Letters

In reply: It saddens us that Winsor’s experiences as a remote visiting specialist are so depressingly familiar, but his nihilism is even more disturbing. There has in fact been improvement in the health of the Indigenous population in remote communities; examples of this include the evidence provided by articles in the very same issue of the Journal, by Margolis and colleagues (falling rates of serious injury retrieval) and Ward and colleagues (declining syphilis rates).1,2 An understanding of the social determinants of health is essential to accepting that we can indeed work towards improving health, perhaps not through focusing on specialist medical services but rather in the broader primary health care context. Our students and patients deserve clinicians and mentors who might inspire and look for solutions, rather than retreat into despair. Progress in closing the gap will be far slower than many imagine, but it is not impossible, as we have already seen. We totally refute that we used a “quasi-scientific methodology”. Our study is a simple retrospective audit with not a P value in sight,3 and it has no pretensions to be otherwise. It aims to present a clear story from a defined group, and to add to the many individual anecdotes, such as Winsor’s, that on their own do not gain the attention of employers, policymakers, or government. By building a body of evidence, surely we will be able to more effectively advocate for systemic changes. Collaborating with interested colleagues such as remote area nurses who have published more widely on their own adverse experiences4 is another key strategy in influencing change. We agree wholeheartedly with Nielsen’s viewpoint that obligations to workplace health and safety legislation and to company policy and procedures should be paramount. However, this breaks down when individuals employed or contracted in various capacities are incompetent, ignorant, stupid or just have a sheer disregard for the rules. In addition, there appears to be a lack of scrutiny in remote areas where lower standards are somehow acceptable, and legal frameworks somewhat more fluid. The romanticisation of the bush and the culture of “making do” is partly responsible for the laissez-faire attitude to occupational health and safety. Perhaps our metropolitan colleagues could assist in challenging the status quo and the deeply entrenched beliefs, attitudes and systems that collude in silencing questioners and burnt-out staff.

Ameeta Patel · Margaret Vigants

To the Editor: Young children are at increased risk of severe influenza compared with the general population. Routine vaccination of children using trivalent influenza vaccine (TIV) is recommended in the United States and Canada. The Western Australian government, with support from vaccine manufacturers, has been providing TIV free of charge to all children aged 6–59 months since 2008.1 In 2010, high fevers and an increased incidence of convulsions were observed in children aged < 5 years after administration of TIV. Most reports of adverse events were from WA, owing to higher uptake of vaccination associated with the free vaccination program. The national influenza vaccination program for children aged < 5 years was subsequently suspended,2 and high rates of fever and convulsions were confirmed.2,3 The majority of adverse events occurred after administration of Fluvax or Fluvax Junior (CSL Biotherapies). More than 50% of parents of children who were administered Fluvax or Fluvax Junior reported high fever after vaccination. The incidence of febrile convulsions after vaccination with Fluvax and Fluvax Junior was 4.4 per 1000 doses, significantly higher than expected.3,4 Fluvax and Fluvax Junior are not recommended for children aged < 5 years in the Australian 2011 influenza vaccination program.5 In response to these events, WA Health established an online registry for vaccine-associated adverse events — the Western Australian Vaccine Safety Surveillance (WAVSS). Health professionals are required and members of the public encouraged to report adverse events. In addition, a prospective safety study of the 2011 TIV in children aged < 5 years has commenced at Princess Margaret Hospital for Children and the WA Central Immunisation Clinic. From 15 March to 29 April 2011, 2227 doses of TIV were administered to children aged < 5 years in WA (2130 doses of Vaxigrip [Sanofi Pasteur]; 97 doses of Influvac [Solvay]). Adverse events in four children aged < 5 years have been reported via WAVSS: two with elevated temperature (≥38°C yet < 39.5°C) within 24 hours of vaccination, one with vomiting and diarrhoea after vaccination, and one with fever (not specified) and convulsions 4 days after vaccination (this child had a respiratory tract infection at the time of vaccination). All four children were administered other vaccines with TIV. In the safety study, 144 children were enrolled between 15 March and 29 April 2011. Adverse events after vaccination were reported in 10 children (7%), two of whom received other vaccines in addition to TIV. All 10 children had fever reported, and one child had a temperature > 39.5°C. Two children developed vomiting. No convulsions were reported and none of the children who had adverse events required assistance from a health care professional. These data demonstrate that the significant adverse events that occurred after administration of TIV in 2010 have not been observed in WA during early 2011. Ongoing surveillance is underway and will continue. Poor uptake of influenza vaccination in Australian children is likely to result in increased influenza-related hospitalisation, morbidity and mortality. Data such as those reported here are required to reassure the community of the safety of this vaccination program before the expected start of the 2011 influenza season.

Christopher C Blyth · Tracy Y Markus · Paul V Effler · Peter C Richmond

To the Editor: Australian influenza notification and hospitalisation rates are highest in children aged under 5 years,1 the group most commonly affected by egg allergy (estimated to affect 8.9% of infants aged 12 months in a recent Melbourne study).2 The ability to safely vaccinate egg-allergic individuals is thus an important public health issue, particularly in the context of potentially pandemic influenza. More than 98% of over 4000 egg-allergic individuals have tolerated vaccination under direct medical supervision in published studies.3-6 As a result, Australian and several international guidelines3,5,6 recommend that influenza vaccination of the egg-allergic individual may be undertaken using a two-step protocol (10%–90% vaccine dose, 30 minutes apart with a final 30-minute waiting period), as long as vaccines contain less than 1 μg egg ovalbumin/dose. Prior allergy testing with the vaccine is not recommended. All currently available influenza vaccines for the 2011 season in Australia have less than 1 μg ovalbumin/dose, specifically Influvac (Abbott Pharmaceuticals, < 1 μg/dose), Intanza (Sanofi Pasteur, < 0.05 μg), Vaxigrip and Vaxigrip Junior (Sanofi Pasteur, < 0.05 and < 0.025 μg, respectively), Fluvax (CSL, < 1 μg), Agrippal (Novartis, < 0.20 μg) and Fluarix (GlaxoSmithKline Australia, < 0.05 μg). Based on current evidence, we suggest that the 2011 seasonal influenza trivalent vaccines can be safely administered in a medically supervised primary care setting as a single dose with a 30-minute observation period (rather than the standard 15 minutes) in those with non-anaphylactic reactions to egg. In those with a history of egg anaphylaxis (or positive allergy tests without a history of ingestion), we recommend a split-dose protocol after discussion with an allergy specialist. We acknowledge that these guidelines are at variance with those in the Australian immunisation handbook,7 but they are consistent with more recent evidence and international recommendations. Whether it is also safe to administer vaccines containing more than 1 μg ovalbumin/dose8 awaits confirmation in a larger patient population and is not currently recommended.

