Letters

To the Editor: E-health’s great promise is to improve health care delivery efficiency and effectiveness1 by enhancing multidisciplinary care planning and information exchange.2 General practice is now largely computerised.3 However, a chain is no stronger than its weakest link, and Australia’s otherwise slow progress towards linking secondary care into a functioning national e-health system is frustrating.1,4 We join the chorus, raising concerns about the e-health readiness of the paediatric sector. We recently surveyed the e-health readiness of paediatricians via the Australian Paediatric Research Network (APRN), a network of about 370 non-tertiary paediatricians broadly representative of all states and territories.5 Established in 2007, the APRN aims to facilitate multisite research into common chronic childhood illnesses where they are most commonly seen — in paediatric secondary care settings. Core to this goal is testing cross-sectoral care models, which requires shared e-health capabilities. The APRN’s annual web-based Multi-Topic Survey in April–May 2010 (n = 181, 48% response) contained a section on computer use with outpatients and in private rooms (Box). Almost all respondents reported having access to a computer at work. However, the reach of e-health is otherwise disturbingly low, its quality is questionable and, when used, it is mainly for clerical purposes rather than patient care. The 27% of respondents using computerised medical records reported more than 10 different systems, suggesting possible future barriers to information exchange and e-health initiatives. We applaud the rapid progress made in general practice,3 but general practitioners do not work in isolation. Our survey shows that, despite similar computer access, Australian paediatricians (and probably other physicians) are a long way behind. This has major implications for policy, shared care programs and the feasibility of e-research. E-health can only provide national benefits in our new world of chronic disease if all health sectors are involved. On a positive note, the current low rate of computerisation in paediatric patient care means that e-health implementation for secondary care could yet be coordinated and integrated from the outset. This opportunity should be seized while still possible. Resources, government funding, planning, a solution focus and the will to move forward are urgently needed. Australian Paediatric Research Network Multi-Topic Survey 2010: computer and e-health use among paediatricians Variable Proportion Computer access Access to computer at work 97% Access in each patient clinic room 85% Internet access at an acceptable speed 71% Computerised patient booking/billing 67% Clinical e-health use Computerised medical records 27% Writing new/follow-up notes 21% Ordering tests 16% Writing scripts/referrals 13%

Melissa Wake · Sarah A Davies · Harriet Hiscock · Gervase M Chaney

To the Editor: Waxman’s prompt recovery after a stroke was probably a stroke of luck,1 unless perhaps Saint Mary MacKillop was involved. Amid the conflicting evidence on the effect of thrombolysis on recovery in ischaemic stroke, one fact is beyond doubt — thrombolysis gives no greater improvement at 24 hours than placebo.2 It is the various measures of recovery at 3 months, and the risks of adverse outcomes from protocol violations in administering thrombolysis, that are less clear. The European Cooperative Acute Stroke Study III (ECASS III) showed that there is a benefit from administering thrombolysis up to 4.5 hours after stroke onset,3 and the complete Safe Implementation of Thrombolysis in Stroke International Stroke Thrombolysis Register (SITS-ISTR) data showed that this benefit can be reproduced in non-trial hospital practice.4 Simpson and colleagues say that the Australian data support this conclusion, even though outcomes show slightly higher mortality compared with rest-of-world data.5 There are several gaps in that line of reasoning. A modified Rankin score (mRS) of 0–1 (zero or minimal disability) is the standard measure of a good outcome. In ECASS III, an mRS of 0–1 was seen in 52.4% of patients who received thrombolysis compared with 45.1% of patients who received placebo.3 However, the SITS-ISTR data showed an mRS of 0–1 in just 40% of patients treated within 3 hours of stroke onset and 44% of patients treated at 3–4.5 hours.4 This is despite lesser stroke severity (National Institutes of Health Stroke Scale score: 10 in the SITS-ISTR cohort v 11.6 in the ECASS III placebo group), selective patient inclusion, and exclusion of patient data with protocol violations known to give worse outcomes. Achieving a worse result than placebo is hardly evidence for safe and effective use of thrombolysis in normal clinical practice. However, the Australian study presents the data differently, using an mRS of 0–2 and thereby concluding good outcomes in patients with greater disability than is the accepted good outcome measure.5 Rather than providing the actual data and the percentage of patients with good outcomes, a novel measure of odds ratio comparison with rest-of-world data is made. Publishing data in the same format as for the full SITS-ISTR report would allay concerns of what may be unfavourable outcomes compared with clinical trial data. Patients deserve to be told what their likely prognosis will be in hospitals that are less experienced in stroke thrombolysis than The Alfred, where Waxman received world-class stroke care.

Brendon J Smith

In reply: We were delighted to hear of Waxman’s “miraculous” recovery, and admire the world-class standard of stroke care which was delivered at The Alfred.1 The Australian data in the Safe Implementation of Thrombolysis in Stroke (SITS) database up to 2008 included tertiary referral centres and outer metropolitan hospitals, and centres with varying experience of using recombinant tissue plasminogen activator (rt-PA) in clinical practice. There was no difference in outcomes according to experience of the treating centres. We believe that the non-trial clinical data presented in our article are a realistic indication of expected outcomes for all patients receiving thrombolysis for stroke in Australia. The choice of a modified Rankin score (mRS) of 0–2 as an outcome measure in our article was largely dictated by the SITS international analysis. The aim of our study was to compare outcomes in Australia with those in the rest of the world; these were also not significantly different when an mRS of 0–1 was used as an outcome measure (mRS 0–1 at 3 months, 34.6% for Australia v 37.8% for the rest of the world; P = 0.13). The original National Institute of Neurological Disorders and Stroke (NINDS) trial data,2 now more than 15 years old, have been analysed and re-analysed and, arguably, it is time to move on from rehashing the data. However, if one wishes to follow this path, there was in fact a significant difference in improvement at 24 hours between patients in the rt-PA and placebo groups. Smith’s statement that thrombolysis gives no greater improvement at 24 hours than placebo is correct in terms of the proportion of patients with an improvement in National Institutes of Health Stroke Scale (NIHSS) score of 4 or more, but this is a low benchmark and many untreated patients also show a relatively mild improvement at 24 hours. If one considers major neurological improvement (MNI, defined as an improvement in 24-hour NIHSS score of 8 or more), this was seen in a greater proportion of patients in the rt-PA group compared with the placebo group.3 Patients with MNI have a much greater chance of achieving minimal or no disability at 3 months, which is by far the most accepted outcome measure for thrombolytic therapy. This major early recovery is frequently seen in patients who receive rt-PA, and has been termed the “Lazarus effect”. Waxman was fortunate enough to experience this effect — but it occurs far too often with rt-PA in stroke to pass the Catholic Church criteria for a miracle.

