Volume 177 Issue 3

It is time to focus on reducing inappropriate test ordering The complexity of modern medicine has promoted an excessive reliance on the results of empirical tests rather than clinical acumen. In Australia, this is reflected in the fact that the rise in the costs of diagnostic testing in pathology and radiology is second only to the rise in cost of pharmaceutical prescriptions, the fastest-growing sector in our healthcare budget. Many reasons have been cited for this increase in clinicians' reliance on pathology and radiology testing. Among community-based practitioners, ordering patterns are most likely to be influenced by medicolegal concerns, time constraints, screening needs, or ingrained practice habits. Among hospital-based clinicians, test-ordering practice may be determined by level of clinical experience, fear of censure for lack of testing, medicolegal concerns, and the desire to provide a "one-stop" service to evaluate all possible physiological parameters.1 In addition, the pressures of shorter consultation times in community practice and diminishing hospital beds have led to the increased use of investigations to fast-track patient throughput. In acute hospital settings, it has been estimated that as many as a third of all tests ordered are inappropriate in terms of their ability to contribute to the diagnosis and treatment of individual patients.2 This overtesting is not without consequences. If a healthy individual is subjected to 10 unnecessary tests, there is a 40% chance of at least one false-positive result.3 As well as exposing the patient to potential harm from unnecessary tests and treatment, this may expose the clinician to an increased, rather than a decreased, medicolegal risk, as patients are exposed to greater risks of complications while they proceed along an unnecessary testing spiral. In a community that is struggling to cope with the financial demands of modern healthcare, the wastage of resources on unnecessary pathology and imaging testing has an adverse effect on the provision of services that are legitimately required. Furthermore, in most settings, it is the relatively cheap, common tests that account for the bulk of testing expenditure. In our own institution, about 80% of the costs of biochemistry and haematology testing are accounted for by full blood counts and testing of electrolytes, urea, creatinine, liver function and cardiac markers. Although more complex investigations, such as gene testing, may individually be more expensive, the sheer volume of common tests drives the overall costs of investigations, and suggests that attempts to reduce inappropriate testing should focus on these tests. In this issue of the Journal, Stuart and colleagues (page 131) report on a comprehensive program of education, audit, feedback and structural change to reduce the number of investigations performed in a public hospital emergency department.4 Although their program focused on reducing inappropriate testing and improving result follow-up in an emergency department, the lessons learned about how to produce sustainable change in clinician practice are equally applicable to the rest of the acute hospital environment, and to the community sector. There has been a plethora of reports on the implementation of educational or other programs aimed at curbing the costs of inappropriate testing. Most describe utilisation of tools such as education programs,5,6 incentives for clinicians,7,8 information about costs of testing, audit of ordering profiles, feedback on ordering patterns, guidelines, decision-support systems, and process changes.9,10 The study by Stuart et al demonstrates the key features required for sustainable improvement in test-ordering behaviour. A multifaceted approach that results in alteration to the core processes of test ordering is more likely to promote lasting improvements than strategies aimed just at increasing awareness or knowledge among individuals. In public hospitals, where the junior medical staff who are responsible for most test-ordering rotate through departments at three-monthly intervals, it is essential that whatever changes are made to improve test-ordering are capable of affecting a mobile workforce. It is unlikely that educational programs alone could cope with the demands of this rostering pattern, unless concomitant process changes are implemented hospital-wide to ensure applicability in all clinical settings. As conceded by Stuart et al, the effects on patient outcomes of attempts to reduce overtesting were not addressed. No data are provided on readmission rates, length of stay, adverse events and rates of missed or incorrect diagnoses. It is possible that attempts to reduce numbers of tests performed could result in harm to patients through underinvestigation of symptoms. Therefore, future studies in this area should include measures of patient outcomes to ensure that an overall improvement in patient care accompanies the reduction in costs of investigation. Computerised systems are widely available in general practice for prescribing, and, in some places, for test ordering, but have yet to be widely implemented in the acute care sector. At present, these systems have focused on facilitating the ordering process rather than ensuring its appropriateness. The future is likely to see implementation of computerised order-entry systems that provide real-time feedback on ordering patterns, guidance on test appropriateness, improved result checking, and information on the costs of tests ordered. Such systems already exist, and are currently being tested in several Australian hospitals. It is hoped that overcoming existing deficiencies in information systems will enable clinicians to order tests and check results more efficiently and more appropriately than they currently do. An academic analysis of current test-ordering practices might suggest that further research is needed into why doctors order tests the way they do, whether there really is such a high rate of unnecessary testing, and what value current ordering patterns add to our highly complex healthcare system. A pragmatic view, however, would suggest that there is enough published evidence that overtesting is a characteristic of healthcare systems in the developed world, and enough information in existing research to guide what should be done to reduce waste and harm resulting from inappropriate testing. It is time that the focus of work in this area shifted to development of practical, sustainable means of improving the appropriateness of testing. Future research may be best directed to understanding the place of sophisticated decision-analysis models, the role of point-of-care guidance and feedback systems, and effective clinical change-management strategies. In the meantime, hospitals around Australia have already embarked upon attempts to change current practice. In Melbourne, the National Institute of Clinical Studies is sponsoring a 12-month project, involving hospitals from four States and Territories, aimed at developing transferable and sustainable changes in test-ordering practices. Similarly, hospitals involved in the Health Roundtable in Sydney have been involved in exchanging information on effective strategies to improve test ordering. The Royal Australasian College of Pathologists is developing undergraduate education programs aimed at improving ordering practices. The lessons learned from these groups should inform national strategies to deal with the problem of inappropriate testing. As in the study by Stuart et al, it is likely that a coordinated, multifaceted, sustained approach to this problem will be required to achieve lasting success.

