Volume 184 Issue 8

Falls and related injuries among seniors are a compelling ongoing priority for Australian health research Falls and fall-induced injuries among older people are a major public health concern worldwide, accounting for over 80% of all injury-related admissions to hospital of people over 65 years.1-3 Falls are also the leading cause of unintentional injury death in these individuals and responsible for appreciable morbidity, including bone fracture, head injury, joint disruption, and soft tissue contusion and laceration resulting in pain, functional impairment, disability, fear of falling, depression, loss of independence and confidence, and admission to residential care.1,4,5 Moreover, this major health problem is likely to increase, as the number and mean age of older people are increasing worldwide and epidemiological studies suggest that, for some types of fall-related injuries, the age-standardised incidence (ie, average individual risk) of injury is also rising.1,6 . . . a hospital setting is not a safe place for elderly people but is actually associated with increased risk of falling. Somewhat paradoxically, a hospital setting is not a safe place for elderly people but is actually associated with increased risk of falling. On admission, the older patient accumulates additional falls risk factors including a new, strange environment with poorly recognised external dangers for falling. This is often combined with confusion, acute illness and balance-affecting medication, in addition to chronic risk factors such as comorbidities, muscle weakness and impaired balance and gait.2,7 A recent systematic review found no consistent evidence for the effectiveness of interventions to prevent falls among older inpatients.8 Since then, two large randomised trials have shed light on this issue. Healey and colleagues,9 using a cluster randomised study design, examined the effect of a simple core-care plan targeting risk factor reduction in elderly care wards of a general hospital. They observed that the relative risk of falls in the intervention wards was 30% lower than in the control wards. Haines and coworkers10 reported that a targeted falls prevention program in a subacute rehabilitation hospital resulted in a 30% reduction in falls after 45 days of observation. Although these studies did not show a significant reduction in fall-related injuries, the results are encouraging and require verification in other hospital settings.5,11 In this issue, Fonda and colleagues12 report the results of a prospective quality improvement project in which they used a hospital-based, multistrategy prevention approach to reduce the risk of falls and fall-induced serious injuries among frail, older patients in hospital aged-care wards. This large study included 1905 inpatients in the year 2001 as a baseline or historical control group and 2056 inpatients in 2003 as the intervention group (mean age of both groups, 82 years). In both time periods, over 60% of the patients were women. The multistrategy intervention, phased in towards the end of 2001, was a hospital staff-led program incorporated into all levels of the organisation. The intervention consisted of various strategies to reduce falls and injuries, including risk screening with the Falls Risk Assessment Scoring System, after-fall assessments, appropriate modifications of patient and environmental risk factors, work practice changes, environmental and equipment changes, and staff and family support and education. Staff compliance with the risk assessment was also studied as part of evaluating the success of implementing the intervention. The total number and incidence (per 1000 occupied bed-days) of falls and fall-induced serious injuries were key outcome variables. The intervention program was associated with a 19% reduction in the risk of falls and a 77% reduction in the risk of falls resulting in serious injury. Staff compliance with completing the falls risk assessment tool increased from 42% to 70%, and 60% of the staff reported that they had changed their work practices to prevent falls. While Fonda and colleagues are to be congratulated on having successfully conducted this important trial, with impressive results, hospitals need to be cautious about applying this type of falls prevention strategy without first weighing up the limitations of the study. Firstly, as the authors point out, the study was not a randomised controlled trial — the “gold standard” of all clinical studies — but a prospective quality improvement project, and so a direct cause and effect relationship between the intervention and reduction in falls and serious injuries cannot be established. Secondly, a critical reader would like to see more detailed analysis of the success in executing the multistrategy falls prevention program. The article does not detail the level of compliance or adherence of the individuals in the intervention group to each recommendation and protective action throughout the 12-month period — information that is crucial to interpret the data. Thirdly, more information about the fallers and the fall and injury data collection system would allow the reader to draw firmer conclusions from the study. The authors note that they recorded many minor events in the follow-up data that were unlikely to have been coded during the baseline year, thus blurring the falls (although not injury) comparison between the baseline year and follow-up year (albeit in favour of underestimating the benefit of the intervention). A limitation of falls prevention research to date has been that fall definition and registration systems have not been standardised. However, the PROFANE (Prevention of Falls Network Europe) Collaboration Group has recently provided soundly based recommendations to address this problem and has suggested strategies for more uniform scientific reporting of falls data and outcomes.13 In various settings, not only in the hospital environment, multifactorial intervention strategies have been shown to prevent falls among elderly adults by 20%–45%,5 but many interesting and important questions remain unanswered.5 Firstly, even in randomised controlled trials, it is not always clear which components of the intervention are effective and which are not. A great deal of time and effort may be put into implementing a complex intervention, when, in truth, using one or two of its components might be equally effective.5,11 Secondly, the cost-effectiveness of interventions is seldom evaluated. Thirdly, little is known about elderly people’s long-term compliance with the recommendations and actions to prevent falls. We may deem the content of an intervention ineffective, when the truth may be that there was insufficient effort to implement the intervention (type III error).5 An additional difficulty with multifactorial falls prevention interventions is that they can be very labour intensive. So, in view of all the above considerations, should we now abandon the results by Fonda and colleagues12 especially since the study was not a randomised trial? Definitely not! Instead, we should pick up all the positive tips from the project, analyse them carefully and try to apply them in the hospital environment. The importance of careful selection of the content of a multifactorial falls prevention program and the target group to which it is applied cannot be overemphasised. The new evidence-based guidelines on preventing falls in older people14 can greatly assist in this implementation. If future clinical experience proves to be as positive as that of Fonda and colleagues, the next step should be a large-scale randomised falls prevention trial, which would probably need cooperation between several centres. The importance of this health problem — falls and related injuries among seniors — makes it a compelling ongoing priority for Australian health research.