Marion A Simpson · Helen M Dewey · Mark W Parsons

To the Editor: We view with concern the listed minimum investigations for chronic suppurative lung disease and bronchiectasis in children and adults recommended in the position statement from the Thoracic Society of Australia and New Zealand and the Australian Lung Foundation, published in the Journal.1 We do not agree with the inclusion of measurement of IgG subclasses in the list. Interpretation of IgG subclasses is fraught with difficulties.2 It is unclear whether the isolated finding of low levels of one or more IgG subclasses is a risk factor for developing severe recurrent bacterial infections. Individuals with complete absence of IgG subclasses due to gene deletions may remain entirely asymptomatic, and the finding of a low or absent response to specific bacterial protein and/or polysaccharide is more closely associated with propensity to infection. In addition, the lack of reproducibility of IgG subclass assays and lack of well standardised age-specific reference ranges hinder interpretation of results. Of major concern is the lack of evidence to provide clear guidance on the efficacy of immunoglobulin replacement therapy in IgG subclass deficiency. In general, the finding of isolated IgG subclass deficiency is not sufficient grounds for commencement of immunoglobulin therapy and is not recommended as an indication for intravenous immunoglobulin therapy in the current Australian guidelines.2 We urge the authors to reconsider the inclusion of IgG subclasses in the list of minimum investigations for chronic suppurative lung disease and bronchiectasis.

David S Gillis · D Sean Riminton

In reply: We thank Gillis and Riminton for their comments highlighting the inclusion of IgG subclasses in the list of suggested investigations when reviewing a patient with chronic suppurative lung disease or bronchiectasis. We agree that a finding of one or more low IgG subclasses in isolation is not an indication for immunoglobulin therapy and that interpretation of serum IgG subclass concentrations is difficult. Indeed, this was debated at length by the position statement authors. However, after considerable discussion, we decided that measurement of IgG subclasses should be included. Although the data are weak, it is an important area of possible aetiology, and there are varying opinions regarding associations with impaired adaptive immunity.1-3 As with some other investigations, an abnormal test result in the context of a child or adult with suppurative lung disease would lead to discussion with an appropriate subspecialist for advice on interpretation and/or further evaluation. Space limitations in the Journal version of our position statement did not permit us to elaborate further.4 In the full document available online,5 we stated that: The benefits of performing IgG subclasses in isolation are particularly controversial as the role of a reduction of a subclass is likely over-diagnosed.[88-91] If IgG subclass is low, assessment of response to vaccinations is advocated.

Anne B Chang

To the Editor: In their paper, Campbell and colleagues list the potential pitfalls of introducing pay-for-performance into Australian primary care.1 They emphasise that, in Australia, the electronic medical records used in general practice would not support the introduction of a scheme such as the Quality and Outcomes Framework (QOF) that is in place in the United Kingdom. In 2009, we demonstrated that it was quite possible to apply a QOF in a large Australian general practice by adapting the in-built search facility of a commonly used medical records program.2 We concluded that the introduction of a QOF in Australia would drive up the quality of our care. The non-clinical standards of a QOF are already similar to those set by the Royal Australian College of General Practitioners for accreditation and could be readily achieved. Campbell and colleagues suggest that the QOF is expensive and without proven benefits.1 This is incorrect. As predicted, the QOF has not only led to a reduction in cardiovascular disease events, but the benefit is greatest in the lowest socioeconomic groups.3 It is now possible to measure the cost effectiveness of a QOF, which is likely to show that it pays for itself by way of reduced morbidity and health service costs.4 Rather than argue for general practitioner remuneration based on pay-for-performance to be less than 20%, one should err on the side of caution, which recognises that 20% has ensured a massive public health gain for the British population. Now that 95% of GPs use computers, at least for prescribing,5 it is plausible that an Australian QOF could be developed, but pay-for-performance may need to include some pay-for-data incentives.

Mark A J Morgan · James Dunbar

In reply: Our article, which related to clinical care, not non-clinical standards, was intended to generate debate, and the points raised by Morgan and Dunbar are important ones. We address the central issue, which relates to the intended purpose of introducing a pay-for-performance scheme, similar to the Quality and Outcomes Framework (QOF) in the United Kingdom, into Australian general practice. Morgan and Dunbar state in their letter, “Now that 95% of GPs use computers for prescribing”; this emphasises that it would not be a level playing field. Even if all indicators only related to prescribing, at least 5% of practices would be disenfranchised. That statement also appears to presume that 95% of practices use compatible and comparable clinical codes. The UK witnessed years of computerisation and clinical code usage across a wide range of clinical issues before the introduction of the QOF. Elliot-Smith and Morgan adapted “the in-built search facility of a commonly used medical records program”, and introducing a QOF-like scheme in Australia would involve this investment in all practices. The percentage of income attributed to pay-for-performance is a political decision, and most people who are involved in the QOF in the UK strongly believe that it is too high. Whatever level is set, it must result in a level playing field for practices.

Stephen M Campbell · Anthony Scott · Rhian M Parker

To the Editor: Although we welcome Boyd and colleagues’ recommendations for changes to infection control guidelines for Australian recipients of human growth hormone (hGH) and human pituitary gonadotrophin (hPG),1 we are concerned about the accuracy of the history provided and do not want it misrepresented. Boyd and colleagues refer to recipients living with anxiety since 1985, when the Australian Human Pituitary Hormone Program (AHPHP) was halted. However, Australian recipients were not aware of the risk until 1991–1992. After the first two recorded deaths from Creutzfeldt–Jakob disease (CJD) of women treated with hPG, their husbands fought for official recognition of the link between their deaths and the AHPHP. In 1992, media attention alerted recipients to the risk and initiated contact from treating doctors. Knowledge that this information had been withheld since 1985 angered recipients. Boyd et al’s article is contradictory in mentioning a possible single, discrete contamination event but also claiming that a higher-risk period is unknown. We challenge this — particularly on behalf of recipients who were informed they had received hormones from a batch identified as likely to have contained the transmissible agent that causes CJD. We dispute the stated lack of availability of detailed treatment information, as the Australian Government Department of Health and Ageing has meticulously obtained and archived patient notes of recipients from their treating doctors, which provide the most accurate source of data. Boyd and colleagues had access to records of the four women whose deaths resulted from AHPHP treatment. The records seem consistent with published data,2,3 confirming that the four women were treated between 1973 and 1978. This surely indicates a high-risk period and gives extra confidence to those treated outside this timeframe. Further, two of the three patients on whom autopsies were performed received treatment from an identical batch of hormones (44); one was treated with this batch only. The third patient received hormones from batches 43 and 45.2 Batch 44 was identified as contaminated, and it was theorised that tainted material was transferred to batch 45 via production equipment. The patient who did not undergo an autopsy received only batch 25, which was produced earlier and indicates another possible contamination event within the 1973–1978 period. Risk estimate percentages do not provide more confidence for recipients than is currently already growing. They do not bring back those who died, take away the guilt of the parents who consented to hGH therapy for their children, or change a history of suicides, broken marriages, anxiety, disgrace and despair. It is important that Boyd and colleagues do not blur the implications of their findings with the continued need for the Australian Government to maintain the Human Pituitary Hormone Trust Account, which was established to provide funding for counselling and support services for recipients, and ongoing support for this group of citizens whose lives changed forever and who continue to battle discrimination and delays when accessing health care. The recommendations inspire hope but provide no immediate relief. The passing of time brings confidence, but the record needs to respect the enormous impact on the lives affected.

