Letters

Lionel L Wilson Principal, Qual-Med, 34B Kangaloon Road, Bowral, NSW 2576. Lwilson10ATbigpond.com To the Editor: Nisselle’s recent editorial on managing medical indemnity raises important issues.1 I would like to comment on some points. The quality movement, in the form of a system of hospital accreditation, actually began via the New South Wales Branch of the Australian Medical Association in the late 1960s. However, credentialling and the delineation of clinical privileges for medical staff are far from the norm that Nisselle claims. In fact, although some hospitals claim to be credentialling medical staff, in most instances this is little more than an exercise in tokenism and is quite incapable of contributing either to quality or to minimising risk. Nisselle also refers to the “safety movement”. While recognising current common usage, to talk of safety as separate from quality in healthcare is tautological. It is not credible to visualise a hospital that claims to provide quality care but tolerates unsafe practices of any description. Similarly, unsafe practices in a facility mean that quality care is not being achieved. In attempting to untangle the semantic problems occasioned by the term “risk management”, Nisselle merely compounds the problem that bedevils this subject. Of course, he is far from alone, and the medical literature further aggravates this confusion. I suggest the following definitions in the hope of introducing some clarity: Quality management: The management of all these issues, as Nisselle points out, is a big task. While the term “clinical governance” is currently in vogue, it means little, I believe, to most doctors. Managing quality is a complex task (as illustrated by Nisselle’s appropriate elephant analogy). So why not call it what it is? Managing quality is largely about avoiding patient harm. Risk management: The same definition should be used whether we are talking about an insurance company or a medical service. It is the minimisation of financial loss. In the case of healthcare, the risk is malpractice litigation directed at both doctors and hospitals. The techniques of risk management are very similar to those of quality management, and risk management is an intrinsic component of quality management.2 Risk management in healthcare is not simply about reducing error, any more than is quality management. It is this focus that leads to so much confusion. Quality assurance: This is the deliberate activity of ensuring that what was done and achieved is what should have been done and should have been achieved. It is another facet of the broader activity of quality management. The management of quality and avoidance of the risk of litigation is difficult enough. It would help if we did not all use the terminology to mean whatever we want it to mean.

Lionel L Wilson

Paul Nisselle Senior Advisor, Risk Management, Medical Defence Association of Victoria, PO Box 1059, Carlton, VIC 3053. nisselpATozemail.com.au In reply: Wilson highlights the confusing taxonomy of quality/risk in healthcare. My editorial distinguished prudential risk management (ensuring insurer solvency) from clinical risk management (reducing medical error).1 The term “clinical governance” combines quality improvement (ie, getting it right more often) and risk management (ie, getting it wrong less often). Wilson writes that “Managing quality is largely about avoiding patient harm”. But quality management is as much about finding more effective ways of doing things as it is about finding safer ones. Quality and safety are separate, albeit overlapping, concepts. Similarly, risk management is more than just “minimisation of financial loss”. Reducing the rate of head injuries by using seat belts has a human benefit, not just a financial one. One trade-off for the “Abbott reforms” to medical indemnity is a demand by government for a real commitment by both medical indemnity insurers and those insured to clinical risk management. Although we may disagree on the language, Wilson and I are in heated agreement on the need for a concerted, systemic approach to quality management. The medical indemnity insurers have a role to play that goes beyond just remaining solvent and keeping indemnity costs down!

Paul Nisselle

Kevin B Orr Surgeon, 3/22 Belgrave Street, Kogarah, NSW 2217. stgeorgedermATbigpond.com To the Editor: I report the case of an unexpected complication of a common cardiothoracic procedure which deserves the attention of the general medical community. An 82-year-old general practitioner required coronary artery bypass surgery. Although retired, he was fit enough to continue visiting patients in a number of nursing homes, and occasionally assisted at operations. His condition after the surgery was good for a few days, but deteriorated, with the development of dyspnoea, shortly before he was due to be transferred to a rehabilitation unit. Whether it was realised that his haemoblobin level had fallen from 150 g/L to 90 g/L over the days before surgery is not known. A blood count several days after surgery revealed a haemoglobin level of 100 g/L. This low level was attributed to insufficient transfusion during surgery. The patient was given two units of blood, which raised the haemoglobin level to 120 g/L. Although a repeat test on the day he was discharged to a rehabilitation unit showed the level was again 100 g/L, this result was not seen by a clinician before the transfer. On arrival at the rehabilitation unit, the patient was unable to complete the scheduled activities. He was breathless, returned to his room, almost fainted and had to be helped back into bed. Later that night, he had massive melaena and died. For some weeks leading up to the bypass surgery, the patient had suffered from dyspepsia and was “living on” antacid. He mentioned this to his general practitioner, who did not initiate any investigations or treatment. On the patient’s admission to hospital, the medical officer prescribed omeprazole, presumably in response to the history of dyspepsia. Whether this doctor was aware of a preoperative drop in haemoglobin level is not known. The most likely cause of this man’s death was a bleeding duodenal ulcer exacerbated by coagulation defects associated with major surgery (no autopsy was performed). Bleeding was initially slow but culminated in a fatal haemorrhage. The lesson from this case is that any suggestion of a serious concurrent illness should be thoroughly investigated before major surgery. In this case, a simple gastroscopy before the bypass surgery might have been lifesaving.

