Letters

To the Editor: The Journal is to be commended for this important discussion on quality improvement (QI) by Millar1 and Runciman.2 It is important to understand that if doctors are not engaged in changes to health service provision, including QI, such changes will be ineffective.3 Not surprisingly, unengaged doctors can “prove” the lack of an effect of a QI initiative and return to doing what they have always done. Millar comments on the “division between QI and clinicians”.1 Why this division? Why is there a lack of engagement, and a lack of common purpose, values, and beliefs? Professional responsibilities as defined by the American College of Physicians (ACP) in 2002 include “commitments” to, among others, “improving quality of care”, “improving access to care”, and “a just distribution of finite resources”.4 The 2009 Royal Australasian College of Physicians Professional Qualities Curriculum provides a very similar list of responsibilities for all physicians.5 It may be time for many doctors to step onto the common ground and out of the ivory tower. It is time that doctors become able to view themselves as only one part of a larger system that exists solely to provide health care for patients and the population. Teamwork and collaboration with non-medical health professionals (including managers) may often be undervalued from a “doctor-centric”, and often “hospital-centric”, perspective. It is also high time that health organisations and many managers become serious about involving clinicians, initiating “true” clinical leadership, and engaging and communicating in a meaningful way. Clinical leadership, clinical governance and “teamwork” have unfortunately become almost slogan-like, stale entities that appear in health policy plans and strategy documents without much meaning or consequence. One day, clinical care may be better and have more resources because of better implementation of QI that actually engages clinicians.

Roland J Meyer

To the Editor: I would have thought that, in 2011, any debate pitting fee-for-service against salary models of remuneration was both stale and futile. These debates, such as the one entered into by Peat1 and Travis,2 have been around since Bismarck introduced health insurance for workers in Germany. Surely we have come to realise, after more than a century of varied health insurance schemes and health services around the world, that it is a matter of horses for courses. A single payment system, whatever it is, will be inappropriate if applied universally in any country. There is a place for fee-for-service delivery, accompanied by insurance; there is a place for salaried service; and there is even (heresy for some!) a place for that form of salary called “capitation”. Each system has its merits and its faults, which have been discussed ad nauseam by health economists too numerous to refer to (two publications serve as examples3,4); there is nothing new under the sun. Debates such as this generalise the behaviour of a few miscreants to all salaried or fee-for-service practitioners. This is clearly unfair to both groups. Australia is fortunate that, back in the 1970s, our profession was able to stave off a Canadian-style, single-payer system. Our graduates can choose their method of remuneration — and, however they have been paid, we have distinguished colleagues who have achieved much and, regrettably, a few rogues. In the latter respect, we are no different from any other profession or trade. Why not abandon the ideologies underlying both sides of the debate, face these facts and have both systems in place, where each is appropriate, rather than trying to apply a single solution everywhere? I am reminded of the wisdom of Anthony Ashley Cooper, third Earl of Shaftesbury; “The most ingenious way of becoming foolish is by a System”.5

Peter C Arnold

To the Editor: The recent article by Hebden and colleagues on the frequency and content of fast-food advertising on Australian television concluded that the industry self-regulatory initiatives currently in place are ineffective in reducing children’s exposure to advertising of non-core foods.1 As the managers of these self-regulatory initiatives, we consider this conclusion to be misleading to your readers. The Australian food and beverage industry recognises the level of community concern in relation to food and beverage advertising to children. There are currently two self-regulatory initiatives in place to moderate advertising of non-core foods and beverages to children: the Responsible Children’s Marketing Initiative, that covers products found in retail outlets; and the Australian Quick Service Restaurant Industry Initiative for Responsible Advertising and Marketing to Children, that covers foods sold in quick-service restaurants. These initiatives are designed to restrict advertisements aimed at children by means of the nature of the advertisement and/or the medium by which it is delivered. Hebden et al base their conclusion on a broad definition of “advertising to children” that captures all advertisements screened between 5.30 pm and 10.30 pm on weekdays, and between 7.30 am and 11 am and 4.30 pm and 11 pm on weekends. Specific time periods are not, in fact, covered in the industry initiatives as these periods capture programs that are watched primarily by adults. If children are watching these programs, they are likely to be doing so accompanied by an adult who can provide guidance on appropriate food consumption. However, industry does recognise that times when children are watching television alone and advertisements that are designed particularly to target children are a different matter, and that it must act responsibly in these areas. The success of the initiatives should not be measured by advertising frequencies during certain time periods, as implied by Hebden and colleagues. Nevertheless, the data presented by Hebden et al actually suggest a significant reduction in the frequency of non-core-food advertisements (excluding fast food) in just the first year of operation of the initiatives, which, in terms of what the authors perceive to be “advertising to children”, should be viewed as a positive finding. The Australian Food and Grocery Council is committed to monitoring the self-regulatory initiatives and makes the results available to all stakeholders to help evaluate the effectiveness of what the initiatives set out to achieve.

Peta E Craig · Geoffrey Annison

In reply: Children’s exposure to advertising of unhealthy foods is of concern because children are exposed to a large volume of such advertisements. The World Health Organization has clearly stated that any efforts to address this issue must reduce children’s exposure to unhealthy food advertising.1 Our research article2 was based on such measures. The viewing times applied in our research were specifically those when the highest numbers of children aged 5–12 years watch commercial television, according to Australian audience data for Sydney commercial television stations, and thus are exposed to advertising. Craig and Annison refer to a decrease in the relative proportion of advertisements for unhealthy fast foods over the first year of the industry initiatives. However, readers should be aware that our research showed that the total amount of fast-food advertising increased over this period, so that the frequency of unhealthy fast-food advertisements that children were exposed to remained the same. To make meaningful changes to what advertising children see, time-based restrictions would form a more responsible approach for regulation than the current industry specifications.