Suzanne L Solvyns · David W Ralston

In reply: We thank Solvyns and Ralston for their thoughtful and heartfelt comments and their assistance in ensuring historical accuracy regarding the issues surrounding iatrogenic Creutzfeldt–Jakob disease (CJD) risk and recipients of the Australian Human Pituitary Hormone Program (AHPHP). Whether there is a need for ongoing support of AHPHP recipients for the foreseeable future was not considered in the scope of our report,1 but we unequivocally support provision of optimal health care services for them, which we believe relaxation of infection control measures will assist. The delays and manner in which many AHPHP recipients learned of their risk of CJD is certainly regrettable, but this was not the universal experience of recipients. Some were made aware of the risk by their treating practitioner in 1985,2 with their heightened personal anxiety commencing from that time. As stated in our report, we agree that the close temporal development of CJD in the four Australian human pituitary gonadotrophin recipients appears consistent with a single, significant contamination event,1 such as from tainting of a limited number of treatment batches — an observation broadly in keeping with the existence of a higher-risk treatment window. However, despite assertions to the contrary, data acquired from various sources by the Australian National Creutzfeldt–Jakob Disease Registry for analysis did not permit confident and consistent delineation of a higher-risk treatment group. This is not synonymous with saying that a higher-risk period was unknown to us.

Alison Boyd · Genevieve M J A Klug · Colin L Masters · Steven J Collins

To the Editor: Dinh and colleagues present data on head injuries among cyclists admitted to the emergency department of Sydney’s Royal Prince Alfred Hospital (RPAH) from 1991 to 2010,1 and conclude with their opinion that legislation mandating the wearing of bicycle helmets should be maintained. However, their data provide poor evidence of the efficacy of helmets and of the effectiveness of legislation requiring helmet use. Almost all studies of helmet efficacy are case–control studies, which, to be of high quality, require a well defined and matched control group. In the study by Dinh et al, the control group was made up of patients who had been wearing a helmet. Many possible explanations for injury severity were not considered. For example, were the non-helmeted cyclists drinking alcohol or riding faster? Were they more likely to be risk-takers? Were the helmet wearers also wearing high-visibility vests or using lights at night? Case–control studies of this kind are a weak form of evidence (ranking just above anecdotal evidence and case studies) and cannot answer questions of causality. The two graphs presented by Dinh et al show that head injury rates among cyclists were very low and fairly stable over most of the time period examined. RPAH treats thousands of trauma patients each year. The study reported on 287 cyclists admitted in a 2.5-year period — an average of 115 per year. Of these, only 14 (eight helmeted; six not wearing helmets) incurred major trauma — about six per year. Given that helmet legislation was in place for the entire study period, these data add no evidence for its effectiveness. In public health terms, the risk of injury needs to be weighed against the benefits of increased physical activity, reduced chronic disease and reduced air pollution due to more people cycling. Because of the low absolute rate of cycling injuries, these benefits are nine to 20 times the size of the risk.2,3 Further, it is well documented that levels of cycling in Australia dropped by 30%–40% when helmet legislation was introduced. This had the unfortunate effect of making cycling less safe for the remaining cyclists because of the “safety in numbers” phenomenon.4 The poor uptake5 of the two public bicycle-hire schemes in Australia (in Melbourne and Brisbane) indicates that helmets are a significant barrier to short-trip and spontaneous cycling, with few potential or casual users carrying a bicycle helmet in case they decide to hire a bicycle. Dinh and colleagues obviously believe in the efficacy of the bicycle helmet, but this does not mean that mandating their use is the best public health policy response. When helmet legislation was introduced, we did not have the epidemics of diabetes and obesity that now threaten to bankrupt state health budgets. Strategies to increase levels of physical activity among the whole population are desperately needed, even if there is a small risk involved.

Chris E Rissel · Paul Martin

To the Editor: About 5% of Australians of Asian, African, Middle Eastern or Mediterranean descent have glucose-6-phosphate dehydrogenase (G6PD) deficiency.1 Affected babies can develop massive haemolysis within hours of exposure to clothes stored with mothballs containing naphthalene. It has long been known that this results in severe jaundice, which may lead to kernicterus2 and profound brain damage, for which the cost is either a lifetime of dependency and very expensive care, or death. We are aware of three cases of kernicterus in babies with G6PD deficiency in Australia in the past 3 years, one of which was associated with exposure to naphthalene in mothballs. One baby died. The exact incidence of severe neonatal jaundice and kernicterus in Australia is unknown, but it is the subject of an ongoing study funded by the Cerebral Palsy Foundation and coordinated through the Australian Paediatric Surveillance Unit. In Australia, packages of naphthalene mothballs must carry a warning that the product is harmful to children. However, clinical directors of neonatal units that comprise the Australian and New Zealand Neonatal Network have unanimously agreed that warning labels give insufficient protection. They have called on the Australian Pesticides and Veterinary Medicines Authority (APVMA) to act in harmony with the European Union, which banned the sale of mothballs containing naphthalene in 2008,3 following a report by the European Chemicals Bureau.4 The adverse risk–benefit ratio for naphthalene provides strong justification for its withdrawal. A submission to this effect has been lodged with the APVMA. Some mothballs contain paradichlorobenzene, a chemical related to naphthalene and associated with haemolysis. Less toxic products that protect clothes against moths exist. Department stores in the United Kingdom have replaced moth repellents containing naphthalene with products containing natural substances, such as sandalwood and lavender. Between 2004 and 2010, the New South Wales Poisons Information Centre reported that it received about one call per week concerning children exposed to naphthalene in moth repellents (Box). The Victorian Poisons Information Centre reported 53 calls in 2008.5 While acknowledging the importance of raising awareness of the dangers of naphthalene, we believe that the safest course is prevention — that is, an Australia-wide ban of mothballs containing naphthalene. Readers who wish to report cases of naphthalene toxicity are encouraged to contact APVMA at aerp@apvma.gov.au. Number of calls to the New South Wales Poisons Information Centre reporting children exposed to napthalene in moth repellents, 2004–2010 Year Number of calls 2004 55 2005 59 2006 65 2007 67 2008 73 2009 45 2010 71 Total (average) 435 (62) Source of data: Judith Kirby, Department Head, NSW Poisons Information Centre, personal communication.

