Volume 188 Issue 6

Medical students should be selected on criteria that include desirable personal qualities, using procedures with demonstrated reliability and validity How best to select medical students (ie, future doctors) is a topic that has rarely been out of the medical journals and the daily newspapers during the past 30 years. In this Journal in 1974, Campbell et al wrote: “Although mounting criticism and concern are expressed for the manner in which our medical students are selected, the status quo continues”.1 The status quo alluded to was selection of medical students solely on the basis of academic marks obtained in high school matriculation examinations. Fifteen years later, John Best, in one of his regular articles for the Journal,2 acknowledged that to be a good doctor required skills and personal qualities additional to academic aptitude, and wrote: The leap of logic that equates high marks in an examination at the terminal end of adolescence with a humane and caring medical profession is a nonsense, but is sustained because nobody has any other solution which is strong enough to combat ... the “high-enough mark method”. The University of Newcastle led a major change in medical education in Australia in the late 1970s by introducing problem-based learning, early clinical skills acquisition, community orientation, and the addition of personal qualities evaluation to the student selection process. The first Newcastle students were admitted in 1978. The Foundation Dean, David Maddison, anticipated the current debate and planned accordingly. The “Newcastle Experiment”3 involved half the students being admitted on the basis of academic marks alone (top 1%–2%), irrespective of personal qualities assessed by test and interview; the other half were admitted on the basis of personal qualities after applying an academic threshold (top 10%). After a 9-year period, prior academic performance and personal qualities at the time of selection were compared with two outcome measures: a negative measure — non-completion of the course — and a positive one — graduation with honours. The results showed no relationship between either outcome and prior academic performance. However, there were important associations for both the negative and positive outcomes with personal qualities at the time of selection. The interview had the most predictive power in the selection procedure — those who did well in the areas of communication skills, motivation to be a doctor, and capacity to provide support to those in distress had a greater likelihood of completing their studies at medical school and of graduating with honours.4 The Newcastle Experiment was followed by another study, on interns in New South Wales hospitals, which demonstrated that Newcastle graduates at the beginning of internship were the equals of graduates of the other NSW medical schools in clinical competence, and had higher scores in the four personal characteristics evaluated5 — a desirable endpoint in the context of being a professional doctor. It is probable that the findings documented in these two studies and others from Newcastle influenced selection procedures across the country, for by the mid to late 1990s nearly all Australian medical schools had begun to select students on the basis of both academic ability and personal qualities assessed by tests and interview. Ten years down the track, the evaluation of personal qualities by interview is now being abandoned by some schools. Why is this happening? A study from the University of Queensland, reported in this issue of the Journal, gives some indication (→ Medical school selection criteria and the prediction of academic performance).6 Its major finding is that criteria other than prior academic grades only modestly predict academic performance in the medical course. That prior academic achievement should predict subsequent academic achievement is no surprise;7 indeed it is almost axiomatic. However, given the current view that graduating doctors should be more than just academically competent, it is of some concern that academic performance was the sole outcome measured in the study. In the present-day context of what we expect in a graduating doctor, the important finding in the Queensland study is the significant association of the interview scores with assessment outcome, especially the increased association for Year 4 (when, presumably, more clinically relevant matters are tested) compared with Year 1. The size of the effect is small, but medicine is accustomed to important small effects, such as the link between passive smoking and lung cancer. The finding that the written Graduate Australian Medical School Admissions Test (GAMSAT) does not predict within-course academic performance is very interesting, particularly given GAMSAT’s emphasis on scientific knowledge and understanding. It is puzzling that the University of Queensland has decided to abandon the interview, given the significant results of their study. Even more puzzling is the stated intention to retain GAMSAT, which had no predictive power at all. In another recent study published in the Journal, GAMSAT was found to be a negative predictor of clinical reasoning.8 The most logical explanation for the proposed selection strategy is one founded on cost. No one questions the fact that having a selection process based on anything other than prior academic performance at school or university is expensive. It is expensive in time and effort for university staff, for community interviewers and for the applicants themselves. It is also politically expensive, especially when applicants with exceptionally high prior academic scores are not selected. The outrage expressed in a number of recent media reports9,10 reflects the passion with which sections of the public regard admission to medical school. Is the interview being abandoned because it is too expensive in terms of time and resources? Is GAMSAT being retained because it costs the medical school nothing, since applicants pay for it, and its numerical scores are a convenient way to differentiate between applicants? The evidence from these two Australian medical schools,3-6 together with community expectations of the skills and competencies of a graduating doctor, supports the retention of methods to evaluate personal qualities during selection. However, this approach, especially the interview, comes at a cost. The question for medical schools is whether the effectiveness is worth the cost. If it is not, we should be honest with ourselves and the public and say that the cost is too much, even though it works. My view is that we should continue to select medical students based on criteria that include desirable personal qualities, using procedures that have demonstrated reliability and validity. We also need to build into medical curricula objective barrier assessments of professional skills and personal qualities relevant to future medical practice. If we do this, we will not only graduate doctors who have the required skills, but we will have the appropriate outcome measures against which to evaluate our personal qualities selection procedure. If we elect not to take these two steps, we will be destined to go through yet another cycle of questioning selection methods. Campbell and colleagues’ 1974 comments1 will be reprised by others.