Pekka Kannus MD, PhD · Karim M Khan MD, PhD, FACSP · Stephen R Lord PhD, DSc

The differences between community-acquired and health care-associated MRSA explained Staphylococcus aureus is one of the most important bacterial pathogens globally. About a quarter of us carry one or other strain at any one time, and, if we develop an infection, our own colonising strain is likely to be responsible.1 All clinicians, from urban general practitioners to remote-area nurses, encounter S. aureus infections. In hospitals, S. aureus is responsible for most surgical-site infections, and their control poses a major challenge. We have no effective vaccine against S. aureus, so for 50 years we have depended on the safe and affordable β-lactam antibiotics. However, in many large Australian hospitals, patients run the risk of becoming colonised with a hospital strain of S. aureus, many of which are β-lactam resistant — “golden staph” in the vernacular.2 As β-lactam resistance is detected in the laboratory using methicillin or oxacillin, microbiologists call these strains “methicillin-resistant Staphylococcus aureus” (MRSA) (see Box 1 for acronyms). All MRSA harbour the mecA gene that encodes a modified cell wall protein to which no β-lactam antibiotic is able to bind.3 Strains of health care-associated MRSA (HA-MRSA) are usually not only resistant to β-lactam antibiotics, but also carry several other resistance genes or mutations. Typically, Australian HA-MRSA isolates are not only “methicillin-resistant” but also “multiresistant”, leaving only vancomycin and a very short list of alternatives as the last line of defence. Fortunately, when clinicians have to prescribe antibiotics for S. aureus infections, the decision has been relatively straightforward — a β-lactam such as flucloxacillin or cephalexin if the infection is community-acquired (because MRSA has been rare in the community), or vancomycin if the patient has recently been in hospital. However, in the article by Nimmo and colleagues in this edition of the Journal,4 this neat epidemiological distinction is under attack. MRSA appears to be at large in the community, and the types of infections we associate with MRSA are changing. What is going on out there? Has MRSA escaped from the hospitals? Evolution occurs far more rapidly in bacteria than in more complex organisms such as humans. Bacteria are constantly deleting and acquiring genes or mutations and trying out their new configurations in new situations. It does not particularly matter from where the genes come; any DNA will do provided it is useful. S. aureus has prospered because it is carried and spread by humans, but there is a silent competition going on between different strains of S. aureus to see which one can colonise and spread most successfully. How do we know this? Using increasingly sophisticated laboratory methods, it is possible to identify and track different strains (or clones) of S. aureus. The data reported from the Australian Group on Antimicrobial Resistance (AGAR) by Nimmo and colleagues reveal the spread in Australia of new strains of MRSA, which may actually be more virulent than HA-MRSA. These “community-acquired” MRSA (CA-MRSA) carry a distinct variant of mecA that is small enough to efficiently move between bacteria. Epidemiologically, a CA-MRSA infection is one that arises in a patient who has not had contact with the health care system (no admissions to hospital in the previous 12 months, no indwelling catheters, and not a resident of a long-term care facility). The AGAR study shows that CA-MRSA has not broken out of the hospitals, but has instead emerged independently when community strains of S. aureus have acquired mecA from other bacteria.4 And S. aureus is not just in the market for antibiotic resistance genes; any DNA that can give a competitive edge is being progressively collected and amplified. One example is the gene for Panton–Valentine leukocidin (PVL), which probably provides some selective advantage to S. aureus, but in humans contributes to necrotising pneumonia and aggressive soft tissue infection. PVL, first described in 1932,5 is now present in more than 90% of the Queensland and south-west Pacific epidemic clones of CA-MRSA reported by AGAR.4 Paradoxically, these “superbugs” are sensitive to more antibiotics than HA-MRSA. β-Lactams such as flucloxacillin and cephalexin are not active, but clindamycin and trimethoprim–sulfamethoxazole may be useful alternatives. This characteristic resistance profile has also led to yet another acronym: “NORSA”, for non-multiresistant oxacillin-resistant S. aureus.6 Confused? The picture is confusing, and it is not static. AGAR has documented the stepwise increase in the proportion of community isolates of S. aureus that are MRSA in Australia, from 4.7% in 2000 to 7.3% in 2004.4 However, these data are drawn from teaching hospitals and private pathology laboratories and do not reveal the true extent of CA-MRSA carriage in the general community. To really understand what is happening, we require a population-based study to document the prevalence and movement of these new strains in the healthy majority. Who is carrying them? Do antibiotic prescribing practices play a role? Can we “profile” the typical CA-MRSA carrier, so that we can better select which antibiotics to prescribe empirically? What if CA-MRSA gets into a hospital; will it spread and replace HA-MRSA and cause even more serious hospital-acquired infections? What will we call it then? The emergence of MRSA infections in patients without apparent risk factors poses a difficult problem for clinicians who see patients with infections likely to be caused by S. aureus, especially if the infections are severe. For patients with mild to moderate infections, obtaining appropriate cultures for susceptibility testing is important. For those with severe infections possibly caused by S. aureus, intravenous flucloxacillin remains the drug of choice, as it is more effective therapy for methicillin-susceptible S. aureus bacteraemia.7 However, if the patient is critically ill or has risk factors for CA-MRSA infection, the addition of intravenous vancomycin is warranted (see Box 2). Fifty years ago, all S. aureus strains were susceptible to penicillin, but 30 years later 80% of community strains worldwide had become penicillin-resistant, forcing us to respond with penicillinase-stable β-lactams, such as flucloxacillin and cephalexin. Nimmo and colleagues have shown that strains of CA-MRSA originally identified in Queensland, Western Australia and overseas do not respect state and national boundaries, and we are likely to see increasing rates of CA-MRSA in coming years. Some of this change results from the overuse of antibiotics, and some is the inevitable result of rapid bacterial evolution to which we will have to adapt. Meanwhile, be alert, not alarmed, but some modification of the standard approach to S. aureus infections is indicated (Box 2). 1 The ABC of MRSA MRSA = methicillin-resistant Staphylococcus aureus CA-MRSA = community-acquired MRSA HA-MRSA = health care-associated MRSA NORSA = non-multiresistant oxacillin-resistant S. aureus (also an MRSA) PVL = Panton–Valentine leukocidin, a virulence factor present in some S. aureus strains 2 Suggested interim guidelines for suspected Staphylococcus aureus infections in community patients Obtain cultures for bacterial identification and drug susceptibility testing whenever possible. Discuss with the microbiology laboratory the patterns of resistance in the local area. Incision and drainage should be considered in all cases, and may be the only treatment required. For mild infections that require antibiotics but not admission to hospital: Prescribe a β-lactam antibiotic initially (eg, flucloxacillin or cephalexin) unless allergy or documented previous CA-MRSA in the patient or the patient’s family. Review the patient. Check the culture result. If CA-MRSA is identified, follow the sensitivity pattern; clindamycin or trimethoprim–sulfamethoxazole are likely to be effective. For severe suspected community-acquired S. aureus infection: Obtain cultures, commence intravenous flucloxacillin empirically. Consider combining flucloxacillin with intravenous vancomycin if the patient is critically ill. Continue flucloxacillin and cease vancomycin if methicillin-resistant S. aureus is excluded, as flucloxacillin is more effective than vancomycin for methicillin-susceptible S. aureus infections.

Paul D R Johnson MB BS, PhD, FRACP(Infectious Diseases) · Benjamin P Howden MB BS, FRACP(Infectious Diseases), FRCPA(Microbiology) · Catherine M Bennett MAppEpid, PhD

A recent review shows how much more we need to find out about this important problem Perioperative ischaemic cardiac events include myocardial infarction, cardiac arrest and cardiac death, and are estimated to occur in 2%–5% of patients over 40 years of age.1 Mortality rates associated with perioperative myocardial infarction and cardiac arrest may be as high as 25% and 65%, respectively.2,3 In the Australian context, precise data on the numbers of patients at risk are not available, but with more than 440 000 general anaesthetics performed annually, this is likely to be an issue facing many physicians. A recent narrative review of the problem is therefore of timely importance.1,4 What is the risk of perioperative myocardial infarction? As the review points out, perioperative myocardial infarction may be difficult to diagnose, and often unrecognised. Three studies were identified totalling 1309 patients, with myocardial infarction diagnosed by creatine kinase MB elevations with new Q waves, with or without autopsy or positive pyrophosphate scan evidence. Myocardial infarction was identified in 30 patients (2.3%); notably, more than half of these did not have symptoms or signs. Creatine kinase MB assays may result in false negative and positive results, and troponin assays — the biomarker currently used in the European Society of Cardiology and American Heart Association guidelines for diagnosis of myocardial infarction — are now preferred. However, in the perioperative setting, troponin elevation may also arise from non-cardiac causes such as pulmonary embolism and renal failure, and limitations exist in the specificity of individual assays.5 Further, the pathophysiology of perioperative ischaemic events may differ from the non-perioperative acute coronary syndromes, and these differences may affect risk prediction and treatment. Non-perioperative acute coronary ischaemia results from rupture of an often mild, non-obstructive atherosclerotic plaque and superimposed coronary thrombosis.6,7 Although such plaque rupture and thrombosis is also thought to occur perioperatively, there are other important influences. The perioperative state is associated with activation and release of multiple inflammatory mediators and cytokines, sympathetic nervous system activation and catecholamine release, hypercoagulability, and hypoxia. These contribute to both plaque rupture and thrombosis. Additionally, the perioperative stress state may contribute to increased myocardial oxygen demand, in the setting of reduced oxygen supply from blood loss, hypoxia, and other factors. This adverse environment may be present up to 3 days into the postoperative period.8 How can we assess this risk? Given this propensity for perioperative ischaemic events, individual preoperative risk assessment has been keenly pursued by surgeons and anaesthetists, often resulting in referral to a cardiologist. Two methods are commonly used: clinical assessment, and noninvasive testing. A number of clinical assessment tools have been advised, a commonly used one being the Lee index.9 This defines a number of features of patient history, physical examination, baseline investigations, and proposed surgical procedure. Based on the presence of one to five of these clinical characteristics, patients’ risk can be stratified from 0.4% to 5.4% likelihood of a major perioperative event.9 Noninvasive exercise or pharmacological stress testing, usually with echocardiographic or nuclear imaging, is generally reserved for those at higher risk. In Australia, dobutamine stress echocardiography is a commonly used technique, achieving sensitivity and specificity of 85% and 70%, respectively, for a positive test predicting perioperative events in a meta-analysis,10 with similar results for nuclear imaging techniques.10 However, the relatively modest sensitivity and specificity of these tests mean a number of high-risk patients will be missed, and many with high risk will not have an event. The advice to patients about their risk must also be tempered by whether the planned surgery is elective or should go ahead regardless of the risk. How can we manage this risk? Coronary angiography is often advised for patients assessed to be at higher risk, but there is uncertainty in how to respond to the finding of significant coronary artery disease. Revascularisation — either percutaneous or surgical — has been suggested for patients with high grade coronary stenosis, particularly for widespread disease.11 However, supportive data are scarce; several retrospective studies suggest benefit, but a large recent randomised trial in selected stable patients undergoing vascular surgery showed no improvement in outcomes, and possibly an increased risk of events.11,12 At a practical level, if revascularisation is performed, observational data support delaying non-cardiac operations for at least a month following revascularisation surgery.13 Following coronary stenting, a window of 6 weeks after bare metal stenting is suggested, to allow endothelialisation of the stent struts and reducing stent thrombosis,14 but also reducing the possibility of in-stent restenosis, occurring maximally at 3–6 months.15 There are as yet no comparative data following drug-eluting stents, although these appear less attractive, given that stent-strut endothelialisation takes longer, and combined antiplatelet therapy with aspirin and clopidogrel is likely to be needed for longer, further increasing perioperative bleeding risk if these agents are continued, and increasing the risk of acute stent thrombosis if they are stopped early to allow surgery.16 Perioperative coronary events: risk management strategies for those at increased risk Consider not performing surgery if elective Smoking cessation: can be advised for all patients β-Blockade: some evidence, but disputed Aspirin, nitrates, statins: little evidence Revascularisation: little evidence of benefit, some evidence of harm; a particular problem with drug-eluting stents Similar uncertainty surrounds pharmacological methods of perioperative risk reduction. β-Blockers, by reducing myocardial oxygen demand and blocking sympathetic and catecholamine responses, would seem a logical option. Their use is widely promoted, and included in the joint American College of Cardiology and American Heart Association guidelines for perioperative management.17 However, these recommendations are based largely on two randomised controlled trials: one, a small unblinded study,18 the second, a larger study, which showed no survival benefit for β-blockade assessed on an intention to treat basis.19,20 Further trials are currently underway.20 Use of aspirin or statins also seems appropriate, given their previous efficacy in prevention of non-perioperative events,21 but aspirin may increase the perioperative bleeding risk,22 and statins have not yet shown robust benefit, although this is likely an area for future investigation. How then, should the physician put together what is at times confusing information? Firstly, perioperative ischaemia is relatively common and often unrecognised. Clinical assessment and non-invasive imaging are useful, but far from perfect, in risk stratification. Stopping smoking before surgery is a useful intervention to reduce risk.23 Revascularisation, while often used for patients with angiographically important disease, has little evidence to support it, delays subsequent surgery, and has a number of associated problems. Lastly, while statins, aspirin and β-blockers may appear intuitive and are commonly used, there is likewise little evidence to support these approaches. The review by Devereaux et al1,4 is a timely reminder of how little is known about such an important problem, a call to obtain better data, and a suggestion to discuss the rationale for surgery and its possible attendant risks carefully with patients.