on behalf of the Advisory Committee of the Australian and New Zealand Neonatal Network

To the Editor: We agree with Mendelson and colleagues1 about the need to ensure radiation doses of computed tomography (CT) are as low as reasonably achievable while maintaining diagnostic quality of the images. Perceived benefit to the patient must be balanced against theoretical small risks from the procedure. The uncertainty surrounding risk estimates at the lower end of the radiation dose range means that it is important for radiologists to take responsibility for monitoring radiation dosimetry. This becomes especially important when imaging young people with chronic disease (such as renal calculi, chronic hepatitis, cystic fibrosis and inflammatory bowel disease), who may have many CT scans while young. As stated by Mendelson et al,1 the theoretical risks are assumed to be cumulative over a lifetime, but diminish significantly the older the person is at time of exposure. We would like to highlight work that the Royal Australian and New Zealand College of Radiologists (RANZCR) has undertaken to support the development of CT scanning standards, professional education, dose optimisation and the establishment of national diagnostic reference levels by the Australian Radiation Protection and Nuclear Safety Agency. CT dose optimisation quality improvement programs have been conducted in Queensland and Victoria. These have been funded through a grant to the RANZCR Quality Use of Diagnostic Imaging (QUDI) Program from the Australian Government Department of Health and Ageing. A dose optimisation project is planned for South Australia in 2011. The RANZCR QUDI program has developed a consumer and referrer information database of diagnostic imaging procedures, including a general item about the theoretical risks associated with ionising radiation. This information is accessible at http://www.insideradiology.com.au and supports informed choices about imaging. While Blecher2 and Mendelson et al1 are correct in indicating that the latest multidetector computed tomography (MDCT) platforms have the potential to deliver acceptably low radiation doses and high-quality images, this is not always seen in practice, based on the evidence from these optimisation programs. Some multiphase MDCT protocols have the potential to give rise to organ doses in the range where there is little doubt that a small increased risk of carcinogenesis exists.3,4 Contrary to the comment made by Blecher,2 our knowledge of the impact of radiation on humans does not arise exclusively from atomic bomb survivors. For example, we have evidence of increased breast cancer risk from patients who underwent multiple fluoroscopic examinations to monitor treatment for tuberculosis.5 Risk estimates from this and other datasets are broadly consistent with those from atomic bomb survivor data. In view of the above, we need to be vigilant in ensuring that CT examinations are clinically justified and, secondly, performed using optimised scanning protocols. Referring practitioners need to know that the potential stochastic effects resulting from CT examinations are cumulative over a lifetime. It is this cumulative effect that is not necessarily trivial.

John C P Heggie · Stacy K Goergen · Michael J Fallon

To the Editor: At a time of apparent increasing concern over radiation exposure, the article by Keijzers and Britton1 unfortunately does not provide any perspective on the clinical necessity of the imaging investigations requested by emergency department doctors. It also contains inaccurate information. Stating that “multidetector CT [computed tomography] scanners have the potential to expose patients to higher radiation doses”, and preceding it with “radiation doses per scan have increased by up to 40%”, is incorrect. CT scanner manufacturers have for some time been producing scanners that have decreased radiation doses by incorporating various techniques,2 including iterative reconstruction (a reconstruction algorithm that corrects image data by using various models, thereby improving CT image quality while reducing radiation dose). The dosage reductions reported by major manufacturers and in the literature2 vary between 25% and 80%. The efficacy of dose-reduction mechanisms and the concepts behind them have been outlined in numerous white papers and scientific articles, leading to the conclusion that “newer scanners have improved technology that facilitates lower patient doses”.3 In their seminal article, McCollough and colleagues caution that “alarmist articles” do the public a disservice. They also state that low-level radiation risk estimates, which are derived primarily from atomic bomb survivors and have considerable uncertainties at low doses (< 100 mSv), give no consideration to the medical benefit of a CT scan.2 While Keijzer and Britton’s research investigated emergency department doctors’ knowledge of radiation exposure, the sample was small, being restricted to one institution, and the study had other limitations, as acknowledged by the authors.1 The alarmist undertones have not been helped by the publication of articles in the lay press, such as “Doctors warned over X-ray risks”.4 The danger is that sensationalising the risks of CT scanning may lead to patients not undergoing scans that are clinically indicated, with consequent patient harm. The Royal Australian and New Zealand College of Radiologists (RANZCR) has issued a position statement on radiation dosage.5 As radiologists, we abide by the ALARA (as low as reasonably achievable) principle, and the RANZCR is actively pursuing ways of decreasing radiation exposure.5 In a clinical context, the risk from CT scans is small compared with health risks arising through other activities. Educating doctors about radiation exposure risks is crucial, but so is up-to-date information and common sense, devoid of sensationalism.

Alain M Lavoipierre

In reply: We thank Lavoipierre for his response to our article.1 He brings up two main points. First, he suggests that our statement that newer computed tomography (CT) scanners emit more radiation is incorrect.2 We acknowledge that actual absorbed doses for exactly the same imaging are lower with newer scanners, but the total exposure of the population may be increasing. In the United States, between 1993 and 2006, the annual number of CT scans increased by more than 10% per year, while the population increased less than 1% per year.3 If some scans are unnecessary for safe clinical care, then unsafe radiation exposure is a consequence. His second point is that we should use common sense and not sensationalise our findings out of concern that some patients may not undergo scans that are clinically indicated. We are surprised by his interpretation of the risk of CT imaging, since we quoted a widely accepted estimate.4 Certainly, for an individual, the absolute risk increase is small and may be outweighed by the benefit the scan can provide. However, patients frequently undergo CT scans on the basis of a questionable clinical indication, or when safer imaging modalities would be superior. These unnecessary scans could be avoided. To that end, we advocate common sense, rational test ordering and appropriate discussion of risks, especially where the expected benefit of CT scanning is limited.