Rohan J H Hammett MB BS, FRACP · Roger D Harris MB BS, FACEM

Surgery shows promise for patients with severe, poorly controlled motor fluctuations Parkinson's disease afflicts around 78 000 Australians. Mortality is almost twice that of age-matched controls1 and the mean disease duration is only 13 years.2 No treatment has yet been shown to slow disease progression. Fortunately, motor disability can be markedly improved with levodopa therapy. However, after 3–5 years, the duration for which each dose of levodopa is effective shortens and many patients begin to experience fluctuations in their motor function throughout the day. Involuntary movements appear, in particular painful posturing of the legs or arms, as the beneficial effect of levodopa wears off ("end of dose dystonia") and writhing choreoathetoid movements that accompany part or even all of the period when levodopa is working ("peak dose dyskinesia"). These problems can be ameliorated to some extent by the addition of dopamine agonists or catechol-o-methyltransferase (COMT) inhibitors. Unfortunately, problems that are not reversed by levodopa, such as worsening of balance and speech, cognitive decline and depression, can also supervene. Patients who never experience sustained benefit from levodopa are likely to have a different underlying pathology from idiopathic Parkinson's disease, such as vascular parkinsonism, progressive supranuclear palsy or multiple system atrophy. It is in patients with severe, poorly controlled motor fluctuations that surgical therapy has re-emerged as a treatment option. In this issue of the Journal (page 142), Iansek and colleagues report the results from 14 patients at their centre who underwent bilateral deep brain stimulation of the subthalamic nucleus for the treatment of Parkinson's disease.3 Motor function was improved with subthalamic nucleus stimulation for at least six months when patients were assessed both with and without levodopa treatment. Dyskinesias were also apparently reduced, and mean levodopa dose was reduced by 30% after surgery. The procedure was not without risk (one patient had a disabling intracerebral haemorrhage, another required relocation of the stimulators to the thalamus), but overall this is an exciting and encouraging development. Data were also collected from the first six patients in the reported series as part of an international multicentre trial, which included another Australian centre, St Vincent's Hospital, Sydney.4 Results from 96 patients who underwent bilateral subthalamic nucleus stimulation showed a median reduction of 49% in motor disability without medication using blinded videotape analysis, a mean increase from 27% to 74% of the day spent with good mobility without involuntary movements, a 58% improvement in dyskinesia scores, and a 37% reduction in mean daily levodopa dose. Similar, but less marked, improvement was seen in 38 patients treated with bilateral pallidal stimulation, although the dose of levodopa was not reduced after surgery in these patients. The incidence of intracranial haemorrhage was 2.5%, and infections requiring electrode removal occurred in less than 1%. These are benchmark figures by which the results of Australian centres offering these procedures can be compared. Surgical therapy for Parkinson's disease is not new, but there have been advances in our understanding of why it works. Loss of dopaminergic projections from the substantia nigra to the basal ganglia results in pathological overactivity of the subthalamic nucleus and globus pallidus. Patients undergoing deep brain stimulation have a wire implanted into the brain that is attached to a programmable battery implanted subcutaneously in the chest wall, much like a pacemaker. Deep brain stimulation mimics the effects of stereotactic lesioning, but has the added advantages of being reversible and allowing postoperative programming to optimise the site of stimulation. However, it is expensive and programming is time-consuming, sometimes requiring months before the optimal stimulating parameters can be established. Economic and geographical constraints limit access to therapy for many patients in whom surgery would otherwise be appropriate; such issues need to be addressed by healthcare providers. At present, there are a number of Australian centres performing subthalamic nucleus stimulation and pallidotomy (lesioning of the globus pallidus); experience in pallidal stimulation is as yet limited. The indications and choice of operation are still evolving. Nevertheless, some general guidelines may be suggested. Who should be offered surgery? Surgically fit patients with severe motor fluctuations or dopa-induced dyskinesia, or both, are the main candidates. Surgery does not significantly improve the patient's best response to levodopa (except by reducing dyskinesias). A good or excellent response to levodopa predicts the response to surgery, and is essential.5,6 The procedure, particularly subthalamic nucleus stimulation, may take hours, during which time the patient remains fully conscious, so a degree of stoicism on the part of the patient is required. For the rare patient with disabling parkinsonian tremor that is poorly suppressed by levodopa, without accompanying akinesia, thalamic surgery can be contemplated. Who should not be offered surgery? Patients who have never responded well to levodopa will not benefit from surgery. The presence of cognitive or psychiatric complications of Parkinson's disease (frequent hallucinations, psychosis, parkinsonian dementia, uncontrolled depression) is an absolute contraindication to surgery; significant cerebral atrophy on computed tomography or magnetic resonance imaging is also a contraindication. Levodopa-resistant symptoms such as impairment of balance or speech can worsen after surgery.7 Which procedure? Overall, subthalamic nucleus stimulation appears more promising than pallidal surgery. However, a randomised trial comparing the two has not been performed, and excellent and sustained improvement following both bilateral subthalamic nucleus stimulation and bilateral pallidotomy is seen.8 Physicians should be guided not only by theoretical considerations, but also by local experience and expertise. Objective evaluation of the results of surgery by a neurology team not involved in patient selection or the surgical procedure is an advantage, and this information should be available to patients and their treating neurologists to aid decisions about therapy.9 Where to refer? The process of optimising therapy for advanced Parkinson's disease, differentiating between idiopathic Parkinson's disease and related disorders, and choosing the appropriate operation, is not always straightforward. For this reason, we recommend that patients considering surgical treatment be referred to a unit with specialist expertise in movement disorders, and that surgery be offered in the setting of a multidisciplinary assessment by teams including a neurologist, neurosurgeon, neuropsychologist and Parkinson's disease nurse specialist.

Victor S C Fung PhD, FRACP Director, Movement Disorders Unit · John G L Morris DM, FRACP, FRCP · Malcolm F Pell MB BS, FRACS Visiting Medical Officer

The NCCI is supporting many projects for improvement Many countries place great importance on their strategy for cancer control. The precedent was set by former US President Nixon's "war on cancer", declared in 1971, with the goal of reducing cancer incidence by 50% by the year 2000.1 This optimistic aim occasioned an unprecedented expansion of the US National Cancer Institute, its budget reaching $3.5 billion in 2001.2 More recently, the UK National Health Service embarked on a comprehensive reform of cancer services.3 The high profile of cancer in Western countries relates to its associated high morbidity, the high level of public awareness of the disease and the rapidity of research advances. In 1997, Dr Michael Wooldridge, the then Federal Minister for Health and Family Services, contracted the Australian Cancer Society (now the Cancer Council Australia) to establish the National Cancer Control Initiative (NCCI). The formation of the NCCI was based on a conviction that a better return for expenditure on cancer could be obtained, and that the time had come to introduce new evidence-based cancer-control measures.4 Although an array of cancer-control activities was already in place, it was envisaged that the NCCI could make these processes less capricious by applying a national focus, establishing agreed priorities and forming strategic partnerships across government and non-government sectors.5 The NCCI sees cancer control as comprising "all actions that reduce the burden of cancer in the community [including] every aspect of care, from prevention and early diagnosis to curative treatment and palliative care, all underpinned by the best scientific evidence available".6 The NCCI is concerned with assessing both existing programs and potential new developments for their clinical effectiveness, cost–benefit and equity. Its brief extends to managing strategic projects concerned with translating new findings into public health and clinical practice. The NCCI's activities have mainly revolved around cancer care, early diagnosis, and information needs. To provide good-quality clinical care, we need to know what good care is, what care is currently being provided, what gaps exist, and what opportunities there are for improvement. Defining good-quality care requires evidence-based clinical guidelines. The NCCI has been involved in various projects in this area, including production of guidelines on colorectal cancer for specialists, general practitioners and consumers; production of consumer guidelines on prostate cancer; development of guidelines for psychosocial care of patients with cancer; and development of an evidence-based model of optimum utilisation of radiotherapy. The assessment of current care requires management surveys, ideally involving all relevant specialties and representative groups of patients. One of the NCCI's initiatives has been the funding, through a Commonwealth grant, of a national survey of over 2000 patients with colorectal cancer. Improving clinical care requires a range of information-dissemination and learning strategies, with incentives to apply best care. In financial and practical ways, the NCCI is supporting many projects for improvement, including a consultative project, sponsored by the NCCI in collaboration with the Cancer Council Australia and the Clinical Oncological Society of Australia (COSA), to assess the limitations of cancer care provision; development of a national consumers' cancer organisation to increase the scope and effectiveness of consumer involvement; a review, in conjunction with COSA and state and federal governments, of the infrastructure needs for cooperative group clinical trials; initiatives to achieve earlier diagnosis, such as (i) federally funded pilot studies of colorectal cancer screening;7 (ii) assessment of new screening methods for cervical cancer, ovarian cancer, lung cancer and melanoma; and (iii) a project to improve GPs' expertise in managing prostate cancer and using prostate-specific antigen screening. collaboration with State and Territory cancer registries to improve the documentation of cancer and its outcomes, particularly with regard to staging. (The NCCI has developed a core clinical cancer data set for hospitals,8 which includes information on stage of disease and primary treatment, and is designed to be compatible with data collected by population-based cancer registries.); development of ways to assess the frequency of non-melanoma skin cancer, Australia's commonest cancer, using survey methods similar to those used previously,9 but also considering any new methods that become available. In the future, the NCCI will continue to take a leadership role by consensus through an inclusive, consultative approach in dealing with nationally identified priorities. The organisation's core purpose is to be an expert reference body providing timely advice, identifying appropriate initiatives and making specific recommendations to the federal government and other groups regarding the prevention, detection, treatment and palliation of cancer for all Australians.