Harry C Lowe FRACP, PhD · Saul B Freedman FRACP, PhD

Objective: To determine whether the rate of falls and associated serious injuries in a hospital aged care setting can be reduced using a multistrategy prevention approach.Design, setting and participants: Three-year quality improvement project comparing data at baseline (2001) and at 2-year follow-up (2003) after interventions to reduce falls. All patients admitted to the Aged Care Services wards at Caulfield General Medical Centre, Melbourne, between January 2001 and December 2003 were included.Interventions: Multistrategy approach phased in over 3 months from September 2001 and involving data gathering, risk screening with appropriate interventions, work practice changes, environmental and equipment changes, and staff education.Main outcome measures: Total number of falls; number of falls resulting in serious injuries (fractures, head injuries, death); staff compliance with the risk assessment.Results: Over a 2-year period, there was a 19% reduction in the number of falls per 1000 occupied bed-days (OBDs) (12.5 v 10.1; P = 0.001) and a 77% reduction in the number of falls resulting in serious injuries per 1000 OBDs (0.73 v 0.17; P < 0.001). Staff compliance with completing the falls risk assessment tool increased from 42% to 70%, and 60% of staff indicated they had changed their work practices to prevent falls.Conclusion: A multistrategy falls prevention program in an aged care hospital setting produced a significant reduction in the number of falls and a marked reduction in serious fall-related injuries. Incorporating a falls prevention program into all levels of an organisation, as part of daily care, is crucial to the success and sustainability of falls prevention.

David Fonda MD, FRACP, FAFRM · Jennifer Cook BSc, BPhysiother(Hons) · Vivienne Sandler BScPhysiother, GradDipBusiness(HlthSci) · Michael Bailey BSc(Hons), MSc(Stats), PhD

Objective: To describe antimicrobial resistance and molecular epidemiology of methicillin-resistant Staphylococcus aureus (MRSA) isolated in community settings in Australia.Design and setting: Survey of S. aureus isolates collected prospectively Australia-wide between July 2004 and February 2005; results were compared with those of similar surveys conducted in 2000 and 2002.Main outcome measures: Up to 100 consecutive, unique clinical isolates of S. aureus from outpatient settings were collected at each of 22 teaching hospital and five private laboratories from cities in all Australian states and territories. They were characterised by antimicrobial susceptibilities (by agar dilution methods), coagulase gene typing, pulsed-field gel electrophoresis, multilocus sequence typing, SCCmec typing and polymerase chain reaction tests for Panton–Valentine leukocidin (PVL) gene.Results: 2652 S. aureus isolates were collected, of which 395 (14.9%) were MRSA. The number of community-associated MRSA (CA-MRSA) isolates rose from 4.7% (118/2498) of S. aureus isolates in 2000 to 7.3% (194/2652) in 2004 (P = 0.001). Of the three major CA-MRSA strains, WA-1 constituted 45/257 (18%) of MRSA in 2000 and 64/395 (16%) in 2004 (P = 0.89), while the Queensland (QLD) strain increased from 13/257 (5%) to 58/395 (15%) (P = 0.0004), and the south-west Pacific (SWP) strain decreased from 33/257 (13%) to 26/395 (7%) (P = 0.01). PVL genes were detected in 90/195 (46%) of CA-MRSA strains, including 5/64 (8%) of WA-1, 56/58 (97%) of QLD, and 25/26 (96%) of SWP strains. Among health care-associated MRSA strains, all AUS-2 and AUS-3 isolates were multidrug-resistant, and UK EMRSA-15 isolates were resistant to ciprofloxacin and erythromycin (50%) or to ciprofloxacin alone (44%). Almost all (98%) of CA-MRSA strains were non-multiresistant.Conclusions: Community-onset MRSA continues to spread throughout Australia. The hypervirulence determinant PVL is often found in two of the most common CA-MRSA strains. The rapid changes in prevalence emphasise the importance of ongoing surveillance.

Graeme R Nimmo FRCPA, FASM, MPH, MSc · Geoffrey W Coombs BAppSc(Med Sc), PGDipBiomedSC · Julie C Pearson BSc(Biol) · Francis G O'Brien BAppSc, PhD · Keryn J Christiansen FRCPA · John D Turnidge FRACP, FRCPA · Iain B Gosbell MD, FRACP, FRCPA · Peter Collignon FRACP, FRCPA, FASM · Mary-Louise McLaws DPHTM, MPH, PhD

Objective: To assess obstetricians’ antenatal screening practice for blood-borne viruses (HIV, hepatitis B and C viruses [HBV and HCV]) and knowledge about management during labour and risk of transmission via breastfeeding for infected women after an educational intervention.Design: Cohort study, with surveys before and after an educational intervention.Setting and participants: Survey 1 was mailed in 2002–2003 to all 767 Fellows registered with the Royal Australian and New Zealand College of Obstetricians and Gynaecologists (RANZCOG), and Survey 2 was mailed in 2004 to the 743 of these Fellows who were still practising.Intervention: Multifaceted intervention with mail-out of survey results and a summary of recommended management, publication of two review articles in the RANZCOG journal, and an oral presentation at the RANZCOG annual scientific meeting.Main outcome measures: Self-reported frequency of antenatal screening for blood-borne viruses, change in practice based on a woman’s infection status, and advice given about risk of virus transmission via breastfeeding in Survey 2, compared with Survey 1.Results: Survey 2 (response rate, 68%) found increases from the previous survey in the proportion of respondents reporting they always offered antenatal screening for HIV, from 51% to 59%, and for HCV, from 60% to 69% (P = 0.001 for both). For women with HIV infection, the proportion of respondents always recommending elective caesarean section increased from 37% to 49% (P = 0.001) and always avoiding rupture of membranes increased from 33% to 49% (P < 0.001). The proportion who reported advising (incorrectly) that breastfeeding is associated with increased risk of transmission to the infant decreased from 34% to 25% for HBV (P = 0.01) and from 47% to 39% for HCV (P = 0.03).Conclusion: The frequency of antenatal testing for HIV and HCV is increasing in Australia. Knowledge about interventions to reduce mother-to-child transmission of HIV and knowledge of the risk of HBV and HCV transmission via breastfeeding improved after a relatively simple educational intervention.

Michelle L Giles FRACP · Suzanne M Garland FRCPA, FACSHP, MD, FRANZCOG · Sonia R Grover FRANZCOG · Sharon M Lewin FRACP, PhD · Margaret E Hellard FRACP, PhD

Objective: To describe how high-cost users of inpatient care in Western Australia differ from other users in age, health problems and resource use.Design and data sources: Secondary analysis of hospital data and linked mortality data from the WA Data Linkage System for 2002, with cost data from the National Hospital Cost Data Collection (2001–02 financial year).Outcome measures: Comparison of high-cost users and other users of inpatient care in terms of age, health profile (major diagnostic category) and resource use (annualised costs, separations and bed days).Results: Older high-cost users (≥ 65 years) were not more expensive to treat than younger high-cost users (at the patient level), but were costlier as a group overall because of their disproportionate representation (n = 8466; 55.9%). Chronic stable and unstable conditions were a key feature of high-cost users, and included end stage renal disease, angina, depression and secondary malignant neoplasms. High-cost users accounted for 38% of both inpatient costs and inpatient days, and 26% of inpatient separations.Conclusion: Ageing of the population is associated with an increase in the proportion of high-cost users of inpatient care. High costs appear to be needs-driven. Constraining high-cost inpatient use requires more focus on preventing the onset and progression of chronic disease, and reducing surgical complications and injuries in vulnerable groups.