David A Powis PhD

Should we be devoting energy and resources to reversing obstructive sleep apnoea in patients without symptoms? Over the past four decades, obstructive sleep apnoea (OSA) has emerged as a prevalent, clinically important disorder. Snoring, which is often a hallmark of OSA, is seemingly ubiquitous in middle-aged men. Over 80% of Australian middle-aged men snore for more than 10% of the night.1 Snoring is also common in women. Although it is undoubtedly an important social nuisance, it remains unclear whether snoring alone (in the absence of sleep apnoea) carries with it any serious health risk. Twenty-five per cent of middle-aged men and 10% of women have OSA, defined as > 5 obstructed breathing events per hour of sleep.2 The prevalence in women rises sharply after menopause. Other risk factors are obesity, older age and a family history of OSA. Population-based studies in China and India indicate that its prevalence is at least as high as that reported in Western countries. A complex interplay between regulation of breathing during sleep, facial anatomy and obesity predicts the development of OSA.2 In contrast to the uncertainty of the effects of simple snoring, OSA clearly has significant health consequences. Many patients with OSA experience excessive daytime sleepiness and impaired cognitive function, increasing the potential for traffic crashes, work accidents and reduced productivity at work.3 Over 50% of Australian truck drivers have mild OSA or worse.4 Moreover, Access Economics has estimated that the cost of sleep disorders to the Australian community is over $7 billion, and much of this cost relates to OSA.5 Increasing awareness of OSA has been followed by an appropriate increase in clinical investigations of sleepy patients with suspected OSA. This is further driven by the availability of cost-effective treatments, notably continuous positive airway pressure (CPAP) and mandibular advancement splints. Recent studies have suggested that OSA is associated with an increased risk of cardiovascular disease.6 Publicity about this research has led to an increasing tendency for people who are not sleepy or who have minimal symptoms to be referred for assessment and treatment of OSA. However, in contrast to the sleepy patient, for whom CPAP usage is reinforced by reduction in sleepiness, asymptomatic patients have more variable compliance.7 Should we be devoting substantial clinical energy and resources to reversing OSA in such patients to prevent cardiovascular disease and death? Certainly, data from cross-sectional and prospective population studies and sleep clinic studies indicate that OSA is associated with a higher prevalence of cardiovascular and cerebrovascular disease and insulin resistance.6 Untreated male patients with severe OSA have significantly greater risks of fatal and non-fatal cardiovascular events than healthy controls (odds ratios, 2.87 and 3.17, respectively).8 However, cross-sectional and observational studies have unmeasured confounders, such as visceral obesity.6 In addition, observational studies can be affected by treatment bias. Patients who refuse to use CPAP and seemingly have higher cardiovascular risk than those who comply with CPAP treatment8 may be the same people who refuse to stop smoking or take lipid-lowering or blood pressure-lowering medication. In contrast, there is good evidence from randomised controlled trials that CPAP lowers blood pressure (mean decrease in systolic and diastolic blood pressure of 2.46 and 1.83 mmHg, respectively), but most studies are relatively short (less than 8 weeks), and treatment effects are hard to demonstrate in patients who are not sleepy.9 The remaining short-term CPAP trials that have focused on other intermediate markers of cardiovascular disease (lipids, glucose control, high-sensitivity C-reactive protein) have been inconclusive. For example, a recent short-term randomised trial failed to show any improvement in insulin sensitivity in patients with type 2 diabetes and OSA.10 No data are available from long-term, well powered, randomised controlled trials assessing the effect of CPAP on hard cardiovascular endpoints, such as myocardial infarction and stroke, in patients with OSA. Medical research is well populated by “positive” results from cross-sectional, observational or short-term intervention studies, but their results have not been reproduced in rigorous, long-term, large-scale clinical trials. To remedy this lack of information, several long-term trials of CPAP treatment in OSA are being planned or have commenced, including one initiated by Australian investigators (Sleep Apnea CardioVascular Endpoints Study [http://www.savetrial.org]). These trials will determine whether treatment of OSA decreases the incidence of new cardiovascular events. In the interim, how should we manage patients with a diagnosis of repetitive OSA who present with complaints of snoring but have minimal or no daytime sleepiness? First, it is important to establish whether such patients are genuinely asymptomatic or simply underreport symptoms that are obvious to their families or work colleagues.11 Second, the disorders of these patients typically are characterised by higher rates of central adiposity, glucose intolerance and other vascular risk factors.6 Given that middle-aged men often neglect to monitor such risk factors, referral for snoring may provide an excellent opportunity for a general health assessment and to institute an intervention, such as advice to exercise and lose weight. Moreover, it would be reasonable to prescribe a trial of CPAP for a patient with asymptomatic OSA and hypertension refractory to maximal medical therapy and to monitor the blood pressure response over 24 hours. Finally, it would be reasonable also to inform asymptomatic patients with severe OSA and coexisting cardiovascular disease of the possible association between OSA and a risk of future vascular events. However, it would be inappropriate to coerce these patients into accepting a treatment that might falsely make them feel secure about future risk and might result in neglect of proven risk factors. Future research, ideally, will enable clinicians to get to the “heart of the matter” when discussing cardiovascular risk management and sleep apnoea with these patients.

Ronald R Grunstein MD, PhD, FRACP · Craig L Phillips BSc

Objective: To examine the relationship between child weight and vehicle booster seat usage in the context of current Australasian booster seat standards.Design, setting and participants: Questionnaire survey conducted between February and April 2005. A convenience sample of parents with children aged 4–11 years in New South Wales and Victoria completed a questionnaire, reporting on the height and weight of their children and the nature of restraint devices used in the family vehicle.Main outcome measures: Proportion of children meeting standard-specified weight and height criteria who are not restrained in booster seats; proportion of children who meet the specified height criteria but whose weight exceeds the specified weight.Results: 699 of 3959 questionnaires were returned (response rate, 18%), of which seven lacked essential details. The remaining 692 responses provided information on 1500 children. Of these children, 633 aged 4–11 years fell within the recommended height range for using booster seats, but only 29% were typically restrained in booster seats, the majority (70%) being restrained in normal seatbelts. A key finding was that 37% of the children who met the recommended height criteria exceeded the maximum weight for booster seats stipulated by the current Australasian safety standard.Conclusion: In view of increasing rates of overweight and obesity in children, it is important to reassess current Australasian standards for child restraints in vehicles. A concerted parental education campaign is also needed to raise awareness of which restraint types are appropriate for children of various heights and weights.

Michael P Fitzharris BA, BSc(Hons), PhD · Judith Charlton BEd, MSc, PhD · Megan Bohensky BA, MPH · Sjaanie Koppel BAppSc(Hons), PhD · Brian Fildes BSc(Hons), PhD

Objectives: To compare results of statistical process-control analyses of in-hospital deaths of patients with acute myocardial infarction by using either administrative or clinical data sources and prediction models, and to assess variation in results according to selected patient characteristics.Design: Retrospective, cross-sectional study comparing variable life-adjusted display (VLAD) curves derived by using administrative or clinical prediction models applied to a single patient sample.Participants and setting: Data from 467 consecutive patients admitted to a tertiary hospital in Queensland, between 1 July 2003 and 31 March 2006, with a coded discharge diagnosis of acute myocardial infarction.Main outcome measure: Statistical estimates of cumulative lives gained or lost in excess of those predicted at the end of the study period.Results: The two prediction models, when applied to all patients, generated almost identical VLAD curves, showing a steadily increasing excess mortality over the study period, culminating in an estimated 11 excess deaths. Risk estimates for individual patients from each model were significantly correlated (r = 0.46, P < 0.001). After exclusion of misclassified cases, out-of-hospital cardiac arrests and deaths within 30 minutes of presentation, replotting the curves reversed the mortality trend and yielded, depending on the model, a net gain of three or seven lives. After further exclusion of transfers in from other hospitals and patients whose care had a palliative or conservative intent, the net gain increased to seven or 10 lives.Conclusion: Appropriate patient selection is more important than choice of dataset or risk-prediction model when statistical process-control methods are used to flag unfavourable mortality trends suggestive of suboptimal hospital care.

Ian A Scott FRACP, MHA, MEd · Peter L Thomson MEngSc, MPH, MBiomedE · Seshasayee Narasimhan MB BS

Objective: To examine differences in psychostimulant prescribing between paediatricians and child/adolescent psychiatrists for treating children with attention deficit hyperactivity disorder (ADHD) in Western Australia.Design: Using whole-population prescribing data, logistic and linear regressions were used to model the number of children (aged 2–17 years) treated with psychostimulants between August 2003 and December 2004 for ADHD and medication dose prescribed by clinical specialty, controlling for age, sex, body weight, and other medication use.Main outcome measures: Mean number of patients treated by specialty; associations between prescriber specialty and patient characteristics; associations between stimulant dose and patient characteristics and prescriber specialty.Results: 54 paediatricians and 23 child/adolescent psychiatrists prescribed stimulant medications for children with ADHD. The mean number of patients treated (per prescriber) was 159.8 (range, 1–1977) for paediatricians and 34.3 (range, 1–166) for psychiatrists. Boys were 32% more likely to be treated with stimulants by paediatricians (P = 0.002). Psychiatrists were 2.9 times (95% CI, 2.4–3.3; P < 0.001) more likely than paediatricians to treat patients with multiple psychotropic medications. When controlled for all other factors, psychiatrists prescribed higher stimulant doses (4.5 mg/day greater; 95% CI, 2.0–7.0 mg/day; P < 0.001) than paediatricians.Conclusion: Treatment of children with stimulant medicines for ADHD differed between clinical specialties. Paediatricians treated more patients per prescriber, a greater proportion of boys, and a younger age demographic, but relied less on combined psychotropic pharmacotherapy and prescribed lower stimulant doses than psychiatrists.