Raymond J Mullins · Michael S Gold

To the Editor: Amid debate about growth in the number of Disability Support Pension (DSP) recipients and the increasing percentage of recipients with mental disorders,1,2 the recent federal Budget announced further welfare reforms and significant investment in mental health services.3 There are, however, limitations in the data informing the current discussion. Administrative data are restricted to coding the primary disability of DSP recipients, and do not assess comorbidity. Further, data on the health of recipients receiving other welfare payments are lacking, precluding thorough understanding of the context of the growth in the DSP population. We recently published an analysis of the 2007 Australian Bureau of Statistics National Survey of Mental Health and Wellbeing, in which we estimated the prevalence of common mental disorders in different categories of working-age welfare recipients.4 The main results showed that just over one-third (34%) of income-support recipients had a 12-month affective, anxiety and/or substance use disorder, compared with 20% of non-recipients; that, despite a decade of reform of the welfare and mental health systems and improved economic circumstances, there had been little change in the overall prevalence of mental disorders among welfare recipients since 1997 (Box, A);5 and that most income-support recipients with mental disorders received payments other than DSP. We compared data from the 1997 and 2007 surveys, focusing on welfare recipients with a mental disorder (12-month common mental disorder assessed by the World Mental Health Composite International Diagnostic Interview). Of the 10 641 and 8841 survey respondents in 1997 and 2007, 667 and 362, respectively, were identified as working-age welfare recipients with a mental disorder.5 We estimated that 31% of income-support recipients with mental disorders were DSP recipients in 1997, but in 2007 this had increased to 45% (Box, B). The increased concentration of recipients with mental disorders receiving the DSP was significant in logistic regression models controlling for age and sex (odds ratio, 1.72; 95% CI, 1.05–2.83).5 The increased profile of mental disorders among DSP recipients may reflect shifts between payments within the welfare recipient population. Although this could be due to financial incentives to receive DSP rather than lower-paying allowances (eg, Newstart Allowance), the results may reflect that some income-support recipients with a mental disorder are unable to comply with the new activity or work requirements introduced by recent policy changes.6 Careful consideration is needed of the potential adverse unintended consequences of welfare reforms for the large number of income-support recipients with mental disorders. Changes that promote DSP as the most appropriate option for people with mental disorders risk entrenching their alienation from the workforce. Mental disorders and welfare recipients (with 95% CIs), 1997 and 20075 DSP = Disability Support Pension.

Peter Butterworth · Philip M Burgess · Harvey Whiteford

To the Editor: The Health Practitioner Regulation National Law Act 2009 (Part 8, Sections 140 and 141) enshrines mandatory notification in the new national registration framework. As registered health practitioners, clinician-researchers are bound by the notification requirements. This raises the question of whether mandatory notification has implications for observational research in health services that is conducted by clinician-researchers. In particular, how likely is it that these requirements will lead to reclassification of one’s observations from “research data” to “notification evidence”? Three initial considerations are important here. First, the Act was designed to make health care safer for patients. Its intent is to limit incidents by ensuring clinicians are more open about and address inappropriate care. Second, serious incidents are rarely isolated, instantaneous and therefore easily observable disasters. When something goes seriously wrong, problems tend to be inherent in how teams practise, communicate and support one another over time. Third, observers may encounter instances of substandard care, but these become notifiable only when the threshold of unsafety is surpassed. This threshold is pegged to relatively high levels of severity, frequency and risk.1 In all, observational research can help clinicians to identify existing risks, but it is unlikely to become a source of notification. Human research ethics committees may also feel obliged to acknowledge and consider the possibility of incident notifications arising from observational research. However, it would not be wise to regard the risk of such notification as detracting from a study’s potential for obtaining ethics approval. The situation calls for specification of: how the observers will deal with incidents if and when observed the observers’ understanding of the definition and threshold of notification how the definition of notification is likely to bear on the study how the design of the study affects the likelihood of notification (eg, does the researcher seek to identify care irregularities or track these irregularities over time?) a projection of the relevant service’s vulnerabilities to notification, and plans for addressing and resolving existing vulnerabilities. In addition, mandatory notification does not mean that observational research will be more difficult to “sell” to ethics committees and frontline clinicians. The aim is generally to stimulate learning and raise awareness of problems. Our experience is that if the research is designed with frontline clinicians, and they contribute to its implementation, analysis and publication,2 it attracts considerable interest and support.3 Frontline staff know that the best way to understand the complexities inherent in their everyday work is through observation. Such research takes seriously their specific and unique circumstances, enabling them to actively participate as analysts and improvers of their own practice. Observation encourages reflection, and this means they become aware of and can proactively resolve their own vulnerabilities. Ultimately, the priority for clinician-researchers involved in observational research in health services, as for patients, is to reduce risks and prevent incidents.

Rick A M Iedema · Donella A Piper

To the Editor: We read with interest the case by Nadeem and Khateeb of an elderly man with migratory lung lesions and the concurrent finding of mixed cryoglobulins.1 We are concerned about attributing this man’s symptoms to mixed essential cryoglobulinaemia. The clinical syndrome described in this patient is not typical of cryoglobulinaemia. The establishment of a diagnosis of essential mixed cryoglobulinaemia in this man is problematic, given a lack of cutaneous findings and no definite evidence of peripheral neuropathy and renal disease. Nerve conduction studies to establish the presence of peripheral neuropathy and renal biopsy to confirm membranoproliferative glomerulonephritis were not carried out. Given his age, the confirmation of membranoproliferative glomerulonephritis would potentially necessitate long-term and possibly intensive immunosuppression to prevent subsequent development of renal failure. The cryoglobulins reported in this case fulfil the criteria for type II cryoglobulins. However, they were of relatively low concentration (0.4 g/L of monoclonal IgM/kappa and 0.1 g/L of polyclonal IgG). As well as hepatitis C, type II cryoglobulins can be detected in association with hepatitis B and Sjögren’s syndrome.2 The absence of anti-Sjögren’s syndrome A and anti-Sjögren’s syndrome B antibodies by no means excludes the diagnosis of concurrent, subclinical Sjögren’s syndrome. In addition, hepatitis B and C have not been excluded as the cryocrit was not analysed for hepatitis B virus DNA and hepatitis C virus RNA. Furthermore, the relatively low concentration of cryoglobulin detected and the findings of chest opacities with very high levels of C-reactive protein (that fell to normal levels with antibiotic treatment) could also be due to an infective aetiology.3 We also note that the thermal amplitude of the cryoglobulins should be investigated in such cases, as it has been well described that cryoglobulins of higher thermal amplitudes are more likely to be clinically significant. In conclusion, given the long duration of this man’s admission, repeat cryoglobulin measurements after he was discharged would have helped to more clearly define the role of cryoglobulins in his disease. We therefore recommend caution when interpreting low levels of cryoglobulinaemia in patients who have a clinical syndrome that may or may not be consistent with clinical cryoglobulinaemia.