Kevin B Orr

Christine Y Lu,* Kenneth M Williams,† Lyn March,‡ James V Bertouch,§ Richard O Day¶ * PhD Candidate, † Deputy Director, ¶ Director, Therapeutics Centre, St Vincent’s Hospital, University of New South Wales, Victoria St, Darlinghurst, Sydney, NSW 2010. ‡ Rheumatologist, Royal North Shore Hospital, The University of Sydney, St Leonards, NSW. § Head, Department of Rheumatology, Prince of Wales Hospital, Randwick, NSW. christine.luATstudent.unsw.edu.au To the Editor: The tumour necrosis factor (TNFα) inhibitors etanercept, infliximab and adalimumab are new treatments for rheumatoid arthritis (RA) subsidised by the Pharmaceutical Benefits Scheme (PBS) under strict criteria. These are based on data supplied by the sponsors and protracted discussions between the stakeholders: the Pharmaceutical Benefits Advisory Committee (PBAC), the sponsors, rheumatologists and consumer representatives.1 One eligibility criterion is that adult patients must be or have been rheumatoid-factor positive. This requirement raises particular concerns. Rheumatoid factor is not exclusively associated with RA. It is found in a number of other autoimmune and infectious diseases, and has been detected in healthy people. Rheumatoid factor is a serological criterion in the American College of Rheumatology classification for RA. However, its presence is not definitive for a clinical diagnosis of RA, with rheumatoid factor being absent in about 30% of patients with RA. Studies suggest that patients who test positive for rheumatoid factor at baseline are more susceptible to relatively severe expression of RA, with development of erosions and functional disability.2 As the PBS already limits access to TNFα inhibitors to patients with severe active RA, the predictive value of rheumatoid factor for severity is redundant. We systematically reviewed 23 clinical trials of TNFα inhibitors available in the public domain (references available on request). The review showed that only the Early Rheumatoid Arthritis trial restricted recruitment to patients who tested positive for rheumatoid factor.3 The aim of this study was to examine the effect of etanercept on the rate of development of erosions in patients with early RA, not whether rheumatoid-factor status affected response. We conclude that the evidence for an association between rheumatoid-factor status and response to TNFα inhibitors in patients with severe RA is inadequate to justify rheumatoid-factor status as a criterion for PBS subsidisation. Similarly, no evidence for an association between rheumatoid factor and response to disease-modifying anti-rheumatic drugs has been reported.4 Nevertheless, potential predictors of response to TNFα inhibitors and such drugs are emerging (eg, polymorphisms of HLA-DRB1, TNFα, and interleukin-10).5 Further analysis of the unpublished individual patient data held by the sponsors is needed to shed light on this question. Clinical studies specifically designed to evaluate the influence of rheumatoid-factor status on response would be helpful. The PBAC may have been provided with these data, but patients and clinicians operating in the public domain have not. This gives rise to an ethical dilemma whereby prescribers cannot provide a plausible explanation for why rheumatoid-factor status is an access criterion. For example, if rheumatoid-factor-positive status was selected to exclude patients with rheumatoid-factor-negative psoriatic arthritis, then the rationale would not appear to be ethically sound. Greater transparency with respect to the rationale and the evidence for the criteria selected for targeting subsidised access to important high-cost pharmaceuticals will enhance confidence in the PBS process.

Christine Y Lu · Kenneth M Williams · Lyn March · James V Bertouch · Richard O Day

Lloyd N Sansom Chair, Australian Pharmaceutical Benefits Advisory Committee, School of Pharmacy, University of South Australia, Adelaide, SA 5000. Lloyd. SansomATunisa.edu.au Comment: I am grateful for the opportunity to put the perspective of the Pharmaceutical Benefits Advisory Committee (PBAC) on this important issue for patients and prescribers using TNFα inhibitors for rheumatoid arthritis. I can confirm that the PBAC based its recommendation to exclude patients who test rheumatoid-factor negative on a meta-analysis of the data presented to it in the sponsor’s reports of two published randomised trials.1,2 The sponsor of etanercept requested a restriction that limited use to patients with rheumatoid-factor-positive status — a proposition that was queried by the PBAC in its evaluation. The sponsor indicated in its response that rheumatoid-factor status was a treatment-effect modifier. As anticipated by Lu and colleagues, the reason for the recommendation was neither to confirm the diagnosis of rheumatoid arthritis nor an attempt to identify patients with more severe disease. The main reason is that there was some statistical support for the contention that, in patients with rheumatoid arthritis, being rheumatoid-factor positive is associated with a better response to treatment with these drugs. Unfortunately, my request to the sponsor to be able to release in this letter the information on which the decision was based was refused. The statistical analysis relied on by the PBAC was based on individual patient data, stratifying trial participants into two groups (rheumatoid-factor positive and rheumatoid-factor negative), and then formally applying a test for interaction against the reported treatment effect compared with placebo. Although a post-hoc analysis, this approach has the advantage of relying on the entire trial dataset rather than increasing the likelihood of detecting spurious differences by conducting a series of post-hoc sub-group analyses. It also differs from the systematic review reported by Lu and colleagues, which sought to examine the question based on the reported eligibility criteria of the trials, and therefore could only be conducted at the level of the overall trial, not the level of the individual patient in the trials. The interpretation of the data available to the PBAC at the time was supported by rheumatologists advising the PBAC about actual restrictions for the subsidy of these expensive agents. It is perhaps noteworthy that many decisions that guide treatment are made purely on the basis of biological plausibility. On this occasion, there was some statistical support, albeit from a post-hoc analysis, to support any biological arguments. There is inevitably an element of judgement about these decisions, as is clear in the letter from Lu et al, who describe “accumulating evidence” in relation to whether gene polymorphisms “may be predictive of clinical responsiveness”. The current situation, as exemplified in this letter, in which the PBAC is unable to give detailed reasons for its decisions, clearly demonstrates the urgent and critical need for greater transparency of the PBAC processes, and underscores the fundamental right of Australian consumers and prescribers to information relevant to decisions about the subsidy of medicines in this country. The PBAC is willing to examine any new evidence relating to the influence of rheumatoid-factor status on health outcomes and the cost-effectiveness of these agents. If there is additional evidence supporting a review of the current listing, the PBAC would encourage the sponsors of these drugs to prepare appropriate submissions to enable us to evaluate these data. As Chair of the PBAC, I intend to continue to work towards the goal of greater transparency, whereby the outcome of any such new evaluation, and its basis, could be made available to Australian consumers and prescribers.

Lloyd N Sansom

Tim Woodruff President, Doctors Reform Society, Suite 207, 320 Victoria Parade, East Melbourne, VIC 3002 twoodruffATbigpond.com To the Editor: It is encouraging to see the Journal continuing its tradition of taking on contentious issues in publishing articles about the negative influence of the pharmaceutical industry.1 With respect to the practical suggestions to address this issue, I suggest that reliance on our profession to substantially improve the situation, although laudable and appropriate, is too optimistic given the gross denial by our colleagues that there is an issue. Our professional bodies simply do not have the support to enforce codes of conduct. The Royal Australasian College of Physicians (RACP) has published guidelines on this issue,2 but I doubt most of its members have read them. I fully support Breen’s comments relating to funding of educational activities, but I suggest that the pharmaceutical pseudo-educational dollar be bypassed by a major expansion in government funding.3 The provision of regularly updated, easily accessible treatment guidelines integrated into prescribing software (which most general practitioners use daily) would go a long way to decreasing our reliance on the drug dollar for information on appropriate treatment. This requires government investment and professional college cooperation, but would lead to recurrent savings to the Pharmaceutical Benefits Scheme and better treatment. Currently, the federal government spends $21 million on drug information to doctors,4 while the drug industry spends $1 billion on marketing.5 To partially redress this imbalance would, however, require both political will and pressure from the profession.