David B Preen BSc(Hons), PhD · Janine Calver BA(Hons) PhD · Frank M Sanfilippo PGradDipPharm, PhD, FPS · Max Bulsara BSc, MSc · C D’Arcy J Holman FACE, FAFPHM, FAIM

Objectives: To investigate the relationship between admission glycaemic status and inpatient mortality in patients with and without pre-existing diabetes.Design: Prospective observational cohort study.Setting: A general medical ward in an Australian tertiary referral hospital.Participants: 903 patients admitted to the general medical ward between February 2003 and July 2004.Main outcome measure: Inpatient death.Results: The overall inpatient mortality was 5.4% (n = 49). In the total cohort, age > 75 years and admission fasting plasma glucose (FPG) levels ≥ 5.6 mmol/L were independent predictors of mortality. For patients without a known history of diabetes, each 1 mmol/L rise in admission FPG was associated with a 33% increase in mortality. In these patients, elevated (> 6.0%) and normal glycated haemoglobin (HbA1c) levels were associated with mortalities of 11.3% and 4.4%, respectively (odds ratio, 2.47; 95% CI, 1.16–5.26). In contrast, in patients with known diabetes, there was no association between admission FPG levels, HbA1c and mortality. Length of stay was not independently associated with FPG, HbA1c, or diabetes status.Conclusions: In patients without known diabetes, the risk of death was increased for admission FPG levels ≥ 5.6 mmol/L. However, pre-existing abnormal glucose metabolism, reflected by elevated HbA1c levels, appeared a more important predictor of inpatient mortality than glucose levels in patients without known diabetes.

Scott T Baker MB BS, BMedSc, FRACP · Cherie Y Chiang MB BS · Jeffrey D Zajac MB BS, PhD, FRACP · Leon A Bach MB BS, PhD, FRACP · George Jerums MB BS, MD, FRACP · Richard J MacIsaac MB BS, PhD, FRACP

Objective: To investigate primary health care service utilisation and health presentations among asylum seekers living in Melbourne.Design and setting: Retrospective audit of files of people who attended three Melbourne asylum-seeker health clinics between 1 July 2005 and 30 June 2006.Main outcome measures: Rates of reasons for the encounter, diagnostic tests or investigations required, treatments prescribed and referrals.Results: Data were collected from 998 consultations corresponding to 341 people. Eighty-eight per cent of visits involved people with no Medicare access, owing to their visa status. The most common reasons for the encounter were general and unspecified symptoms or problems (rate, 59.9 per 100 encounters; 95% CI, 55–65), followed by musculoskeletal conditions (27.1; 95% CI, 24–30), and psychological problems (26.5; 95% CI, 23–30). The rate of referrals was 18.3 per 100 encounters (95% CI, 16–21).Conclusions: The three clinics providing services to asylum seekers in Melbourne are delivering care to a considerable number of people with complex health needs. A substantial number of asylum seekers present to clinics with psychological and social problems. Most cannot access government-subsidised health care. This must be addressed urgently by policy change at the federal and state and territory levels.

Ignacio Correa-Velez MB BS, PhD · Vanessa Johnston MB BS, MPH · Joanne Kirk RN · Angeline Ferdinand BA

Objective: To assess how well prior academic performance, admission tests, and interviews predict academic performance in a graduate medical school.Design, setting and participants: Analysis of academic performance of 706 students in three consecutive cohorts of the 4-year graduate-entry medical program at the University of Queensland.Main outcome measures: Proportion of academic performance during the medical program explained by selection criteria, and correlation between selection criteria and performance. Selection criteria were grade point average (GPA), GAMSAT (Graduate Australian Medical School Admissions Test) score, and interview score. Academic performance was defined as overall total in all examinations combined, in first and fourth year examinations, and in individual written, ethics and clinical components.Results: Selection criteria explained 21.9% of variation in overall total score, falling from 28.2% in Year 1 to 17.7% in Year 4. This was highest for the written examination in Year 1 (30.5%) and lowest for the clinical examination in Year 4 (10.9%). GPA was most strongly correlated with academic performance (eg, for overall score, partial Spearman’s correlation coefficient [pSCC], 0.47; P < 0.001), followed by interviews (pSCC, 0.12; P = 0.004) and GAMSAT (pSCC, 0.07; P = 0.08). The association between GPA and performance waned from Year 1 to Year 4, while the association between interview score and performance increased from Year 1 to Year 4.Conclusion: The school’s selection criteria only modestly predict academic performance. GPA is most strongly associated with performance, followed by interview score and GAMSAT score. The school has changed its selection process as a result.

David Wilkinson FRACGP, FAFPHM, DSc · Jianzhen Zhang PhD · Gerard J Byrne MB BS, PhD, FRANZCP · Haida Luke PhD · Ieva Z Ozolins MB BS, PhD · Malcolm H Parker MLitt, LLM, FACLM · Raymond F Peterson PhD

Objective: To review the evidence for the effectiveness of complementary and self-help treatments for anxiety disorders and situational anxiety in children and adolescents.Data sources: Systematic literature search using PubMed, PsycINFO and the Cochrane Library for 111 treatments up to February 2006.Study selection: There were 11 treatments for which intervention studies had been undertaken and reported.Data extraction: Studies on each treatment were reviewed by one author and checked by a second. A consensus was reached for level of evidence.Data synthesis: Relevant evidence was available for bibliotherapy, dance and movement therapy, distraction techniques, humour, massage, melatonin, relaxation training, autogenic training, avoiding marijuana, a mineral–vitamin supplement (EMPower +) and music therapy. Findings from case–control studies, individual cohort studies or low quality randomised controlled trials indicated that several treatments may have potential to reduce anxiety, including bibliotherapy, massage, melatonin, and relaxation training.Conclusions: Although some complementary and self-help treatments might be useful for children and adolescents with anxiety, they need to be tested adequately through randomised controlled trials before they could be recommended.

Ruth Parslow PhD · Amy J Morgan BASc, BAppSci(Psychol)(Hons) · Nicholas B Allen BSc(Hons), MSc, PhD · Anthony F Jorm PhD, DSc · Colin P O’Donnell MB BCh, BAO, MRCPsych · Rosemary Purcell PhD

In 2007, the National Health and Medical Research Council (NHMRC) released a revised National statement on ethical conduct in human research. Public submissions in the review process leading to the 2007 statement highlighted four main areas of concern: children’s competence to consent, mature minors and the requirement for parental consent, whether children can refuse to participate, and the provision of information to children. A useful addition to the statement is the concept of levels of maturity, which help determine whether a child or young person’s consent is necessary and/or sufficient for participation in research. Changes in terminology (“capacity” instead of “competence” and introduction of the term “vulnerability”) have the potential to create confusion, as the new terms are not clearly defined, and capacity is used in several senses.