Carl A Kennedy · David Gillis · Richard C W Wong

To the Editor: Katelaris recently asserted: In our society the response to medical error is typically legal, rather than investigative and remedial. This should be deplored by both the profession and the public.1 This polarised orientation seems more political than objective. It acknowledges neither the reticence of medical professionals regarding investigative reviews, nor the costs to patients’ families. Katelaris notes that defensive approaches encourage the concealment of errors. I have long advocated clinical reviews of critical incidents. Having personally set up Queensland Health’s original Suicide Register, I released statewide patient suicide data to health services. Reactions from service providers were decidedly underwhelming, despite the gravity of the outcomes. Katelaris did not explain how clinical reviews can address the problem of income replacement or other major costs associated with catastrophic outcomes for patients’ families. In the 1990s, I reviewed all Australian litigation for failure to prevent suicidal behaviour in care, through a survey of insurers and defendant solicitors.2 Of the 13 non-fatal cases identified, paraplegia occurred in seven patients, with other serious injuries in the remaining six. These were not trivial complaints. I also reviewed what might be learnt from the international literature3 and made known my availability to assist with clinical reviews of patient suicides. Despite having been an expert witness at the Royal Commission into Aboriginal Deaths in Custody and a Royal Australian Navy inquiry into the loss of a sailor who disappeared overboard in 2002, among others, no medical services have sought my assistance over more than 20 years! I understand, from personal experience, how distressing trivial and vexatious complaints against doctors are. I have even received a complaint for providing a report to a plaintiff’s solicitor, in relation to failure to prevent suicidal behaviour, in which I asserted that reasonable care had been provided. I now run a personal-injury psychiatric practice, with alleged medical negligence featuring in about 3% of cases. Mostly I am called by the plaintiff’s side, often following devastating surgical outcomes. Referral bias operates, in that negative surgical outcomes with psychiatric consequences are likely to have been more serious than those without. The outcomes have often been both emotionally and financially devastating to those affected. I long to see a medically mature culture develop with respect to clinical reviews of critical incidents, but my experience suggests we still have a way to go. But even when or if such a medical utopia is achieved, how will the financial disadvantages to patients’ families be overcome?

Christopher H Cantor

To the Editor: I was extremely surprised to note that there was no mention of the Australian Council on Healthcare Standards’ (ACHS) extensive national clinical database (http://www.achs.org.au/ClinicalIndicators) in the recent article by Evans and colleagues on clinical-quality registries.1 Since 1993, commencing with a small set of generic indicators that were of limited value, the ACHS has been collecting clinical data through its clinical indicator (CI) program as part of its accreditation process. Now, with over 300 CIs in use and around 670 health care organisations (HCOs), including some from New Zealand, contributing data, the scope of the ACHS national clinical database is unique in the world. Its longevity makes it one of very few national programs that can display longer term trends in processes and outcomes — both desirable and undesirable — of medical care. The clinical indicators, which form the basis of the database, were all developed in conjunction with providers of medical care, namely, the medical colleges. The validity, reliability and effectiveness of the indicators were established (and published) subsequent to introduction of the more specific indicators into the accreditation process.2 In addition to providing aggregate and peer-comparative data to the contributing HCOs, the ACHS publishes aggregate data with detailed analyses on an annual basis.3 As with similar databases, problems have arisen regarding maintenance of currency and relevance, timelines for reporting, and other issues. However, it seems extraordinary that this valuable aid to determining the quality of health care standards — envied by many countries — could be ignored by Evans et al, as it was similarly ignored by the authors of a recent special MJA supplement that reported on gathering patient-centred health care data aimed at improving care.4

Brian T Collopy, AM

To the Editor: Cancer Voices NSW, a leading organisation for health care consumers, welcomes the coverage in the 18 April issue of the Medical Journal of Australia of gaps in and barriers to research endeavours into cancer. We particularly commend Olver’s editorial which, among other things, calls for more consumer-friendly clinical trial registries to play a role in enhancing patient recruitment by making it easier for them to find suitable trials.1 Cancer Voices NSW (http://www.cancervoices.org.au), the voice of people affected by cancer in our state, has long advocated for such a resource, both centralised and reliable. We are delighted to advise Journal readers that an initiative of ours, the Australian Cancer Trials website (http://www.australiancancertrials.gov.au), is now up and running. It has been publicly available since its launch by Professor Jim Bishop, Australia’s Chief Medical Officer, in November 2010 and is hosted by Cancer Australia. In partnership with consumers, the development of the project was led by a research team that included members from the University of Sydney, the Australian New Zealand Clinical Trials Registry (ANZCTR), Cancer Voices NSW and Cancer Australia. Consumers had considerable input to the website’s development through consultation with members of Cancer Voices NSW and Cancer Australia’s National Consumer Advisory Group. The Australian Cancer Trials website was funded by Cancer Australia with partial funding from the National Health and Medical Research Council project grant (grant reference number 512380). The Australian Cancer Trials website’s consumer-friendly portal offers open access information held on both the ANZCTR and the United States ClinicalTrials.gov registers (http://clinicaltrials.gov/). It currently lists over 1000 cancer trials, and it is updated every day. Consumers can do a “simple search” by cancer type or keyword or an “advanced search” using criteria including cancer status, trial focus, phase of clinical trial, recruitment status and age category. Information about each trial is displayed in a user-friendly format. All cancer trials registered with ANZCTR in Australia for which a few consumer-friendly additional cancer fields are completed at registration will find recruitment easier. Patients with cancer and their specialists will have much easier access to up-to-date clinical trial information. This website is a successful model that can be translated to other diseases and conditions, and indeed, generically.

Sally Crossing

To the Editor: The association between poor hand hygiene of health care workers and nosocomial infection is well established.1 The National Hand Hygiene Initiative2 has been established to improve hand hygiene among health care workers, and the use of ethanol- or isopropanol-based hand sanitisers has been widely adopted in the hospital setting. To encourage their use by health care workers, many hospitals have undertaken extensive education programs and made hand sanitisers with high alcohol content readily available at all points of patient care. An unanticipated but potentially adverse outcome of this campaign is the intentional consumption of hand sanitisers by patients. We report the case of a 45-year-old man, with a history of polysubstance misuse, who was admitted to our institution with epigastric pain in the setting of acute-on-chronic alcohol intake. No evidence of pancreatic or biliary disease was found and the diagnosis of probable alcohol-related gastritis was made. On Day 3 of admission, the patient became increasingly drowsy. Clinical examination showed that he was rousable, and had a Glasgow Coma Scale score of 13. There were no other significant findings. Some hours later, six near-empty 375 mL bottles of Aqium Gel (Ego Pharmaceuticals, Melbourne, Vic), an antibacterial hand sanitiser that has an ethanol content of 66%, were found by the patient’s bedside. Excipients in this gel include thickener, dexpanthenol, dl-alpha-tocopheryl acetate, fragrance, pH neutraliser and water.3 On direct questioning, the patient admitted to intentionally consuming the contents of the hand sanitiser bottles. This was supported by a breath test performed about 40 minutes after the bottles were found, which showed a blood alcohol concentration of 0.271%. Following advice from the Poisons Information Line, supportive therapy was instigated and the patient made an uneventful recovery. Intentional consumption of ethanol- and isopropanol-based hand sanitisers by hospitalised patients has been described in overseas settings and serious adverse outcomes (including the need for intubation) have occurred.4-6 In one emergency department, all removable bottles of alcohol-based hand sanitiser in patient care areas were replaced with non-removable, self-contained dispensers.6 Experience at our institution over the past 6 months suggests that consumption of alcohol-based hand sanitisers by inpatients may be an increasing problem in Australian settings — we are aware of a further three patients who have consumed these products while at our institution. An increased awareness of this practice is required among health care workers in Australia, as it has the potential to create diagnostic dilemmas and lead to serious outcomes, and preventive measures need to be identified and implemented.