Janine Calver PhD · Kate J Brameld PhD · David B Preen PhD · Stoney J Alexia BA(Hons) · Duncan P Boldy MSc, PhD · Kieran A McCaul MPH

The aetiology and management approach for cough in children differs greatly to that in adults, so the empirical approach commonly used in adults is unsuitable for children. Clinical evaluation of cough in children should include an assessment of environmental factors, particularly tobacco smoke, parental concerns and expectations. Most children with acute cough are likely to have an uncomplicated viral acute respiratory tract infection, but the possibility of a more serious problem, especially aspiration of foreign material, should always be considered. Isolated chronic cough in children is rarely asthma, and the term “cough variant asthma” should not be used. Over-the-counter and prescription medications are ineffective for the symptomatic relief of acute cough. Treatment for chronic cough should be based on aetiology. Because of the favourable natural history of cough, a “positive” response in medication trials should not be assumed to be due to the medication. Children should be reassessed within the expected timeframe of response to therapy.

Anne B Chang MPHTM, PhD, FRACP · Lou I Landau MD, FRACGP · Peter P Van Asperen MD, FRACP · Nicholas J Glasgow MD, FRAGP · Colin F Robertson MD, FRACP · Julie M Marchant MB BS · Craig M Mellis MD, MPH, FRACP

Staphylococcus aureus bloodstream (SAB) infections are common and serious causes of morbidity and mortality that incur considerable health care costs and are potentially preventable. It should be relatively easy for hospitals to collect data on the incidence of SAB episodes, to determine whether infections were acquired in hospital or in the community, and to establish whether they were health care associated. The proportion of SAB infections caused by methicillin-resistant S. aureus strains should be a useful indicator of the level of control of antibiotic resistance in the community and in the health care setting. Continuous monitoring of infection incidence would enable health care facilities to determine the effectiveness of interventions designed to minimise SAB infections.

Peter J Collignon FRACP, FRCPA, FASM · Irene J Wilkinson BSc(Hons), MPH, MASM · Gwendolyn L Gilbert MD, FRACP, FRCPA · M Lindsay Grayson MD, FRACP, FAFPHM · R Michael Whitby FRACP, FRCPA

Haematopoietic stem cell transplantation is an accepted curative therapy for many cancers and inherited non-malignant diseases, including bone marrow failure syndromes, haemoglobinopathies, and inborn errors of metabolism. Stem cells can be used from the bone marrow or blood of matched siblings or appropriately matched unrelated volunteers, but many patients do not have a suitably matched donor. Umbilical cord blood (UCB) has been successfully used as an alternative stem cell source. It has the advantage of tolerance for a degree of human leukocyte antigen (HLA) incompatibility not possible with adult bone marrow, resulting in greater likelihood of finding an appropriate match. UCB is also stored fully tested and cryopreserved, leading to rapid availability. Greatest clinical experience in UCB transplants has been in treating paediatric leukaemia. Results using well matched UCB grafts are equivalent or better than with unrelated bone marrow transplant. Cell dose and the degree of HLA matching are critical determinants in the success of UCB transplant. The use of UCB in older children and adult patients has been limited by the fixed, low cell dose available in a UCB unit, relative to recipient weight. This can be overcome by strategies such as using two or more UCB units. Early animal studies suggest that UCB may have the potential to differentiate into other cell types, including nervous tissue, and may in future play a role in the treatment of disorders such as Alzheimer disease and Parkinson disease.

Tracey A O’Brien FRACP, MB ChB, MHL, BSc · Karin Tiedemann OAM, MB BS, FRACP · Marcus R Vowels AM, MB BS, MD, FRACP

Setting You bump into a junior medical officer you know. She looks tired and harassed. She has been working long hours and spent much of the previous evening sorting out a sick patient without getting help from anyone. She felt she had made some mistakes. You wonder whether the JMO in your unit has ever been in the same situation. Work in medicine has many stressors.1,2 Failing to cope well with these stressors can lead to emotional exhaustion and burnout.1,2 Junior medical officers (JMOs) who can’t cope with stress make significantly more errors.3 This leads to increased costs as a result of JMO absenteeism and litigation by patients against hospitals because of suboptimal care.4,5 As outlined in “Tips 11”, the causes of poor performance may lie with the person, the system, or the supervisor.6 Supervision is often perceived to be inadequate by JMOs and lack of supervisors one of their greatest stressors.7 The concept of supervision is more global than clinicians providing episodes of help with patient care, teaching at ward rounds or performing at outpatient clinics or in operating rooms.8 It means planning to ensure that JMOs provide high-quality patient care all the time, that the term in a clinical service provides a good professional experience for them, and that potential problems are anticipated and prevented.8-10 What are the qualities of a good supervisor of JMOs?2,8-10A good supervisor: Ensures that he or she and the JMO are clear about their respective roles and responsibilities for the term, particularly with regard to patient care (see below). Informs the JMO how supervision will occur — that time will be set aside to observe the JMO’s performance. Provides feedback in a positive way. Unless weaknesses are tackled in a clear, unambiguous way, JMOs won’t get the message. Makes time to get to know the JMO as a person, as someone who has a life outside medicine as well. It can be interesting and impressive to learn what JMOs can do, along with letting them learn something of your own life. Recognises that there are power factors (eg, age, gender, sexuality, race) that may influence the relationship. If this causes a problem that can’t be satisfactorily resolved, a different supervisor should be found for the JMO. What makes a happy junior medical officer?2,4,5,7,8 Being supported, especially out of hours Being given responsibility for patient care Good teamwork Receiving feedback Having a supportive learning environment Being stimulated to learn Having a supervisor take a personal interest in him or her Another way of considering the qualities of a good supervisor is to examine the factors that are associated with a happy JMO (Box). Supervising patient care8-11When it comes to supervising patient care, you should: Be available. Check that the JMO knows how to contact you at all times. Be approachable to discuss problems. Don’t give JMOs a hard time — be empathetic, respectful, supportive, focused and practical. Be aware of the type of environment in which the JMO is working. Supervision is harder when JMOs work in circumstances in which they are isolated in patient care (eg, an outpatient or community setting) compared with the ward setting, where there may be a range of people who can offer advice. You may need to take more time to ensure care is appropriate. Directly observe the JMO carrying out patient care. For example, allow the JMO to lead the interaction with patients on rounds, set aside one clinic every 3 months in which you sit in with the JMO, or watch the JMO perform procedures. Those who are more often observed and observe their seniors gain skills more rapidly. Think where mistakes often occur in your unit and watch out for these (eg, check medication charts for prescribing errors, which are common). Handle any errors made with a no-blame approach, exploring all contributing factors and discussing how to prevent a similar problem next time. Turn the experience into a good learning opportunity. Recognise that errors often occur out of hours. Ensure that your unit has out-of-hours cover and that communication is good (not “Ring me when there is a problem” but “Feel free to ring me at any time”). Ask your JMO, “Have you ever felt out of your depth and unable to get help?” Impact of good supervision Take-home message Good supervision improves patient outcomes, reduces the stress on junior medical officers (JMOs) and increases JMO learning. A good supervisor clarifies what is expected of both parties and ensures good communication on training and personal issues. When supervising patient care, clinicians should ensure that JMOs feel supported and have someone to contact at all times. They should directly observe work and be on the lookout to prevent common JMO errors. A mentor is ideally not the supervisor or a person involved in assessment, but someone chosen by the JMO to mentor over a long period. Evidence shows that following these principles of good supervision has a positive impact on patient outcomes8,12 and JMO learning.2 When there is more supervision, patient satisfaction is higher, there are less patient-reported problems with care, and lower death rates occur in areas such as surgery and anaesthesia. The effect is greater when the trainee is less experienced and the cases more complex.8 Good supervision reduces JMO stress and increases learning.2 JMOs don’t mind working long hours as long as they receive good support.8 MentoringMany of us have had mentors at various stages of our lives. Mentoring overlaps with supervision, but has some specific differences.13 A mentor is someone who can confidentially discuss difficult issues and guide and encourage trainees in their career — usually over a long period, not just the 3–6 months of a standard clinical rotation. Ideally, the mentor should be chosen by the JMO and not be involved directly in supervision or assessment, allowing the mentor to stand aside and provide support.