Gerben B Keijzers · Charles J Britton

To the Editor: Douglas and other senior epidemiologists have described the imminent demise of the Master of Applied Epidemiology (MAE) program.1 This program has produced around 160 graduates, at least 104 of whom (65%) are working in the broad area of infectious diseases epidemiology. It may be thought, therefore, that there is no further scope for employing MAE graduates. My experience indicates otherwise and I would be very surprised if it were unique. In a small epidemiology unit of a state reference laboratory, two of the six staff members are MAE graduates. One past employee, also an MAE graduate, is a close collaborator. Last year, on very short notice, this person was able to take over coordination of the infectious diseases epidemiology course in the Master of Public Health program (MPH) at the University of Melbourne after the previous coordinator, also an MAE graduate, accepted a position as Head of the School of Health and Social Development at Deakin University. The MAE graduates from the epidemiology unit contributed to the MPH teaching program as guest lecturers. The University of Melbourne was unable to attract a full-time infectious diseases epidemiologist to the coordinating position, suggesting a lack of suitably trained and experienced people in this discipline. There is no doubt that the MAE program produces suitably trained and experienced people, as attested by Douglas et al1 and Kelly et al in the Journal.2 It also fits with my experience as an employer of MAE graduates and a collaborator with other graduates and staff from the program. Continued funding of the MAE program was recommended by independent reviewers.3 There are many who believe that, not only should the MAE program continue, it should continue as part of a national infectious diseases prevention and control program.2 It is appropriate that similar Australian programs already exist for heart disease, cancer and diabetes. In a letter to the Journal, Givney eloquently described the arcane processes of interlocking acronym-rich, mandate-limited committees that constitute Australia’s approach to the national coordination of infectious diseases.4 This description would be recognised by many, who would agree with Givney and Kelly et al that the time has come for Australia to establish its own independent expert body for monitoring and control of infectious diseases.

Heath A Kelly

To the Editor: Trachoma control guidelines from the World Health Organization1 and Communicable Diseases Network Australia (CDNA)2 recommend the “SAFE” strategy that includes surgery for trichiasis, antibiotic treatment, facial cleanliness and environmental improvement. Lack of access to antibiotics in isolated areas should not be a major contributor to the persistence of trachoma in Australia because special Pharmaceutical Benefits Scheme arrangements (SPBSA) under section 100 of the National Health Act 1953 for the supply of medicines to remote-area Indigenous health services should enable a ready availability of azithromycin. The 1999–00 to 2001–02 evaluation of the SPBSA suggested that the program had led to major increases in the supply of medicines in remote areas, but that the supply of azithromycin did not change as a result of the introduction of the program.3 We assessed the relationship between reported azithromycin treatment of people with trachoma, their household contacts, and community members; levels of treatment recommended by WHO and CDNA guidelines; and the total number of courses of azithromycin available through the SPBSA. The National Trachoma Surveillance and Reporting Unit (NTSRU) provided 2008 data on treatment with azithromycin and trachoma prevalence in the Northern Territory, South Australia and Western Australia (refer to the report for limitations of the data).4 Data for 2007–08 on the supply of azithromycin to health services under SPBSA were obtained from Medicare Australia. The WHO guidelines recommend treatment of an entire community if the prevalence of active trachoma among children is above 10%.1,5 The CDNA guidelines2 recommend that contacts (> 6 months of age) of infected children within a household be treated. Our estimate of trachoma treatment according to CDNA guidelines is based on multiplying the number of infected children (from the NTSRU data) by the average number of members in remote Indigenous households.5 The impact of shared and multiple residence on estimates of household contacts could not be taken into account. The Box shows the numbers of azithromycin courses available through the SPBSA to remote-area Aboriginal and Torres Strait Islander health services in the three states. In the NT, the reported number of courses given (3069) fell well below the level recommended by both WHO (by 34%) and CDNA (by 41%) guidelines. In SA, reported courses of azithromycin given (7) fell well below the 45 suggested by the CDNA guidelines. The prevalence of trachoma did not exceed 10% in any SA community, so no treatment was required under WHO guidelines. In WA, the reported number of courses given (2917) also fell below recommended levels, although the deficit (WHO, 35%; CDNA, 81%) varied substantially depending on which guidelines were used. Reported treatment with azithromycin was below levels recommended by the CDNA and the WHO despite health services having sufficient courses available to them to mostly meet these targets. All aspects of the SAFE strategy are important in the eradication of trachoma. However, improving the supply and distribution of azithromycin should be relatively easy to implement, fund and monitor. Azithromycin courses* available, 2007–08;† courses given, 2008;‡ and WHO- and CDNA-recommended courses,§ in three Australian states with remote-area Indigenous health services WHO = World Health Organization. CDNA = Communicable Diseases Network Australia. * Azithromycin courses are given to those with active trachoma, their household contacts, and community members. † Under special Pharmaceutical Benefits Scheme arrangements and reported by Medicare Australia. ‡ Reported by the National Trachoma Surveillance and Reporting Unit (NTSRU). § Based on NTSRU data and using community population estimates.

Margaret Kelaher · Angeline S Ferdinand · Hugh R Taylor

To the Editor: Girgis and Seibel1 are to be congratulated as endocrinologists for raising the important issue of bisphosphonate therapy and femoral fractures. This is a relatively new phenomenon that even a couple of years ago, although already documented, did not seem to be on many endocrinologists’ radar. However, I question the authors’ statement that such fractures are rare. In my small outpost of the orthopaedic world (Northeast Health Wangaratta), three cases have been seen in 12 months. All patients characteristically had a spontaneous non-traumatic fracture, a short oblique or transverse fracture in the subtrochanteric area, and had been on alendronate for more than 5 years. If a journeyman orthopaedic surgeon is seeing a cluster of cases, I suggest that these fractures are not rare. On the other hand, a review of our audit figures in Wangaratta in north-eastern Victoria (where we have a stable rural population of about 17 000) provides an interesting statistic. Over 15 years (1993–2008), Northeast Health Wangaratta admissions for fractured neck of femur fell steadily from 74 to 35 a year. This trend continues. We should not throw out the baby with the bathwater — osteoporosis treatment is likely partly responsible. Also, a deeper level of community aged care support and much better comorbidity management may have helped to reduce falls. The real question is whether all patients who have been on alendronate (or any bisphosphonate) for 5 years need to have a mandatory holiday from the drug. In line with Wolff’s law (bone will adapt to loads under which it is placed), the precursor femoral stress lesions will heal by remodelling, as long as bisphosphonate therapy is suspended. I suggest that the suspension should be for 2 years, which is the time required for full fracture remodelling. I agree with Girgis and Seibel that these drugs have been effective in reducing fracture incidence; however, their long-term use needs further study.