J Mark Elwood MD DSc FFPHM · Paul D Ireland PhD

With our high standards of sanitation and healthcare, how important is breastfeeding? Any breastfeeding advocate can rattle off a list of the advantages of breastfeeding to infants, their mothers and society. The list of benefits ranges from better emotional attachment to a lower risk of childhood leukaemia or dental malocclusion. However, claims of benefit have been contentious, with many studies failing to demonstrate a clear advantage and some even showing increased risk of a negative health outcome with breastfeeding. The constituents of human milk suggest that it has evolved to promote infant health and human growth, particularly to protect children from infections and to support the rapid growth of the human brain. Despite advances in science and manufacturing, infant formula will always be a poor copy of human milk. It is improbable that a substitute will ever reproduce the full spectrum of human milk proteins, milk sugars (numbering over 100), live white cells and antibodies programmed by infections in the infant's environment, together with constant variations in milk content to meet the needs of the growing infant. But does this matter in a developed country such as Australia? Is there justification in the argument that women are being pushed too hard to breastfeed, or is there more to infant nutrition than the provision of clean water and biologically safe artificial feeds? Many studies reporting the effects of breastfeeding, both positive and negative, have major methodological flaws. Indeed, robust studies are difficult to carry out. Random allocation of study participants to either a "breastfeeding" or an "artificial feeding" group is unethical, especially if we accept the belief that "the epidemiologic evidence is now overwhelming that, even in developed countries, breastfeeding protects against gastrointestinal and (to a lesser extent) respiratory infection, and that the protective effect is enhanced with greater duration and exclusivity of breastfeeding".1 So evidence for the effects of breastfeeding must rely largely on observational cohort and case–control studies. Blinding to the intervention group is difficult, except at the analysis level. Moreover, mothers who elect to breastfeed differ from those who don't — the former group are generally better-educated women of higher socioeconomic status, who are more likely to have partners and less likely to smoke. All of these factors are likely to be independently associated with positive health outcomes, so failure to adequately adjust for these confounders generally favours positive breastfeeding outcomes. On the other hand, apparently poorer outcomes may result if mothers preferentially breastfeed more vulnerable infants. Difficulties with defining terms such as "breastfeeding" and "exclusively breastfed", and with defining endpoints such as "atopic disease", also make comparisons between studies difficult. So, have the roughly 2000 papers on breastfeeding and human milk listed in Medline since the year 2000 helped answer the question of whether or not it matters if a term infant born in a country like Australia is breastfed? I will confine my comments to the three most common health problems in Australian children: infection, obesity, and asthma. In Australia, there are almost 20 000 hospital admissions a year for acute gastroenteritis in children under five years old. Rotavirus accounts for about half of these episodes and is also one of the most important nosocomial infections in paediatrics. A Belarussian study2 (involving 17 000 healthy mother–infant pairs intending to breastfeed) showed that, in centres randomly assigned to deliver support for breastfeeding (as outlined by the Baby Friendly Hospital Initiative3), there were increases in exclusive and continued breastfeeding and reductions in episodes of gastrointestinal infection. In an Italian study4 of infants aged 1–18 months admitted to an infant ward, fewer breastfed infants contracted rotavirus infection (10.6% v 32.4%), and none of these became symptomatic. It has been shown that human milk lactadherin prevents symptoms in breastfed infants infected with rotavirus by binding to the virus and inhibiting its replication.5 Obesity is the commonest chronic health problem in Australian children. This has health implications both in and beyond childhood, as about half of obese children become obese adults. The effect of breastfeeding on later overweight/obesity remains contentious. A 2001 review of 18 studies6 concluded that most studies examining the effects of breastfeeding on later obesity had found an insignificant effect, although two of the studies actually found a positive association between breastfeeding and later body fatness. Since that review, four large studies7-10 (involving between 2000 and 14 000 children) have shown a lower prevalence of overweight in previously breastfed children, with several showing decreasing risk with longer duration of breastfeeding. The three studies of older children (aged 5–14 years)8-10 also found a negative association between breastfeeding and obesity (with adjusted odds ratios [ORs] ranging from 0.66 to 0.8). Similar results in these three studies, despite differences in method, suggest that the finding may be robust. The second most common chronic health problem in Australian children is asthma. A large Western Australian study showed a substantial reduction in risk of childhood asthma, as assessed at six years of age, if exclusive breastfeeding is continued for at least the first four months of life.11 This was included in a systematic review with meta-analysis of 12 prospective studies,12 which gave a summary OR of 0.70 (95% CI, 0.60–0.81) for asthma among children who had been breastfed, with a greater effect in children from families with a history of atopy (OR, 0.52; 95% CI, 0.35–0.79). The studies were mainly of younger children but included children up to 8.4 years. Another prospective study of more than 330 000 children followed to age 24 months supported these findings: breastfeeding of less than nine months' duration was associated with an increased risk of asthma or wheezing, and a dose–response effect was observed with breastfeeding duration.13 However, a recent report has suggested that atopic children with asthmatic mothers are more likely to develop asthma in later childhood if they have been exclusively breastfed.14 There may be interesting possibilities for intervening to further reduce atopy in at-risk families. Mothers of infants who develop atopic sensitisation have a higher intake of saturated fat,15 and their breast milk is much lower in some long-chain unsaturated fatty acids (which may have antiallergenic properties16). Perhaps improving maternal diets and the use of probiotics17 may reduce the prevalence of atopic disease in their children. I have selected three childhood conditions for which small changes in prevalence or disease severity would have a major impact on the health of the nation. The US Department of Agriculture, Food and Nutrition chose otitis media, gastroenteritis and necrotising enterocolitis, and estimated that the United States would save a minimum of US$3.6 billion dollars a year if breastfeeding rates increased by 10% at initiation and by 20% at the age of six months.18 While we should be careful not to convey to mothers that breastfeeding will make their child a trim, non-atopic, infection-free genius, the balance of the evidence is that breastfeeding is of benefit in many ways. Every healthcare professional in contact with young children and parents should be familiar with their responsibilities under the World Health Organization Code19 to encourage and promote breastfeeding — for the health of the nation.

Patricia McVeagh MB ChB FRACP

Objective: To evaluate an intervention developed to improve test-ordering practice.Setting: Public hospital emergency department with an annual census of 42 500. The study comprised a six-month pre-intervention stage (November 1998 to April 1999), which was compared with a similar post-intervention period (November 1999 to April 2000), and trends were examined over an 18-month post-intervention period (May 1999 to October 2000).Intervention: The intervention comprised three integrated components: implementation of a protocol for test ordering; education program for medical staff; and audit/feedback process.Main outcome measure: Test utilisation (assessed as cost per patient).Results: There was a 40% decrease in the ordering of investigations in the emergency department (95% CI, 29%–50%), with test utilisation falling from a mean of $39.32/patient to $23.72/patient. The decrease was similar for both laboratory and imaging tests and was sustained for the duration of the 18-month follow-up.Conclusions: Our intervention appears to have produced long term modification of test ordering in the emergency department of a public teaching hospital.