Fiona R Lake MB BS, FRACP, MD · Gerard Ryan MB BS, FRACP

Government-subsidised access to effective medicines in Australia is provided via the Pharmaceutical Benefits Scheme (PBS). Decisions to subsidise medicines are based on assessment of cost-effectiveness (“value for money”) by the Pharmaceutical Benefits Advisory Committee (PBAC).1 In effect, the PBS is “purchasing” health outcomes. As the majority of medicine use is publicly funded via the PBS, there is an obligation to monitor the outcomes to determine whether the expected health improvements are actually realised. Monitoring the outcomes of medicine use is a core component of the National Strategy for Quality Use of Medicines,2 a pillar of Australia’s National Medicines Policy. Review of the cost-effectiveness of subsidised medicines is also an initiative of the federal government.3 The Drug Utilisation Sub-Committee advises the PBAC on patterns and changes of drug use associated with subsidy restrictions. However, there is minimal evaluation of health outcomes. This article discusses the problem of accessibility to data needed to examine the outcomes and use of high-cost medicines in Australia. Targeting access to high-cost medicinesThe PBS has complex controls to ensure cost-effective use of high-cost medicines by targeting access to subsets of patients. PBS restrictions are based on evidence and a collaborative effort between the PBAC, the respective pharmaceutical companies and representative medical specialists.4 Patients must meet criteria for both starting therapy (severe disease inadequately controlled by existing cheaper treatments) and continuing therapy (substantial clinical improvement). Prescribers must provide documentation to support patients’ eligibility. The eligibility of individual patients for initiating or continuing treatment is assessed by Medicare Australia (previously the Health Insurance Commission), which administers the PBS and other health programs. PBS restrictions thus enforce monitoring and documentation of patients’ clinical outcomes from using specialised drugs such as imatinib for treating chronic myeloid leukaemia, and infliximab and etanercept for treating ankylosing spondylitis. Accessibility to data on the use of biological disease-modifying antirheumatic drugs (bDMARDs: etanercept, infliximab, adalimumab, and anakinra) for treating rheumatoid arthritis provides an illustrative example to raise important issues. Information on the clinical status of each patient that is required as part of an application for bDMARDs (Box 1) could be helpful in evaluating the long-term efficacy and safety of the medicines as well as determining the effectiveness, utility and appropriateness of targeted access schemes. The following are examples of questions that could be answered by researchers with access to such information: What are the health outcomes of patients who have commenced, continued, switched between, or withdrawn from biological treatments? What are the associations between use of biological agents and rheumatoid factor status, disease duration, and conventional antirheumatic drugs usage, and are they predictive of patient response? How many rheumatoid-factor-negative patients have been approved to commence biological treatment since the removal of rheumatoid-factor-positive status as an eligibility criterion? How does the cost of these medicines compare with the cost savings in other health programs? Data available on medicine use and health outcomesMedicare Australia maintains electronic databases of claims from pharmacies for subsidised medicines. The databases also store details of “authority prescription” requests and reimbursements (Box 2, A). These data are potentially accessible at both aggregated and de-identified individual level, including the related prescription claims (medicine usage profile). Requests for access to the data for legitimate research can be made, but the process is slow and difficult. Monthly aggregated prescription volume and expenditure statistics on each PBS item are available in the public domain through Medicare Australia’s website (Box 2, B). While these aggregated data provide some indication of the uptake of bDMARDs,5 the actual number of patients using a bDMARD can only be approximated (eg, a crude approximation was that more than 2000 patients had been commenced on bDMARDs by March 2005).6 However, the proportion of patients that was approved to continue these medicines cannot be determined. It is also not possible to examine the effects of the “interchangeability rule”, which allows eligible patients to switch between different bDMARDs — an important initiative under the PBS. We recognise that the primary responsibility of Medicare Australia is to deliver government health programs. On the other hand, its role as a major information source to assist effective health decision making is becoming increasingly apparent.7 The limited usefulness of currently accessible administrative data has been discussed previously.8 Our further concern, in the case of high-cost medicines, is that invaluable health information on each individual patient submitted to Medicare Australia (Box 1) is not captured in its electronic databases and is, therefore, inaccessible for research purposes. Unfortunately, the information on individual clinical status is regarded as merely supportive of a patient’s eligibility for access to high-cost medicines. The existing Medicare Australia databases only capture the “standard” information from an authority prescription (Box 2, A). The value of the clinical information is recognised by Medicare Australia, to the extent that some of this information is recorded manually in an Excel spreadsheet. However, these data do not comply with Medicare Australia’s own validated procedures and are not released because the reliability, accuracy and quality of the data are not controlled. This information, which is also required by Medicare Australia’s Program Review Division for auditing prescribers, is apparently just as difficult for the Division to obtain. Data on the use of high-cost medicines managed under the Highly Specialised Drugs Program (eg, infliximab, imatinib) are accessible on request through the Pharmaceutical Access and Quality Branch of the Australian Department of Health and Ageing — but, again, data on health outcomes are unavailable. A recent review of the extent to which information from the PBS and Medicare claims databases can be linked9 is a welcome step towards better monitoring of the use of medicines and informing health policies, as well as identifying possible risks and health outcomes resulting from their use. Comprehensive and comparable datasets on drug usage, clinical details and health outcomes are held by the Department of Veterans’ Affairs. The ability to link de-identified datasets is an encouraging example of what can be achieved. These datasets could be used to examine the outcomes of taking specific medicines. However, the uptake of bDMARDs in this special population is low, thereby limiting the usefulness of the data for this drug group. The Department of Health and Ageing, which holds de-identified data from PBS and Medicare claims and performs policy and program review, could provide useful feedback to prescribers and patients to enhance patient management. In an attempt to complement the minimal information available through Medicare Australia, rheumatologists have established a voluntary database (the Australian Rheumatology Association Database) to track patient outcomes. However, only about 35% of patients treated with bDMARDs are registered, which may partly reflect the additional administrative burden on practitioners of reporting this information. Some patients do not participate because of the regular questionnaires required and privacy concerns. This emphasises the need for public discussion to address concerns about privacy and to highlight the value of health outcomes research. The way forward: a need for better access to comprehensive dataEvaluation of drug use and health outcomes can provide important evidence of the effectiveness of medicines in the “real world”, where many factors affect the outcome other than the medicines themselves. Analyses of international health outcome data from large observational databases are useful. However, patients treated with high-cost medicines in Australia are likely to have more severe disease than patients treated with these medicines in other countries, as a result of our generally more restrictive criteria. Therefore, it is important to be able to separately analyse the health outcomes of the Australian patient population. External, independent examination of the PBS system of access to high-cost medicines from the perspective of system improvement, clinical outcomes or cost-effectiveness is currently impossible. Allowing sufficient access to information that is already collected on drug use and health outcomes should be the basis for improving the quality of the system. We consider that a review and enhancement of Medicare Australia databases, with liberalisation of access to administrative data for approved research, is essential if we are to increase the accountability, transparency, and efficiency of allocating public resources for pharmaceuticals. It would also enhance community confidence in the PBAC’s decisions. Better access to accurate, comprehensive and reliable measures of the value of pharmaceutical expenditure and health gains obtained are urgently needed in the interests of better health for all Australians. 1 Information required by Medicare Australia For initiating bDMARD therapy Patient’s Medicare number, name, and dates of previous biological treatment History of trialled disease-modifying antirheumatic drugs (name, dosage, duration, reasons for treatment withdrawal) Levels of inflammatory markers: erythrocyte sedimentation rate, C-reactive protein “Active joint” counts (any joints that are swollen and tender are indicated on a diagram) For continuing bDMARD therapy Patient’s Medicare number, name, and dates of previous biological treatment Baseline and current levels of inflammatory markers: erythrocyte sedimentation rate, C-reactive protein Reduction of “active joint” count (any joints still swollen and tender are indicated on a diagram) bDMARD = biological disease-modifying antirheumatic drug. 2 Administrative data currently available from Medicare Australia A. Records related to “authority prescription” requests and claims De-identified-patient identifier PBS code, generic/brand name and strength of item Date authority lodged with Medicare Australia Prescriber unique identifier Dosage and quantity Number of repeats Authority reason (eg, “authority only drug”/increased quantity/increased repeats) Authority assessment outcome (approved/rejected/pending) Officer initials State or territory Approval number Date of approval Whether original prescription has been supplied Pharmacy identifier Date of claim Claim identifier Whether the claim is for an original or repeat prescription Cost reimbursed Payment category (general, concession, entitlement) B. Statistical reports* Prescription counts by item Cost reimbursed by PBS/RPBS Monthly aggregated data (for each state and territory) Aggregated data by patient category (general, concession, entitlement) PBS = Pharmaceutical Benefits Scheme. RPBS = Repatriation Pharmaceutical Benefits Scheme. * Available at the Medicare Australia website (http://www.medicareaustralia.gov.au/providers/health_statistics/statistical_reporting.htm).

Christine Y Lu MSc · Kenneth M Williams PhD · Richard O Day MD, FRACP

A 41-year-old man was referred for open biopsy of a 3 cm left lung lesion. The lesion had been discovered incidentally on chest x-ray (Box, A) and investigated with a computed tomography scan of the chest (Box, B) and a fine needle aspiration biopsy under radiological guidance that was inconclusive. The patient had a history of smoking and had also sustained a ruptured left diaphragm and a pulped spleen (with subsequent splenectomy) in a motor vehicle accident 13 years previously. A left thoracotomy was performed and the mass removed. During surgery, the mass was noted to be closely applied to the left phrenic nerve and apparently deriving blood supply from the phrenic pedicle. A smaller mass was discovered posteriorly, adjacent to the descending aorta. Histological examination of the mass revealed encapsulated lymphoid tissue, with lymphoid foci surrounding central hyalinised vessels. The lymphoid foci were separated by a broad region of erythrocyte-filled sinuses. The appearances were of splenic tissue and there was no evidence of malignancy (Box, C). Thoracic splenosis is a rare condition in which ectopic splenic tissue exists in the thoracic cavity, more commonly on the left side.1 It occurs in some patients who have experienced thoraco-abdominal trauma with resulting splenic and diaphragmatic injury. Fragments of splenic tissue implant themselves within the thorax and derive a blood supply.2 Often this occurs at multiple sites within the thorax and abdomen. These ectopic spleens remove aged and abnormal red blood cells from the circulation. So, despite having had a splenectomy, a patient with this condition may have normal red cell morphology on blood smears. Nuclear medicine studies with either 99mTc sulphur colloid, 111I-labelled platelets or 99mTc heat-damaged erythrocytes demonstrate an increased uptake of the radioactive isotope in ectopic splenic tissue. The 99mTc heat-damaged erythrocyte study is more specific because of reduced uptake of 99mTc in otherwise normal liver tissue.3 When a localised area of uptake corresponding to the mass is detected — supporting the diagnosis of thoracic splenosis — no further treatment is required.1-3 Imaging and histopathological findings A: Chest x-ray showing the incidental finding of a left hilar mass (arrow). B: Computed tomography scan showing a well encapsulated mass (arrow) adjacent to the mediastinum. C: Histological section of the left hilar mass demonstrating lymphoid foci (arrows) surrounded by splenic red pulp.