Michael P Falkenberg

In reply: We thank Falkenberg for his comments in reference to our article in the Journal.1 Two recent large-scale population-based studies have suggested that subtrochanteric femur fractures are rare both in the general population and among bisphosphonate users.2,3 While personal experience may often suggest otherwise, a cluster of atypical fractures cannot be used as an indicator of true incidence in the absence of data on the frequency of bisphosphonate use in a particular population. It is certainly safe to say that atypical fractures occur much less frequently than osteoporotic hip fractures. In a 5-year retrospective analysis of femur fractures at our centre, osteoporotic hip fractures outnumbered atypical fractures by a factor of greater than 60.4 Given the body of high-quality evidence on the antifracture efficacy of bisphosphonates, we agree that discarding an effective class of drugs because of a presumed association with an uncommon fracture pattern would be like throwing out the baby with the bathwater. Should we routinely advise patients to take a drug holiday after, say, 5 years of bisphosphonate therapy? There is no good evidence for that either. Although bisphosphonates bind to bone for extended periods, severely suppressed bone turnover or signs of mechanical failure (microcracks) are rarely, if at all, seen in patients chronically treated with bisphosphonates. Similarly, the few bone biopsy studies in patients with atypical fractures do not uniformly support the hypothesis of severely suppressed bone turnover as a cause of these fractures.5,6 Instead of being based on the theoretical assumption of an uncertain risk, the decision for a drug holiday should be made on a case-by-case basis, guided by factors such as the patient’s on-drug fracture history, the presence of other relevant risk factors for osteoporosis, and changes in bone density and bone turnover. Many questions remain unanswered regarding atypical femoral fractures and their biomechanical evolution. Until further research is conducted, the fear of the unknown, namely the impact of bisphosphonates on bone remodelling and microfracture accumulation, should not replace strong evidence in support of their antifracture efficacy.

Christian M Girgis · Markus J Seibel

To the Editor: Point prevalence studies have been used for many years as markers of antimicrobial consumption,1,2 but they have suffered from a lack of standardisation with regard to the populations studied and the data collected. These deficiencies make it difficult to generalise the data outside the study populations. In recent years, the European Surveillance of Antimicrobial Consumption (ESAC) has sought to overcome these weaknesses by implementing a web-based point prevalence survey in 20 European countries using standardised definitions for site of infection, indication and quality indicators, such as whether the indication for prescription is documented in the case notes.3 As Australian studies of this type have not been published, we undertook a pilot study to assess whether this point prevalence tool is feasible and useful in an Australian setting. All surgical inpatients (excluding intensive care patients) in Sydney’s Royal North Shore Hospital (a 541-bed tertiary referral hospital) at 8 am on a single day in December 2009 were included. Current prescriptions for antimicrobials were captured from the medication prescription charts, and data on duration of therapy, dose and route of administration were collected for that point in time to give a “snapshot” of prescribing on that day. We reviewed patients’ medical records to establish site of infection, indication for treatment, and whether the reason for the antimicrobial was documented. ESAC codes for site of infection and indication were used. Of 178 patients, 95 (53%) had been prescribed 140 antimicrobials (ESAC mean, 30% of patients; range, 19%–59%).3 Cephazolin was the most commonly prescribed antimicrobial (32/140; 23%), and 115 antimicrobials (82%) were administered intravenously. Intra-abdominal sepsis (31/140; 22%) and cellulitis or wound infection (21/140; 15%) were the most common anatomical sites requiring treatment. Of the 140 prescriptions, 48 (34%) were for community-acquired infections, 29 (21%) were for postoperative infections, and 35 (25%) were for surgical prophylaxis. Of the 35 prescriptions for surgical prophylaxis, 14 (40%) were administered for more than 1 day (ESAC, 57%).3 The reason for initiation of the antimicrobial was documented in the patient’s medical notes for 95 of 140 prescriptions (68%) (ESAC, 64%).3 Use of the ESAC methodology allowed us to benchmark our results against published international reports. However, it gave no information on the appropriateness of the prescriptions or whether they adhered to antimicrobial guidelines. The ESAC point prevalence tool is easily applicable to the Australian health care system and provides useful information on antimicrobial consumption and quality indicators at an institutional level. Addition of questions regarding appropriateness of prescribing could be incorporated to give further relevant information.4 Use of the same methodology in other Australian centres would enable comparison across institutions and, potentially, national and international collaboration.

Jennifer A Kieran · Rosaleen G O’Doherty · Bernard J Hudson

To the Editor: It is regrettable that research published by Studdert and colleagues suggests that barriers remain to the open disclosure of medical error in Australia.1 Although all states have enacted legislation to protect defendants who apologise to plaintiffs, such protection is variable and inconsistent across Australia.2 Most significantly, the definition of what constitutes an apology varies greatly from jurisdiction to jurisdiction, as do the various protections afforded to the apology. Unfortunately, this only serves to complicate what should be an open and candid discussion of the circumstances surrounding a medical error. However, the fear of legal action is not the only barrier preventing doctors from disclosing harm-causing medical errors to patients and their families. Acknowledging that an error has caused serious harm to a patient is extremely distressing to doctors, most of whom enter the medical profession with the aim of relieving the suffering of others. When their actions inadvertently result in harm to patients, the impact can be devastating.3 The emotional reaction to a medical error is usually one of intense anxiety and concern for the patient’s welfare, then deep reflection on how the error occurred and how the outcome might be mitigated. This may be followed closely by the doctor’s anxiety about his or her own welfare and the professional and legal consequences of the mistake, including the potential loss of reputation or even job. Consequently, doctors are sometimes tempted to rationalise away their role in causing harm or minimise their responsibility for disclosing mistakes and failures.4,5 However, an apology is a powerful tool to facilitate healing of the emotional scars of a patient’s injury. Furthermore, from the perspective of a medical indemnity insurer, while open and transparent disclosure of medical error would seem an improbable risk-management strategy, there is no doubt that a truthful and compassionate explanation of some errors that cause harm may actually reduce the risk of litigation.6 So, as Studdert and colleagues conclude, doctors should be and are supported and encouraged to enter into these difficult discussions by their insurer, without a presupposed fear that the actual process of open disclosure might contribute to the risk of litigation. One hopes that stakeholders will continue to work towards removing barriers to this process, with a greater focus on clinical risk management and less on recrimination and blame within the Australian health care system in years to come.