Merle P Spriggs PhD · Lynn H Gillam PhD

Worldwide, over 80% of primary liver cancers are attributable to chronic infection with hepatitis B or C virus. Over the past two decades, primary liver cancer incidence rates have been consistently rising in Australia. In New South Wales, the standardised incidence ratios for primary liver cancer in males born in Vietnam, Hong Kong and Macau, Korea, Indonesia and China and in females born in Vietnam and China are 6–12 times those in Australian-born populations. The incidence of liver cancer is likely to continue to increase unless a coordinated approach to disease control can be developed. Effective programs for chronic hepatitis B management need to link prevention, treatment and care, and enhance opportunities for research and surveillance activities. The evidence that suppression of hepatitis B virus replication could limit disease progression needs to inform the development of a public health response. Lessons learned in the development of the National Hepatitis C Strategy and the experience of international hepatitis B control programs need to inform this process.

Monica C Robotin FRACS, MApplEpid · Jacob George FRACP, PhD · Rajah Supramaniam BSc, MPH · Freddy Sitas MSc, DPhil · Andrew G Penman MACP, MPH

We report the case of a 59-year-old severely obese man with coexisting type 2 diabetes, hypertension and dyslipidaemia who was treated with a very-low-calorie diet (VLCD) program for 12 months. He continued to lose weight during the treatment, with marked improvement in his comorbidities and no adverse effects. This case demonstrates that prolonged use of a VLCD under close medical supervision is safe and effective in certain obese patients. Clinical recordA 59-year-old severely obese man was admitted to hospital with a 3-day history of gradually progressive paraesthesia and mild weakness affecting all four limbs, with a background of polydipsia, polyuria and fatigue over the previous 4 months. On examination, his weight was 169.5 kg and his height was 1.90 m (body mass index [BMI], 47.0 kg/m2). He was hypertensive (167/80 mmHg) and afebrile. He had mild weakness in a pyramidal pattern in the legs. Upper and lower limb reflexes were brisk, ankle jerks were absent, plantar responses were upgoing bilaterally, and sensation was reduced in a stocking distribution. The cranial nerves and speech were unaffected and visual fields were normal. Cardiovascular, respiratory and abdominal examinations were unremarkable. The presence of acanthosis nigricans and a fungal toenail infection were noted. Initial laboratory investigations revealed a random blood glucose level of 22.2 mmol/L (reference range, 3.3–5.5 mmol/L) and a glycated haemoglobin (HbA1c) level of 12.2% (reference range, 4.3%–6.0%). Urinary ketones were not detected. Levels of electrolytes, inflammatory markers and vitamin B12 were normal. Liver function tests showed a mild generalised elevation, and lipid levels were raised (Box 1). An electrocardiogram (ECG), non-contrast computed tomography brain scan, lumbar puncture and carotid Doppler ultrasound were normal. Nerve conduction studies showed an axonal sensorimotor neuropathy, with the lower limbs more severely affected than the upper limbs. Neurological findings remained stable during the hospital stay, and a provisional diagnosis of a cervical myelopathy with peripheral neuropathy was made. Magnetic resonance imaging of the spine could not be performed because of the patient’s large size. The patient was treated with aspirin 100 mg daily, simvastatin 20 mg daily and metformin 500 mg twice daily. On the day of discharge (Day 6), he commenced a very-low-calorie diet (VLCD) (Optifast VLCD, Novartis Consumer Health Australasia, Melbourne, Vic) three times daily. Blood glucose readings at discharge were 6–8 mmol/L. After discharge, he commenced a daily exercise program. Over the following 12 months, the patient attended the weight control clinic at our hospital. He continued on an intensive regimen of Optifast VLCD three times a day for 5 months, and then began a transition phase (two Optifast VLCD meals plus one low-fat meal per day). Over the 12 months, the patient’s weight fell steadily (Box 2, Box 3). At 1-year follow-up, he had lost 43% of his initial weight and was down to 96.5 kg (BMI, 26.7 kg/m2). He was normotensive (125/80 mmHg), and his fasting blood glucose and HbA1c levels were in the non-diabetic range. Full blood examination, electrocardiographic readings, and levels of electrolytes, calcium, magnesium, folate, vitamin B12, vitamin D and uric acid were normal. Liver function tests had normalised, and the lipid profile had improved significantly (Box 1). Bone mineral density (measured by dual energy x-ray absorptiometry) was normal at 6 and 12 months after commencement of the VLCD. Neurological symptoms improved, with persistence of limb weakness and sensory loss. Planned management was to gradually reduce the Optifast diet and enter a supervised weight maintenance phase, which would include an education program about lifestyle changes, frequent clinic visits and close observation of weight. DiscussionVLCDs involve replacement of meals with foods or formulas providing 1675–3350 kJ/day. They are commonly used in medically supervised weight reduction programs for patients with BMI > 30 kg/m2 (or > 27 kg/m2 with obesity-related comorbidities), or for whom rapid weight loss is necessary. Several formulations are available without prescription (Box 4). VLCDs should provide at least 0.8 g protein per kilogram of ideal bodyweight per day (to preserve lean body mass1), along with the recommended daily allowances of minerals, vitamins, trace elements and essential fatty acids. Around 10 g/day fat is recommended to stimulate gallbladder contraction.2 Although optimal caloric and carbohydrate intakes are unknown, 50 g carbohydrate daily has been suggested as a suitable quantity to maintain normoglycaemia and to prevent loss of electrolytes and protein.2 There is no advantage in reducing energy intake below 3350 kJ/day.3 Treatment duration varies but is usually 8–16 weeks.1 To our knowledge, our report is the first to document the use of a VLCD for 12 months. There is concern about the safety of VLCDs, most of which stems from the occurrence of over 60 deaths associated with a popular liquid protein diet, available in the 1970s, that consisted entirely of solutions of collagen or gelatine hydrolysates.4 Many of the deaths occurred in people with pre-existing comorbidities.4 However, 17 deaths (16 in women) occurred in relatively young (median age, 35 years) and otherwise reasonably healthy people. These 17 people, who were severely obese (mean BMI, 40.6 kg/m2), remained on the diet for an average of 5 months and lost a large amount of weight (mean, 35%). Postmortem findings were consistent with the cardiac effects of protein-calorie malnutrition (which include myocardial atrophy, QT prolongation and ventricular arrhythmias).5 In contrast, VLCDs in current use contain high-quality protein and appear to be safe.1 In 1998, Rössner described the case of a patient who had lived solely on a VLCD preparation for 46 weeks without medical supervision, in whom no adverse events occurred other than cholelithiasis and one episode of palpitations, after which ECG monitoring over a 24-hour period showed no abnormality.6 Common minor adverse effects associated with VLCDs, which include cold intolerance, dry skin, hair loss, constipation, headaches, fatigue and dizziness, are generally self-limiting and transient. Other potential effects are gallstones, increased serum uric acid levels, precipitation of gout and reduced bone mineral density. When beginning a VLCD, liver function tests, lipid profile measurements, a full blood count and iron studies should be carried out, and levels of electrolytes, creatinine and uric acid should be measured. Testing of electrolyte and creatinine levels should be repeated about 6 weeks after commencement, or earlier if more careful monitoring is required (eg, in patients who have renal impairment or are using diuretics). If the VLCD is to continue for more than 12 weeks, it is advisable to repeat the baseline tests at least every 2 months.7 Obese people typically achieve a mean weight loss of 1.5–2.5 kg per week using a VLCD. A 2001 meta-analysis concluded that, after using a VLCD, subjects maintained a significantly greater weight loss at 4.5 years (mean loss, 6.6% of initial weight) than after a hypocaloric balanced diet (mean loss, 2.1% of initial weight).8 Taking meal replacements once or twice daily in conjunction with a reduced-calorie diet is also effective for long-term weight maintenance.9 Advantages of VLCDs include the motivating effect of rapid weight loss, the convenience of meal replacement (which improves adherence compared with an ad-libitum low-fat diet)10 and a mild ketosis, which may suppress hunger.7 VLCDs also help with several obesity-related comorbidities by reducing levels of total cholesterol, low-density lipoprotein, triglycerides and blood glucose and by reducing blood pressure, insulin resistance1 and hepatic steatosis.11 All of these benefits were obtained by our patient. To date, bariatric surgery has been the most effective long-term treatment option for obesity. The Swedish Obese Subjects Study, a large prospective controlled study of severely obese patients, found significantly greater weight loss in the surgically treated group than the control group (23.4% bodyweight lost [surgical group] v 0.1% gained [control group] at 2 years, and 16.1% lost [surgical group] v 1.6% gained [control group] at 10 years).12 Similar weight reductions after surgery were reported in a study of mildly to moderately obese subjects13 and in a meta-analysis of bariatric surgery trials.14 Pharmacotherapy for weight loss has only modest benefits, with loss of around 3%–5% bodyweight over 1–4 years reported in a recent meta-analysis.15 The 43% weight loss achieved by our patient at 12 months is comparable with results reported for surgery. Weight maintenance will be his next major challenge. Increasing evidence indicates that physiological changes occur after diet-induced weight loss, including decreased levels of leptin, glucose, insulin, free fatty acids, cholecystokinin and triiodothyronine (T3), and increased levels of reverse T3 and ghrelin. Many of these changes would be expected to reduce satiety and increase hunger, possibly contributing to the weight regain frequently seen after weight loss. Our patient may continue to replace one meal a day with Optifast in the longer term to assist with weight maintenance. As there is growing evidence of physiological adaptations after weight loss that encourage weight regain, pharmacotherapy will be introduced if lifestyle changes prove insufficient to maintain his current weight. Bariatric surgery could also be considered if his weight loss cannot be maintained. Our report shows that, under close medical supervision in certain obese patients, a VLCD may be used safely and effectively for a period of at least 12 months. Prevention of weight regain remains difficult. 1 Blood biochemistry measurements Biochemical levels At baseline At 6 months At 12 months Reference range Total cholesterol (mmol/L) 7.9 3.9 4.8 < 5.5 Triglycerides (mmol/L) 2.4 1.6 0.5 < 2.0 High-density lipoprotein (mmol/L) 1.0 0.8 1.4 > 1.0 Low-density lipoprotein (mmol/L) 5.8 2.4 3.2 < 2.5 Fasting glucose (mmol/L) 16.5 4.5 4.5 3.3–5.5 Glycated haemoglobin (%) 12.2 4.8 4.7 4.3–6.0 Potassium (mmol/L) 4.1 3.9 4.0 3.5–5.0 Creatinine (μmol/L) 107 85 89 30–110 Albumin (g/L) 34 39 40 36–48 Bilirubin (μmol/L) 31 22 20 < 18 Alkaline phosphatase (U/L) 100 70 68 32–91 Alanine aminotransferase (U/L) 88 23 22 < 45 γ-Glutamyltransferase (U/L) 113 21 27 < 55 2 Patient’s weight loss during maintenance of a very-low-calorie diet over a 12-month period 3 Patient at baseline and after 12 months on a very-low-calorie diet 4 Comparison of available very-low-calorie diet (VLCD) formulations* Product† Energy (kJ) Carbohydrate (g) Protein (g) Fat (g) Optifast VLCD‡ 1908 45.0 51.9 6.9 OptiSlim 2000§ 1958 48.1 48.4 4.7 KicStart¶ 2636 58.2 74.7 8.4 * Values given are per 3 × 40 g sachets of chocolate shake prepared as directed. Figures in the table are daily amounts, but do not take into account the additional vegetables recommended along with the VLCD. † All three products are available without prescription. ‡ Novartis Consumer Health Australasia, Melbourne, Vic. § OptiPharm, Melbourne, Vic. ¶ Pharmacy Health Solutions, Sydney, NSW.