Tim Woodruff

Linda V Graudins Senior Pharmacist (projects), Prince of Wales Hospital, High Street, Randwick, NSW 2031 graudinslvATsesahs.nsw.gov.au To the Editor: Thank you for publishing the Viewpoint by Breen regarding pharmaceutical industry relationships with the medical profession1 — but please do not coin the word “pharmaproof”. This word unintentionally casts aspersions on fellow clinicians — pharmacists — who share the dilemma of aggressive pharmaceutical marketing influencing professional decisions. The relationship between the industry and pharmacists is actually more complicated, as we are not only advocates for patients and advisers to doctors on the safe and evidence-based use of medicines, but also the buyers of the pharmaceutical products. This last function means that most pharmacists cannot be removed from the business side of medicine supply and must work with the manufacturers to obtain supplies in a timely fashion and at the best price. In my work as a hospital pharmacist, the pharmaceutical industry helps in planning financial aspects of medicine supply, sponsoring various activities that the public health system and universities are unable to, and providing specific product information — be it for marketed, unregistered or trial medicines. Most pharmacists cannot choose to not see industry representatives. The formation of such relationships can indeed insidiously affect our clinical decision-making, as outlined by Breen. Unfortunately, the issue of industry’s influence on pharmacists’ decision-making has only rarely been discussed in the pharmacy literature.2-4 Both medical and pharmacy clinicians must be aware of this influence and act accordingly. Peter Mansfield’s Healthy Skepticism (www.healthyskepticism.org) is a good starting point to increase this awareness. However, the movement must include physicians and pharmacists on the same side. I have often been told that we must have the latest new drug on the hospital’s formulary because . . . and have been given a hefty manufacturer-prepared dossier as the sole reason for the request. I urge physicians to work with pharmacists and be “pharma(cist)friendly”, yet also “industryaware”.

Linda V Graudins

Scott Masters General practitioner, Musculoskeletal Medicine, Caloundra Spinal and Sports Medicine Centre, 39 Minchinton St, Caloundra, QLD 4551 cfmpATozemail.com.au To the Editor: The Journal recently published three interesting articles on the relationship between the medical profession and the pharmaceutical industry.1-3 With Medicines Australia (the pharmaceutical manufacturers’ association) setting up a strict code of conduct (tighter than for any other industry I know), a better balance seems to be on the horizon. Breen reminded us of our responsibilities to protect ourselves and our patients from slick marketing by pharmaceutical companies.1 One technique our surgery has found useful is to have a personal code of conduct. Our surgery has a guide for pharmaceutical reps (copies available from the author). It advises reps that we are not interested in seeing their promotional material, especially those useless coloured graphs. However, we are very happy to look at published trials regarding their product and associated diseases. Personally, I have found the resources available from many reps useful and time-saving. Breen is concerned about our professional leaders being in denial about the influence of the pharmaceutical industry on doctors’ prescribing habits. If this is so, then the same leaders have complete amnesia and catatonia about another influence that potentially threatens to engulf us. The sale of supplements and complementary medicines in Australia is a billion-dollar business now. Every month I receive more requests to use supplements for conditions varying from heart disease, cancer and fatigue to non-specific therapies such as detoxification, immune support, metabolic enhancer and anti-ageing. I can sell all these products directly to consumers (patients) at a mark-up I consider reasonable. Alternatively, I can recruit patients to become sellers in a multilevel marketing scheme (similar to pyramid selling). One doctor who practises nutritional medicine full-time has told me he buys $10 000 worth of vitamin E at the start of the year and manages to sell it over the ensuing 12 months for $100 000. I imagine most of that doctor’s patients are recommended vitamin E for their health complaints or health maintenance. This is entirely legal, although there are major ethical concerns about conflict of interest. To date, there has been little debate among our leaders regarding proper guidelines and regulation of this behaviour. With the enormous potential of the complementary industry to be a useful partner in health management, this needs to be sorted out sooner rather than later.

Scott Masters

Rosanna Capolingua Chair, Ethics and Medico-Legal Subcommittee, Australian Medical Association, PO Box 6090, Kingston, ACT 2604 Comment: I commend Masters on his personal code of conduct in dealing with the pharmaceutical industry. I also share his concerns about the ethical minefield that lurks in the interface between complementary and conventional medicine. Some of the issues involved have recently been explored in the Journal’s series on Complementary and Alternative Medicine.1 However, his scenario of a doctor selling vitamin E to patients raises specific concerns, and the Australian Medical Association’s Code of Ethics2 provides some ethical principles in this regard. Specifically, it states that a doctor should: “make sure that you do not exploit your patient for any reason” “exercise caution in publicly endorsing any particular commercial product or service not covered by the Therapeutic Goods Advertising Code”3 and “when referring your patient to institutions or services in which you have a direct financial interest, provide full disclosure of such interests”. Translating these principles into daily professional conduct means the practitioner must at all times declare pecuniary interest in the sale of products and be aware of the evidence base of the commercial recommendation so as to not mislead the patient. This involves clear communication of potential benefit, adverse effects, and possible drug–drug interactions of whatever product is promoted. But, above all, the whole thrust of the AMA Code of Ethics is to ensure that perverse incentives remain foreign to the patient–doctor relationship. Ultimately, it is an individual doctor’s choice.

Rosanna Capolingua

Hugh G Dickson Chair, Human Research Ethics Committee, South Western Sydney Area Health Service, Locked Bag 7103, Liverpool BC, NSW 1871. Hugh. DicksonATswsahs.nsw.gov.au To the Editor: Roberts et al1 state that the National Health and Medical Research Council’s National statement on ethical conduct in research involving humans2 clearly outlines that, once approval has been gained from one human research ethics committee (HREC), other sites should accept that approval. Nowhere does the national statement state this. What Roberts et al appear not to appreciate is that research projects may consume resources within a health service. The HREC might also have the responsibility of ensuring that the tasks required for successful completion of research can be performed without compromising the standard of care of the health facilities in which the research is to be performed. The project in question required the extraction of medical records — someone has to do this and be paid for the task. While centralisation of human research ethics approval might make the task of approval of research faster, each administrative unit has to be able to decide whether to allow participation in a project given its current level of service demand. Approval for multicentre research will therefore still take time whether or not central ethics approval is obtained, and researchers will not find an easy solution to this.