Peter J Stuart MB BS, FACEM · Shelley Crooks BA(Hons.Psych) · Mark Porton BAppSc

Objective: To investigate whether late referral to a nephrologist of patients with chronic renal insufficiency influences the likelihood of both transplantation and mortality among those who survive at least one year on dialysis.Design: Retrospective national cohort study, using data from the Australia and New Zealand Dialysis and Transplant Registry database.Participants: All patients with end-stage renal disease who started renal replacement treatment in Australia between 1 April 1995 and 31 December 1998, excluding those who received transplants or who died in their first year of dialysis. Patients referred "late" were defined as those who needed to commence dialysis within three months of referral to a nephrologist.Main outcome measures: Length of patient survival, and whether patients received a transplant at any time between one year after starting dialysis and completion of the study on 31 March 2000.Results: Of the 4243 patients included in the study, 1141 (26.9%) were referred late. Late-referral (LR) patients were significantly less likely to receive a transplant in their second and subsequent years on dialysis (adjusted rate ratio, 0.78; 95% CI, 0.64–0.95). LR patients were at significantly increased risk of death after their first year on dialysis (adjusted hazard ratio, 1.19; 95% CI, 1.04–1.35).Conclusions: Late referral is associated with increased mortality, even among those who survive their first year on dialysis. Improving the quality of pre-dialysis care might improve access to transplantation and long-term survival. General practitioners could minimise late referrals through targeted screening of high-risk individuals.

Alan Cass FRACP · Joan Cunningham ScD · Zhiqiang-Wang PhD · Wendy Hoy FRACP · Peter C Arnold MB BCh · Paul Snelling FRACP

Objective: To measure bone turnover in Muslim women with vitamin D deficiency.Design: A cross-sectional study of a random sample of Muslim women aged 20–65 years, evaluated over a 6-month period from November 1999 to April 2000.Setting and participants: 146 women living in an urban community in south-western Sydney with adequate opportunities for sun exposure.Main outcome measures: Bone turnover as measured by urinary deoxypyridinoline (DPYD) excretion rates; and vitamin D status as determined by 25-hydroxyvitamin D (25OHD) levels, serum calcium levels and parathyroid hormone (PTH) concentrations.Results: We analysed data on 119 Muslim women (mean [SEM] age, 46.6 [1.1] years) who met the inclusion criteria. There were 81 (68.1%) women with serum 25OHD levels < 30 nmol/L (defined as "severe" vitamin D deficiency). Fifty-five (46.2%) women had evidence of high bone turnover (urinary DPYD excretion > 6.5 nmol/mmol creatinine). The women with "severe" vitamin D deficiency had significantly higher serum PTH levels (7.3 [0.3] v 5.4 [0.5] pmol/L; P = 0.001) and higher urinary DPYD excretion (7.2 [0.3] v 5.4 [0.2] nmol/mmol creatinine; P = 0.003) than women with serum 25OHD levels ≥ 30 nmol/L. No significant differences were seen in their ages, menopausal status or serum calcium and phosphate measurements. The risk of developing high bone turnover was significantly greater in the women with "severe" vitamin D deficiency (relative risk = 5.52; 95% CI, 2–14.8; χ2 = 12.95; P = 0.0003).Conclusion: High bone turnover occurs in Muslim women with vitamin D deficiency.

Terrence H Diamond MB BCh, MRCP, FRACP · Sherel Levy MB BCh · Angelina Smith BSc · Peter Day PhD

Objective: To evaluate the effects of bilateral deep brain stimulation in the subthalamic nucleus for symptomatic relief of advanced idiopathic Parkinson's disease.Design: Prospective cohort study.Setting: Patients were assessed and received medical treatment at the Kingston Centre, Southern Health, Melbourne. Surgery took place at Melbourne Neuroscience Centre, The Royal Melbourne Hospital. Both are tertiary public institutions.Subjects: 14 patients with Parkinson's disease with intact cognition and difficult to manage motor symptoms who were referred to Kingston Centre between 1996 and 2000 and were eligible for surgical intervention.Interventions: All patients were assessed both after 12 hours' withdrawal from and while taking their levodopa medication on two occasions before surgery. Further assessments were carried out one, three, six and 12 months after surgery.Main outcome measures: The Unified Parkinson's Disease Rating Scale motor exam and gait parameters, such as stride length and velocity, were compared at six months after surgery with neither stimulation nor medication, with stimulation only, with medication only, and with stimulation and medication.Results: Stimulators were explanted in one patient after intracranial haemorrhage and relocated to the thalamus in a second. Extraneous factors prevented two patients from attending at six-month follow-up. Motor performance improved significantly with stimulation alone in the 10 remaining patients. Further significant gains were seen with stimulation and medication combined, with an apparent reduction in side-effects such as dyskinesia.Conclusions: Bilateral deep brain stimulation of the subthalamic nucleus significantly improves motor performance in advanced Parkinson's disease, despite a rather high complication rate.

Robert Iansek PhD, BMedSci, MB BS, FRACP · Jeffrey V Rosenfeld MB BS, MS(Melb), FRACS, FRCS(Ed), FACS, FACTM · Frances E Huxham DipPhysio, GradDip(HealthResMeth)

Objective: To examine the potential of the New South Wales baby-walker regulation to reduce injury.Design: Injury surveillance data were used to reconstruct baby-walker injury incidents, which were examined in conjunction with the 2000 NSW baby-walker regulation, which requires a specified level of stability and a gripping mechanism to stop the walker at the edge of a step.Setting and participants: Injury surveillance data on injuries to 381 babies collected from hospital emergency departments in South Australia and Victoria, 1986–2000.Main outcome measure: Injury events that would still have occurred with the regulation in place.Results: About half (46%; 95% CI, 32.5%–59.8%) of the serious baby-walker injuries (ie, requiring admission to hospital) are caused by the walker enabling babies to reach hazards other than steps and stairs.Conclusion: The New South Wales regulation has the potential to eliminate only about half the baby-walker injuries. Banning baby walkers altogether is preferable.

Peter G Thompson CertMechEng, MPH

The main source of vitamin D for Australians is exposure to sunlight. Thus, levels of serum 25-hydroxyvitamin D3, the indicator of vitamin D status, vary according to the season and are lower at the end of winter. In Australia and New Zealand, the prevalence of vitamin D deficiency varies, but is acknowledged to be much higher than previously thought. One study found marginal deficiency in 23% of women, and another frank deficiency in 80% of dark-skinned and veiled women. The groups at greatest risk of vitamin D deficiency in Australia are dark-skinned and veiled women (particularly in pregnancy), their infants, and older persons living in residential care. Only a few foods (eg, fish with a high fat content) contain significant amounts of vitamin D. In Australia, margarine and some milk and milk products are currently fortified with vitamin D. The average estimated dietary intake of vitamin D for men is 2.6–3.0 µg/day and for women is 2.0–2.2 µg/day. The estimated dietary requirement of vitamin D is at least 5.0 µg/day and may be higher for older people. Adequate intake of vitamin D is unlikely to be achieved through dietary means, particularly in the groups at greatest risk, although vitamin D-fortified foods may assist in maintaining vitamin D status in the general population. An appropriate health message for vitamin D needs to balance the need for sunshine against the risk of skin cancer.

Caryl A Nowson PhD, DipNut · Claire Margerison BSc(Hons), MND

Diagnostic laboratories are increasingly seen as no more than "factories" that generate fast, reliable test results. The dangers of complacency about the use of tests are highlighted by recent cases of unnecessary surgery and chemotherapy based solely on false-positive test results. There are many causes of misleading laboratory data that can potentially lead to clinical mismanagement. Re-emphasis of the value of patient-relevant communication between the requesting doctor and the laboratory, and better undergraduate and postgraduate education about the appropriate use of tests, will help reduce the risks of test results leading to harm.