Lachlan M Batty · Anna J Brischetto · Ajay C Kevat · Michael J Oldmeadow

To the Editor: A 44-year-old female nurse with a 4-year history of hand dermatitis was referred to an occupational dermatology clinic in Melbourne. In 2009, her hand dermatitis had worsened when she started working in a neonatal intensive care unit, where she used antimicrobial hand gel more frequently. Her hands improved when she spent time away from work but worsened again within 2 days of returning. Patch testing was conducted using our baseline patch test series as well as rubber accelerators (used in manufacturing rubber gloves), antiseptics and the patient’s own samples (eg, gloves, moisturiser, etc). She developed positive reactions to formaldehyde and the formaldehyde releasers quaternium 15, imidazolidinyl urea and diazolidinyl urea, as well as the hand gel she had been using — Microshield Antimicrobial Hand Gel (Johnson and Johnson Medical, Sydney, NSW) — a gel containing 30%–60% water, and diazolidinyl urea as a preservative. (Diazolidinyl urea is not listed on the safety data sheet for this product as it is in a concentration of < 1%.) A negative result for a radioallergosorbent test indicated it was unlikely the patient was allergic to latex. She was advised to use a waterless, alcohol-based hand cleaner without preservatives and was given advice about general skin care, especially use of moisturising cream.1 She complied with this advice, and her condition subsequently improved. Diazolidinyl urea is a preservative commonly used in cosmetic products. Once absorbed into the skin, it releases small amounts of formaldehyde. Individuals may become sensitised to diazolidinyl urea, formaldehyde, or both. This can occur at any stage, even if the individual has been exposed to the product for years. At our occupational dermatology clinic we have patch tested 2688 patients and diagnosed 1461 of these with allergic contact dermatitis (ACD) over the past 16 years. Nine health care workers have been diagnosed with ACD to diazolidinyl urea contained in products they used at work. Thirty other patients have had ACD caused by this preservative from other sources, usually their skin care products. Many workers will simply accept their hand dermatitis as part of the job, or begin treatment without patch testing. It is only with patch testing that an accurate diagnosis can be made. Waterless hand cleaners are an important part of hand hygiene in health care settings,2 and they minimise irritation caused by washing hands with soap and water and drying with paper towels.3 Alcohol-based liquid hand-disinfectant solutions are more efficacious than gels.4 Our report provides another reason to use these products as, generally, alcohol-based liquids do not contain preservatives such as diazolidinyl urea.

Jennifer L Cahill · Rosemary L Nixon

To the Editor: Weight fluctuations may lead to significant changes in a patient’s treatment, so it is vital that hospital scales are accurate. A literature review revealed that calibration,1 accuracy2 and centralised hospital quality control3 of hospital scales were issues that are being recognised and addressed around the world. We audited all scales at the Royal Melbourne Hospital, city campus, to assess their accuracy and identify the types of scales that are likely to be most accurate. A preliminary survey identified all scales on the wards and in outpatient departments. On a single survey day, each scale was categorised and photographed. Scales were “zeroed” and standard weights of 5 kg, 10 kg, 15 kg and 20 kg, and a person whose weight had been established elsewhere as 106 kg, were then weighed on each scale. Our primary measure of accuracy was the difference between 106 kg and the recorded weight of the person, as this most closely approximated the weight of an average patient (rather than using the 5, 10, 15 and 20 kg weights). Forty-three of 50 scales identified in the hospital were tested. Scales that were excluded were either not working or not able to be tested with the weights we used. All scales in the outpatients department were digital (22). On the wards, there was a mix of sit-on (6) and stand-on (15), and digital (9) and analogue (12) scales. The digital scales had an accuracy (range around the standard weight) of − 1 kg to +1.5 kg, compared with an accuracy of − 3.5 kg to +1 kg for the analogue scales (P = 0.006; Wilcoxon signed rank test). Interquartile ranges were − 0.45 kg to +0.07 kg for digital scales and − 2 kg to +0.5 kg for analogue scales. The mean deviation from the correct weight was 0.06 kg for digital scales and 0.55 kg for analog scales. The most accurate scales were in the renal wards, used by dialysis outpatients and inpatients. Some areas had scales that were unusable by patients, such as sit-on scales in the geriatric ward (Box 1) that were difficult to mount. A haematology ward, where decisions are often made on the basis of changes in weight, had five sets of scales, with significant inaccuracies and differences between them. In one ward, no scales could be located, and five out of 23 outpatient rooms had no scales. The digital scales were more accurate than the analogue scales (Box 2). In areas where treatment decisions are made on the basis of changes in weight, scales should regularly be checked for accuracy, and patients should be weighed on the same scales each time they are weighed. For greater accuracy and consistency in measuring patient weights, we recommend that all scales be upgraded to digital scales throughout the hospital. 1 Sit-on analogue scale at Royal Melbourne Hospital, unusable for some patients 2 Weight variations in 43 digital and analogue scales at Royal Melbourne Hospital * As measured using standard weights of 5 kg, 10 kg, 15 kg, 20 kg and a 106 kg person.

Rimma Goldberg · Geoffrey Hebbard

To the Editor: Atypical femur fractures appear to be an emerging adverse outcome of long-term use of bisphosphonates. Although analyses of epidemiological data suggest that subtrochanteric and diaphyseal fractures per se are rare,1,2 the true incidence of atypical fractures (a distinct subset of such fractures) is unknown. In a recent 5-year retrospective study, we reviewed individual radiographs of 152 patients with subtrochanteric and diaphyseal femur fractures and identified 20 atypical fractures.3 Seventeen of these 20 atypical fractures had occurred in patients treated with oral bisphosphonates. In light of these findings, we sought to calculate the incidence of atypical femur fractures in the population served by our large tertiary referral hospital in Sydney. According to the Australian Bureau of Statistics 2006 Census, the hospital’s catchment population (as defined by the New South Wales Department of Health) was 174 448. The annual incidence of atypical femur fractures in 2006 was therefore estimated to be 0.23 per 10 000 in the general population, and 1.6 per 10 000 in people aged over 65 years. These estimates, based on a stringent radiological definition of atypical femur fractures, confirm that, on a population basis, these fractures are indeed rare. We also sought to define the mean annual incidence of atypical femur fractures in patients treated with oral bisphosphonates. Thus, we obtained data on the wholesale purchase of alendronate and risedronate by pharmacies within the hospital’s catchment area over the 5 years of the original retrospective study (1 June 2003 to 30 May 2008) from IMS Health Australia (market researchers for the global pharmaceutical and health care industries). A mean number of 2860 patients per year were prescribed alendronate and 1265 patients per year were prescribed risedronate. This corresponded to a mean annual incidence of atypical femur fractures of 10 per 10 000 in patients taking alendronate and three per 10 000 in those taking risedronate. The use of a relatively small number of cases to calculate these incidences is a particular limitation of our research, and is a reflection of the rarity of these events. Furthermore, our estimates need to be considered within the wider context of the established beneficial effects of bisphosphonates in patients with osteoporosis. On the basis of randomised trials, it has been estimated that treating 1000 women with oral bisphosphonates for 3 years prevents 100 fractures.2 Also, several meta-analyses have confirmed significant reductions in the risk of osteoporotic vertebral and non-vertebral fractures in patients treated with oral bisphosphonates.4,5 In spite of two recent large database studies that showed a greater incidence of atypical fractures among long-term bisphosphonate users,6,7 atypical fractures are rare and the risks of using this class of drugs appears to be strongly outweighed by their proven efficacy in preventing fractures.