Hugh G Dickson

Kerry J Breen Chair, Australian Health Ethics Committee, National Health and Medical Research Council, PO Box 9848, Canberra, ACT 2601. kerrybreenATaccess.net.au Comment: It is correct that the National Health and Medical Research Council’s National statement on ethical conduct in research involving humans1 (paragraph 3.4) does not say that other sites should accept ethics review of a research proposal from another human research ethics committee (HREC). However, the national statement is written to permit and encourage this, but not to enforce it. Dickson’s letter also raises the issue of the terms of reference of HRECs. He alludes to an additional role — as gatekeeper of an institution’s resources — which some may feel is beyond the domain of HRECs. The national statement provides the framework for the composition and role of HRECs in their work of ethical review, but does not prevent an institution from asking its committee to also be the steward of access to resources regularly used (eg, medical records, pathology laboratories). The national statement requires an institution to set out the terms of reference for its HREC, “including the scope of its responsibilities” (paragraph 2.2). The prime function of HRECs is to make recommendations about whether a research proposal is ethical, but the final approval about whether the research can proceed rests with each individual institution. Thus, there is more to getting approval for a research proposal than just the ethical review.

Kerry J Breen

David J Maxwell,* Karen I Kaye† * Project Officer, † Executive Officer, New South Wales Therapeutic Advisory Group, PO Box 766, Darlinghurst, NSW 2010. tagprojectATstvincents.com.au To the Editor: We are currently coordinating the New South Wales arm of a national quality assurance (QA) project to improve the management of community-acquired pneumonia in Australian hospital emergency departments (CAPTION project: Community-Acquired Pneumonia: Towards Improving Outcomes Nationally, funded by the National Prescribing Service). In the project drug usage evaluation methods are used, and it involves an audit (retrospective review of patient medical records) as well as feedback and targeted education of healthcare professionals about national management guidelines for community-acquired pneumonia.1 There is no direct patient contact at any stage. Because this is a QA project, we did not request that participating NSW hospitals seek human research ethics committee (HREC) review. However, we did request that the project proposal be supported by HRECs as a QA activity. Further endorsement from the Chief Executive Officer, Director of Emergency, Director of Pharmacy and other key people and groups was also required. According to the National Health and Medical Research Council (NHMRC),2 an appropriately planned QA activity can proceed without HREC review and patient consent if: there is consistency with National Privacy Principle 2.1(a); and all people involved in the activity are unlikely to suffer burden or harm. To assist hospitals reviewing this QA project proposal, we developed a number of tools that explicitly outlined the nature of the project and provided answers to the questions in the NHMRC document. 2 These tools were provided to emphasise that this QA project was consistent with NHMRC requirements. The NHMRC further describes the establishment of hospital policies to allow efficient review of QA proposals that involve minimal risk, burden, alteration of care or invasion of privacy. It is recommended that a member of the HREC be appointed to review such proposals. Despite the NHMRC recommendations and the provision of tools as described above, full HREC submissions have still been required by four out of eight hospitals to date (recruitment still ongoing). After receipt of an initial expression of interest, completing the HREC submission and obtaining approval in three of these hospitals has taken an average of 5 months. The HREC review has not yet been completed in the fourth hospital. As the project is only funded for a 2-year period, this has resulted in a significant delay in the progress of the project. We do not challenge the vital role of HRECs, and we value the importance of ensuring the safety and privacy of all involved in human research. If QA coordinators and HRECs work together within the NHMRC recommendations, valuable time and resources could be saved, for both parties. In doing so, the Australian Research Ethics Committees’ belief that “quality assurance activities are an essential and integral part of health care delivery that should be encouraged and facilitated” would be one step closer to becoming a reality.

David J Maxwell · Karen I Kaye

Martin B Van Der Weyden Editor, The Medical Journal of Australia, Locked Bag 3030, Strawberry Hills, NSW 2012. medjaustATampco.com.au Comment: The distress conveyed by Maxwell and Kaye is the latest in a litany of concerns and complaints to the Journal over recent years about the workings of ethics committees.1 At the centre of the protests is the perceived tardiness and inefficiency of human research ethics committees (HRECs) in Australia.2,3 But the past decade has also seen reform. The National Health and Medical Research Council (NHMRC) has clarified the relationship between research and quality assurance and when quality assurance proposals require ethical scrutiny.4 Furthermore, the NHMRC’s National statement on ethical conduct in research involving humans is clear in its advice that HRECs must establish working procedures that include “timely consideration and review of research protocols”, and it also outlines procedures for expediting review of minimal-risk research.5 On multicentre research, the statement is also clear, stressing the need to minimise unnecessary duplication in review of such research, and calling for “prompt and efficient consideration of multi-centre research protocols” and adoption of “other administrative procedures to accelerate timely consideration and avoid unnecessary duplication”.5 With such clear enunciations, what could go wrong? But, as Maxwell and Kaye attest, things do go wrong. It seems that either the NHMRC recommendations have yet to be translated into reality or the “silo” mentality of HRECs is deeply ingrained. The time may well have arrived to consider performance indicators for HRECs, or even an accreditation process. After all, clinical research and quality assurance should not be at the mercy of inefficient HRECs.

Martin B Van Der Weyden

Gordon R W Davies Psychiatrist, 33 Smith St, Wollongong, NSW 2500. alienistATihug.com.au To the Editor: The recent article on obesity by Proietto and Baur in the Journal1 coincided with another by Campos in New Scientist,2 in which he criticised the conventional view of the risks of obesity and the norms usually accepted. Campos quoted evidence suggesting that, in fact, the group in the overweight range (body mass index [BMI], 25–30 kg/m2) are healthier than those with a BMI below 25 kg/m2. He also noted that between 1990 and 2002, despite a further increase in the prevalence of obesity in the United States, the incidence of type 2 diabetes hardly changed, while cardiovascular death rates fell. According to Campos, similar claims about the risks of obesity have been repeated over the past 50 years and relate more to cultural and political factors than to reliable scientific evidence. Clearly, this view is inconsistent with that articulated by Proietto and Baur. While Campos’ view obviously does not apply to the grossly obese, there is a strong suggestion that the overall evidence base is inconsistent. This may be because the assumption of a linear relationship between excess weight and illness is false. It is further likely that there is confounding of variables, with weight a proxy for lack of exercise. As Campos points out, large-scale observational studies are inevitably poorly controlled. If this is so, then it may well be more useful for the medical profession to emphasise exercise and lifestyle rather than weight loss. It may be much easier to obtain and reinforce behavioural change in these areas, and avoid the common feeling of hopelessness (“why bother”) expressed by people who find it hard to diet and to lose weight.