Lana Hebden · Lesley King · Anne Grunseit · Bridget Kelly · Kathy Chapman

To the Editor: Outpatient non-attendance remains a major problem that significantly drains the ability of hospitals to provide efficient and effective outpatient services.1,2 Our earlier pilot study demonstrated the effectiveness of short message service (SMS) text message reminders in improving attendance at the outpatient department in Melbourne’s Royal Children’s Hospital (a 250-bed tertiary referral hospital).3,4 We present the results of a follow-up retrospective cohort study that examined the effect of the following eight factors on failure to attend (FTA): sex, native language, distance lived from hospital, day of appointment, time of appointment, wait time (days from scheduling to appointment), socioeconomic status (SES), and SMS reminders. Data included all outpatient appointments (65 535) in the period July 2005 to January 2006. Incomplete data meant that 44 appointments were excluded, leaving 65 491 episodes for the analyses. The patients were classified into three SES groups: low (G1), middle (G2) and high (G3). This classification was based on the Jarman score (a proxy for SES) derived from the patient’s residential postcode.5 Similarly, patients were classified into three groups based on distance between the patient’s residence and the hospital: < 25 km, 25–50 km and > 50 km. Univariate and multiple logistic regression analyses confirmed that all factors other than sex were significantly associated with FTA. We also found that the two populations with and without SMS reminders were significantly different. We conducted a stratified analysis for the two groups and the summary results are presented in the Box. Our analysis shows that FTA rates improve by 5.34% (from 14.85% to 9.51%), and confirms the effectiveness of SMS reminders in lowering FTA. It shows that native language, distance lived from hospital, SES and wait time are significantly associated with FTA across both groups. Although SMS reminders resulted in higher improvement in attendance for non-English speaking patients compared with English speakers (8.33% versus 4.1%), those patients still had higher odds of missing an appointment. Lower SES was associated with an increased likelihood of defaulting. Longer waits until the appointment resulted in lower odds of attending, and odds of attending improved with increased distance from the clinic. Together these results suggest that in addition to SMS reminders, interventions targeted at specific groups may improve attendance rates and cost effectiveness. Stratified analysis of factors contributing to outpatient failure-to-attend rates, by SMS reminder No SMS reminder (n = 20 871) SMS reminder sent (n = 44 620) Factor FTA OR FTA OR Aggregate 14.85% 9.51% Native language English 13.04% 1* 8.94% 1* Non-English 21.35% 1.62† 13.02% 1.30† Distance lived from hospital < 25 km 15.89% 1.36† 10.28% 1.51† 25–50 km 13.77% 1.20†† 8.71% 1.28† > 50 km 11.36% 1* 7.16% 1* Socioeconomic status Low (G1) 17.51% 1.37† 12.28% 1.57† Middle (G2) 14.84% 1.34† 9.26% 1.22† High (G3) 12.11% 1* 8.26% 1* Wait time (from scheduling to actual appointment) < 15 days 8.40% 0.42† 5.94% 0.45† 15–30 days 16.40% 0.90‡ 9.48% 0.74† > 30 days 18.13% 1* 12.40% 1* SMS = short message service. FTA = failure to attend. OR = odds ratio. * Baseline comparison group: OR = 1. † OR significant at P < 0.001. ‡ OR significant at P < 0.05.

Sean R Downer · Kannan Sethuraman · Devanath Tirupati

To the Editor: Kinner and colleagues described the high proportion of deaths among recently released prisoners in Australia.1 I had a patient with a history of intravenous drug use who, after a prolonged stay in hospital for osteomyelitis complicating a diabetic foot ulcer, including extensive inpatient rehabilitation, died due to drug overdose on the first weekend after discharge. This tragic death suggests a mortality risk for people with a history of drug misuse who are released from any long-stay institution, including hospitals. It may be appropriate for medical practitioners to discuss this risk frankly with such patients at discharge.

Emma L Duncan

To the Editor: We wish to report Queensland data regarding vitamin D levels during pregnancy, to contribute to the debate on screening during pregnancy raised in Lau and colleagues’ article1 and Ebeling’s accompanying editorial.2 In 2009, we measured serum 25-hydroxyvitamin D (25[OH]D) levels, using a DiaSorin radioimmunoassay (DiaSorin, Stillwater, Minn, USA), in 75 women who attended general antenatal clinics at the Royal Brisbane and Women’s Hospital (RBWH) and Mater Mothers’ Hospital. Both institutions’ Human Research Ethics Committees approved the study. Participants gave written consent. The RBWH Private Practice Fund covered pathology expenses. Fifty-seven of the 75 women were white; the remainder were Asian (five), Indian Subcontinental (seven), Polynesian (four), Middle Eastern (one) and black African (one). Mean age was 28.6 years (SD, 5.4 years), mean gestational age was 28.7 weeks (SD, 2.7 weeks) and mean body mass index was 26.4 kg/m2 (SD, 5.5 kg/m2). Median serum 25(OH)D level was 92 nmol/L (interquartile range, 74–118 nmol/L). Using cut-offs of < 25 nmol/L for deficiency and < 50 nmol/L for insufficiency, two women were vitamin D deficient (one was Middle Eastern and one was South-East Asian) and five women were vitamin D insufficient (three were white, with lowest serum 25[OH]D level of 40 nmol/L, and two were Indian Subcontinental). The result of a Fisher exact test suggested an association with ethnicity (P = 0.01). A χ2 value of 21.36 (P < 0.001) confirmed that the proportions of deficiency and insufficiency in our study population were significantly different to those of Lau et al’s study population. The majority of serum samples (40) were obtained in winter, followed by spring (21), summer (10) and autumn (three). Six of the seven results of deficiency and insufficiency were from samples obtained in winter; the other was from a sample obtained in September. Excluding autumn, categorical and continuous analyses showed borderline significant variation of 25(OH)D level by season (Mann–Whitney U test [P = 0.08] and Kruskal–Wallis test [P = 0.08], respectively). Several factors may account for the difference in vitamin D deficiency and insufficiency prevalence between our study and that of Lau et al. The most obvious is the “Sunshine State” factor, because several studies in southern states have reported higher prevalence of vitamin D insufficiency than in our study.3-5 In Lau et al’s study, a large proportion of women were at high risk of vitamin D deficiency (only 19% were white) and the women were recruited from a gestational diabetes mellitus clinic. Care should be taken in extrapolating such findings to the wider population. Although our study was not population based, it included a majority white and healthy general obstetric population, rather than sampling at a clinic where women are at high risk of vitamin D insufficiency. We are not asserting that gestational vitamin D levels are unimportant. The increasing incidence of rickets in Australia,2 along with other potential hazards, dictate that increased awareness is mandatory. However, as opposed to routine screening in all pregnancies, our data suggest that local assessment of vitamin D status and demographic risk factors (in gestational diabetes mellitus and general obstetric populations) should be the priority.