Priya Sumithran MB BS, FRACP · Joseph Proietto MB BS, FRACP, PhD

Clinical record We report the case of a 54-year-old woman who presented with a painful and swollen left eye 3 days after receiving zoledronate. The patient had been diagnosed with locally advanced breast cancer 3 years earlier. This was managed with four cycles of neoadjuvant chemotherapy (with adriamycin and cyclophosphamide) followed by breast-conserving surgery and axillary dissection. Histological sections from the surgical specimen revealed a 10 mm grade 3 infiltrating ductal carcinoma that was negative for both oestrogen and progesterone receptors. Eight out of 10 axillary lymph nodes were positive for malignancy. The patient went on to receive four cycles of adjuvant chemotherapy (paclitaxel) and postoperative radiotherapy. The patient remained well until a month before presentation, when she developed right hip pain. An x-ray and bone scan showed a suspicious bone lesion within the ischium on the contralateral side to the pain. A computed tomography scan of the chest, abdomen and brain revealed a 1.5 cm right upper lobe lung lesion as well as multiple brain lesions. A biopsy of the lung lesion confirmed the presence of adenocarcinoma consistent with metastatic breast cancer. She commenced oral dexamethasone treatment 4 mg three times daily and, because of the symptoms associated with bone metastases, also received a 4 mg intravenous dose of zoledronate. Three days later, she was reviewed by her local ophthalmologist when she presented with an acutely swollen and painful left eye with associated blurring of vision. On the basis of a moderate cellular infiltrate in the anterior chamber, she was diagnosed with acute iritis and commenced on homatropine 2% three times daily as well as ocular dexamethasone hourly. Two days later, the patient noted increasing pain in the eye, worsening blurring of vision and onset of photophobia. She was reviewed by the ophthalmology department at the hospital where she was undergoing whole brain radiotherapy. She was noted to have reduced visual acuity in the left eye, an injected conjunctiva, a hazy and oedematous cornea, and cells in the anterior chamber. Fundoscopy was unremarkable. A diagnosis of acute anterior uveitis and anterior diffuse scleritis was made. She was continued on homatropine drops but the dexamethasone drops were changed to 2-hourly prednisolone acetate/phenylephrine hydrochloride drops. The patient was reviewed regularly in the ophthalmology clinic over the following 2 weeks. At the time of discharge from the clinic, her visual acuity had improved and the anterior chamber was clear of cells. She had ceased homatropine treatment and was on a weaning dose of ocular steroids. Three months later, she had ceased ocular steroid therapy and her vision had returned to normal. She received no further doses of bisphosphonate after the first administration. Bisphosphonates are indicated for treatment of a number of conditions, including osteoporosis, Paget’s disease, hypercalcaemia associated with malignancy, and bone metastases. Their mechanism of action is via inhibition of osteoclast activity, leading to reduced bone resorption. Common side effects of bisphosphonate treatment are dysphagia, heartburn and oesophagitis. Lessons from practice Bisphosphonates are used to treat a number of clinical conditions, including osteoporosis, Paget’s disease, hypercalcaemia of malignancy, and bone metastases. Various ocular complications of bisphosphonate use have been reported, including conjunctivitis, scleritis, iritis and uveitis. These complications are rare and are readily treatable. Management usually involves cessation of the bisphosphonate and treatment with an ocular topical mydriatic drug and steroids. Since the early 1990s, there have been a number of case reports documenting various ocular complications of bisphosphonate use, including conjunctivitis, scleritis, iritis and uveitis.1-9 In most cases, ocular symptoms began within 72 hours of administration of the bisphosphonate, and symptoms generally improved after local therapy and cessation of the drug. Usually it is the nitrogen-containing bisphosphonates that have been implicated (alendronate, pamidronate, zoledronate, risedronate), but in one report uveitis was associated with a non-nitrogen-containing bisphosphonate (clodronate).5 The mechanism of the inflammation is unclear, but it is known that the nitrogen-containing bisphosphonates cause elevated levels of pro-inflammatory cytokines, including tumour necrosis factor α and interleukin-6.10 The factors that predispose some patients to develop ocular symptoms are not known. Management of patients with ocular complications of bisphosphonate use includes treatment with an ocular topical mydriatic drug and a steroid. In most of the cases described in these case reports, the bisphosphonate treatment was stopped, and, in one case, ocular symptoms recurred on rechallenge with the drug.5 In another case, in which the original bisphosphonate was replaced by a different drug of the same class, eye inflammation was reduced and eventually resolved with continued use, suggesting the development of immunological tolerance.11 Between 1997 and April 2004, there were nearly 6 million Pharmaceutical Benefits Scheme prescriptions filled in Australia for bisphosphonates.12 This figure underestimates overall use, as it does not capture bisphosphonates administered to hospital inpatients. Bisphosphonates are an extremely useful class of drugs, and the point of our case report is not to advocate lesser use, but to highlight the importance of early recognition of potentially sight-threatening ocular conditions, as they are readily treatable.