Tinte Itinteang MB BS · James R McGiven MB ChB, FRACS · Catherine B Koleda MB BS · Graham D McCrystal MB ChB

To the Editor: During a national multicentre study of snake bites — the Australian Snakebite Project (ASP), involving over 40 hospitals — we have recently noted a high rate of early allergic reactions following the administration of tiger snake antivenom in Australia. People with suspected or definite snake envenoming are recruited to ASP, and laboratory and clinical data and serial blood samples are collected to measure venom and antivenom concentrations. From 1 November 2005 to 31 January 2006, 14 patients who had been given tiger snake antivenom (CSL Limited, Parkville, VIC) were recruited. These patients are briefly described in the Box, and include bites from several different groups of snakes. Of the 14 patients, 11 exhibited immediate systemic hypersensitivity reactions to antivenom infusion. Reactions were mild in five patients, moderate in three, and severe in three, according to the grading system by Brown.1 The six patients in the moderate and severe groups fulfilled the criteria for anaphylaxis according to a recent consensus definition.2 All patients required specific treatment in addition to ceasing antivenom therapy, and nine were treated with adrenalin. Antivenom was recommenced in all patients at a slower rate, although an adrenalin infusion was required in four of these and repeat doses of intramuscular or subcutaneous adrenalin in another four while the antivenom infusion continued. Over the same period, there were seven administrations of brown snake antivenom (over 30 vials of antivenom) reported to ASP without any hypersensitivity reactions. There has been a previous report of allergic reactions to tiger snake antivenom in a single hospital,3 and we are concerned that there may be a particular problem with tiger snake antivenom. The reaction rate in this series is similar to reported rates in parts of the world where high reaction rates have been attributed to relatively impure antivenom preparations.4,5 The reactions here were traced to at least four different batches of tiger snake antivenom. We have informed CSL of this high rate of reactions and the antivenom batch numbers, and we have encouraged the treating doctors to make formal reports of each adverse reaction to CSL and the Adverse Drug Reactions Advisory Committee. Health care professionals treating patients with tiger snake antivenom need to be aware of the possible higher risk of anaphylaxis with tiger snake antivenom and be prepared to treat with adrenalin. Recommendations for the diagnosis and treatment of anaphylaxis have recently been reviewed.6 However, this current problem with CSL tiger snake antivenom should not cause health professionals to reduce or cease its use. In all patients described here, control of the adverse reaction and continuation of antivenom was possible. The rapid identification of this problem over a short period was only possible because of our large multicentre collaborative study, and supports such studies for recognising uncommon envenoming syndromes. Fourteen patients administered tiger snake antivenom for snake envenoming Age/sex Previous antivenom Snake Clinical features Grading Treatment of reaction 47 M No; SH BHS No reaction Nil Nil 13 M No TSG No reaction Nil Nil 17 M No TSG Nil Nil Nil 20 M No TSG Generalised erythema, urticaria, tachycardia Mild IM adrenalin (0.5 mg), then IV adrenalin infusion 12 M No RBBS Generalised erythema Mild IM adrenalin (0.2 mg × 3) 12 M No RBBS Generalised erythema, urticaria Mild IM adrenalin (0.25 mg 3 2) 28 F No TSG Pruritus, erythema and moist cough (no wheeze) Mild Promethazine (10 mg) 53 M No TSG Generalised pruritus Mild Promethazine (25 mg) 32 M No TSG Dizziness, chest tightness, tachycardia, vomiting Mod. SC adrenalin (0.3 mg) 21 M Yes; SH SBS Generalised rash and pruritus, vomiting Mod. IV adrenalin infusion for 1 hour 9 M No SBS Urticarial rash, chest tightness Mod. IV adrenalin infusion 55 M No; SH PHS Generalised pruritus, diaphoresis, confusion, hypotension Severe SC adrenalin (0.5 + 0.5 + 1 mg), IV fluid, IV hydrocortisone (100 mg) M No RBBS Rash, wheeze and hypotension Severe Adrenalin, IV fluid, antihistamines, steroids 45 F No TSG Hypotension, sweaty and unwell appearance Severe IV adrenalin infusion BHS = Broad-headed snake (Hoplocephalus bungaroides); IM = intramuscular; IV = intravenous; Mod. = moderate; PHS = Pale-headed snake (H. bitorquatus); RBBS = Red-bellied black snake (Pseudechis porphyriacus); SBS = Stephens’ banded snake (H. stephensii); SC = subcutaneous; SH = snake handler; TSG = Tiger snake group (any snake from the Notechis, Hoplocephalus, Tropidechis, and Austrelaps genera).

Geoffrey K Isbister · Alan Tankel · Julian White · Mark Little · Simon G Brown · David J Spain · Chris F Gavaghan · Bart J Currie

Comment: Thank you for the opportunity to comment on the letter by Isbister et al regarding hypersensitivity reactions to tiger snake antivenom. CSL has been notified about the cases of hypersensitivity reactions to tiger snake antivenom in general, but has only received two individual case reports. We have been in contact with the study investigators and have requested more detailed information on the other patients so that we can further our investigations. A thorough check of product manufacturing records revealed no deviations from approved specifications for tiger snake antivenom. It is important to note Isbister et al have advised health professionals not to reduce or cease the use of tiger snake antivenom. We would like to draw physicians’ attention to the approved Product Information before use of the product. The tiger snake (and other antivenom) Product Information lists the possibility of both anaphylactic and anaphylactoid reactions. Hypersensitivity and skin reactions (including urticaria, rash, hypotension, bronchospasm, anaphylaxis and delayed serum sickness) are listed as common, and are more likely to occur in people who have had previous exposure to equine-based products. In addition, the Product Information describes an anaphylactoid reaction which can occur because the antivenom has the ability to bind complement. The risk of this reaction can be minimised by adequate dilution of the antivenom (1 : 10 for adults and 1 : 5 in small children) before infusion. Further, the Product Information states that a syringe already loaded with 1 : 1000 adrenalin must be available during antivenom therapy. CSL is continuing to monitor this situation closely and is awaiting further details on the patients from the reporting physicians. In the meantime, we encourage users of all antivenom products to report any untoward reaction to CSL so that these can be fully evaluated.

Jane Leong

To the Editor: Community strains of methicillin-resistant Staphylococcus aureus (MRSA) are increasingly seen in Australia, particularly in certain population subgroups, such as Pacific Islander1 and Aboriginal2 people. We report the case of an African with community MRSA to highlight its existence in yet another subgroup. Given the increase in people arriving in Australia from Africa under the Humanitarian Program (with around 8500 arrivals from Africa in 2004–2005)3 and their wide dispersal around the country, it is possible that African community MRSA will be seen increasingly in Australia. A 53-year-old Burundi refugee presented with an infected wound overlying the left lateral malleolus after laceration 6 weeks previously in a Tanzanian refugee camp. An unknown antibiotic was given for 2 weeks before travel to Australia. On the patient’s arrival in this country, the wound appeared purulent, erythrocyte sedimentation rate was 82 mm/h (reference range [RR] < 10 mm/h), and C-reactive protein level was 9 IU/L (RR < 5 IU/L). Plain x-rays and bone scans suggested osteomyelitis. A wound swab grew S. aureus, Streptococcus pyogenes and Pseudomonas species. The patient was initially given intravenous cefazolin, and then definitive therapy (for MRSA and S. pyogenes, ignoring the colonising pseudomonad) with oral clindamycin (450 mg three times daily). Clinical resolution was complete, and levels of acute-phase reactants returned to normal. The antibiotic sensitivity pattern of the S. aureus isolate raised suspicion that it might be an unusual strain: it was resistant to methicillin, tetracycline and trimethoprim–sulfamethoxazole, but sensitive to erythromycin, clindamycin, ciprofloxacin, gentamicin, vancomycin, linezolid, mupirocin, rifampicin, fusidic acid and chloramphenicol. The mecA gene was detected by polymerase chain reaction testing, confirming methicillin resistance. The organism possessed staphylococcal cassette chromosome mec (SCCmec) element type IV. The Panton–Valentine leukocidin gene, staphylococcal enterotoxins A to E and toxic shock syndrome toxin-1 were not detected. As DNA fingerprinting with standard pulsed-field gel electrophoresis showed a novel banding pattern, the “gold standard” of multilocus sequence typing was used for identification. This confirmed an ST140 allelic profile, which has not been seen previously in Australia.4 On the balance of probabilities, the isolate represents an African community MRSA strain, not previously detected in Australia. Non-multiresistant community MRSA is not widely recognised in African countries. Hospital MRSA rates vary widely in Africa (eg, between 21% and 30% of all S. aureus isolates in Nigeria, Kenya and Cameroon, and fewer than 10% in Tunisia and Algeria5), but most are multiresistant. Medical practitioners in Australia who treat African refugees need to be aware that pyogenic soft tissue infections could be caused by community MRSA, and these MRSA strains may have a different antibiotic sensitivity profile to Australian community MRSA strains. It is essential to take appropriate specimens for microbiological analysis (wound swabs and possibly blood cultures and/or tissue samples), as antibiotic susceptibility profiles are increasingly unpredictable.