Donald S A McLeod · Katherine A Scott · Karin M C Lust · H David McIntyre

To the Editor: We published a case in the Journal in 2009 titled “Spontaneous chylothorax in a 2-year-old child”.1 Subsequently, it has come to our attention that trauma is likely to have been the cause of the chylothorax. At the time of caring for the child, and submission of our article to the Journal, we had no evidence of this. We had specifically asked for a history of trauma and looked for external signs of injury. The chest x-ray and computed tomography (CT) scan had been reviewed with our radiology staff at the time and we did not detect abnormalities of the vertebrae or paravertebral tissue, and no such abnormalities were detected during surgery. However, the child presented with serious injuries 9 months later and died on arrival at hospital. At autopsy, a CT scan showed a paravertebral haematoma and vertebral injury in the lower thoracic vertebrae where the thoracic duct traverses the diaphragm and ascends on the right side (it was a right-sided chylothorax). On further review of the original chest x-ray and CT scan, it was possible to see that some of these findings were evident at the initial presentation with chylothorax. At the time of submission of our article, we speculated that vomiting could have caused injury to the thoracic duct. We now wish to highlight that apparently spontaneous chylothorax may be due to trauma. In children, non-accidental injury must be considered as a possible cause.2

Manuel E Soto-Martinez · Vanessa Clifford · Tom Clarnette · Sarath Ranganathan · R John Massie

To the Editor: A 38-year-old man with genotype 1b chronic hepatitis C infection had been treated with 48 weeks of pegylated interferon (IFN)-α and ribavirin. Autoimmune serology performed just before treatment showed positive perinuclear antineutrophil cytoplasmic antibodies (ANCA) accompanied by an elevated antimyeloperoxidase antibody level (22 U/mL; reference range [RR], < 5 U/mL). Notably, the patient was ANCA-negative 12 months previously. The treatment course was uneventful. One month after the completion of therapy, the patient presented with a subacute onset of fever, haemoptysis, breathlessness and generalised arthralgia. Laboratory investigations demonstrated raised levels of C-reactive protein (128 mg/L; RR, < 5 mg/L) and creatinine (159 μmol/L; RR, 64–104 μmol/L), low albumin concentration (28 g/L; RR, 35–46 g/L), a low haemoglobin level (64 g/L; RR, 135–180 g/L), and microcytic hypochromic anaemia. Autoimmune serology showed persistence of a positive ANCA and an elevated antimyeloperoxidase antibody level (29 U/mL). A high-resolution computed tomography scan of the chest showed features of interstitial lung disease (Figure, A) and a renal biopsy demonstrated pauci-immune necrotising glomerulonephritis (Figure, B). These findings were consistent with a diagnosis of microscopic polyangiitis. Despite treatment with intravenous cyclophosphamide and pulse methylprednisolone, the patient deteriorated and was admitted to the intensive care unit for ventilatory support, haemodialysis and plasmapheresis. This admission lasted 4 weeks and was complicated by line-related sepsis and persistent anaemia requiring multiple blood transfusions. The patient remains clinically well 14 months after discharge, with negative ANCA and negative hepatitis C virus RNA polymerase chain reaction consistent with a sustained viral response. Autoimmune disease is a well recognised complication of IFN-α therapy in chronic hepatitis C infection. The clinical manifestations of IFN-α-related autoimmune disease can be either organ-specific (thyroiditis, psoriasis) or, less commonly, systemic (rheumatoid arthritis, lupus-like disease, sarcoidosis).1 IFN-α-based treatment in chronic hepatitis C infection unmasks silent autoimmune processes, or induces de novo autoimmune diseases or autoantibodies.2 A predisposition to autoimmunity, together with the presence of baseline auto-antibodies, has been demonstrated in most instances of IFN-α-mediated autoimmune diseases,1 as observed in our case. Although rare, the diagnosis of microscopic polyangiitis needs to be considered in patients treated with IFN-α-based therapy for chronic hepatitis C infection presenting with skin rash, fevers, arthritis, an active urine sediment, renal failure or pulmonary haemorrhage. One could consider reducing the duration of therapy in patients who achieve negative RNA polymerase chain reaction at Week 4 of treatment. There is emerging evidence that 24 weeks of response-guided therapy in genotype 1b chronic hepatitis C infection is as effective as the standard-of-care treatment for 48 weeks in rapid responders.3 We also suggest that, in the presence of a positive ANCA at baseline screening, a chest x-ray and urinalysis be performed before initiating IFN-α-based treatment, and that patients be monitored clinically and with urinalysis during treatment. A chest x-ray should also be performed at the completion of treatment. The presence of auto-antibodies alone is not a contraindication to IFN-α therapy, but it does mandate careful monitoring and a high index of suspicion of an immune diathesis. A: High-resolution computed tomography scan of the patient’s chest showing patchy foci of ground glass opacification and nodules bilaterally. B: Renal biopsy showing focal crescentic necrotising glomerulonephritis (haematoxylin-eosin stain; original magnification x 400).

Stephen Y Oh · Brett E Jones · Suran L Fernando

To the Editor: In a recent article that appeared in newspapers such as Melbourne’s The Age and Sydney Morning Herald on 19 Jan 2011,1 one of us (P Z) argued that it is both ineffective and inaccurate to blame those who are overweight and obese for their health problems. It was highlighted that our social, economic, cultural and physical environments are all “obesogenic”,2 acting as barriers to achieving a healthy lifestyle. The article by Proietto in the August 2011 issue of the Journal similarly argued that the obesogenic environment, and its interaction with a person’s genetic make-up, is to blame for the increasing prevalence of overweight and obesity.3 Neglecting to address the role of environmental factors in lifestyle disease may lead to a number of unintended negative consequences. First, healthy eating and being physically active are not easy choices. If attempts are not as successful as first hoped, and if the response from health professionals is simply “try harder”, feelings of guilt and despair can result, which then make it even harder to engage in healthy behaviours. Second, a sole emphasis on individuals’ responsibility for their own health has led governments at all levels in Australia to be passive on this issue. Governments seek to protect us in other ways (eg, legislation to restrict the use and advertising of tobacco), so they now need to be encouraged to take steps towards reducing the obesogenic nature of our environment (eg, introducing policy that ensures affordable and sustainable fruit and vegetable production).4 Finally, focusing on individual health behaviours alone may create or reinforce a social stigma around obesity and related chronic conditions, such as type 2 diabetes.5 When individual behaviour change is the sole focus of prevention and management efforts, the subtext is that the individual is to blame if he or she develops the condition. The astonishing and immediate public response to the aforementioned newspaper article — almost 300 comments were posted online on The Age and Sydney Morning Herald websites alone within hours — reflected an entrenched attitude of blame towards people who are overweight or obese. Given that type 2 diabetes can only be prevented in about 60% of cases,6 these comments reveal and perpetuate a limited understanding of the multiple causes of lifestyle diseases. It remains critical to encourage people to pursue healthy lifestyle choices. However, addressing the obesogenic elements of our environment is just as important. Encouraging patients to become involved in organisations such as The Parents’ Jury, an online network dedicated to improving children’s food and physical activity environments (www.parentsjury.org.au), or to become familiar with community-based initiatives such as Victoria Walks (www.victoriawalks.org.au) may be beneficial. More broadly, it is important for health professionals and their professional bodies to make known to governments their support of policy and other initiatives that make our environ-ment conducive to healthy choices.

