the function of neutrophils. Mice in which the IFRD1 gene was deleted showed delayed clearance of bacteria from the airways, but also less inflammation and disease. The authors comment that the identification of IFRD1 could be a potential lead in future therapy for cystic fibrosis. Nature 2009; 458: 1039-1042 Virtual reality surgery Virtual reality training for surgeons learning to perform laparoscopic procedures im-proves performance and decreases operation time, say Canadian and Danish researchers. In a randomised controlled and blinded trial, registrars in obstetrics and gynaecology were allocated to two groups — laparoscopic salpingectomy training using a virtual reality simulator or a control group following standard clinical education. When performing an actual procedure, the simulator-trained group demonstrated increased proficiency comparable to the experience gained after 20-50 laparoscopic procedures, as opposed to fewer than five procedures in the control group. The virtual reality-trained registrars also showed a significant reduction in operation time. The authors conclude that virtual reality simulator training can improve patient safety and operating theatre efficiency. BMJ 2009; 338: b1802 Keratitis cluster A severe keratitis caused by Acanthamoeba, a common free-living amoeba, is becoming more common worldwide, and a cluster of cases has been recently described in Brisbane, say Australian ophthalmologists.1 In response to an observed increase in patients with Acanthamoeba keratitis, the authors conducted a retrospective, consecutive case-series study. Although the infection appeared to be associated with the use of soft contact lenses and a type of contact lens solution implicated in a previous outbreak in the US, the small number of patients precluded any definite conclusions as to the association. An accompanying review emphasises the importance of early diagnosis of this potentially devastating keratitis, and advises clinicians to have a high level of suspicion when presented with an atypical keratitis.2 1 Clin Exp Ophthal 2009; 37: 181-190 2 Clin Exp Ophthal 2009; 37: 232-238 Oestradiol and heart failure The role of oestrogens in chronic heart failure (CHF) has been clarified by the results of a Polish prospective observational study involving over 500 men with CHF or reduced left ventricular ejection fraction. Working from the established finding that androgen deficiency is common in men with CHF, researchers measured serum concentrations of oestradiol and androgens in all participants and collected data on mortality during the 3-year follow-up. Results showed a U-shaped outcome in relation to oestradiol concentrations: low and high levels of oestradiol were significant predictors of poor prognosis, independent of other prognostic indicators. Differences in clinical characteristics of men with low and high oestradiol were observed. The authors note the question of whether oestradiol is a causative factor or a marker of disease progression. JAMA 2009; 301: 1892-1901

Tanya Grassi