Christian M Girgis · Markus J Seibel

To the Editor: Harper and Ko recently suggested radically changing the way we investigate patients with stable coronary artery disease (CAD), stating that they should initially undergo computed tomography coronary angiography (CTCA), with subsequent stress testing if CTCA shows atherosclerosis.1 To save costs, they recommend excluding stress nuclear myocardial perfusion imaging (MPI) because it has similar accuracy to stress echocardiography and involves ionising radiation. To suggest that the available evidence supports CTCA as the first-line investigation of stable CAD is premature, and likely to cause more therapeutic confusion than it resolves. Of particular concern is the assertion that all patients with any detectable atherosclerosis on CTCA should undergo intensive medical therapy for CAD. The clinical significance of mild atherosclerosis detected on CTCA in patients with chest pain that is unlikely to be of cardiac origin is uncertain, with no clinical studies demonstrating a benefit of medical management for CAD based on CTCA findings. Conversely, were such patients investigated first with a stress test, those with a negative test could be reassured that their chest pain is not cardiac and their intermediate-term prognosis is excellent. Importantly, the directive for unproven lifelong medical therapy for CAD is averted. It is also incorrect to imply that different stress-testing modalities may be seen as equivalent because they have comparable diagnostic accuracies, because their strengths and weaknesses remain complementary. This allows referring physicians to choose the modality that most suits the individual patient. For example, stress echocardiography is more operator-dependent, with known limitations in patients with obesity, airways disease, arrhythmias, poorly controlled hypertension, and contraindications for β-blocker cessation. It also cannot be fused with CTCA images, as myocardial perfusion images can.2 While we agree that measurement of fractional flow reserve (FFR) is an extremely important advance in interventional cardiology, it has the limitation of underestimating ischaemia in patients with small-vessel disease (eg, patients with diabetes).3 We agree that demonstrating ischaemia is the critical component in the decision to perform either percutaneous coronary intervention or coronary artery bypass graft surgery — and until now the largest body of evidence has been accumulated with MPI.4 Moreover, demonstration of regional ischaemia on MPI associated with an angiographic stenosis obviates the need for FFR. Electrocardiographic stress testing alone cannot provide these localising data. The advent of CTCA promises to reshape how we assess and manage CAD in the future, but today we should be guided by the clinical evidence, and be mindful not to put the cart before the horse.

Victor Kalff · Stephen J Duffy · Andrew J Taylor

To the Editor: Harper and Ko have ignored significant facts regarding myocardial perfusion scintigraphy and made unsubstantiated conclusions regarding computed tomography coronary angiography (CTCA) and fractional flow reserve (FFR).1 Their investigation algorithm for suspected and known stable coronary artery disease (CAD) is flawed. By definition, stable CAD patients cannot be categorised into a “suspected CAD” subgroup. CTCA is not an appropriate first-line investigation for patients presenting with atypical chest pain or equivalent syndromes. Being purely anatomical, CTCA cannot determine the functional significance of CAD, rendering it ineffective in intermediate disease. Furthermore, CTCA often overestimates stenoses due to partial voluming and blooming. Guidelines from the United Kingdom National Institute for Health and Clinical Excellence (NICE) state that “questions remain about the ability of multislice CT coronary angiography to accurately identify stenoses of functional significance ... in people with stable chest pain”.2 Harper and Ko’s algorithm will lead to more investigation, provide no differentiation over and above Step 2 (functional imaging), and increase radiation dose, contrast burden and delays between presentation and definitive treatment. The real potential of CTCA lies in its ability to non-invasively assess plaque burden and therefore help rationalise long-term pharmacotherapy in high-risk, asymptomatic patients. However, because there is a lack of evidence for this approach, it has been largely ignored and instead the CTCA community has been “sidetracked” into comparing CTCA with functional imaging. Harper and Ko claim that additional costs from the inevitable increase in CTCA scans would be “minor in comparison to the savings”. This is unproven, and not supported by NICE.2 For atypical symptoms, Harper and Ko recommend “the less expensive ECG [electrocardiogram] exercise test” to risk-stratify patients; however, stress ECG testing is poor at predicting the degree of myocardium at risk, a key factor in risk-stratifying patients. The exercise ECG lacks specificity, leading to unnecessary invasive testing, and many patients are unable to comply. NICE has abandoned exercise ECG testing completely.2 The authors state that a “wealth of data has validated the accuracy of FFR”. The original papers demonstrating a significant FFR of 0.75 were based on perfusion imaging.3,4 The review cited quotes a lower sensitivity and specificity of FFR compared with perfusion scintigraphy, and lists scintigraphy as the “clinical gold standard of ischemia”.5 This is because scintigraphy is the most sensitive technique for identifying functionally significant CAD, as it detects the first abnormality in the ischaemic cascade (reduced myocardial perfusion). Furthermore, the exact level of FFR significance (0.75 v 0.80) is debated. In practice, there is a large degree of operator “discretion” in deciding to revascularise, irrespective of the FFR value, which is often “intermediate” in itself. Harper and Ko question the cost of scintigraphy; however, it is more than $300 cheaper than FFR measurement. They overstate the cost of a standard guidewire by threefold.1 In just one study of over 5000 patients (three times the population of a recent FFR meta-analysis6), increasingly abnormal perfusion scans predicted death and myocardial infarction. There was a reduction in death following revascularisation according to defect severity.7 The nuclear substudy of the COURAGE trial confirmed this.8 No study of CTCA or FFR has been able to predict survival with revascularisation, as the technology is unable to define area at risk. Despite this, Harper and Ko conclude that the Medicare rebate for nuclear testing should be abolished. The authors state that “instituting these changes would undoubtedly result in improved outcomes and substantial savings”. This comment is opinionated, inflammatory and not based on current evidence. The only reasonable conclusion is that before a rebate for CTCA is even proposed, it should be proven diagnostically and prognostically equivalent to myocardial perfusion scintigraphy in predicting ischaemia.