Jessica L Browne · Paul Zimmet · Jane Speight

To the Editor: A daunting idea for health care providers is the statistic that, for many medications, only about half of the patients given standard doses will receive the desired therapeutic benefit.1 In the past decade or so, it has been argued that some of this variation in response may be attributed to genetic differences between individuals in mechanisms responsible for the pharmacokinetics and pharmaco-dynamics of many drugs.2 The disparity in health standards among Aboriginal and Torres Strait Islander people compared with non-Indigenous groups is a cause for concern, and requires a concerted political effort to instigate adequate solutions.3,4 Some of the problems include a higher rate of diseases such as hypertension, diabetes, obesity, cardiac disease and depression.3,4 The range of medicines prescribed for these conditions is broad, and some people may not receive the full therapeutic benefit, or may have more severe side effects compared with others. Genetically determined variables contribute to the pharmacokinetics and pharmaco-dynamics of these drugs. Many medications used to treat such diseases are metabolised by the cytochrome P450 (CYP) hepatic enzyme systems, and/or their pharmacokinetics are altered by drug influx and efflux systems. Many of these mechanisms are under genetic control and their efficiency may vary between individuals. Despite this, there are few data on the pharmacogenetics of Indigenous populations generally, and the data on Aboriginal and Torres Strait Islander populations are particularly scant.5 Of the few genetic studies of Indigenous Australians, one found that CYP2C19 and CYP2D6 allele frequencies in a group from remote north-western Australia differed significantly from those for Australians of European ancestry, but were similar to those for East Asian populations.5 An altered CYP2C19 allele could mean alterations in levels of drugs such as phenytoin and clopidogrel, and an altered CYP2D6 allele could mean alterations in levels of drugs such as tricyclic antidepressants, selective serotonin reuptake inhibitors, codeine and tamoxifen. We urgently need to identify clinically relevant issues relating to the capacity of people from these groups to metabolise certain medicines. Screening for genetic variations in drug metabolism and transport mechanisms may highlight significant variations in capacity. This may influence whether people benefit from or are harmed by commonly prescribed medications for hypertension, type 2 diabetes, cardiac disease and depression. The high and increasing prevalence of these diseases among Aboriginal and Torres Strait Islander populations supports a detailed, methodical assessment of the genetics of their drug-metabolising capacity.

Joseph D Tucci

To the Editor: NSW Health’s latest initiative, www.emergencywait. com.au, is a website that presents real-time information about estimated waiting times at 58 emergency departments (EDs) in New South Wales. Similar websites have been used in other Australian states, including South Australia, Western Australia and Victoria, as well as overseas, in Ontario, Canada, and in Memphis, Tennessee. I am concerned that this initiative will be counterproductive and will add further congestion to our already overcrowded EDs. Extended waiting times are a longstanding problem at EDs. They have traditionally been attributed to staff shortages, delays in pathology and imaging tests,1 and inadequate funding. However, there is another major contributor to waiting times that rarely attracts attention in the lay media — the overwhelming number of patients who inappropriately seek medical attention in EDs and would be better served by a general practitioner. Much of the work in EDs involves treating patients with non-acute and non-urgent problems. Recent examples from my personal experience include a man requesting a prescription for antiepileptic medication, a perimenopausal woman with many months of irregular menstrual bleeding, and a young man with a common cold. All of these patients bypassed their GPs, despite their attendances being within normal business hours. A logical outcome of www. emergencywait.com.au is an increase in the number of non-acute, non-urgent presentations to EDs that are seen to be “quiet”. For alongside each hospital’s estimated waiting time, the website presents a list of nearby hospitals with the number of patients waiting at each, thereby enabling patients to compare EDs and attend the least busy one. Formal studies are scant, but crude American data indicate a 6%–10% increase in ED patient volume since waiting times were publicised.2 Although the transparency of www.emergencywait. com.au may help our EDs to share more equitably the burden of inappropriate patient attendances, I expect that it will increase the overall number of such attendances and ultimately increase waiting times. Australian EDs provide excellent, prompt care for patients who have been in accidents or emergencies, but they are neither equipped nor designed to look after individuals who meet neither of these criteria. The solution to overcrowded EDs lies not in websites that publicise waiting times, but in convincing the public that emergency rooms are for emergencies.

Alexander M Owen

To the Editor: Recently, there has been an increase in the popularity and use of baby slings to transport infants. A sling is a soft fabric carrier, worn around a parent or caregiver’s neck, in which the infant is suspended. Slings are often promoted as a secure and easy way to carry an infant, that maintains close contact with the child. An issue has arisen concerning the safety of such devices, in that infants may be placed in a position where there is excessive flexion of the neck (chin-to-chest positioning) or obstruction of the mouth and nose that may cause suffocation. Warnings have recently been issued by the Australian Competition and Consumer Commission.1 Sixteen deaths attributed to the use of slings have occurred in the United States and Canada,2,3 resulting in calls for mandatory standards by the US Consumer Product Safety Commission.2 We report a South Australian case of a 2-day-old boy, born at 38 weeks’ gestation by normal vaginal delivery, who was placed into a cloth sling worn under his mother’s shirt and jumper and was subsequently noted by his mother to be cold and not breathing. At autopsy, there were no significant abnormalities identified, with no injuries visible on x-ray or physical examination. Results of toxicological, metabolic, virological and bacteriological studies were normal. In the absence of definitive pathological findings, the cause of death was undetermined, although the baby sling was considered a risk factor. It is well recognised that infants placed in certain positions, such as in car safety seats, may be at risk of significant oxygen desaturation, and even death, due to upper airway compromise. This applies particularly to preterm and low-birthweight infants.4 It appears that a similar situation occurs with certain slings, albeit rarely, as the soft and rounded sleeping surfaces may promote a potentially dangerous posture that impedes normal respiration. Certain infants may also be quite vulnerable to airway occlusion, with deaths being reported while breastfeeding, for example.5 Given the cases of infant death associated with baby slings in North America, and this Australian case, it is important that parents and carers are made aware of potential safety issues with the use of these devices, particularly in very young infants. Constant monitoring of infants in slings is advised, to ensure that the infant’s head is facing outwards, with no covering of the face.