Gordon R W Davies

Ray C McHenry,* Richard W Gilhome,* Chris Hensman* * General Surgeon, Eastern Surgical, Suite 7529, Police Road, Mulgrave, VIC 3170. To the Editor: We take issue with the recommendations on treatment of morbid obesity in the otherwise excellent article on obesity management by Proietto and Baur.1 Like most non-surgical clinicians involved in the management of obesity, they fail to differentiate between the treatment of obesity (body mass index [BMI], 30–35 kg/m2) and morbid obesity (BMI > 35 kg/m2). The literature is crystal clear — non-surgical treatments are unsuccessful in achieving and maintaining weight loss in morbid obesity.2,3 We are unaware of any branch of medicine, other than morbid obesity management, where respected clinicians routinely recommend treatments (drugs, diet and lifestyle modification) which have been proven not to be effective. We challenge all clinicians to accept what the evidence clearly shows, that: the only known effective treatment for morbid obesity is surgery;2,3 and laparoscopic adjustable gastric banding is much safer than bypass/diversion surgery4 and just as effective; it is the treatment of choice for morbid obesity.

Ray C McHenry · Richard W Gilhome · Chris Hensman

Huy A Tran Director of Clinical Chemistry, John Hunter Hospital, Hunter Region Mail Centre, Locked Bag No 1, New Lambton Heights, NSW 2310. huy.tranAThunter.health.nsw.gov.au To the Editor: I read with interest the recent article on obesity in Australia by Proietto and Baur1 and would like to comment on the issue of proteinuria and measurement of insulin level in obese patients. Proteinuria in obesity, commonly referred to as obesity-related glomerulopathy, is a clinical syndrome with an estimated incidence of about 2% in obese subjects.2 With a fifth of the population being obese,1 the sheer number suspected to have this condition will create an enormous management and cost burden. Furthermore, the incidence of this condition appears to have increased disproportionately to the incidence of obesity.2 The syndrome of obesity-related glomerulopathy comprises the triad of morbid obesity, marked proteinuria without oedema, and normal serum albumin concentration. It can occur in any degree of obesity but is more common in the morbidly obese group (body mass index > 40 kg/m2; Class III obesity). It often presents as proteinuria on urinary dipstick testing, with marked proteinuria seen on confirmatory testing (up to 32 g/day).2 Other features of the nephrotic syndrome do not occur, and the cholesterol level is often lower than that in patients with nephrotic syndrome. However, glomerular filtration rate is raised, and glomerulosclerosis is seen on biopsy. The pathogenesis is unknown. Obesity-related glomerulopathy is a diagnosis of exclusion: secondary causes of proteinuria should be fully eliminated, including hypertensive renal disease and undetected type 2 diabetic renal disease. More often than not, biopsy will be required to guide management, with cost implications. Although the condition is said to be benign, in a small proportion of patients it progresses to end-stage renal failure requiring replacement therapy, further adding to the cost of management. Fortunately, the condition is readily reversible with weight loss, which is an important emphasis in management. 3 My second comment relates to the case of the overweight adolescent described by Proietto and Baur. In this patient, measurement of insulin level is not indicated.4 There is no standardised insulin immunoassay, the sample has to be collected and processed correctly to produce a valid result, and the result would not add to or alter the management of the condition. It is doubtful if normative data exist for adolescents, but the clinical picture suggests the insulin resistance syndrome. As the primary goal would be to detect disordered glucose metabolism, appropriate testing of glucose level is all that is required.

Huy A Tran

Joseph Proietto,* Louise A Baur† * Endocrinologist, Department of Medicine, Repatriation Hospital, Heidelberg, VIC 3081; † Paediatrician, Children's Hospital at Westmead Clinical School, Sydney, NSW. j.proiettoATunimelb.edu.au In reply: We agree with McHenry and colleagues that, until very recently, surgery was the only effective treatment for morbid obesity. However, the development of effective pharmacotherapy that targets the underlying cause — increased hunger — may well change this situation, as evidenced by the effect of leptin treatment in leptin-deficient children.1 In the not-too-distant future, a medical alternative may be possible. The issue of the relative merits of surgery to insert a foreign body (gastric band) or permanently alter the anatomy of the gastrointestinal tract versus lifelong pharmacotherapy will need to be considered. However, economic as well as health issues may be important, and, as McHenry and colleagues suggest, may still favour surgery as the preferred therapy. We thank Davies for bringing to our attention Campos’ book The obesity myth, in which he claims that overweight individuals are in fact healthier than those of normal weight.2 While many of the book’s other claims can be challenged (such as the statements that the prevalence of type 2 diabetes is not rising in the United States, and that bald men have higher testosterone levels), the fact that there is no simple linear relationship between body mass index (BMI) and illness is correct. Sex, race and fat distribution can all influence the relationship. Moderately overweight women with gynoid (hip and thigh) fat are not at increased risk of illness.3 In contrast, South Asian people have an increased risk of developing diabetes at lower BMI values than people of European background. We agree with Davies that maintaining fitness through regular exercise is very important in minimising the health consequences of obesity. Tran raises the issue of whether it is useful to measure insulin levels in children. It is not unreasonable to assume that insulin levels are raised in most obese children, but this is not always the case. The National Health and Medical Research Council clinical practice guidelines for management of overweight and obesity in children and adolescents state that: “Fasting insulin and glucose should be considered in obese children or adolescents, particularly those with a family history of type 2 diabetes, those with acanthosis nigricans and those from certain ethnic backgrounds”.4 In the presence of insulin resistance, serum glucose level remains normal because of high insulin levels. Thus, glycaemia cannot be used to monitor improvement in insulin sensitivity.