William J van Gaal · Kevin Allman

To the Editor: Although Harper and Ko’s effort at proposing an algorithm1 to reduce unnecessary cardiac catheterisation and stenting is laudable, it is concerning that they advocate investigating patients with stable coronary artery disease (CAD) using computed tomography coronary angiography (CTCA), with an algorithm, furthermore, that has not been validated in terms of patient outcomes. The COURAGE trial demonstrated that percutaneous coronary intervention (PCI) provided no survival advantage or reduction in myocardial infarction over 5 years of follow-up compared with optimal medical management in patients with chronic stable angina.2 PCI provided a relative symptomatic benefit only within the first 3 years. Therefore, it is debatable whether imaging most of these stable patients — much less catheterising them — provides any enduring favourable patient outcomes. For those who do require intervention, fractional flow reserve (FFR) measurement does obviate unnecessary stenting during a cardiac catheterisation. But why perform CTCA — which cannot diagnose ischaemia — in the first place, only to then perform an expensive invasive catheterisation to compensate for it? Why not diagnose ischaemia with an initial non-invasive stress test (nuclear or echocardiography) and only proceed to catheterisation if revascularisation is warranted, thus also lessening the radiation dose? Modern gamma cameras allow nuclear stress studies with radiation doses as low as 2–3 mSv. Yes, CTCA can (as opposed to does) achieve comparable doses with prospective gating, but without the left-ventricular function analysis that nuclear or echocardiography studies provide. Advocating the elimination of the rebate for nuclear stress studies is thus premature, if not ill informed. Harper and Ko’s algorithm relies on the assumption that medical therapy is appropriate in asymptomatic patients for any degree of coronary atherosclerosis, hence justifying the use of CTCA for its detection. However, there is considerable uncertainty about the benefits of medical therapy for primary prevention in low-risk patients.3 Furthermore, the use of CTCA has not been validated as a determinant of appropriate medical management leading to favourable patient outcomes. This contention remains speculative. Indeed, contrary to the claims of CTCA supporters, the United States Centers for Medicare and Medicaid Services has declared that there is uncertainty regarding any potential health benefits or patient management alterations from including coronary CTA [computed tomography angiography] in the diagnostic workup of patients who may have CAD. No adequately powered study has established that improved health outcomes can be causally attributed to coronary CTA ... the body of evidence is of overall limited quality and limited applicability ... in community practice.4 Consequently, the technology also poses significant potential to unnecessarily increase the population radiation burden.5

Peter Karamoskos

To the Editor: Harper and Ko stress the importance of differentiating the presence of atherosclerosis from ischaemia,1 a concept that has been well understood for years. We agree that identifying myocardial ischaemia is important in the management of atherosclerosis; there are a variety of well validated non-invasive tools for this, including exercise electrocardiography, stress echocardiography, and nuclear myocardial perfusion imaging (MPI). However, we have concerns about some of the sweeping changes suggested by the authors — in particular, replacing nuclear MPI with stress echocardiography. While published studies report similar accuracy for these modalities, it is clear that each has strengths and weaknesses. Stress echocardiography is an excellent tool that will often suffice but it is operator-dependent, while MPI is more accurate for single-vessel ischaemia. It is well known that a diagnostic stress echocardiogram cannot be achieved in some patients, so an alternative modality may be required. This is particularly problematic in Australia, where there is no mechanism in place to fund the use of ultrasound contrast imaging. MPI remains a widely accepted technique globally, with a substantial evidence base to support its diagnostic and prognostic impact. For instance, a negative MPI study is generally associated with a cardiac event rate of < 1% in the following year.2 Further, its role in directing the mode of treatment on the basis of extent of ischaemia and its cost-effectiveness as the “gatekeeper” to cardiac catheterisation have been amply demonstrated.3 The use of radiation in medical procedures is always subject to the ALARA (as low as reasonably achievable) principle, and prescribed doses in Australia are typically lower than those quoted in the American literature cited by Harper and Ko. Recent advances in hardware and software with MPI have achieved additional gains in reducing radiation exposure.4 The cost of MPI is greater than stress echocardiography, but remains less than angiography and fractional flow reserve (FFR) measurement. Further, Harper and Ko’s proposed cost savings will not be realised with their call for an increased use of computed tomography coronary angiography and FFR measurement. The job of a good clinician is to choose the right test for the patient; in some cases this is a stress echocardiogram but it is often an MPI study, as supported by international guidelines.5 Thus, readers should be mindful that Harper and Ko’s views about replacing nuclear stress tests with stress echocardiography and abolishing the Medicare item number for nuclear stress tests are personal and may be contrary to sound evidence.

Nathan Better · Myles B Webb · David L Prior · Steven A Unger · George Larcos

In reply: We thank the authors of these letters for their comments on our article. In response to Kalff and colleagues, we firmly believe stress testing should be reserved for the diagnosis of ischaemia in patients with known coronary artery disease (CAD), and computed tomography coronary angiography (CTCA) is the investigation of choice for anatomical diagnosis of CAD in patients with suspected CAD. In this, we are supported by recent guidelines from the American Heart Association and others.1 Most heart attacks occur as a result of plaque rupture in coronary lesions of insufficient severity to cause ischaemia on stress testing, but that would be detected on CTCA.2 In view of the undoubted benefits of medical therapy in both primary3 and secondary prevention of CAD events, do Kalff et al seriously suggest that coronary atherosclerosis detected on CTCA should not be treated with proven anti-atherosclerotic therapy? Regarding comments made by van Gaal and Allman, and Karamoskos, we believe the upfront use of CTCA in our proposed algorithm would substantially decrease downstream referrals for both stress testing and invasive angiography in patients with suspected CAD. The current practice of referrals for invasive angiography based on clinical assessment and functional tests results in a low yield of obstructive disease.4 Furthermore, we believe the responsible use of CTCA can be promoted by restricting its use to the anatomical diagnosis of CAD as a once-only investigation. Once the diagnosis is established, further functional testing can be pursued if clinically indicated. Multicentre studies designed to determine the optimal role of CTCA are underway and will provide important insights regarding our viewpoint.5 Van Gaal and Allman place considerable emphasis on the 5000-patient study of myocardial perfusion imaging.6 We point out, however, that this was an observational study. In contrast, the FAME study on which we base our views of fractional flow reserve (FFR) was a randomised study.7 In addition, we are bemused by their statement that “The review cited quotes a lower sensitivity and specificity of FFR compared with perfusion scintigraphy, and lists scintigraphy as the ‘clinical gold standard of ischaemia’”. To quote directly from the review article: ... scintigraphy, although considered the clinical gold standard of ischemia, has limitations in identifying the hemodynamic significance of individual lesions in patients with multivessel CAD.8 Regarding comments made by Better and colleagues, we believe both stress echocardiography and nuclear stress testing are overused in clinical practice. In most circumstances, a standard electrocardiographic stress test is sufficient to exclude significant ischaemia and thus to determine who should undergo invasive angiography. In circumstances requiring stress imaging, our preference is to perform stress echocardiography, as its accuracy is comparable to nuclear stress testing, with no additional radiation. Notably, in multilesion CAD, none of the stress testing modalities are sufficiently accurate to determine which lesions require intervention.9,10 Only FFR, a proven cost-effective investigation, can decide this.9,10 Rather than putting the cart before the horse, as suggested by Kalff et al, our algorithm provides a horse with the potential to win the Melbourne Cup.