Roger W Byard · John D Gilbert

To the Editor: Few reports have been published on bone mineral density (BMD) among randomly sampled populations. Organisations such as Osteoporosis Australia and the Australian and New Zealand Bone and Mineral Society rely on research to supply reliable data that are representative of the Australian community. This information informs practitioners, researchers and policymakers of the size of the problem of osteoporosis in Australia. Our study aimed to document the proportion of individuals who have reduced BMD. The Geelong Osteoporosis Study recruited a random population-based sample of individuals from the Barwon Statistical Division, an area surrounding Geelong, Victoria. This region is well suited to epidemiological research as it is geographically well defined and has a large, stable population (259 000) with sufficient socioeconomic diversity for it to be representative of the Australian population.1,2 Age-stratified random samples of 1494 women (median age 54.0 years; range 20–94 years; recruited 1994–1997)3 and 1467 men (median age 56.0 years; range 20–97 years; recruited 2001–2006)4 were drawn from electoral rolls. Participation rates were 67% for men and 77% for women. We measured BMD at the spine and femoral neck by dual energy x-ray absorptiometry (Lunar; GE Healthcare, Madison, Wis, USA). Reference ranges for BMD in men4 and women3 have been published previously. We categorised BMD as normal (T score, > − 1.0), osteopenia (T score, − 2.5 to − 1.0) or osteoporosis (T score, < − 2.5) using the osteoporosis and osteopenia thresholds developed for postmeno-pausal women. Among those with discordant BMD, the site with the lower BMD was used in this classification. Normal BMD was predominant among men aged < 50 years (Box). A consistent proportion of men older than 50 years, including those aged > 80 years, had osteopenia (range, 49%–64%); 19% of those aged > 80 years had osteoporosis. Most women aged < 55 years had BMD in the normal range. Osteopenia was most prevalent among those aged 55–79 years, and osteoporosis dominated (51%) among those aged > 80 years. The osteoporosis and osteopenia thresholds developed for postmenopausal women may not be the most appropriate cut-points for diagnosis in younger women and in men; however, we used them because they are the currently accepted thresholds. Although sex-specific thresholds for defining osteoporosis might best be defined on the basis of absolute fracture risk, until such data are available, T-score criteria continue to be used. After standardising for age and sex to the 2006 Australian population,5 we found that 5.9% of men and 22.8% of women aged 50 years and over, and 12.9% of men and 42.5% of women aged 70 years and over, would be classified as having osteoporosis. Proportion of participants in the Geelong Osteoporosis Study with osteoporosis or osteopenia, by age group, according to bone mineral density at the spine or femoral neck Men* (no. [%]) Women† (no. [%]) Age group (years) Osteoporosis‡ Osteopenia§ Normal¶ Osteoporosis‡ Osteopenia§ Normal¶ 20–24 0 (0) 14 (15.7%) 75 (84.3%) 1 (1.0%) 21 (20.6%) 80 (78.4%) 25–29 0 (0) 24 (26.1%) 68 (73.9%) 0 (0) 24 (22.2%) 84 (77.8%) 30–34 1 (1.1%) 29 (30.9%) 64 (68.1%) 0 (0) 25 (22.5%) 86 (77.5%) 35–39 0 (0) 31 (30.7%) 70 (69.3%) 2 (1.7%) 41 (35.3%) 73 (62.9%) 40–44 4 (3.8%) 36 (34.3%) 65 (61.9%) 1 (0.9%) 32 (29.9%) 74 (69.2%) 45–49 4 (3.9%) 34 (33.3%) 64 (62.7%) 2 (1.8%) 32 (28.1%) 80 (70.2%) 50–54 3 (2.5%) 60 (50.0%) 57 (47.5%) 5 (4.7%) 43 (40.6%) 58 (54.7%) 55–59 2 (1.9%) 61 (58.7%) 41 (39.4%) 9 (8.9%) 57 (56.4%) 35 (34.7%) 60–64 4 (3.9%) 50 (48.5%) 49 (47.6%) 22 (21.0%) 54 (51.4%) 29 (27.6%) 65–69 6 (5.7%) 67 (63.8%) 32 (30.5%) 24 (24.0%) 48 (48.0%) 28 (28.0%) 70–74 9 (7.5%) 72 (60.0%) 39 (32.5%) 43 (32.6%) 70 (53.0%) 19 (14.4%) 75–79 14 (13.1%) 63 (58.9%) 30 (28.0%) 32 (42.7%) 33 (44.0%) 10 (13.3%) 80+ 34 (18.5%) 107 (58.2%) 43 (23.4%) 105 (51.0%) 88 (42.7%) 13 (6.3%) * Recruited 2001–2006. † Recruited 1994–1997. ‡ T score, < − 2.5. § T score, − 2.5 to − 1.0. ¶ T score, > − 1.0.