Graham H White PhD, MAACB

In cases of multiple impalement injury, the extent of damage to the body can be underestimated. A 26-year-old man sustained a fivefold impalement injury after falling three metres onto metal reinforcement rods. When the emergency medical services arrived at the scene, the patient was in severe distress, pale with clammy and moist skin, increased respiratory and heart rate and tenderness in the lower abdomen. Motor and sensory responses were normal. The emergency physician would not permit the steel rods to be cut until adequate fluid resuscitation (lactated Ringer's solution 1500 mL and hydroxyethylstarch 1000 mL) and analgesia (ketamine hydrochloride 50 mg) were established. During the extrication process, the patient was covered with a blanket and supported from the back (Figure A). Within 53 minutes of the fall, the patient was admitted to the emergency department. Abdominal x-ray indicated that two rods had entered the abdominal cavity (Figure B). Surgical investigation revealed, in addition to laceration of the right femoral artery, major trauma to the abdomen (perforated rectum, jejunum and duodenum, incomplete rupture of the spleen, and injury to the head of the pancreas). The patient recovered from severe infection of the abdominal cavity with concomitant septicaemia, and was discharged from hospital three months later. Multiple impalement is a potentially life-threatening injury that requires perfect cooperation between technical and medical personnel on the scene.1-3 Stabilisation of vital functions, analgesia, and extrication must be performed simultaneously. On-site emergency management must be judged on an individual basis. The question arises whether a scoop-and-run policy — with presumably shorter prehospital treatment time — is justified. In cases involving prolonged rescue, manipulation, or even removal, of the impaling objects has been reported as an exception to the general rule that an impaling object should remain in situ while the patient is transported to an operating theatre.4,5 In our patient, removal of the impaling objects was especially tempting, as successful compression of bleeding vessels from outside the body was anticipated. However, intra-abdominal injury was clearly underestimated at the scene. Major injuries to the upper abdomen by protruding rods were not clinically suspected before operation. This shows that the entry site does not necessarily reveal the extent of damage to the body. A: The patient was supported from behind while the penetrating rods were cut. B: Rods were found to have penetrated the abdomen. This was not suspected until the patient had reached the hospital.

Wolfgang Lederer MD, DTM · Hans C Jeske MD · Kroesen Gunnar MD

Clinical record An 86-year-old woman presented initially with pain on swallowing and tongue ulceration. While awaiting an appointment with an ear nose and throat surgeon, she developed tongue infarction, with associated mild frontal headache and blurred vision. She was then referred to a consultant physician, with symptoms of severe dysphagia, weight loss and dehydration. Examination revealed that she was afebrile, cachectic, and dehydrated, with a blood pressure of 110/70 mmHg and a pulse rate of 88 beats/min. Her tongue was ulcerated, and the anterior third was black with grey-white slough (Box 1). She had wasting and moderate abduction weakness in the shoulder girdle (power 3/5), but her reflexes were intact and she had no sensory loss. Her temporal arteries were palpable and tender, without pulsations. Right-eye acuity was 6/60 (unchanged from a previous assessment). Left-eye acuity was reduced to finger counting. Funduscopy, after dilation, revealed an old right retinal artery occlusion and a recent left retinal artery occlusion. The patient's erythrocyte sedimentation rate (ESR) was 164 mm/h, with an associated microcytic anaemia (mean cell volume, 67 fL) and elevated platelet count (475 x 109/L). Iron studies were consistent with inflammation (ferritin, 762 μg/L [normal range, 20–300 μg/L]; serum iron, 2.8 μmol/L [normal range, 9–23 μmol/L]; transferrin, 2.1 g/L [normal range, 2.0–3.6 g/L]. Tongue biopsy showed necrotic tissue with multiple thrombosed small vessels. Temporal artery biopsy showed classical features of temporal arteritis (Box 2). In light of the severity of the disease, the patient was given intravenous hydrocortisone (100 mg, 6 hourly, for 5 days), then oral prednisolone 75 mg daily. Enteral feeding, subcutaneous morphine, xylocaine mouthwashes and prophylactic antibiotics were instituted. On discharge at one month, acuity of both her right and left eye was 6/60. Her tongue had healed, but 10% of the tongue mass had been lost. Her shoulder-girdle weakness had improved, and her ESR was 35 mm/h (taking 20 mg prednisolone). Over the next four years, numerous attempts to withdraw prednisolone failed, and each relapse responded to steroid increase. Recurrent headache, lethargy, tongue ulceration and pain on swallowing occurred with relapses, with concomitant elevations in her ESR (Box 3). At 42 months from diagnosis, she was asymptomatic taking 5 mg prednisolone. Lingual infarction is an atypical manifestation of temporal arteritis, with fewer than 30 cases reported since 1966.1 Temporal arteritis causes inflammation of medium- to large-sized arteries, particularly branches of the carotid artery. It occurs predominantly in white women over 55 years old and is associated with polymyalgia rheumatica. The two conditions are considered to be part of the spectrum of the one vasculitic disorder.2 Diagnosis of temporal arteritis is a clinical challenge given that atypical presentations occur in up to 40% of patients. Furthermore, there are differing opinions about treatment.2 Its incidence in the over-50 age group is 22.2 per 100 000.3 Given the ageing population in Australia, the spectrum of presentation of temporal arteritis warrants renewed discussion and awareness. Presentation of temporal arteritisClassically, temporal arteritis presents as a recent-onset headache with scalp tenderness over the temporal arteries.2 The headache can be mild to severe.2 In a meta-analysis of patients with biopsy-positive temporal arteritis, jaw claudication was the most specific symptom, but was present in only 34% of patients.3 Tongue sensations, such as burning or sudden increases in size and/or necrosis of part of the tongue, have been reported in 25% of patients.1 Paroxysmal blanching on eating may herald tongue infarction. Symptoms of tongue claudication, such as jaw or tongue pain on chewing, and pain on swallowing, can be misdiagnosed as temporomandibular dysfunction or dental problems,2 and may also herald critical stenoses secondary to atherosclerotic disease of the carotid artery. Facial paresis, acoustico-vestibular symptoms and amaurosis fugax (a transient episode of monocular or partial blindness) can be associated with lingual infarction and, as in our patient, features of polymyalgia rheumatica may also be present.1 These include pain, tenderness, wasting and weakness in the shoulder girdle, with systemic features of anorexia, weight loss and fever.2 Delayed diagnosis and complicationsRecognition and early treatment can prevent complications. In our patient, the lack of recognition of the cause of her tongue symptoms led to diagnostic delay: three weeks elapsed while she waited for review by an ENT surgeon to exclude malignancy and infective causes, during which time lingual and retinal infarction occurred. Complications of visual loss occur in 15%–20% of untreated cases4 and can be abrupt or progress over days.4 Prompt steroid treatment is required and referral for temporal artery biopsy. In a series from the Mayo Clinic, only 1% of patients treated with steroids developed new visual loss over five years.3 The search for new, less invasive diagnostic tools is ongoing. Ultrasound can be reliable, but is highly operator dependent.2 Magnetic resonance imaging is used for assessment of larger-vessel involvement, and the usefulness of positron emission tomography is being explored.2 Temporal artery biopsy Temporal artery biopsy is positive in 60%–80% of patients with temporal arteritis.3 As vasculitis is patchy, small biopsies may miss active disease; bilateral segments more than 2 cm long are preferred. The characteristic histological appearance persists for days after commencement of prednisolone; thus, delays in treatment should not occur if clinical suspicion is high.5 An erythrocyte sedimentation rate (ESR) over 50 mm/h increases clinical suspicion, while a normal ESR significantly reduces the possibility of temporal arteritis.3 The following features (from a meta-analysis) increase the likelihood of a positive biopsy result: acute onset of symptoms (mean, 3.5 months); jaw claudication; diplopia (present in 9%); beaded, prominent temporal arteries; and an ESR over 100 mm/h.3 Treatment, follow-up and specialists involvedBecause of the wide spectrum of presenting symptoms, many specialist groups treat this condition, including rheumatologists, ophthalmologists, neurologists, general physicians and general practitioners. This can result in a wide range of therapeutic regimens, depending on the predominant symptoms. Initiation of steroids is imperative to avoid visual loss. Standard therapy is oral prednisolone 50–75 mg/day initially.2 Intravenous steroids have been used when visual loss has occurred within 24 hours and is severe, although no randomised controlled trials of the value of intravenous steroids have been performed. Most patients respond quickly to high dose oral therapy and maintenance therapy for 12 to 24 months.2 The median duration of treatment is 1.8 years;2 however, relapses occur, and further treatment may be required for several years. Long-term prednisolone is associated with complications (eg, osteoporosis, infections, and peptic ulcer disease), especially in the elderly, and careful monitoring is required. Studies of combination therapy with steroid-sparing agents, such as methotrexate, have been commenced, but further research is needed.2 Lessons for practice Temporal arteritis may present with oral symptoms, such as tongue symptoms or jaw claudication. If temporal arteritis is suspected, measure erythrocyte sedimentation rate (low levels do not completely exclude the diagnosis), and refer for opinion and biopsy. Delays in recognition and treatment can lead to permanent loss of vision. Long-term treatment with prednisolone requires close follow-up and supervision. 1: An 86-year-old woman with tongue infarction 2: Biopsy of the temporal artery Biopsy showed fragmentation of internal elastic lamina, with infiltration of histiocytes, lymphocytes, epithelioid cells and multinucleated giant cells, and accompanying intimal proliferation occluding the lumen (original magnification x100). (Courtesy of Mr Aldo Anile, Pathology Manager, Melbourne Pathology.) 3: Response to treatment over time in a woman with temporal arteritis — erythrocyte sedimentation rate (ESR) and prednisolone dose