Melissa M Moore BA, BSc, MB BS(Hons) · Jane M Beith PhD, FRACP

To the Editor: Panton–Valentine leukocidin (PVL) is a potent necrotising toxin, which, although produced by less than 5% of all Staphylococcus aureus strains, is strongly associated with pathogenic isolates that cause recurrent furunculosis and severe necrotising pneumonia.1 The virulence of PVL-positive community-associated methicillin-resistant S. aureus (CA-MRSA) causing necrotising pneumonia was recently highlighted in the Journal.2 Conversely, PVL produced by methicillin-sensitive S. aureus (MSSA) is uncommon.1 Here, we describe a case of fulminant necrotising pneumonia caused by PVL-positive MSSA, which, to our knowledge, is the first reported case in Australia. A previously well 33-year-old man presented to the emergency department with a 48-hour history of pleuritic chest pain, fever and productive cough. On presentation, the patient was hypotensive, and in acute renal failure and hypoxemic respiratory failure (type I). Chest x-ray showed bilateral widespread air space consolidation. Despite treatment with intravenous fluid resuscitation and early broad-spectrum antibiotics (ceftriaxone, azithromycin, vancomycin and co-trimoxazole), the patient’s condition rapidly deteriorated, requiring intubation and inotropic support. Multiple blood and sputum cultures isolated MSSA. Bronchoscopy revealed widespread airway haemorrhage. A trans-oesophageal echocardiogram excluded endocarditis. Progressive leukopenia developed. Septic shock and respiratory failure worsened, despite treatment with flucloxacillin as well as maximal inotropic and ventilatory support. The patient died 72 hours after presentation from fulminant pneumonia. Polymerase chain reaction testing subsequently identified the PVL gene in the isolated MSSA. Rising rates of CA-MRSA causing recurrent furunculosis and severe necrotising pneumonia have been reported worldwide.3 Necrotising pneumonia often affects children and young adults,1 and, despite current treatments, mortality rates are over 50%.4 Our patient exhibited two major factors predictive of increased lethality: leukopenia and airway bleeding.4 PVL has been well described in CA-MRSA; it is present in at least 96% of the two predominant strains in south-east Australia.3 There is some evidence that PVL is the major pathogenic factor of CA-MRSA, although this remains controversial.5 The precise pathogenesis of PVL has not yet been discovered; however, a severe inflammatory response secondary to PVL’s cytolytic effects on polymorphonuclear leukocytes, as well as the induction of other bacterial virulence factors, are possibilities.1 Therapies directed against the PVL toxin, including antibiotics such as clindamycin that target the bacterial ribosome, or intravenous immunoglobulin, have been suggested but have little supportive data.2,3,6,7 In contrast to CA-MRSA, the PVL gene is found much less frequently in MSSA, being present in only 2% of isolates in one French study.1 Specific Australian prevalence data are lacking, but PVL-positive MSSA isolates have similar potential to cause severe invasive disease.1,6 Most cases of severe necrotising staphylococcal pneumonia and recurrent furunculosis are caused by CA-MRSA, and empirical therapy for these conditions should cover this organism. This case involving MSSA highlights the role that PVL may play in the pathogenicity of these conditions, and shows that the development of novel therapeutics directed at PVL may be of value.

Ada S-Z Cheung · Craig A Aboltins · John R Daffy · Peter A Stanley

To the Editor: Predicting research quality on the basis of past research publications is clearly imprecise, as noted by Nicol et al in their recent article on National Health and Medical Research Council (NHMRC) grant applications.1 They note that assessor ratings of applicants’ “track records” correspond poorly with the bibliometric data for authors, and that there is vast variability between discipline panels. For immunology, the correlation between track record scores and journal impact or citations was high, at over 0.7. For public health, the correlation was actually negative. The authors consider some possible reasons for the wide discrepancies, such as poor coverage of public health publications in the journals captured by Institute for Scientific Information citation indexes. Nevertheless, they are at a loss to explain why the variation is quite so great, and conclude by suggesting that the time is right for an automated approach to assessing quality. We need to consider the implications of this suggestion carefully. Track record within NHMRC project grants is assessed relative to opportunity, with regard to factors such as legitimate career interruptions, administrative and teaching load, and typical publication rates for the field in question. In the fellowship or program grants schemes, there appears to be less emphasis on relativity, which may explain some of the closer correspondence between actual and expected citation rates. We need to be clear that the use of an “automated” system that uses surrogate measures of research quality will disadvantage individuals who experience a period of illness, take maternity leave, change their research area, or carry a period of heavy administrative or teaching load, as well as those who publish books, book chapters or government publications. It will also disadvantage teams in which feasibility requires fieldwork collaborators whose applied work does not readily translate into peer-reviewed journal publications. For instance, much public health research is based in the community or takes advantage of data collections in the public health system. Collaborators working in this context often have relatively limited opportunities for peer-reviewed publication. Nevertheless, their active collaboration is often critical for achieving a feasible research plan. Also disadvantaged would be teams with a new or junior investigator, particularly if the new team member was the first named investigator. On the other hand, a move to an automated system of quality assessment would further advantage grant applicants who work in research-dedicated institutes, those engaged in basic research, and those who do not require external collaboration. Given these reservations, I suggest further investigation, by discipline, of what makes a “good” track record, before recommending a single assessment formula.