Margaret J Henry · Julie A Pasco · Geoff C Nicholson · Mark A Kotowicz

To the Editor: Childhood communication disorders (CCD) affect up to 20% of 4-year-old children.1 Early intervention is important2 and a variety of health and education professionals may provide assistance, including speech pathologists (SPs), paediatricians, general practitioners and others. The type and amount of help provided to preschool-aged children in Australia is unknown, nor are the costs empirically described. Using data from the Early Language in Victoria Study (ELVS),1,3 a prospective study of a large Australian cohort of children, we describe the use of services for CCD, out-of-pocket costs to families and costs to the health system. ELVS participants were recruited at 8 months of age, at routine child health checks in maternal and child health centres in Melbourne during 2002. Parents completed questionnaires at baseline (when the child was 8 months of age) and at each birthday.3 In-depth questions about use of services were included for the first time at 5 years. These questions covered SP assessment and treatment, visits to other professionals for CCD concerns, and out-of-pocket expenses for all services, within the preceding 12 months (ie, when children were in their fourth year). Of the original cohort, 983 families (51%) completed the service-use questionnaire. Sixteen per cent had used services (one-third of whom used more than one service); 11% had accessed SP treatment, and 6% had accessed other professionals. The number of service occasions per year for each professional, and the associated costs, are shown in the Box. Children accessing SP treatment received a median of 10.8 therapy hours within 12 months (interquartile range, 4.3–17.3; range, 0.5–104); 28% received ≤ 5 hours and 13% received > 25 hours. Costs of all services accessed in the period, including health system costs and parent out-of-pocket expenses, varied from $34 to $16 546. Our data show that some children received very little intervention for CCD within a 12-month period. Given the critical importance of communication skills to school achievement, this is of concern. We also demonstrate a substantial financial outlay associated with the treatment of CCD in Australia. These data are likely to be generalisable given the nature of this prospective cohort and the reliability of our health care cost estimates. The results highlight the immense variability in service use and the potential burden of cost to government and families associated with CCD. Our data do not describe service use before 4 years of age, nor have we included indirect costs such as travel and parental time away from work. Thus, they represent a starting place for understanding total costs. Costs to the health care system and families for childhood communication disorders services provided to children aged between 4 and 5 years in the Early Language in Victoria Study cohort Cost per family for 1 year using the service Service Median number of visits per year (IQR; range) Health care system cost* per visit ($) Median health care system cost ($) (IQR; range) Median out-of-pocket costs ($) (IQR; range) Median combined costs (health care system + out-of-pocket) ($) (IQR; range) Speech pathologist (treatment) 15.2 (6.5–26; 1–52) 49 742 (318–1273; 49–2545) 498 (173–1040; 0–4117) 1061 (472–2256; 49–6662) Paediatrician 2 (1–3; 1–10) 119 (initial) 59 (subsequent) 178 (119–237; 119–296) 250 (120–320; 0–500) 328 (178–511; 119–776) General practitioner 2 (1–4; 1–10) 34 (standard) 67 (34–151; 34–336) 40 (0–75; 0–294) 101 (34–181; 34–495) Psychologist 3 (1.5–4.5; 1–8) 49 147 (61–233; 49–392) 575 (105–889; 0–1300) 502 (157–1027; 49–1545) Otolaryngologist 2 (1–3; 1–8) 119 (initial) 59 (subsequent) 178 (119–237; 119–534) 210 (120–358; 65–1200) 239 (119–438; 119–1734) Hearing specialist 1 (1–2; 1–4) 49 49 (49–98; 49–196) 0 (0–2; 0–1000) 50 (49–98; 49–1098) Early intervention† 10 (1.5–28; 1–48) 240 2400 (300–8160; 240–11 520) 112 (0–600; 0–720) 2400 (300–8638; 240–12 240) All services na na 661 (238–1273; 34–14 426) 413 (91–1306; 0–4500) 1061 (335–2460; 34–16 546) IQR = interquartile range. na = not available. * Health care system costs were Medicare Benefits Schedule (MBS) fee rates charged at the applicable rebatable level (ie, 100% for GP services and 85% for other services).4 † Early intervention services, which are not covered by the MBS, were estimated from existing cost estimates.5

Jemma Skeat · Lisa Gold · Melissa Wake · Obioha C Ukoumunne · Sheena Reilly

To the Editor: Australian bat lyssavirus (ABL) has the potential to cause fatal encephalitis in humans exposed to infection through bat bites or scratches. There is no cure for rabies currently available, so postexposure prophylaxis with rabies vaccine and rabies immune globulin is recommended following potential human exposure, such as after bites or scratches. People who work with or handle bats should be vaccinated, should regularly monitor their rabies antibody levels to ensure maximum protection, and should seek immediate medical attention for all potential ABL exposures.1 We report the case of a 42-year-old man bitten by a black flying fox (Pteropus alecto) during the retrieval of the bat from a suburban Brisbane, Queensland, backyard. The bat had been found on the ground in the daytime, vocalising and acting aggressively. The patient was a member of a local organisation which cares for injured bats. The Logan and West Moreton Public Health Unit was notified the day after the incident. The patient reported that he had been vaccinated against rabies previously, and that his rabies virus-neutralising antibody titres were adequate. However, the patient’s available titres were below 0.50 IU/mL in 2002 and 0.43 IU/mL in 2008 (no boosters were given), both of which were below the World Health Organization recommended level that confers protection against rabies virus.2 The bat was euthanased for testing (because it had bitten a person, as per Qld Health protocol), and tests on the brain tissue showed it to be reactive for lyssavirus antigen (using an immuno-fluorescence antibody test) and lyssavirus RNA (using a TaqMan assay). In view of the patient’s recent serological tests indicating subprotective antibody levels and definite exposure to an ABL-positive bat, he was given postexposure prophylaxis comprising rabies immune globulin into the wound and five doses of rabies vaccine. He is currently well. The Public Health Unit determined that others were not potentially exposed to the bat. The prompt reporting of all potential ABL exposures to public health units is especially important because bat carers may underreport potential ABL exposures.3 Current guidelines recommend that bat carers with ongoing potential exposure to ABL should check their rabies virus-neutralising antibody titres every 2 years and have a booster if the titre is reported as inadequate (< 0.5 IU/mL). Alternatively, booster doses may be offered every 2 years without determining antibody levels.1 Further education of the bat-handling community and their doctors is necessary to maintain awareness and best practice to protect the people who do this potentially dangerous work.