Joseph Proietto · Louise A Baur

Richard X Davey Chemical Pathologist, Melbourne Health Shared Pathology Service, Western Hospital, Gordon Street, Footscray, VIC 3011. richard.daveyATwh.org.au To the Editor: In 1996, the Journal published my assessment of the scientific validity of a 1994 decision by the Australian Health Insurance Commission (HIC) to limit the Medicare rebate payment for assessment of thyroid function to thyroid-stimulating hormone level (TSH), except in certain more complex clinical conditions.1 For these, levels of TSH and of other indicators of thyroid function, such as thyroxine, are tested simultaneously and a rebate given for the group of tests. Although discussion concerning this diagnostic strategy persists,2 nearly a decade later it is appropriate to assess the outcome of this initiative. Publicly accessible HIC data3 on privately ordered, then publicly refunded, thyroid function tests in Australia for the fiscal years 1994–2002 were retrieved and are presented graphically (Box). Figure A shows the change in thyroid function test ordering sought by the HIC occurring in 1997 through to 2000 and probably now consolidating. Overall, before the initiative, there were 1.55 TSH tests ordered for each thyroid function group test, and in 2002 this increased to 2.65. The outcome in the elderly is similar, but the change is even more noticeable for thyroid testing in young women and men (with ratios of about 5 to 1 and 7 to 1, respectively). Clinicians have presumably come to accept the high negative predictive value of a normal TSH result for ruling out primary thyroid disease as both necessary and sufficient to finalise thyroid diagnoses in the young. By contrast, thyroid disorders are more common among the elderly, who thus more readily satisfy the HIC requirements for thyroid function group tests. The approximately fourfold increase in absolute terms in the number of single TSH tests performed over 9 years (from 2731 per 100 000 persons per annum in 1994 to 10 763 in 2002) can also be seen as vindicating the HIC’s decision to run with a “TSH first” testing protocol. The same pattern is seen in the age and sex groups illustrated (15–24 years and 75–84 years). The present speed, ease and relative economy of obtaining a TSH test, and the reliability, particularly at low TSH levels, of using this measure for thyroid disease case finding, make ordering a TSH test no longer an indulgence,4 but a clinical necessity. The national cost-of-living index for 30 June of each fiscal year5 was used to standardise the annual expenditure on thyroid function tests to 1994 dollar values, thus allowing comparison across the decade (Figure B). From 1995 to 2002, the HIC has contained annual expenditure to under $20 million for thyroid function group testing. This is both desirable and appropriate. That this has been sustained for 7 years in the face of increasing numbers of first-line TSH tests is both astonishing and commendable. Most of the increase in costs of TSH testing is probably explained by the acceptance of its use as a first-line test. Between the 1996 and 2001 censuses, the population grew from 17.9 to 18.8 million, and the proportion over 65 years also increased (from 12% to 12.5%). Both these trends are continuing,5 and both also explain some of the increase in ordering of TSH tests. It is unclear if any of this change is also due to testing moving from the totally public, hospital sector, not funded by the HIC, to the HIC-funded sector. Effect of changes to the Health Insurance Commission rebate for thyroid function testing A: Ratio of the number of single tests ordered (thyroid-stimulating hormone [TSH]) to the number of thyroid function group tests ordered (TSH and thyroid hormones). Data are tests per 100 000 persons per annum. B: Annual expenditure on thyroid function testing in Australia.

Richard X Davey

Jan R Stockigt Senior Endocrinologist, Alfred Hospital, Commercial Road, Prahran, VIC 3181. jrsATnetspace.net.au Comment: In his timely review of changing patterns of thyroid function testing, Davey suggests that Australian Health Insurance Commission (HIC) policy is responsible for the increased emphasis on a “TSH-first” strategy, with consequent containment of costs for other thyroid function tests. While this may in part be true, the trend towards initial TSH testing has been advocated worldwide1 following the development of TSH assays sufficiently sensitive to distinguish the typical suppressed TSH levels of thyrotoxicosis from normal levels. The developments documented by Davey are a consequence of technological development, perhaps enhanced by selective rebating as a result of HIC policy. It is unfortunate that current HIC policy is sometimes described as prohibiting more complete thyroid function testing, unless TSH level is abnormal. Rebate policy does not prohibit any line of testing and it is because the “TSH-first” approach has some serious, well-documented deficiencies.2 Measurement of levels of thyroid hormone in addition to TSH is clearly sanctioned in HIC regulations when TSH level alone can be misleading, for example in suspected pituitary dysfunction, or in monitoring the treatment of thyroid dysfunction. The adverse consequences, both human and financial, of relying on TSH measurement alone in such situations can be serious and may outweigh the savings achieved by restrictive testing. It must be noted again that a normal concentration of immunoreactive TSH has no predictive value in ruling out potentially life-threatening hypopituitarism,3 which may present with prominent hypothyroid features. The effective integration of clinical and laboratory investigation of potential thyroid dysfunction requires an active laboratory–clinical interface. There are over a dozen patterns of thyroid function — some trivial or inconvenient, some quite serious — that can be misdiagnosed or incorrectly managed if communication across this interface is inadequate.4 Effective communication requires relevant information from the clinician and a response to this information within the laboratory. It is a reality that current patterns of investigation in Australia frequently fall short of this ideal. If, as a result of automation and effective competition, the unit cost of assays can eventually be reduced in relation to the total cost of medical care, it may become appropriate to revert to a more complete panel of initial testing that integrates tropic hormone and target gland secretion, a strategy that remains the cornerstone of definitive endocrine investigation.

Jan R Stockigt

Peter J Gilbar,* Christine V Carrington† *† Co-Chair, Committee of Specialty Practice in Oncology, The Society of Hospital Pharmacists of Australia, Suite 3, 27-33 Raglan Street, South Melbourne, VIC 3205. peter_gilbarAThealth.qld.gov.au To the Editor: The national media recently highlighted the tragic consequences of the inadvertent spinal administration of the antineoplastic drug vincristine. The 7.30 Report (ABC Television) detailed the case of a young man erroneously administered vincristine intrathecally instead of, as intended, intravenously, resulting in progressive neurotoxicity, paralysis and death.1 Since the first report in 1968 of unintentional intrathecal administration of vincristine,2 many, invariably fatal, cases have been described. These have involved a combination of human and system errors affecting the medical, nursing and pharmacy professions. On behalf of the Society of Hospital Pharmacists of Australia, we recommend the following strategies to reduce the opportunity for error: Only specifically trained and designated oncology staff should prepare, dispense and administer cytotoxic medication. Intrathecal chemotherapy should only be administered during normal working hours, and in an area where no other cytotoxic drugs are given or stored. Medical staff must use a formal checking procedure, involving an oncology-trained nurse, to ensure the right drug is given at the right dose, by the right route, to the right patient. Intrathecal drugs must be packaged separately and clearly labelled both on the syringe and outer container “For intrathecal use”. Specifically designated containers should be used for transportation of intrathecal drugs from the pharmacy and for storage on the ward. Intrathecal doses should be delivered separately and preferably administered after drugs to be given by other routes have been supplied to the ward and administered. Vincristine should be prepared in a small-volume intravenous bag rather than a syringe.3 For adults, prepare vincristine in an intravenous bag in 50 mL of sodium chloride 0.9% and administer it as a short intravenous bolus over 5–10 minutes. Smaller volumes and a slower administration rate are suggested for children. While this method has been criticised as potentially increasing the risk of extravasation injury, this has not been reported as a problem. Vincristine should be clearly labelled both on the intravenous bag and outer container “For intravenous use only — fatal if given by other routes”. Negative labels, such as “Not for intrathecal use”, must never be used. Many hospitals currently use syringes for vincristine and increase the diluent volume in the syringe as a deterrent to intrathecal administration; however, fatalities have occurred after the administration of vincristine supplied in 10 mL4 and 20 mL5 syringes. The safest method of eliminating the potential for spinal instillation of vincristine remains the abolition of the syringe as a means of administration.