Michael J Davies

To the Editor: Abdulla and Ward’s excellent article on tako-tsubo cardiomyopathy (TTC)1 raises two important issues. The first issue is the diagnostic dilemma faced by emergency physicians and cardiologists in differentiating TTC from ST-elevation myocardial infarction (STEMI) in centres that lack coronary angiogram capabilities. In patients presenting with chest pain and ST elevation on electrocardiography, the diagnosis of TTC might be suspected on recognition of risk factors and the common psychological, physical and emotional stressors that precipitate TTC.1 Supporting evidence can be obtained by demonstration of basal hyperkinesis and apical or midventricular hypokinesis on transthoracic echocardiography. This modality is now available in many centres without coronary angiography. However, if the diagnosis is incorrectly made as STEMI rather than TTC, the patient runs the risk of unnecessary thrombolysis. Alternatively, after risk–benefit analysis, the clinicians may transfer the patient to a facility with coronary angiography to confirm TTC. The second issue is the therapeutic dilemma facing intensivists treating TTC-related shock with adrenergic inotropes. Although cardiogenic shock in TTC is uncommon, it can still occur (4.2%).2 As increased endogenous catecholamines are thought to be central to the pathophysiology of TTC,3 treating shock with inotropes puts the clinician in a quandary. Agents such as adrenaline, dobutamine, dopamine, milrinone and noradrenaline increase cyclic AMP within the myocardial cell, and are commonly used to restore blood pressure and cardiac output. However, in TTC, inotropes may theoretically delay resolution of the apical ballooning. A recent echocardiographic study showed no improvement in apical and midventricular akinesis with the use of low-dose dobutamine.4 Levosimendan is a calcium sensitiser that has been used successfully to stabilise shock secondary to TTC (with and without use of an intra-aortic balloon pump).5 Levosimendan is non-adrenergic and allows earlier introduction of β-blockers than would be possible with adrenergic inotropes. I agree that prospective trials are needed to guide management in this intriguing condition.

Laven Padayachee

In reply: I thank Padayachee for his interest in our review.1 We read Padayachee’s published case series of the use of levosimendan to help recovery of left ventricular dysfunction in tako-tsubo cardiomyopathy (TTC)2 after our review was published. I agree that levosimendan is the inotropic agent of choice in this situation, and this approach has been used successfully in my hospital on two occasions. This is, in fact, what we meant by “In our experience, β-blockade in conjunction with non-adrenergic inotropes can prevent this vicious cycle and allow the ventricle to recover (unpublished data)”. As Padayachee rightly points out, definitive evidence on this point would require a proper randomised trial, which would be very difficult to organise, given the low incidence of tako-tsubo cardiomyopathy and the small fraction of patients who develop cardiogenic shock requiring inotropic support. I think that it is probably better to simply state that levosimendan therapy works and makes scientific sense, so “just do it”. However, Padayachee also surmises that, if the patient has a typical wall-motion abnormality and a typical history, it might be possible to avoid unnecessary thrombolytic therapy in cases of TTC. Unfortunately, my understanding is that this is not the case. Occlusion of the left anterior descending artery (LAD) may result in the classic TTC wall-motion abnormality if the LAD extends far beyond the apex (usually with a non-dominant right coronary). As myocardial infarction can be precipitated by stressful events, and the evolution of electrocardiographic changes in TTC is similar to that seen with an anterior infarct after thrombolysis, there is still no clear way to discriminate between the two diagnoses apart from immediate coronary angiography. Whether computed tomography (CT) angiography can accurately discriminate remains to be seen — this might be useful in centres that have CT but not a cardiac catheterisation laboratory. Until then, I believe it is probably less harmful to give TTC patients thrombolysis than to withhold thrombolysis from patients with large anterior infarcts. Lastly, I invite Padayachee and other interested clinicians who frequently manage these patients to participate in an ongoing study of genetic predisposition to TTC for which we are currently enrolling participants.

Michael R Ward

To the Editor: It is a worthy aspiration for Australia to become the world’s healthiest country, but it will take revolutionary leadership to prevent and manage the effects of obesity that will reverse the previous gains in reducing heart disease.1 In addition, we have to overcome the adverse impact on the health of young people caused by fundamental changes in Australia, highlighted by Eckersley.2 He also identifies medical practitioners as a potential obstacle in that we are overfocused, with government approval, “on an individual, biomedical, disease-centred approach to health at the expense of a more social, preventative model”. He also calls for an increase from the current investment in prevention and public health programs, 1% of health expenditure — but that will only occur if his more radical suggestion is adopted: that governments change their focus from wealth to health creation. It was Japan that embraced this concept, with a health creation policy developed in 1978. It led to a law ensuring that at least 5% of their compulsory health insurance expenditure is allocated to preventive activities. If we are going to achieve Ring and O’Brien’s vision, we are going to have to do more than adopt Japan’s healthy diet. Other keys to their success are: good antenatal care; reinforcement of high breastfeeding rates by provision of small incentive payments; routine home visits to women during pregnancy and during the postpartum period by maternal and child health care workers; and all parents having their own maternal child health record. While these and other measures have probably contributed to Japan having the lowest infant mortality in the world, these interventions are also likely to have influenced their longevity by preventing the Barker hypothesis from being applied. This hypothesis, or developmental origins theory, was derived from observations of infants who are small at birth being at higher risk of increased blood pressure and other adverse cardiovascular endpoints later in life.3 It is interventions during the early years that have evidence of high returns on investment — whereas attempts to influence adult behaviour are difficult, and can fail.4,5

Bret Hart

In reply: Our paper demonstrates the considerable potential for improving Australia’s already competitive international mortality ranking by focusing on several selected conditions and inequalities in their distribution among Australians.1 Hart recognises the aspirational nature of the paper and proposes several challenges and opportunities to improve the health of the mothers, babies and young children of Australia. We agree. As shown by our evidence, Australia’s performance on mortality in infancy and early childhood is less than stellar. We acknowledge that our ranking on some childhood risk factors, such as obesity (which can confer lifelong health disadvantage and may affect future mortality), may well be similar or even worse. A critique of these was beyond the scope of our paper, as we confined our analysis to measures of past mortality. There is ample evidence of effective interventions for infants, children, adolescents, adults and older people, and for various population groups. The interventions include preventive or clinical services — as the Journal’s own repository of guidelines shows.2 We contend that rather than being alternatives, childhood and adulthood interventions are complementary (as are biomedical and social interventions), and we have to advance simultaneously on many fronts. Australia has accelerated to be among the world’s leaders on mortality and life expectancy, but, as Hart presages, this will not remain the case merely through a continuation of current trends. It may take a revolution, but we can at least be clear about how we compare in these areas and what we need to achieve.