Heidi J Carroll · Bradley J McCall · David Looke · Bruce Fraser

To the Editor: There is international recognition of the substantial threat that global warming presents to human health and of the challenges that it poses to health service delivery. The World Health Organization has estimated that global warming and climate change-related natural disasters account for over 60 000 deaths globally per year.1 Global warming will also have implications for surgery and surgical practice. The Victorian “Black Saturday” bushfires of February 2009 saw 414 people presenting to hospital emergency departments, stretching hospital resources,2 and 173 deaths were attributed to the bushfires. Nineteen patients were admitted to the Alfred Hospital (Melbourne’s burns service) with burns to more than 30% of their bodies. The care of severe burns victims is complex and highly labour-intensive, often with a patient–nurse ratio of 1 : 1. There would have been even more burns victims if the fire had been less ferocious and had not resulted in such a high loss of life.3 In other words, there were fewer injuries because this intense fire killed people outright; a less intense fire may kill fewer people but leave more injured. The extreme weather that led to the fires is an example of the type of event that may become more frequent as global warming increases. The Garnaut climate change review predicts more frequent extreme wind, rain and intense tropical cyclones, and predicts that category 3–5 storms are likely to increase in intensity by 60% by 2030, and by 140% by 2070.4 Increasing population densities along the northern Queensland coast will also expose more people to the risks of floods, storms and cyclones. These natural disasters often produce wounds which are highly contaminated, and primary wound care services may face increased demand. One of the practical implications of research in the field of surgery and climate change will be the need for modelling of future demands for surgical intervention in Australia. The range of trauma impact due to climate change needs to be defined, and the incidence with which this is likely to occur needs to be determined, based on climate change modelling. With this information, models of future demand for surgical interventions can be determined.

Joseph W Smith · Guy J Maddern

To the Editor: Scott and Guyatt are absolutely correct that as much transparency as possible is required in the process by which any clinical guidelines are formulated.1 I also agree that this must include careful management of conflicts of interest, particularly in the selection of the members of the expert panels required to formulate guidelines and in the functioning of those panels.1 However, transparency does not necessarily require adopting the GRADE (Grading of Recommendations Assessment, Development and Evaluation) system or any other hierarchical system for formulating guidelines, nor does it necessarily require seeking formal feedback from external stakeholders. The GRADE system, like most hierarchical systems, assumes there is at least some evidence in the literature that addresses the relevant clinical problem — thus, it gives its lowest grade to observational studies with a very uncertain estimate of effect. But, often, practitioners most want help with the complex and multifaceted clinical problems on which there are not even formal observational studies. The GRADE system would presumably put these problems in the category of “You’re on your own, chaps, and don’t expect us to help you”. Recommendations on the problems that are most vexing to practitioners will be mainly (and inevitably) based on clinical experience and circumstantial evidence — in other words, expert opinion. Most practitioners looking for guidance will be well aware that such recommendations are likely to be based on expert opinion rather than excellent formal evidence. When deciding whether or not to trust the recommendations, they will be much more concerned that any conflicts of interest for the experts making the recommendations have been recognised and appropriately redressed, rather than that the level of evidence has been rigorously graded. Seeking formal feedback from stakeholders is also a separate issue from transparency. Potential users should be well represented on any writing panel, and their feedback is obviously essential — there is no point in producing guidelines that don’t address the problems that the potential users are facing. However, many stakeholders — for example, the pharmaceutical industry — will have much more serious conflicts of interest than do the members of the expert panel, and these can be impossible to deal with. Of course, feedback should be sought where appropriate, but to make it an absolute requirement under the guise of transparency seems nonsensical. It is clearly essential that users of clinical guidelines must be able to have confidence that they have been developed as rigorously as possible, but an excessively doctrinaire approach to their development will almost certainly lead to a decline in usefulness without a counterbalancing increase in trustworthiness.

Robert F W Moulds

To the Editor: Bismark, Spittal and Studdert observed that complaints clustered around certain doctors.1 They state that, in Victoria, extrapolations from their findings indicate that 1% of the medical workforce in private practice accounts for nearly 20% of complaints, and that male surgeons who have practised for more than 30 years are the doctors who are most complained about.1 Bismark and colleagues established that complaint-prone doctors are more likely to be male, surgeons or psychiatrists, to have trained in Australia and to have been in practice for at least 30 years. They agree with previous studies that suggest that the inherent risks of surgical procedures and the relative visibility of poor surgical outcomes are likely to play a role, and also note that the potential for power imbalances between doctor and patient is high in both surgery and psychiatry. That training outside of Australia was found to have a “protective effect” may seem surprising, but this fits my view about what most often motivates a patient to complain about a doctor when something goes a little astray. My belief, based on a long period of surgical practice and of observing other doctors, largely surgeons, is that a common stimulus to make a complaint when there is a degree of dissatisfaction is a perception that the doctor was overconfident, perhaps to the point of arrogance, and had little personal interest in the patient’s welfare. The lower self-confidence of some overseas-trained surgeons could therefore lessen the likelihood of complaints being made about them, whereas the supreme confidence of some highly experienced Australian-trained surgeons may go against them when something goes wrong. Good manners, kindness, demonstrations of personal interest and concern, and a degree of humility all discourage complaints! In an article subtitled “Arrogance: the biggest sin of all”,2 in the United Kingdom Telegraph, in 2009, Dr James LeFanu appropriately commented, “The virtues of generosity, cheerfulness and discretion should be the hallmark not just of medicine, but of all the liberal professions. How many doctors live up to these ideals is, of course, impossible to quantify, but certainly some readers of this column take a rather jaundiced view”.2

John A Buntine

To the Editor: Recent media reports queried whether Australia could experience a serious outbreak of foodborne disease, such as the massive outbreak in May this year of Shiga toxin-producing Escherichia coli (STEC) serotype O104:H4 in Germany.1 Australia is potentially vulnerable to foodborne disease outbreaks from contaminated fresh produce, and health and food safety authorities need to plan for these events and assess our capacity to respond. Australian health agencies investigate 100–150 outbreaks of foodborne illness each year, although < 10% are associated with fresh produce.2 Australia has a very high-quality food supply, but we are still vulnerable to outbreaks. In 1991, norovirus-contaminated orange juice served by airlines infected 25 000 people, despite the juice being sourced from a single small factory.2 Foodborne outbreaks can become very large and spread internationally before health agencies identify a vehicle of transmission. In 2009–2010, an outbreak of hepatitis A infection in more than 400 people in multiple Australian states, France and the Netherlands was associated with consumption of semidried tomatoes from Turkey.3 The recent outbreak of STEC O104:H4 also occurred in other European countries and was associated with a common source of fenugreek seeds used for growing sprouts.4 Seed sprouts have caused many outbreaks of foodborne illness, including two outbreaks of Salmonella Oranienburg in Western Australia and Victoria in 2005–2006 where alfalfa sprouts were implicated.2 STEC outbreaks overseas have implicated seeds originating from Australia.5 Seeds may become contaminated during plant growth, particularly due to livestock and feral animal grazing, or during storage, neither of which can be effectively controlled by disinfection at sprouting facilities.5 In light of the recent European STEC outbreak, Australian food safety agencies should urgently assess the risks posed to the food supply by sprouted seeds. Australia does have well functioning plans to respond to multijurisdictional outbreaks and national food safety incidents,2 but has not had to respond to a massive outbreak. German investigators reported 3222 outbreak cases of STEC, including 810 cases of haemolytic–uraemic syndrome, in less than 2 months.1 The health system resources required to manage such an outbreak would be immense and costly. In Australia, treatment and other costs for two cases of haemolytic–uraemic syndrome totalled an estimated $14 000 each, despite neither patient requiring dialysis, developing end-stage renal disease or requiring a transplant.6 As with other national plans for responding to epidemics, government agencies need to ensure that possible impacts on the health system and industry are taken into account.