Eliza A Tweddle MB BS(Hons) · Amanda K Gilligan MB BS(Hons) BSc, FRACP · Paul W Fogarty MB BS, FRACP

To the Editor: Bupropion hydrochloride was listed on the Pharmaceutical Benefits Scheme (PBS) on 1 February 2001 for use as short-term adjunctive therapy for high nicotine dependence, with the goal of maintaining abstinence. Supply is limited to one application per year, with no repeats, and a maximum quantity of 120 tablets at a dispensed cost of $238.95. From the beginning of February to the end of December 2001, 351 772 bupropion prescriptions had been processed by the Health Insurance Commission (HIC) at a cost of $83.14 million.1 This is equivalent to about 2% of total PBS-related drug expenditure in Australia.2 Given this high cost, it is reasonable to consider the extent to which this investment represents value for money. An important first step is to assess the penetration of bupropion into the population of regular smokers in Australia. One indicator of this is the proportion of regular smokers who have filled a bupropion prescription (Box). Estimates suggest that 22.8% of the population aged 20 years and over (25.2% males and 22.8% females) are current regular smokers.3 Seventy-three per cent (14 099 273) of the Australian population were aged 20 years or over in June 2001.4 Combining population and age-specific smoking prevalence estimates results in an estimated 3 198 738 current regular smokers aged 20 years and over. Given that the PBS guidelines allow for only one prescription of bupropion per smoker per year, an estimated 11% (351 772 prescriptions divided by 3 198 738 smokers) of current regular smokers filled a prescription for bupropion in 2001. Excluding smokers aged less than 20 years will have minimal effect on this estimate, as the incidence of high nicotine dependence in this group is likely to be low. Applying this method to each State and Territory reveals marked variation between them in the apparent proportions of smokers filling a prescription for bupropion. For example, an estimated 16.5% of all smokers in Tasmania had such a prescription filled, compared with 8% in Victoria. Although data from the HIC may be incomplete,5 the same method is applied to each jurisdiction in compiling them. Key unanswered questions relate to the extent to which (i) smokers complete a full course of bupropion, (ii) the field effectiveness of bupropion in aiding smoking cessation is comparable with abstinence rates achieved in clinical trials, and (iii) bupropion is used in conjunction with a comprehensive treatment program. We are currently conducting research to examine such questions. Characteristics of bupropion use in Australian States and Territories, February to December 2001, inclusive ACT WA Vic Tas SA Qld NT NSW Total Population (≥ 20 years) 225 797 1 372 378 3 550 348 338 108 1 110 897 2 602 539 131 542 4 767 664 14 099 273 Current regular smokers (≥ 20 years) 53 448 316 608 804 455 74 507 245 553 593 268 33 254 1 077 132 3 198 225 Bupropion prescriptions processed 4 470 46 186 64 482 12 279 32 455 81 619 3 803 106 478 351 772 Total cost of prescriptions processed $1 043 863 $10 854 828 $15 253 431 $2 920 481 $7 713 913 $19 237 576 $881 709 $25 238 851 $83 144 652 Proportion of current regular smokers who used bupropion 8.4% 14.6% 8.0% 16.5% 13.2% 13.8% 11.4% 9.9% 11.0%

Christopher M Doran · Anthony P Shakeshaft · Jennifer A Gates · Julia E Fawcett · Richard P Mattick

To the Editor: Cyanocobalamin and hydroxycobalamin are synthetically derived preparations of vitamin B12. Allergy to vitamin B12 injection is infrequent, but may be serious. We describe a patient with allergy to hydroxycobalamin, without cross-reaction to cyanocobalamin. Our patient was a 45-year-old woman with vitamin B12 deficiency. She had positive antiparietal cell antibodies and normal results of Schilling's test after addition of intrinsic factor. Otherwise she was in good health, with no other evidence of autoimmune disease. Her allergy commenced after an intramuscular injection of hydroxycobalamin, with onset of mild generalised pruritus. Subsequent monthly 1 mg injections of hydroxycobalamin were followed by incrementally worsening pruritus, and then frank urticaria. The last of nine injections was followed by urticaria, bronchospasm and oropharyngeal angioedema, which responded to administration of adrenalin. The patient underwent skinprick and intradermal testing with hydroxycobalamin and cyanocobalamin. Wheal-and-flare reactions occurred with injection of dilutions of hydroxycobalamin, suggesting an IgE-mediated response. No reactions were evident with dilutions of cyanocobalamin (Box). Subsequently, the patient had no reaction to a challenge of subcutaneously administered cyanocobalamin 0.1 mL (100 μg), and then intramuscularly administered cyanocobalamin 0.5 mL (500 μg). Her macrocytic anaemia resolved with ongoing monthly injections. After one year of treatment, the patient described an episode of delayed urticaria after a routine cyanocobalamin injection. The skinprick and intradermal tests were repeated, with negative reactions to cyanocobalamin, and wheal-and-flare reactions to hydroxycobalamin. She has since tolerated monthly intramuscular cyanocobalamin for over 12 months. Vitamin B12 allergy is rare, but has been reported.1-3 Positive results of basophil histamine release assay and skin testing suggest an IgE-mediated mechanism.2 Desensitisation is therefore theoretically possible; however, anaphylaxis during desensitisation has occurred.3 In Australia, both hydroxycobalamin (Neo-cytamen, David Bull) and cyanocobalamin (Cytamen, David Bull) are available. The excipients of each preparation are identical — sodium chloride, glacial acetic acid, and sterile water. Although the risk of severe allergy is low, adequate facilities for resuscitation should be available when parenteral vitamin B12 is administered. One approach to dealing with vitamin B12 allergy is to use the alternative compound after skin testing to exclude cross-reactivity. If cross-reactivity occurs, then desensitisation may be considered. Alternatively, oral administration of vitamin B12 may also be used.4 Results of skinprick and intradermal testing with hydroxycobalamin and cyanocobalamin* Dilution Saline (negative control) Morphine (positive control) Hydroxycobalamin Cyano-cobalamin Skinprick 1 : 1000 Negative Positive Positive Negative Intradermal 1 : 100 Negative Positive Positive Negative Intradermal 1 : 10 Negative Positive Positive Negative * A positive reaction was a wheal greater than that of the positive control.