Peter J Gilbar · Christine V Carrington

Nat Lenzo Head, Department of Nuclear Medicine, Royal Perth Hospital, Wellington Street, Perth WA 6000, and Co-ordinator, WA PET/Cyclotron Service, Sir Charles Gairdner Hospital, Nedlands, WA 6009 nat.lenzoAThealth.wa.gov.au To the Editor: I read with interest the article by Ware et al1 and the response from Davies.2 Let me first commend Ware and his colleagues on an excellent piece of investigative journalism. For the readers’ information, there are about 200 operational positron emission tomography (PET) scanners in the United States, and the United Kingdom has recently committed to 50–60 PET scanners within the next 5–10 years.3 This is based on the vast amount of published evidence with respect to the benefit of PET for the diagnosis, staging and monitoring of a range of malignancies and other disorders. Despite more than 15 000 publications3 and the fact that some countries reimburse for many indications not covered in Australia (eg, breast cancer restaging, dementia assessment), our authorities request “Australian data” before allowing expansion of the Medicare benefit for PET in Australia. The issuing of only eight Medicare licences (ie, about 1 per 2.5 million population) also impedes access to what may be the most important imaging development of the past 20 years. What was not mentioned by Ware et al is the grossly inadequate amount paid for PET services under the Medicare Benefits Scheme in Australia. Currently, the reimbursement for a fluorodeoxyglucose PET scan in the US is about US$2000/scan. In Australia, the Medicare Benefits Scheme pays about $900. This makes our reimbursement one of the cheapest in the world. So cheap that it makes no economic sense for private entities to provide PET services in this country (note: isotope cost, about $350/patient; cost of PET set-up, $2.5–5 million). So the Commonwealth has no need to worry — it already has done much to slow the growth of clinical PET in Australia. Before Davies replies that we need “Australian data”, cost-effectiveness data, etc, before allowing new technology expansion, I ask: are Australian data so much better than those from our colleagues overseas? And what is the level of evidence for much of what we currently do and get paid for in clinical practice? For example, what is the rationale behind the reimbursement, without limit, of regular computed tomography scanning in the follow-up of patients with treated lymphoma? I direct readers to the articles by Guppy et al4 and Dryver et al5 to see what little benefit there is in this practice. Of course, these are British and Canadian studies, so surely they cannot be taken seriously.

Nat Lenzo

Robert E Ware,* Hilton W Francis,† Kenneth E Read‡ * Nuclear Medicine Physician, 49 Augusta Road, Lenah Valley, TAS 7008; † Rheumatologist, Hobart; ‡ Barrister, Malthouse Chambers, Hobart. robwareATtrump.net.au To the Editor: In light of our article examining the Australian Government’s review of positron emission tomography (PET),1 it is interesting to note that the accompanying official response is attributed to the Department of Health and Ageing (DOHA).2 When asked to clarify its role in the review of PET, DOHA had previously persuaded the Commonwealth Ombudsman that it had contributed only secretarial support to the process. With no accountability for policy decisions or the review itself, is it any wonder that DOHA’s response does not address the hard evidence that the politicians are “misusing” evidence-based medicine. The comment that “one of the concerns that has been raised about the PET reviews is that the government did not follow the views of individuals who were involved in the process” does not relate to our text. We are aware that individual opinion is considered very low-level evidence. Our argument is that the supporting committee made a decision that PET was safe, clinically effective and potentially cost-effective on the basis of the evidence it reviewed. The Medical Services Advisory Committee (MSAC) itself did not review any evidence, so, by changing the decision of its supporting committee, MSAC’s own opinion was substituted without any sound scientific basis. Therefore, the decision at a ministerial and government level to restrict Medicare funding for PET is purely a political decision, and must not be misrepresented as “evidence-based”. Indeed, the evidence suggests that the policy decision to restrict Medicare funding for PET prejudiced the objective analysis of the evidence by MSAC. The suggestion that “the government is funding the collection of data by service providers to improve the evidence base related to the use of PET in a wider range of indications” is misleading. To improve the level of evidence for PET would require, in the words of the permanent medical adviser to MSAC, “very large randomised trials, which are probably not feasible”. The current data collection is not a randomised trial. For many of the indications being examined, the validity of the PET findings and consequent management changes will not be assessed. There is no plan to evaluate cost-effectiveness. Therefore, the process is not going to improve the level of evidence for subsequent decision-making. Perhaps this is the outcome envisaged for 2006! The problem with the PET review was a fundamental disregard for the promised standards. The ongoing problem is that MSAC is not an appropriately legislated body (unlike the Pharmaceutical Benefits Advisory Committee). MSAC is secretive and its process and decision-making are difficult and costly to penetrate. Unless the structure, process and accountability of MSAC are changed, history is likely to repeat itself. The official response to our article only serves to heighten our concerns.