Martyn D Kirk

To the Editor: Echoing Scott and colleagues’ recent call for caution regarding the use of hospital standardised mortality ratios for benchmarking and public reporting,1 we have concerns about the use of infection rates as hospital quality indicators. The National Healthcare Safety Network (NHSN) at the United States Centers for Disease Control and Prevention defines central line-associated bloodstream infection (CLABSI) as occurring where the patient has “a recognized pathogen cultured from 1 or more blood cultures and organism cultured from blood is not related to an infection at another site”.2 This and other criteria (for organisms associated with skin contamination and in children) are also used as quality indicators by VICNISS (the Victorian hospital-acquired infection surveillance system) and the Australian Commission for Safety and Quality in Health Care. The infection prevention unit at Alfred Health in Melbourne recently assessed three cases of hospital-acquired bacteraemia as having met the NHSN/VICNISS definition of CLABSI. This assessment was disputed by Alfred Health’s intensive care unit and we sought further opinions from other infectious diseases physicians and infection control practitioners to adjudicate, in the absence of established criteria to determine whether the bacteraemia was due to infection at a site other than the central line. We received conflicting advice. These three cases would have comprised a third of the CLABSI cases at our hospital in the 6 months to April 2011, and thus significantly impact on our reported quality assurance indicators. Similar common situations may arise in considering cases of bacteraemia in patients who have central lines in the context of chemotherapy-related mucositis; in patients with extensive burns; where cultures are only taken from central lines (rather than from peripheral venepuncture); where there are single blood cultures of enterococci of doubtful clinical significance; and where there are unconfirmed clinical foci of deep infection.3 Previous published work suggests that interrater agreement remains poor, despite changes to the definition of CLABSI.4 Other infection rates are associated with other problems as outlined by Scott and colleagues.1 For example, the current NHSN risk stratification system for infection (http://www.vicniss.org.au/Resources/HCWType1Manual/Type1Manualv6_0708.pdf) related to coronary artery graft surgery is poorly discriminatory, as most patients fall into risk index categories 1 or 2, and statistical calibration of this system is poor.5 Interrater reliability of classification of superficial infections has also been shown to be poor.6 The relatively low rate of infections in patients undergoing coronary artery surgery may result in large stochastic variation, particularly in hospitals performing relatively few such procedures. Public reporting of infection rates is probably inevitable. However, such data should be restricted to indicators that have been shown to validly reflect preventable infections, using definitions that are reliable, and with the appropriate caveats regarding their limitations.

Allen C Cheng · Pauline Bass · Carlos Scheinkestel · Tim Leong

To the Editor: Australia is already a hot country and the frequency of hot spells looks set to increase over coming decades.1 Health care professionals will therefore need to consider the effect that medications can have on people’s capacity to respond to hot conditions. Medications can directly increase body temperature by altering thermoregulatory mechanisms, pharmacological action, idiosyncratic reactions, or hypersensitivity reactions.2-4 Uncommon side effects — including toxic states, anticholinergic poisoning syndrome, serotonin syndrome and neuroleptic malignant syndrome — can also generate heat. Indirect impairment of physiological response to thermal stress may occur by preventing adjustment to hypotension, or by interfering with behavioural responses. Despite these risks, hyperthermia and reduced sweating each rate only one mention in the 2010 Australian medicines handbook (in relation to anticholinergics).5 The handbook does not list heat stress as an adverse reaction to dexamphetamine,5 which can impair thermoregulation by increasing metabolic rate. Medications can affect thermoregulation by:2-5 impairing sweating triggered by the parasympathetic nervous system — eg, anticholinergics, phenothiazines; impairing sweating by carbonic anhydrase inhibition — eg, topiramate, zonisamide; impairing cardiac output or causing hypovolaemia — eg, antihypertensives, alpha-blockers, diuretics; impairing behavioural responses to heat (such as drinking or taking cooling action) — eg, sedatives and hypnotics, anxiolytics, phenothiazines, illicit drugs; or rarer effects, such as increasing metabolic rate — eg, monoamine oxidase inhibitors, thyroxine, amphetamines, cimetidine. Elderly people with impaired thermoregulation, the socially disadvantaged and people with mental illness have been identified as being most at risk from heat stress.6 Although the risk of medications directly impairing physiological responses to heat is low, thermoregulatory effects can be cumulative. People in certain occupations (eg, outdoor labourers and tradespeople, indoor workers in hot industries such as metal manufacturing) may be at increased risk of heat exposure, and there are anecdotal reports of tourists suffering heat stress in climates that are hotter than those to which they are accustomed. There is a need to educate workers, the public and health practitioners about the relationship between certain medications and heat. Professional associations and trade unions have a responsibility to warn and educate their members. It may be helpful for the Therapeutic Drugs Administration to actively solicit reports of adverse events related to medicine use, heat and thermoregulation via the Australian Adverse Drug Reaction Reporting System. Carers of elderly and chronically ill people might flag patients on certain medications for extra care during hot spells. Additionally, health practitioners can ensure that these people are on appropriate heatwave notification and emergency support lists, which are being developed by Australian state and territory health departments and emergency service agencies.

Peter W Tait

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

Joanna R Sutherland

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

Alan E O’Connor

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

Mark R Nelson