Annabelle Donaldson MB ChB · Iain B Gosbell MD, FRACP, FRCPA

To the Editor: We recently treated two patients with invasive meningococcal disease presenting with cellulitis. This presentation contributed to a delay in diagnosis and appropriate antibiotic treatment. The first patient was a 33-year-old woman, recently diagnosed with nephrotic syndrome, who had been unwell for a week with mild upper respiratory tract symptoms. During this time, her nephrologist began treating her with prednisolone (15 mg daily). The day before presentation, she developed abdominal pain, vomiting, chills, myalgia and headache. A rash developed on the day she presented to hospital. The temperature was 39.2°C, heart rate 148 beats per min, and blood pressure 146/57 mmHg. She had an area, measuring 20 cm × 20 cm, of tender cellulitic rash on the right thigh (Box) and mild neck stiffness. The diagnosis was initially unclear, leading to a delay of several hours before ceftriaxone was administered, and a lumbar puncture performed. Cerebrospinal fluid (CSF) examination revealed a leukocyte count of 4500 × 106/L (98% polymorphs) (reference range [RR], < 5 × 106/L), gram-negative diplococci, and protein concentration of 2073 mg/L (RR, 150–450 mg/L). The patient subsequently required intensive care admission for non-invasive ventilation and inotropic support. Neisseria meningitidis serotype C was detected in the CSF by polymerase chain reaction testing. The patient was discharged well except for mild headache and lethargy after 6 days. At 1-week review, she remained lethargic but was otherwise well. The rash was slowly resolving. The second patient was a 51-year-old woman with fever and a 2-day history of progressive pain, swelling and erythema of the anterolateral area of the neck. The temperature was 38.5°C, heart rate 115 beats per min, and blood pressure 134/86 mmHg. There was no evidence of upper airway involvement. The anterior area of the neck and upper chest wall were swollen, erythematous, tender and warm. No fluid collections or masses were detected on ultrasound examination. The patient was admitted to hospital with a diagnosis of cellulitis, and treatment was begun with intravenous flucloxacillin and metronidazole. After 17 hours, culture of blood taken on admission showed N. meningitidis serotype W135. Antibiotic treament was changed to ceftriaxone. After 5 days, the patient had mild residual inflammation and tenderness of the neck. She completed another week of treatment with oral amoxycillin. Only 14 cases of N. meningitidis cellulitis have been published.1-3 Seven cases involved children with periorbital cellulitis. In adults, three cases involved the face and neck, and four the limbs. N. meningitidis was isolated from blood (eight patients), conjunctival swabs (three), aspirates of the cellulitic areas (two) or CSF (one). There was one death: an elderly woman with bacteraemia and cellulitis of the face and neck.2 As illustrated by our cases, the many guises of meningococcal disease continue to challenge clinicians. Cellulitis in Patient 1 Cellulitic area on the right thigh of a 33-year-old woman with Neisseria meningitidis meningitis.

Karina J Kennedy MB BS · Jhumur Roy MB BS, FRCPA · Paul Lamberth MB BS, FACEM

To the Editor: The CanMEDS 2000 report1 and its 2005 revision2 have emphasised that effectiveness as a medical specialist requires competencies in addition to clinical and medical expertise. These include being a communicator, collaborator, manager, health advocate, scholar and professional. Building the non-clinical skills of doctors has been the focus of a professional development project in Australia that is targeting registrars. Junior doctors usually step up to the role of registrar in the 3rd year of their prevocational training. A national workshop convened by the Postgraduate Medical Council of Victoria in March 2004 agreed on a framework for the professional development of registrars, comprising the following 10 competencies: leadership; communication skills; supervision; mentoring; teamwork; self-awareness and empathy; time management; problem solving; professionalism and ethics; and safety and quality.3 To provide content for these competencies, a job-shadowing exercise involving two registrars at two different Victorian hospitals was undertaken in April 2005 to get a first-hand understanding of the roles of medical registrars as managers. The registrars were voluntary participants, and permission was obtained from all participants. I shadowed the two registrars during their entire 9-hour shifts. No major issues arose in relation to the shadowing process itself, and the consultants overseeing the two registrars were extremely accommodating in this process. The two observed registrars authenticated the veracity of the recorded observations. The observations from the job-shadowing exercise were clustered into competencies using the framework developed for the professional development of registrars discussed above. The Box summarises these observations and highlights the range of registrar interactions that are influenced by non-clinical competencies. While the small number of registrars is an obvious limitation of the study, this job-shadowing exercise did demonstrate that managerial skills, knowledge and behaviour represent a significant component of the work of clinicians, especially as they move up the medical hierarchy. This assertion should not be misconstrued as suggesting that the clinical skills and knowledge become any less important. As noted in the 2005 CanMEDS framework, the medical expert role is the central role for doctors. It is also worth noting here that some pilot professional development programs conducted recently as part of the registrar project show that registrars welcome training that enhances their non-clinical skills, especially when provided professionally in an environment conducive to learning. Observations during job-shadowing of two registrars at two Victorian hospitals Competency Observed interactions Supervision Reviewing patient treatment plans and test results and prescribing a course of action Ensuring that procedures are followed Coaching intern on test procedures, completion of patient records, etc Giving ongoing feedback to intern Delegating tasks to intern Coordinating patient treatment with other units Leadership Dealing with other health professionals, some of whom take directions from the registrar, as well others over whom there is no formal authority Providing advice to intern and role modelling desired behaviour Demonstrating the ability to respond quickly and with confidence Involving subordinates and providing opportunities for them to participate in decision making Using networking skills with other departments Using negotiating skills in dealing with other departments, hospitals, etc Communication skills Using communication skills with patients, intern, medical colleagues, other health care professionals, and service departments Dealing with cross-cultural diversity issues with patients, their families, and staff Using negotiating skills in dealing with other departments, hospitals, patients, and family members Using recording skills to ensure treatment plans properly documented for others Time management Prioritising patient list for ward rounds The constant need to re-assess priorities during ward rounds, in light of time constraints The ability to deal with constant interruptions from other colleagues, to provide necessary clarifications Problem solving Making decisions on patients’ continued treatment or discharge, and stipulating any follow-up action Task contingency management skills to deal with patient treatment plans not proceeding as planned Dealing with information gaps in patient historical records Involving intern and other staff to assist in the decision-making process and raising issues with consultant Professionalism and ethics Dealing with demarcation issues with other doctors and professionals Role modelling professional behaviour to patients, staff, and the public Balancing the interests of patients with hospital needs, without sacrificing patient trust Obtaining patient consent for procedures Teamwork Coordinating treatment plans with other doctors and health professionals Sharing information and agreeing on treatment plans with allied health staff Joint meeting with other colleagues to advise a patient and family members on surgical procedures and associated risks Ability to work in both collaborative and individual modes during the day Mentoring Providing advice to intern to be more assertive and confident when dealing with consultant Self-awareness and empathy Patience and empathy in giving bad news to family Dealing with patients who are aged or mentally or physically challenged Safety and quality Knowledge and application of safe practices in relation to patient management Ensuring that procedures are followed, such as obtaining consent, ordering of tests, etc Reviewing records before dispensing treatment Recording treatment plans and medications