Ian T Ring · John F O’Brien

John (“Jack”) Henry Alpers died on 2 November 2007 at his home in Adelaide after battling all year with leukaemia. He was one of the founding leaders of the Flinders University School of Medicine and its major teaching hospital, Flinders Medical Centre. Jack was born on 3 April 1936 in Mannum, South Australia, where his father was a general practitioner. When Jack was 8 years old, the family moved to Adelaide, where he continued his education at St Peter’s College. He then followed his father to study medicine at the University of Adelaide. After graduating in 1960, Jack undertook his initial training at the Royal Adelaide Hospital. This was followed by further formative experiences in Papua New Guinea (New Britain and Port Moresby), the United Kingdom (Hammersmith Hospital, London), the United States (University of Colorado Medical Center, Denver, Colo) and Sweden (Karolinska Hospital, Stockholm). He qualified as a consultant physician with a subspecialty interest in respiratory medicine. Before arriving at Flinders University, he worked as a consultant in Adelaide, Papua New Guinea and Canada. In August 1976, Jack joined the staff of the recently opened Flinders Medical Centre as Head of Respiratory Medicine and Deputy Head of the joint Flinders University/Flinders Medical Centre Department of Medicine. He continued in both roles until his retirement in 2001. An excellent leader in his own clinical discipline, with a commitment to the highest standards of teaching hospital medicine, Jack built a team of talented clinicians, clinical scientists, nurses and administrative staff. He was a gifted and compassionate physician with a particular human touch and a quietly flamboyant personal style. His lifelong interest in social justice was greatly appreciated by all his patients, particularly those with occupational lung disease. An excellent and highly respected clinical teacher and mentor to several generations of medical students and junior doctors, he was also a committed leader in the Flinders School of Medicine and highly valued as a great “team player”. Flinders University appropriately recognised Jack’s contributions by his promotion to Professor in 1997, the award of Emeritus Professor status on his retirement, and the presentation of a Vice-Chancellor’s Award for Excellence in Teaching in 1998. In 2002, he was nationally recognised by the award of Membership of the Order of Australia. Jack is survived by his wife Liz, his children Sarah, John and Liza, and his brother Michael, also a medical graduate and a world authority on kuru.

Lindon M H Wing

Textbook of regional anesthesia and acute pain management. Admir Hadzic, editor. New York: McGraw-Hill Medical, 2007 (xviii + 1259 pp). ISBN 978 0 07 144906 X. In this text, Hadzic aims to provide the scientific basis for the practice of regional anaesthesia, integrating it into the multimodal approach to acute pain management. He has selected 126 contributors, most of whom are American, to write the 83 chapters, nearly all of which are multiauthored. The result is a well coordinated treatise on every aspect of regional anaesthesia, serving as an excellent introduction to the postgraduate study of the subject. No topic is ignored — community practice, the austere environment, and the principles of statistical methods of research are unique inclusions. As well, the new techniques of ultrasound-guided nerve blocks are well covered. The management of postoperative pain introduces latest concepts including multimodal analgesia (although the organisation of an acute pain service has a rather rigid North American approach). The book is very well laid out, punctuated with coloured boxes containing “Clinical pearls” and tabular summaries. It is profusely illustrated with anatomical diagrams, photographs of positioned patients, equipment and some anatomical dissections. While these break up the text into easily readable bites, the photographs are occasionally overdone; repetitive images showing slightly different needle positions add little to the clear descriptions. Some anatomical drawings are too diagrammatical and do not give an easy understanding of the point being made. A final minor criticism: there are slight inaccuracies in the description of the surface anatomy of some nerve blocks, particularly those of the ilioinguinal and iliohypogastric nerves, and of the greater occipital nerve. A newcomer to the art of regional anaesthesia needs three guides — clear textbooks, access to accurate recent concepts and helpful teachers. This textbook admirably fills the first two requirements.

Ken W Sleeman

Bend it like Beckham Watching exciting soccer games can be dangerous to your health, according to German researchers. Acute cardiovascular events involving over 4000 people were analysed during the World Cup soccer tournament of 2006 and compared to a control period. The incidence of cardiac emergencies, including myocardial infarction, unstable angina, and cardiac arrhythmia, increased significantly (by a factor of 2.66) on days when the German team were playing in matches. The proportion of cardiac emergency patients with known coronary heart disease was also greater on these days compared with the control period. Although the study did not allow the identification of the exact triggers provoking the additional observed cardiovascular events, the authors hypothesise that the additional emergencies were triggered by emotional stress related to watching soccer matches involving the national team. N Engl J Med 2008; 358: 475-483 Lighter not brighter Commercial skin-lightening creams can have dangerous side effects for users who are unaware of the components. These creams can potentially contain toxic substances such as steroids and hydroxyquinone. In a report by UK authors, a 28-year-old woman presented to clinicians suffering from symptoms and signs of apparent Cushing’s syndrome, including central obesity, pigmented striae, thin, bruised skin, infertility and hirsutism. On investigation, the patient was found to have very low levels of cortisol and corticotropin. The diagnostic dilemma deepened when she denied taking any medications or illicit drugs, but was eventually solved when she admitted to using a skin-lightening cream daily for 7 years. The cream had been bought from an unauthorised source and was found to contain clobetasol, a potent topical corticosteroid. The authors warn clinicians that the use of skin-lightening agents is common, and that the potential for toxic additives causing health problems should be considered. Lancet 2008; 371: 596 Stents v grafting Since their introduction in 2003, the use of drug-eluting stents has provoked considerable controversy. In an observational study involving over 17 000 patients, US researchers have compared the adverse outcomes for patients receiving drug-eluting stents and those undergoing coronary artery bypass grafting (CABG). Patients with three-vessel and two-vessel disease were studied, and data analysed for rates of mortality and myocardial infarction. In comparison with the use of a drug-eluting stent, CABG appeared to be associated with lower rates of death and of myocardial infarction over 18 months in patients with multivessel disease. Lower rates of repeat revascularisation were also apparent in the group undergoing CABG. The authors comment that they used analyses aimed at overcoming the potential bias of such observational studies, after which the relative outcomes associated with the two procedures remained about the same. N Engl J Med 2008; 358: 331-341 Here kitty A kitten with rabies caused a public health nightmare in South Carolina when it was taken to a softball tournament, potentially exposing hundreds of people to the disease. In a report from the Centers for Disease Control and Prevention, the convoluted story of the movements and subsequent euthanasia of the animal is used to illustrate the importance of a coordinated multistate investigation in such cases of exposure. Interestingly, it was the mother of one of the children involved, herself having been bitten by the animal, who alerted authorities and instigated the investigation. Eventually, 27 people were considered potentially at risk and given post-exposure prophylaxis. The report is also a timely reminder for Australian travellers that rabies is still alive and well in the United States. MMWR Morb Mortal Wkly Rep 2008; 56: 1337-1340 Not the supernanny A program aimed at improving problem parenting appears to have a modest but limited value, Australian researchers have found. A randomised trial set in Melbourne studied the responses of over 600 mothers of children ranging in age from 8 to 15 months over the study period. The intervention group attended a three-session course targeting parenting risk factors for childhood behavioural problems, including unreasonable expectations, harsh parenting, and lack of nurturing parenting. The control group received the usual care from a child health centre. Main outcome measures were maternal mental health, parenting style, and maternal report of child externalising behaviour, such as oppositional defiance and aggression. After 24 months, child behaviour scores, nurturing parenting, and maternal mental health were similar in the two groups but intervention group parents were slightly less likely to report harsh or abusive parenting. BMJ 2008; 336: 318-321

Tanya Grassi

Med J Aust 2008; 188 (6 Suppl).