David Heyworth-Smith · Patrick G Hogan

To the Editor: Safety is a rather subjective concept, so to use the word without definition, as Clarke et al did,1 is somewhat misleading. One possible definition is that the complication rate for general practitioners is no greater than for anaesthetists in the same circumstances. In the study by Clarke et al,1 the GPs were allocated the lower-risk cases and the anaesthetists were allocated the more difficult ones. Direct comparison was made without any adjustment for this difference. The data suggest that the GPs had similar or higher rates of adverse events or interventions despite handling lower-risk cases. The most recent data on anaesthesia-related mortality reports 20 deaths at endoscopy from 1994–1996, with a note that this is likely to be an underestimate.2 Using the authors' denominator of 430 000 endoscopies per year, an estimated risk of anaesthesia-related death is therefore about 1 in 64 000. The risk of anaesthesia-related death for all surgery is quoted as 1 in 63 000, which implies that anaesthesia for endoscopy is of average risk. The sample size of 28 000 lacks sufficient power to make any comment on safety as regards the risk of death. Although I applaud the clinical standards of the authors' institution and fully agree that propofol has many clinical benefits over other agents, Clarke et al do not prove safety in the use of propofol by non-anaesthetists.

Patricia Mackay · Patrick J Hughes

To the Editor: We read with interest the article by Clarke et al1 and the accompanying editorial by Knoblanche,2 and are concerned that they may be interpreted as endorsing the use of the anaesthetic agent propofol in sedation techniques by personnel inadequately trained in anaesthetic techniques. Cases reported to the Victorian Consultative Council on Anaesthetic Mortality and Morbidity confirm the risk of serious morbidity and mortality associated with these procedures. Our report for the triennium 1997–1999 will include two deaths at endoscopy where a non-specialist administered the sedation or anaesthetic. In both of these cases, propofol was used. The circumstances described by Clarke et al are exceptional. They combine a scrupulous adherence to the professional guidelines3 and a significant involvement by the administration of the endoscopy centre in the selection, education and on-going training of the general practitioner sedationists. They include incident reporting of adverse events and non-standard treatments as part of a quality assurance program. Although not specified, there is also, presumably, access to high-quality back-up. This level of attention to detail is by no means universal. We would like to endorse several observations made in the articles: For a procedure to be considered sedation, it is imperative that the drugs used are not intended to, and do not, cause loss of consciousness or the loss of protective reflexes or spontaneous ventilation; by definition, this would be anaesthesia. Proper selection and careful medical assessment of patients is very important, and training must enable the identification of patients at higher risk. People administering sedation must have knowledge of the pharmacology of the agents being administered and modifications necessary because of concurrent therapeutic regimens or disease states. They must also ensure adequate intraprocedure monitoring is provided, that they have experience in interpretation of abnormal indices, and that they can manage any complications arising from the procedure, with particular emphasis on airway management and cardiovascular resuscitation. There may be benefits with the use of propofol, but the guidelines, designed for patient safety, clearly state: "Intravenous anaesthetic agents such as propofol must only be used by an anaesthetist."3 Technological advances in non-invasive and minimally invasive procedures have led to an explosion in demand for sedation of increasing complexity in areas removed from the traditional operating room environment. Consequently, demand for sedation by non-anaesthetists is likely to grow. It is important that the standard of care and patient safety be maintained in all these circumstances. The concern is not whether the practitioner administering the sedation is a general practitioner or a specialist, but whether he or she has the training and skills necessary to function as an anaesthetist. The terms "general practitioner sedationist" and "non-anaesthetist" might give an impression of diminished risk, which is not supported by the experience of this committee.

Jon P Clarke · Anthony C Clarke FRCP, FRACP · Lybus C Hillman MD, FRACP

In reply: We thank Clarke and Mackay and Hughes for their interest and comments. We accept that a sample larger than the 28 000 endoscopies we reported1 would be required to establish the true incidence of death or other catastrophic complications of our sedation service. As the mortality rate is expected to be so low, it would take many years to achieve an adequate sample size. It is even difficult to determine the mortality from endoscopy in Australia, as quantifying all the endoscopies performed is problematic, and the Royal Australian and New Zealand College of Anaesthetists believes that not all deaths occurring from endoscopy are reported to anaesthetic mortality committees.2 It is essential that any sedation service is carefully planned, and that all doctors providing sedation receive adequate training and follow the protocols and guidelines of the endoscopy centre. However, we challenge the opinion that only anaesthetists should use propofol. We have not been able to find any clinical safety studies that demonstrate that only anaesthetists are able to use propofol safely. We believe the results of our study show that, when propofol is used in the manner described in the article, the rate of ventilatory and other complications is low (but clearly not zero). There is no reason to believe that the propofol component of the sedation regimen increased the rate of ventilatory problems. Indeed, it might, through its short duration of action, minimise such problems. To arbitrarily exclude the use of propofol by appropriately trained GP sedationists would deny many patients the manifest benefits of this drug. Importantly, our GPs have been shown capable of successfully managing the problems of airway obstruction and apnoea that were encountered — whatever the cause. We agree with Mackay and Hughes that the GP sedationists need to have the anaesthesia skills necessary to maintain patient ventilation, as well as an excellent understanding of all the drugs they use. Anaesthetists play a major role in improving safety standards in the provision of sedation for endoscopy through codifying the standards required,3 assisting the training of staff, and delivering sedation services to high-risk patients. But many patients can be successfully sedated without a specialist anaesthetist being present. We argue there is no evidence that these patients should receive a suboptimal regimen. Most specialist anaesthetists have a more valuable role to fill than providing sedation for straightforward endoscopies.

Jon P Clarke

To the Editor: The study by Douglas et al1 reports that the purposeful hastening of death in terminal illness is both widely practised and an acceptable method of palliative care for over a third of Australian surgeons. Yet the study is based on a questionnaire strongly favouring theoretical scenarios rather than actual practice. The framing of the questions maximises reporting bias towards "hastening death" by the use of absolute terms (eg, "Have you ever . . .?"; "[Are] there any circumstances . . .?"1). The study also fails to determine the stage in a terminal illness at which hastening of death had been, or might possibly be, acceptable to the surgeons, nor the reason for its implementation. If the patient's symptoms are already adequately controlled and the dying process is not prolonged, we do not see why it is necessary to administer doses in excess of those required to control symptoms. Whose symptoms are we treating?