Julian L Rait · Elizabeth H Van Ekert

To the Editor: Readers of the Journal’s editorial on the importance of clinical patient-outcome monitoring asking “Where are the clinical data?”1 will be pleased to know that the state of Victoria collects considerable data on surgical outcomes. Since 2001, the Department of Health’s Victorian Surgical Consultative Council (VSCC; http://www.health.vic.gov.au/vscc/) has monitored surgical outcomes in the state’s public hospitals. Monitoring of both morbidity and mortality outcomes is combined with voluntary and mandatory case reporting and a high level of participation of hospitals and surgeons. It is compulsory for hospitals to report a range of sentinel adverse events and undertake corrective strategies. Data about surgical inpatients are obtained from discharge coding in medical records statewide, and the chief executive officers and directors of surgery of health services with “outlying performance” are invited to analyse the case records and provide their findings to the VSCC. A VSCC subcommittee, the Surgical Outcomes Information Initiative, promulgates the conclusions in a de-identified manner to hospitals, surgeons and trainees, with a view to improving safety, systems and surgical outcomes. Since 2008, deaths of public hospital patients that occur under surgical care are monitored by the Victorian Audit of Surgical Mortality (VASM, derived from the VSCC), which covers most surgical specialties, and is soon to embrace private hospitals and, hopefully, gynaecological surgery as well. De-identified educative information from autopsies and case analyses is offered to surgeons and trainees, whose participation in case reporting and assessing is now a professional requirement of the Royal Australasian College of Surgeons (RACS). Surgical mortality as monitored by the VASM is now bi-nationally compared through the RACS’s overarching Australian and New Zealand Audit of Surgical Mortality. Victoria’s Department of Health has longstanding collections of data for anaesthetic, obstetric and perinatal outcomes, with similar consultative councils. Several surgical specialties have for over a decade collected and promulgated their morbidity and mortality information. The Melbourne Vascular Surgical Association requires its members to participate in clinical outcome audits, as does the Australian and New Zealand Society for Vascular Surgery. Other specialties that audit outcomes are orthopaedic surgery (the bone and joint registry), transplantation surgery and cardiac surgery. Surgeons’ general experience of clinical patient-outcome monitoring is that of enthusiasm for its professional and community benefits, including the benefit of knowing that Australia’s overall surgical standards are comparable with the world’s best. The incentive remains to improve data capture, patient safety and eternal clinical vigilance, and these endeavours deserve support.

Peter L Field

To the Editor: We would like to report the deaths of three young children in Australia as a result of hanging from bicycle helmets. Our aim is to draw attention to this rare but entirely preventable cause of childhood death. Helmets are required to be worn when bicycles are ridden, and have been the subject of mandatory standards since 1989.1 A number of accidental deaths have, however, been reported in the United States, Scandinavia and Canada as a result of young children becoming suspended by their bicycle helmets while playing on playground equipment. This has led to a series of warnings about not allowing children to wear helmets in playgrounds.2,3 The National Coroners Information System (NCIS)4 is an electronic database containing information on coronial cases from all Australian states and territories since 2001. We undertook a review of the NCIS for all deaths of children in Australia that were associated with bicycle helmets from 2001 to 2009. Three cases of deaths due to hanging were identified; these involved a 2-year-old boy who was suspended by his helmet strap between a bunk bed and a wall (in 2003), a 3-year-old boy who was suspended by his helmet strap when he tried to climb out of a home window (in 2007), and a 5-year-old boy who was suspended from an overhead clothesline while jumping on a trampoline (in 2009). These cases show that accidental hanging is still occurring among young children who wear bicycle helmets while engaging in activities other than bicycle riding. Importantly, hanging from bicycle helmets can occur in places other than playgrounds, sometimes by quite unusual mechanisms. Although such deaths are rare,5 it is important for parents and child carers to ensure that bicycle helmets are only worn by children for their intended purpose, and not during other activities.

Roger W Byard · Allan Cala · Donald Ritchey · Noel Woodford

To the Editor: We read with interest the letter by Baschera et al1 regarding the retrieval of non-permanent inferior vena cava filters (IVCFs) in trauma patients. With the advent of retrievable devices, there has been a renewed interest in the use of prophylactic IVCFs after trauma. Retrievable IVCFs are a particularly attractive option for trauma patients, who are often young, with only a transient predisposition to develop venous thromboembolism (VTE). They theoretically provide prophylaxis against pulmonary embolism (PE) in high-risk patients for whom chemoprophylaxis is contraindicated, while avoiding long-term complications associated with permanent IVCFs. However, we share the authors’ concern about low retrieval rates of IVCFs due to loss of patients to follow-up.2,3 The decision to place an IVCF in a patient who has undergone trauma is based on a risk–benefit ratio. If such decisions are made on the presumption that IVCFs will be retrieved, while in practice many IVCFs are not retrieved, the increasing popularisation of retrievable filters may be under false pretences. At our institution, a level 1 trauma centre, all IVCFs are inserted by interventional radiologists under fluoroscopic guidance. At the time of insertion, patient and device details are entered into a purpose-built IVCF database that is run and maintained by the Department of Radiology. At this time, a follow-up appointment is also booked for the patient to attend the IVCF outpatient clinic run by the interventional radiologists. Here, ongoing VTE risk factors are evaluated and the timing of IVCF retrieval is determined. The timing of IVCF retrieval after trauma is controversial, and the occurrence of PE after retrieval is well documented. The risk period for PE after trauma is difficult to quantify, but likely to extend beyond the discharge date for many patients, especially if ongoing surgery is scheduled. For this reason, our practice is to retrieve IVCFs in the outpatient setting 3–4 months after injury. Prolonged IVCF dwell times must be balanced against the increasing difficulty of retrieval because of IVCF endothelialisation, but we feel that a timeframe of 3–4 months does not compromise retrieval rates. Successful retrieval of filters has been reported up to 317 days after insertion.4 As in the case described by Baschera et al,1 it is not uncommon to find a clot in the filter at the time of attempted retrieval, for which multiple causes have been proposed.5 In this situation, it is our practice to rebook patients for a repeat cavogram and second retrieval attempt after therapeutic anticoagulation for 1–2 months.