Robert E Ware · Hilton W Francis · Kenneth E Read

Joshua P Hanson,* Carmel T Taylor,† Ann R Richards,‡ Ina L Smith,§ Craig S Boutlis¶ *Registrar, ¶ Physician, Cairns Base Hospital, PO Box 902, Cairns, QLD 4870; † Scientist, § Research and Development Coordinator, Public Health Virology, Queensland Health Scientific Services; ‡ Public Health Nurse, Tropical Public Health Unit, Cairns, QLD. joshua_hansonAThealth.qld.gov.au To the Editor: The Japanese encephalitis flavivirus is the most common cause of encephalitis in Asia. Death occurs in 25% of clinical cases, and permanent neurological deficits occur in up to 50% of survivors.1 Infection is transmitted from amplifying hosts (primarily waterbirds and pigs) by Culex mosquitoes. Although the virus has been isolated in the Western Province of Papua New Guinea,2 and clinical cases have been described in the Western Province and suspected in the Milne Bay region,3 to our knowledge cases have not been reported from around Port Moresby. In January 2004, a 66-year-old man of European background was evacuated to our hospital with a 7-day history of fever and confusion. On examination, he had generalised upper motor neurone signs and a Glasgow coma score fluctuating between 6 and 10. Computed tomography and magnetic resonance imaging showed multiple non-specific white-matter lesions bilaterally. An electroencephalogram (EEG) demonstrated diffuse slowing in the delta to theta range in both hemispheres, with preserved response to painful stimulation. Lumbar puncture showed clear cerebrospinal fluid (CSF), with a leukocyte count of 65 × 106 cells/L (81% mononuclear) (reference range [RR], < 5 × 106 cells/L), normal erythrocyte count, raised protein level of 0.79 g/L (RR, 150–500 mg/L); glucose level of 4.3 mmol/L (RR, 2.8–4.0 mmol/L) and negative bacterial and fungal cultures. The CSF was also negative for cryptococcal antigen and by polymerase chain reaction (PCR) testing for enterovirus and herpes simplex, Japanese encephalitis, Murray Valley encephalitis and Kunjin viruses. Serological tests were negative for syphilis and human immunodeficiency virus infection. Paired sera from Days 2 and 19 of admission were tested in parallel against a panel of flaviviruses using a haemagglutination inhibition assay.4 This showed fourfold rises in antibody titre against dengue virus serotypes 1, 3 and 4, and Japanese encephalitis, Murray Valley encephalitis, Kunjin, Alfuy and Kokobera viruses, and twofold rises in titre against dengue virus serotype 2 and Stratford virus. Overall, these results were diagnostic of recent flavivirus infection but were non-specific. IgM antibody responses to the same flaviviruses were measured in sera and CSF using an in-house enzyme-linked immunosorbent assay (ELISA), with strongest reactivity demonstrated to Japanese encephalitis virus (Box). The patient had lived in Papua New Guinea since 1970, predominantly on a church-run farm at Bootless Bay, about 20 km from Port Moresby. He had not travelled outside this region in the month before his illness, and had no history of Japanese encephalitis vaccination or of dengue fever. The farm was situated about 150 metres from a piggery. The patient had no direct contact with this piggery. His accommodation was poorly screened against mosquitoes. After 3 weeks of primarily supportive intensive care, the patient was discharged to a general ward. His neurological recovery was slow. After 5 months, he was able to walk with assistance and required a tracheostomy to protect his airway. He was judged likely to experience permanent neurological deficits. The clinical, epidemiological, radiological, EEG and serological features of this case strongly support a diagnosis of Japanese encephalitis. Japanese encephalitis virus is difficult to detect in CSF by isolation or PCR because of neutralising antibodies and the limited duration of viraemia, which may have accounted for the negative PCR result in this case, despite the use of a highly sensitive method.5 This case highlights the desirability of further defining the epidemiology of Japanese encephalitis in the Port Moresby region, as well as reconsidering the current recommendation to vaccinate Australians only if they intend travelling to the Western Province of Papua New Guinea.1 IgM antibody levels, measured against a panel of flaviviruses by enzyme-linked immunosorbent assay (ELISA) JE = Japanese encephalitis. MVE = Murray Valley encephalitis. * IgM levels were measured as the P/N (positive/negative) ratio (ratio of the absorbance of the test sample to the absorbance of a negative control sample tested against the same antigen).

Joshua P Hanson · Carmel T Taylor · Ann R Richards · Ina L Smith · Craig S Boutlis

To the Editor: The Australian Technical Advisory Group on Immunisation (ATAGI) is responsible for maintaining and updating the Australian immunisation handbook, on behalf of the National Health and Medical Research Council (NHMRC).1 At its 25th meeting, in April 2004, ATAGI discussed data (then unpublished) presented by Hanson and colleagues on evidence for the spread of Japanese encephalitis virus beyond the Western Province of Papua New Guinea to the Port Moresby region.2 ATAGI believes it is probable the virus has spread to other parts of Papua New Guinea. The current (8th) edition of The Australian immunisation handbook states on page 179: “Current understanding of the ecology of the JE [Japanese encephalitis] virus elsewhere in Papua New Guinea is fragmentary and unsubstantiated. Therefore no definitive recommendations about JE vaccination for travellers to other parts of Papua New Guinea can be made at the current time.” ATAGI agreed that the evidence provided by Hanson and colleagues was compelling, and sufficient to warrant expanding the current recommendation for Japanese encephalitis vaccination. ATAGI is proposing the recommendation be changed to include travellers staying more than one month in all parts of Papua New Guinea, not just those planning to stay in the Western Province. A public consultation process to change this recommendation is being conducted as part of the requirements of the NHMRC Act 1992. A public consultation paper is available from the Immunise Australia Program website (www.immunise.health.gov.au). Submissions close on 17 September and can be directed to Ms Letitia Toms, Assistant Director, Immunisation Section, Department of Health and Ageing, MDP 14, GPO Box 9848, Canberra, ACT 2601 (letitia.tomsAThealth.gov.au).

on behalf of the Australian Technical Advisory Group on Immunisation (ATAGI)

Tarney J Spencer,* Ben Clark† * Ophthalmology Registrar, † Ophthalmologist, Geelong Hospital, Ryrie St, Geelong, VIC 3228. drtarnAThotmail.com To the Editor: We are concerned about the recent number of patients presenting to our hospital after accidentally applying superglue to their eyes. Of the four cases in February and March 2004, two arose from patients mistaking cosmetic nail adhesive for their regular ocular lubricant, and applying it to the inferior ocular fornices, creating a tarsorrhaphy. Superglues are cyanoacrylate derivatives. Those used domestically are lower-alkyl derivatives than those designed for medical use and have higher tissue toxicity. The two patients who mistook nail glue for ocular lubricant both required surgical separation of the upper and lower eyelids, and both had significant corneal abrasions, periocular dermatitis and temporary loss of lashes as a result of the reparative surgery. Both were treated with chloromycetin ointment until the abrasions had healed. We examined the bottles containing the nail adhesives. They were remarkably similar to many ocular lubricant bottles, with no significant difference in size, colour or feel (Box). As both products are often kept together in a cosmetics area of the bathroom, accidental ocular application can occur. Similar cases have been reported in other countries over the past 20 years.1-3 The risk of accidental ocular (or potentially aural) application could be reduced by changes to bottles containing superglue, including: childproof cap to prevent conventional opening of the bottle; colour coding of the bottles; different bottle shape; and distinctive odour and/or colouring of the glue. Superglue and eye lubricant bottles Examples of bottles of synthetic nail adhesive (two on left) and eye lubricant (two on right), showing similar appearance and feel.

Tarney J Spencer · Ben Clark