Jagdishwar Singh PhD

To the Editor: We were pleased to read Turnbull and Parisi’s short piece on the effectiveness of shade structures, highlighting the challenges of ensuring adequate and effective shade protection, particularly in children’s settings.1 Cancer councils in various states have long recognised these challenges and provided assistance to those who design or manage facilities for children, in the form of training workshops, resources and guidelines. Epidemiological evidence indicates that childhood exposure to ultraviolet (UV) radiation is a strong determinant of risk of melanoma but there is also evidence of its contribution to the development of non-melanocytic skin cancer.2,3 It is estimated that living in Australia for the first 15 years of life contributes about two-thirds of the lifetime risk of melanoma of a lifelong resident.4 Sun exposure in childhood, especially that leading to sunburn, is the main environmental determinant of the number of melanocytic naevi. An individual’s number of naevi is the strongest measurable predictor (after age and ethnicity) of risk of melanoma.5 Our publication, Under Cover, referred to by Turnbull and Parisi, is one such resource, developed as a comprehensive reference tool for anyone involved in shade planning and design in New South Wales and has been adapted for use in other states by state cancer councils.6 Turnbull and Parisi comment that Under Cover provides inappropriate advice regarding the use of deciduous trees, as solar UV radiation levels can be hazardous during winter in subtropical Queensland. As might be expected, the NSW edition of Under Cover does not address winter solar protection issues in northern Queensland. We note that the “requirements for effective shade” cited by Turnbull and Parisi are identical to those prescribed in Under Cover. For those interested in determining when UV protection is required throughout the year in different locations, an interactive shade planning software program will be available shortly at <www.webshade.com.au>. In it, ShadeCalendar recommends what type of shade would be most appropriate for comfort and solar protection in different months of the year. The Bureau of Meteorology now issues the SunSmart UV Alert when the UV Index is forecast to reach 3 or above, highlighting when sun protection is required (www.bom.gov.au/products/uvindex_national.shtml). The SunSmart UV Alert is reported in most newspaper, television and radio weather forecasts across Australia. Shade is only one of a range of sun protection strategies recommended by the Cancer Council. With Australia having the highest skin cancer rates in the world, general practitioners play a pivotal role in providing sun protection counselling advice to parents of children aged 1–13 years.7 The Cancer Council NSW recommends a range of sun protection measures including UV avoidance during the peak UV times (10:00–14:00 or 11:00–15:00 during daylight saving time), shade, clothing, hats, sunglasses and use of sun protection factor 30+ broad spectrum, water resistant sunscreen.

Kay R Coppa MPH · John S Greenwood

To the Editor: Investigators in the recent Canberra Heart Study1 highlighted the importance of improving the detection of heart failure in the community, given the high proportion of people with preclinical disease. The accompanying editorial2 expressed concern about the lack of major Australian initiatives that focus on the prevention and treatment of this disease. We fully endorse the authors’ view that under-recognition and under-treatment of heart failure is an important national issue. While we support their call for sustained and adequately funded programs, we feel it is important to note that there are initiatives under way to attempt to improve the situation. The National Prescribing Service, the National Heart Foundation of Australia and the National Institute of Clinical Studies joined forces in 2004 to improve the diagnosis and management of heart failure in primary care. A national program, undertaken in partnership with 45 divisions of general practice, began in October 2004 and will conclude in early 2006. Nationally, the program provided newsletter materials to all general practitioners, pharmacists and physicians.4 In participating divisions, educational outreach visits and interactive small group meetings involved over 1600 GPs and local specialists in discussions of the role of echocardiography in diagnosis, and pharmacological and lifestyle management issues. Patient education materials were also widely disseminated.5 Outcomes of this large-scale quality improvement program are currently being evaluated, and results are expected to be available in early 2007. Other groups have also recognised heart failure as an important issue — for example, it is one of the featured conditions in the Department of Veterans’ Affairs Medicines Advice and Therapeutics Education Services program.6

Heather H Buchan MBChB, MSc, FAFPHM · Susan M Phillips DPhil · Lynn M Weekes BPharm, MSc, PhD · Judith M Mackson BPharm, MMedSci(ClinEpi) · Andrew N Boyden MB BS(Hons), MPH, FRACGP · Andrew M Tonkin MB BS, MD, FRACP

Anti-Atkins advice US experts have advised that low-carbohydrate diets, such as the Atkins diet, should not be recommended for weight loss as they fall short of being indisputably safe.1 Steffen and Nettleton said that low-carbohydrate diets are associated with ketosis, constipation or diarrhoea, halitosis, headache and general fatigue; further, the Atkins diet is not nutritionally balanced. They were commenting on a case report of life-threatening ketoacidosis in an obese woman.2 In this patient, an underlying ketosis — due to strictly following the low-carbohydrate, high-protein Atkins diet for a month — was thought to have been exacerbated by a mild illness which compromised her oral intake. 1. Lancet 2006; 367: 880-8812. Lancet 2006; 367: 958 Northwick Park reactions Recently in the UK, eight healthy volunteers were the first human beings to receive a new humanised monoclonal antibody — TGN1412, a superagonist of a T cell receptor, designed to mitigate autoimmune disease and immunodeficiency. The six men who received the active component rapidly developed catastrophic multisystem failure. The tragedy has sparked a renewed call for an open culture in medical research, as prior disclosure of the trial protocol may have flagged potential problems — for example, the ethical issue of giving an agonist drug targeted at compromised immune systems to individuals with intact immune systems.1 It has also retaught us the lesson of thalidomide — relative lack of severe toxicity in animal models should never be construed as a guarantee of safety in people. Meanwhile, researchers in the relevant discipline expressed concern a tragedy of another kind might occur — that is, that the very potency of monoclonal antibody therapies, possibly demonstrated so forcefully by recent events, might hinder or even prevent the rapid future development of these agents.2 1. BMJ 2006; 332: 677-6782. Lancet Online, 24 March 2006 Perineal protection Australian authors Beckmann and Garrett say doctors should advise their pregnant patients of a simple, inexpensive practice which may help prevent tears to the perineum and reduce the need for episiotomies during vaginal delivery — manual perineal massage. They conducted a systematic review of trials of this practice, now in The Cochrane Library and reported in JAMA. In three trials involving 2434 women, there was a 15% reduction in the number of episiotomies among women who had practised perineal massage, which involved gently stretching the perineum, during the last 4 or 5 weeks of pregnancy. The benefit was greatest in women experiencing their first vaginal delivery. JAMA 2006; 295: 1361-1362 Another “gift of life” The first child born to a solid-organ transplant recipient is now 48 years old; since that first birth in 1958, about 14 000 births among women with transplanted organs, including the liver, heart, lung and pancreas-kidney, have been reported worldwide.1 Debate has shifted somewhat from whether such women should have a baby to when they should fall pregnant.2 Nevertheless, a review article says that we still lack sufficient data and knowledge about risks and outcomes, particularly in the long term, for both mothers and their offspring.1 1. N Engl J Med 2006; 354:1281-12932. N Engl J Med 2006; 354: 1313-1316 The mother-child nexus Vigorous treatment of depression in mothers may benefit their children’s mental health, according to US researchers. Weissman and colleagues studied 151 mother-child pairs; in each pair, a depressed mother was being treated with medication. After 3 months of treatment, remission of maternal depression was associated with reduced symptoms of behavioural and emotional disorders in the children; the greater the maternal response to treatment, the fewer current diagnoses and symptoms in the children. Conversely, unremitting maternal depression was linked with an increase in child psychopathology. These study findings are particularly timely, given the many concerns about the safety of treatment of psychiatric disorders in children. JAMA 2006; 295: 1389-1398 Ethics in space Should female hormones be given to male astronauts to obviate the need for shaving in space? Should training for spaceflight involve prolonged sensory deprivation? Should an astronaut’s legs be amputated in order to enhance tolerance to gravitational forces? UK ethicist Gibson considers all of these actions to be ethically unacceptable, irrespective of whether or not an astronaut has given informed consent, as either the benefit is too small or the risk or harm too great to warrant such measures. He supports his recommendations with references to unethical practices in the past, such as a prototype British full pressure suit which bolted the pilot to the aircraft, giving no means of escape. Gibson aims to assist today’s aviation medical practitioners to develop a morally justifiable code of practice that will effectively balance society’s needs with individual ambitions and corporate goals. J Med Ethics 2006; 32: 129-132

Ann Gregory

Looking Good. The Australian guide to skin care, cosmetic medicine and cosmetic surgery. Dr Laurence Anderson. Sydney: MJA Books, 2006 (v + 112 pp) ISBN 0-85557-044-X . “— an excellent publication that gives an accurate overview of what is available for the cosmetic medicine consumer. It is interesting, informative, well set out and easy Cosmetic medicine and cosmetic surgery have come of age. We can remove wrinkles and blemishes, straighten teeth and noses, and sculpt our bodies into works of art. We have the power to make ourselves beautiful and are not afraid to use it. These days, cosmetic procedures are varied, mainstream and affordable, and the line between beauty treatments and cosmetic medical options is blurred. In Looking Good, Dr Laurence Anderson, a member of the Cosmetic Physicians Society of Australasia, clearly explains how to look after our skin and demystifies the many cosmetic and plastic surgical procedures available. Looking Good answers the Australian public’s questions. A registered cosmetic physician and long-term GP, Dr Anderson covers skin anatomy, sun protection, diet, cosmetics and other general information in the first half of the book, then tackles available cosmetic procedures in the second half. These are broadly divided into minor or office procedures valued at around $1000 or less, and the major procedures costing up to $15,000 or more and often requiring a general anaesthetic. Various practitioners have contributed high quality “before and after” photographs, and the text is liberally illustrated with line drawings and other photographs. There are sections on overseas travel to get cosmetic medicine and how to prepare yourself and your family when you are considering surgery. Looking Good is not a shopfront for cosmetic practitioners and is quite candid about the downfalls, both physical and emotional, of this growing cultural phenomenon. While people have the right to maximise their attractiveness, the book points out that there is also the danger that for some cosmetic medicine may become an unhealthy obsession or be mistaken as the answer to life’s problems. Order this book

Med J Aust 2006; 184 (8 Suppl).