Richard W Harper · Brian S Ko

To the Editor: Handelsman and colleagues raise concerns1 about medical confidentiality with regard to legislation in New South Wales and a recent National Health and Medical Research Council (NHMRC) guideline. We wish to correct some of their statements related to the NHMRC guideline. The NHMRC recently released two documents about the use of genetic testing and genetic information in health care. The first describes the mandatory process by which clinicians can utilise new provisions in federal privacy legislation.2 This guideline was the subject of our editorial3 in the same issue of the Journal as Handelsman et al’s Viewpoint article. The second document is an information paper on medical genetic testing, including reference to disclosure of information, and directs readers to relevant resources.4 Handelsman et al cited the second document, but their concerns pertain to the first. Disclosure of genetic information without consent for the benefit of relatives was considered by the Australian Law Reform Commission (ALRC) in 2001–2003. The Commission consulted widely in preparing its two-volume report on genetics and ethics.5 The Commission recommended amending the Privacy Act 1988 (Cwlth) to allow disclosure in certain circumstances. It is incorrect to suggest that the proposal had the potential to “silently harm individuals who do not form sufficiently clamorous rights-demanding groups”.1 The federal government responded by amending the Privacy Act, and the NHMRC was charged with drafting a mandatory guideline2 for clinicians using the amendment. We were members of the working committee who, together with the NHMRC and the Office of the Australian Information Commissioner, ensured the guideline complied generally with federal privacy legislation and reflected the intent of the ALRC. The guideline was subject to public and targeted consultation — it does not represent an arbitrary standard, as suggested by Handelsman et al.1 The guideline emphasises the importance of confidentiality and the need to balance the rights of patients and genetic relatives. It carefully defines what information can be used or disclosed, and to whom. In contrast to Handelsman et al’s assertion, the legislation does not allow disclosure of a patient’s identity or genetic status. Disclosure is only permitted after extensive, documented consultation. It is incorrect to suggest that disclosure occurs at the “sole discretion” of a doctor or is the “lazy path”. Disclosure without consent represents a major change in the use of medical information, and best practice involves communicating with patients to avoid the very situation that the legislation and guideline address. But we must also recognise that, for each of us, our genetic heritage — and the right to access that heritage — is something that we share with our relatives.

Graeme K Suthers · Elizabeth A McCusker · Samantha A Wake

To the Editor: I write to clarify the National Health and Medical Research Council’s (NHMRC’s) role in supporting the dissemination of the Privacy Act 1988 (Cwlth), which regulates information privacy, and to correct some statements made by Handelsman and colleagues in their Viewpoint article.1 The process of using or disclosing genetic information to a patient’s genetic relatives in circumstances where patient consent is not given is complex. In 2006, the Privacy Act was amended to enable a health service provider to disclose the genetic information of a patient (and not specific information about an individual) to their genetic relatives. This may be done in certain circumstances and in accordance with guidelines2 developed by the NHMRC to assist health practitioners faced with the difficulty of making decisions about use or disclosure. The guidelines, approved by the Privacy Commissioner and then released in December 2009, establish when, by whom and in what manner the use or disclosure of genetic information may take place, with particular reference to the statutory test set out in the National Privacy Principles. That test provides for use and disclosure when there is: a serious threat to the life, health or safety of a genetic relative; and the use or disclosure is necessary to lessen or prevent that threat. The NHMRC agrees that such situations are likely to occur rarely, as patients in the great majority of cases agree to communicate their genetic information to relatives, particularly if there is potential for that information to benefit their relatives’ health. Furthermore, the amendments do not oblige use or disclosure. Rather, they provide the framework for this to occur in certain circumstances. Handelsman et al’s criticism of the guidelines and interpretation that “disavowal of patient confidentiality [is] at a doctor’s sole discretion” suggest they may have confused the guidelines with another NHMRC document titled Medical genetic testing: information for health professionals.3 This document discusses the legislative amendments briefly but aims, more broadly, to provide a source of information for health professionals and to assist them in communicating with patients when genetic testing is being considered. It provides support for the ordering and interpretation of results in the context of clinical decision making. The guidelines, in contrast, explore the complex issues associated with disclosure, and provide practical tools, including scenarios, key points for good practice, and flowcharts to assist in decision making. Disclosure is only permitted if it is in accordance with the guidelines, and is likely to be a lengthy and involved process.

Warwick P Anderson

To the Editor: Suthers and colleagues raise a number of significant ethical issues regarding patients’ right to privacy and the passing of genetic information to relatives.1 Although the National Health and Medical Research Council guidelines relate specifically to private practice and living patients,2 similar dilemmas arise during medicolegal autopsies. Forensic pathologists regularly encounter conditions in deceased individuals that may have implications for surviving family members. Examples include advanced coronary artery atherosclerosis in a young individual, raising the possibility of a familial dyslipidaemic syndrome; pulmonary thromboembolism, suggesting a hereditary thrombophilia;3 and haemochromatosis. However, there are no national guidelines, let alone nationally consistent laws, for the appropriate handling of such information. It would seem obvious that a deceased person’s relatives should have access to information of possible significance to their health. If a family wishes to receive such information, then mechanisms to pass it on should exist. These might range from contact with the forensic pathology service itself, to referring the family to a general practitioner or physician who has been briefed by the service. Whoever takes on this responsibility should be aware of the subtleties and pitfalls of genetic counselling. For example, the relevant condition may be an incidental finding rather than what caused the death (eg, haemochromatosis in a person killed in a road accident). The issues concerning the identification of, and appropriate medical response to, serious familial conditions at autopsy involve: accurately establishing the potential significance of postmortem findings;4 determining whether the family wish to be made aware of this information; disclosing the information to family members when a patient is deceased and not able to give consent; and deciding on the mechanisms by which this should be done. A complicating factor is the role of the coroner, as autopsies and subsequent reports are performed and written under coronial, not medical, authority. However, the authors of these reports are first and foremost doctors, and many feel a therapeutic obligation to the families of those whose autopsies they have performed. Many of these pathologists feel that the autopsy is indeed for the family — even if it is formally for the coroner and the public interest. However, it is no part of the coroner’s legislated responsibility to look after the health of surviving family members. It would therefore be a useful service to accommodate these issues in future iterations of the national guidelines.2