Lachlan M Batty · Jim Koukounaras · Stuart M Lyon

To the Editor: Significant morbidity and mortality are associated with excessive alcohol use, which, for Aboriginal Australians, generally occurs within a context of disadvantage. During 2007–2009, we assessed cognitive and psychological factors (using CogState1 and Strong Souls2 [CogState Ltd, Melbourne, Vic]) of 21 men and 11 women on admission to a 2-month Aboriginal residential treatment program in the Northern Territory. Participants’ mean age was 32 years (SD, 8.7 years) and the mean length of time for which they had used alcohol was 13.3 years (SD, 7.7 years). To determine the effect of age, number of years of drinking and other factors on continued alcohol use, we reinterviewed and reassessed participants in their home community with the same cognitive and psychological measures used at the initial assessment after a mean period of 11 months (SD, 4.4 months). At both baseline and follow-up, the number of participants for whom data were available varied for some characteristics. The Human Research Ethics Committee of the Northern Territory Department of Health and Community Services and Menzies School of Health Research (including the Aboriginal Ethics Sub Committee) approved the study. At baseline, 14 of 23 alcohol users reported drinking every day or most days, and 26 of 31 drank more than 10 standard drinks on each occasion. At follow-up in the community, 23 had resumed drinking at the same level, and nine had reduced their use (six had stopped using alcohol, and three had resumed drinking at lower levels). Compared with users who reduced their alcohol intake, users who did not showed poorer paired associate learning at the time of admission for treatment, and poorer performance at follow-up in visual attention, learning and executive function, visual learning and recall, and paired associate learning tasks (Box). This suggests that while subtle cognitive impairment may be a risk factor for continued heavy alcohol use after treatment, heavy alcohol use is also a likely cause of additional cognitive deficits.3 While reduced alcohol use may be associated with improvements in cognitive function, continued use may lead to further cognitive decline. Alcohol users who resumed drinking at the same level were significantly more likely to experience the psychological symptom “worry” after treatment (4/6; Fisher exact test, P < 0.05) than were users who reduced their alcohol use (0/6), which suggests that alcohol may have been used for self-medication or that excessive alcohol use may mask underlying psychological problems. Interestingly, a greater proportion of alcohol users who resumed drinking at the same level (10/16) were also using cannabis at follow-up, compared with those who reduced their use (1/9; Fisher exact test, P < 0.05). Cannabis use has been independently associated with psychological symptoms in other Australian studies, but with no impact on cognition.2,4 Our data indicate that there is a need to treat mental health problems concurrently with alcohol misuse problems among alcohol users undergoing treatment. Alcohol users who resumed drinking at the same level were less likely to return to remote communities with restricted alcohol availability (11/23), compared with those who reduced their alcohol use (9/9; Fisher exact test, P < 0.01), lending some support to the effectiveness of alcohol restrictions. Overall, our data show that cognitive problems and alcohol availability may be underlying factors in ongoing alcohol misuse by Aboriginal Australians. Charactersitics of alcohol users who resumed drinking at the same level and those who reduced their alcohol use after a 2-month residential treatment program, at baseline and at follow-up (n = 32) Characteristic Unchanged alcohol use, median Reduced alcohol use, median Z Significance No. of alcohol users 23 9 Age at baseline, years 31.3 29.0 − 0.15 ns Years of drinking, at baseline 13.0 11.6 − 0.59 ns Visual attention, speed (log transformed)* Baseline 2.81 2.76 − 1.67 ns Follow-up 2.79 2.71 − 2.10 P = 0.04 Working memory, accuracy (arcsine transformed)† Baseline 0.70 0.70 − 0.19 ns Follow-up 0.80 0.74 − 0.53 ns Psychomotor speed, moves per second† Baseline 0.77 0.95 − 0.35 ns Follow-up 1.17 1.37 − 0.75 ns Learning and executive function, moves per second† Baseline 0.44 0.47 − 0.39 ns Follow-up 0.58 0.76 − 2.32 P = 0.02 Visual learning and recall, moves per second† Baseline 0.48 0.46 − 0.21 ns Follow-up 0.73 0.84 − 2.20 P = 0.03 Paired associate learning, duration (seconds)* Baseline 307.81 214.11 − 2.52 P = 0.01 Follow-up 286.51 168.48 − 2.67 P = 0.008 ns = not significant; P > 0.07. * Higher values indicate poorer performance. † Higher values indicate better performance.

Kylie M Dingwall · Paul Maruff · Sheree Cairney

To the Editor: The article by Philip Sambrook et al on the impact of adverse news media on prescriptions for osteoporosis1 contains a number of serious errors and ignores more recent data. Their article quotes the estimated incidence of osteonecrosis of the jaw (ONJ) after oral bisphosphonate treatment for osteoporosis to be between 1 in 10 000 and 1 in 100 000 patient treatment-years. This is in fact a gross underestimate.2 The results of an independent study funded and conducted by the United States Food and Drug Administration (FDA) found an incidence of between 1 in 537 and 1 in 1537.3 This result is similar to that of an independent Australian study, which found an incidence of 1 in 296 to 1 in 1130.4 Thus, there is evidence that bisphosphonate-associated ONJ is much more common in patients treated with oral bisphosphonates for osteoporosis than the authors claim. Bisphosphonate-associated ONJ is also much more serious than presented. Patients with ONJ can be affected for years. The condition causes considerable morbidity, with greater interference in a patient’s life than the condition of osteoporosis and vertebral fractures. It should be noted that the FDA study3 and the Australian study4 were based on documented cases of ONJ, whereas the study by Sambrook et al1 was not based on actual fractures. It is unfortunate that, despite the wording of the Pharmaceutical Benefits Scheme (PBS) regulations, the Pharmaceutical Benefits Advisory Committee has let it be known that osteoporosis diagnosed by bone mineral density is not a requirement for PBS-supported bisphosphonate therapy — all that is required is a minimal trauma fracture, although it is well known that most patients with minimal trauma fracture do not have osteoporosis (however that is defined).5 The issue of adverse effects of bisphosphonate treatment for osteoporosis is currently being tested by a US class action. In the bellwether case of Boles v Merck & Co,6 the issue being tested is whether it was appropriate to prescribe alendronate for a patient with osteopenia but no fractures, and how much this treatment contributed to the patient’s end-stage ONJ. The plaintiff had exposed bone, constant pain, a pathological fracture, and pus dripping from her chin. The New York Supreme Court found in her favour. Despite the claim by Sambrook and colleagues that unbalanced media coverage “has the potential to do more harm than good”,1 the media do have an important role to play in exposing to the public the risks of pharmaceutical products and the actions of some pharmaceutical companies. It should be noted that Professor Sambrook was not only involved in The 7:30 Report current affairs program, but was also subsequently granted the unusual right of reply on that program. Following these two programs, the public made its decision based on facts about the incidence and morbidity of ONJ that have been confirmed by recent independent studies.3,4,6

Paul J Sambrook · B E Christopher Nordin · Alastair N Goss