Roger W Byard · Stephen M Cordner

To the Editor: In Natural history of infectious disease,1 Macfarlane Burnet emphasised that poliomyelitis was the one infective disease of advanced countries that had failed to respond to improvements in the standard of living, leading to epidemics in the first half of the 20th century that increasingly involved young adults, who developed severe paralyses. There was also an abnormally high death rate among young adults. However, in tropical countries where the poliovirus was endemic, the virus spread among infants “with a minimal number of paralytic cases”. Burnet therefore defined a “safe” period in the first year of life, when infection was not likely to lead to paralysis. Burnet also described the features of the “so-called ‘virgin soil’ epidemics” that occurred in remote islands and Arctic communities. In these places, the population had not been exposed to the virus in infancy, but the “brunt of the disease was borne ... by adolescents and young adults”. In an Eskimo community, the paralysis rate was 40% and the mortality rate 14% of the whole population.1 When, in 1988, the World Health Organization decided to eliminate the poliovirus using the oral, live attenuated virus Sabin vaccine, it apparently ignored Burnet’s observations, concluding that polio was in fact a serious disease in tropical countries. As a result of the vaccination program, the wild virus was eliminated from Africa, except in Nigeria.2 However, re-infection has occurred in several African countries, leading to epidemics since 1993 in which young adults have become severely paralysed and the mortality rate has been high,3 because the population’s first contact with the wild virus has no longer occurred in infancy. Burnet predicted that young adults aged between 15 and 25 years would be the main group affected in any polio epidemic.1 He based his observations on the natural history of the disease. The current approach to the epidemiology of polio infection has, however, relied on mathematical models and molecular biology. Both of these approaches have failed to predict that epidemics would occur.4,5 In fact, Anderson and May claimed that the decision to advocate vaccination was justified — that “programmes of mass immunization against poliomyelitis in developing countries are unlikely to do harm”.4 Nearly 40 years earlier, Burnet wrote: Any escape into circulation that was not immediately dealt with could grow into the almost unimaginable catastrophe of a ‘virgin-soil’ epidemic of poliomyelitis involving all the populous regions of the world. [...] The great epidemics represented the entry of virulent strains into populations containing a high proportion of older children and adults who had escaped natural immunisation infection.6 The loss of naturally acquired immunity to the wild virus as the result of oral vaccination could have disastrous results. While it is now too late to stop vaccination, it should be extended to young adults as well as children, because current epidemics are affecting this age group, as Burnet predicted.1

Colin L Crawford

To the Editor: Grills eloquently informs readers on the dangers of the Easter bunny and chocolate, and reminds us that Easter eggs may pose a choking hazard.1 It is worth noting that the foil used to wrap Easter eggs also poses a health risk. This was demonstrated in the case of a 20-year-old woman who presented to hospital with respiratory distress after inhaling foil wrapping from an Easter egg.2 The foil wrapper had been pushed inside the woman’s salbutamol inhaler by her 2-year-old son and subsequently occluded her left lower lobe bronchus after she used her inhaler.

Mark Naunton

To the Editor: A recent study of adult bodyweights recorded in 199 countries showed an increase in mean body mass index (BMI) of 0.4 kg/m2 per decade between 1980 and 2008.1 The increase in Australia was even greater: 0.9 kg/m2 for men and 1.2 kg/m2 for women.1 This increase in BMI, sometimes referred to as an “obesity epidemic”, has also been reported in coronial cases in South Australia, with the percentage of morbidly obese individuals (BMI > 40 kg/m2) undergoing autopsy rising from 1.3% to 4.8% between 1986 and 2006.2 While attention is often focused on complications of obesity such as diabetes mellitus, hypertension and cardiac disease, there is also a link to pulmonary thromboembolism (PTE). A recent prospective forensic autopsy series found that 24 of 32 cases of fatal PTE were in individuals who were overweight or obese.3 To examine this association further, we performed two analyses. First, we recorded the numbers of sudden deaths subject to coronial autopsies in SA from 2000 to 2009 (inclusive) where the cause of death was PTE. These were divided into two periods (2000–2004 and 2005–2009) and expressed as the percentage of the total number of coronial autopsies. Second, we analysed all deaths due to PTE that were the subject of coronial autopsies in SA in 2008 (the most recent year for which complete autopsy data were available at the time that the study was initiated). Age, sex and BMI were recorded, and the group was compared with an age- and sex-matched control group taken from other coronial autopsy cases. Despite considerable yearly fluctuations, the death rate due to PTE showed a small increase over time (Box). The rate of deaths due to PTE per total number of autopsies increased from 3.59% (198/5521) in 2000–2004 to 3.71% (239/6442) in 2005–2009. In 2008, there were 44 individuals (21 men, 23 women) with PTE as cause of death. The age range of this group and the 44 matching controls was 27–93 years (mean, 67 years). The mean BMI for individuals dying of PTE (29.6 kg/m2; range, 19.0–51.8 kg/m2) was significantly higher than for the controls (25.9 kg/m2; range, 17.7–44.6 kg/m2) (Student t test, P < 0.05). If PTE is conclusively found to be associated with BMI, there may be significant effects on hospital diagnostic services, coronial forensic investigation units and public expenditure in the future. Coronial cases in South Australia where death was due to pulmonary thromboembolism, 2000–2009

Roger W Byard · Hannah Rosenfeld

To the Editor: Colchicine is an alternative to anti-inflammatory agents for the treatment of acute gout.1 It is potentially toxic and can cause multiorgan dysfunction, including hepatotoxicity, neutropenia, acute kidney injury, rhabdomyolysis and hypotension. We report three cases of toxicity from supratherapeutic dosing that occurred within 2 weeks of each other. In each case, no alternative diagnoses (in particular, sepsis) were considered likely. An 87-year-old man presented with vomiting after 3 days of profuse diarrhoea, nausea and generalised myalgia without other infective symptoms. He had been prescribed 0.5 mg colchicine daily, but he was taking 1.0 mg four times daily. Clinical features included generalised abdominal tenderness, pancytopenia, rhabdomyolysis and hepatic dysfunction. These resolved over 5 days with supportive treatment. A 67-year-old woman presented with lethargy, diaphoresis, fever, nausea, vomiting and diarrhoea. She had been prescribed 1.0 mg colchicine initially, then 0.5 mg every 6 hours “until diarrhoea develops”. She was taking colchicine every hour despite diarrhoea. Initial clinical features included tachycardia, hypotension, tachypnoea and fever. Multiorgan dysfunction developed rapidly and despite aggressive resuscitation, including an intra-aortic balloon pump and broad-spectrum antibiotics, she died within 24 hours. A 77-year-old woman presented with nausea, vomiting and profuse diarrhoea. She had been prescribed 1.0 mg colchicine three times daily “until diarrhoea develops”. On presentation, she was dehydrated but haemodynamically stable, with mild renal and hepatic dysfunction and creatine kinase level elevation. These resolved over 4 days with supportive treatment. A recent randomised controlled trial demonstrated that low-dose colchicine (1.8 mg over 1 hour) was as effective as a higher dose (4.8 mg over 6 hours). Further, the adverse effects of the lower dose were similar to placebo and significantly less than those of the higher dose.2 Adapting to the Australian formulation, 1.0 mg initially and 0.5 mg 1 hour later is now recommended.3 In contrast, repeat doses of 0.5 mg until clinical improvement or side effects (in particular, diarrhoea) was previously recommended. In the cases above, the apparent dosing regimen differed significantly from current recommendations. Ineffective patient education may have also contributed to the conditions of patients 1 and 2, who up-titrated their dose. Patients 2 and 3 persisted with dosing despite gastrointestinal symptoms. Health professionals should be aware of the new dosing recommendations. These are highlighted by the National Prescribing Service4 and the Australian medicines handbook.3 Patients with renal or hepatic impairment, or concomitant use of cytochrome P450 3A4 or P-glycoprotein inhibitors (eg, clindamycin), are at increased risk.5

Myles W H Smith · Darren M Roberts · Siobhann M Ritson · Richard O Day