Mathew Piercy · Gerald B Fogarty · Aubrey W Jansz · David M Gawler · Luis Vitetta · David Kenner · Avni Sali

To the Editor: We wish to comment on the article by Douglas et al about surgeons hastening death.1 Recently, Ray2 noted that, historically, surgeons have had to witness their patients' pain probably longer than any other medical specialty. Hence, it is not surprising to read Douglas and colleagues' report1 that more than a third of surgeons surveyed performed life-terminating events without explicit and persistent requests. The desire for death, as perceived by doctors and patients, has been correlated with ratings of pain, depression and poor family support.3,4 Surgeons, while intending "no harm", could be seen to be palliating themselves (relieving their own distress) as well as their patients' when performing life-terminating events. Helplessness, hopelessness and negative attitudes toward life-sustaining treatments are common and understandable in palliative care, and experienced by both doctors and patients.3,4 Surgeons are relatively new to palliative care and could have a significant contribution to make to the psychosocial support of cancer patients with terminal illness. Decisions by surgeons about hastening death may be modified by greater interaction with their patients' families and with other healthcare providers working with terminally ill patients. A clinical-outcomes study of 102 consecutive deaths of terminally ill patients admitted to hospice care during 1997–1999 highlights the importance of family support in the outcomes immediately before death.5 The study period coincided with a time of heightened awareness of euthanasia in Australia. Fifty-six per cent of the patients had received continuous family support and 44% sporadic support; these patients appeared to have less distress and better preterminal outcomes, despite 10% experiencing significant family conflict and distress. However, no spontaneous or other requests for euthanasia were recorded in patient files or notes by staff. This could reflect, in part, family support received in an environment conducive to positive interactions between patients, their families and health professionals. Involving such palliative care teams in surgeons' care for terminally ill patients may have a significant effect on both pre-terminal outcomes and hence requests for euthanasia.

Mathew Piercy MB BS · Gerald B Fogarty BSc, MB BS(Hons) · Aubrey W Jansz MB BS, FRACS · David M Gawler MB BS, FRACS, FRCS · Luis Vitetta · Avni Sali Professor and · David Kenner

To the Editor: We were interested to read the recent supplement on preventing osteoporosis.1 We could find only one reference to cigarette smoking, on page S13, where it is noted that "the role of lifestyle changes (including specific exercise regimens, changes in diet and quitting smoking) has not been evaluated adequately". The orthopaedic literature is replete with information and evidence on the adverse effects of cigarette smoking on bone density, healing of fractures, incorporation of bone grafts, etc. A meta-analysis2 has suggested that smokers have greater bone loss over time than non-smokers. Granted, there may as yet be no direct evidence that quitting smoking reduces "the fracture burden". However, to discuss osteoporosis and management of fractures without discussing the major adverse effects of cigarette smoking is akin to discussing the prevention of melanoma and the outcomes of treatment without discussing unprotected exposure to sunlight (for example). Could the "writing group" tell us what steps are being taken to inform Australians of the adverse effects of cigarette smoking on their bones, quite apart from the other public health issues surrounding this extraordinarily harmful habit?

Roy PL Carey · Walter E Plehwe · Peter R Ebeling

In reply: On behalf of the writing group, I wish to thank Carey and Plehwe for their perceptive comment on the effects of cigarette smoking on bone health. The focus of our supplement was the prevention of fragility fractures, and unfortunately there is no evidence that smoking cessation reduces fracture rate. However, the authors are correct to emphasise the negative impact of cigarette smoking on fracture healing, bone graft incorporation and bone density, the last factor being a strong predictor of fragility fracture. The meta-analysis that Carey and Plehwe refer to1 showed that hip bone mineral density (BMD) in current smokers was one-third of a standard deviation below that of people who had never smoked. This meta-analysis and another recent study2 showed that these effects are greatest in men and are dose-dependent. Prospective studies also show that smokers have higher rates of bone loss than non-smokers. Extrapolations from these BMD data suggest smoking increases the lifetime risk of vertebral fracture by 13% in women and 32% in men, while hip fractures are increased by 31% and 40%, respectively. In response to the question of what steps are being taken to publicise the effects of smoking on bone health, we would like emphasise that further prospective studies are urgently required to assess the effect of smoking cessation on fracture risk, BMD and bone turnover; and the message that smoking has a negative impact on BMD should be incorporated into public education campaigns run by government and non-government organisations for both osteoporosis prevention and smoking cessation. This area of bone health is eminently suited to successful intervention.

Roy PL Carey FRACS · Walter E Plehwe MB BS FRACP PhD · Peter R Ebeling MD FRACP

To the Editor: I applaud the ideology of the Journal in its pursuit of evidence-based excellence, drawn to our attention by Rosselli in a recent letter.1 Based on data that the MJA is at the top of the list of English-language journals publishing "evidence-based medicine" references, Rosselli asks "could it be that MJA readers are three times more interested in EBM-related topics than BMJ readers?". My response is that the editors (and perhaps also reviewers) of articles for the MJA may well be more interested in EBM than their BMJ counterparts, but this does not necessarily apply to readers. Without actual evidence of what interests MJA readers, it is not possible to draw any conclusions. Perhaps the readers should be asked?

C Ross Philpot

To the Editor: It was a most interesting idea to call for a list of favourites books.1 I have some of my own to add. The death of Ivan Ilyich, by Tolstoy — all the different responses to a dying man handled in the way only Tolstoy can. Interestingly, the most comforting presence was that of his illiterate man-servant, Gerassim. The doctor, his patient, and the illness, by Michael Balint — this was introduced to me by a very thoughtful medical student when I was a surgical registrar in England 40 years ago. A new edition edited by Balint's son has appeared in the past year or two. Contrary imaginations, by Liam Hudson — the advice in this book on selecting medical students and introducing first-year students to clinical medicine is now being carried out by many teaching schools 35 years after it was written! A long season in hell, by Gail Graham — the story of a mother's fight to rehabilitate her head-injured son. This book has all the characters that a doctor should be aware of — good doctors, bad doctors, unimaginative bureaucrats and politicians, helpful people and an inspiring physiotherapist who lost her husband, apparently through suicide, during the period she was fighting for her son. The book would be an ideal seminar topic for medical students and ethics discussion groups. Lastly, Intellectual impostures, by Sokal and Bricmont — a book with little medical content, but which should be read by every intelligent person. Sokal submitted pretentious gobbledygook to a postmodern journal, which was published. He then exposed the hoax, creating an enormous stir. This book is an expansion of that exposure.

Aubrey W Jansz

Richmond Rikard-Bell, a pioneer in the field of human sexuality studies, was born on 25 April 1922 in Sydney. He was educated at the King's School, Parramatta, and enrolled in medicine at the University of Sydney in 1941. When war broke out in the Pacific in 1942, he took leave from his medical studies to enlist in the RAAF and saw active service in the Pacific. He completed his medical degree in 1950. Richmond worked as a Resident Medical Officer at St George Hospital, then spent five years in a country practice at Captain's Flat, near Canberra. He then moved to Sydney, where he established the first medical practice in the Peakhurst–Lugarno area, as well as a practice at Brighton-le-Sands, where he remained until his death. It was a family practice with a strong emphasis on mothers and babies. Early on, he noted that the young couples whose babies he delivered were often extremely ignorant about marriage, birth and sexual technique, and that this often led to much unhappiness. In setting out to rectify this, he became a pioneer in the field of human sexuality studies, giving courses of instruction to young couples and lecturing at the University of New South Wales to third- and fourth-year medical students. His book, Loving sex, published in 1991, has been widely acclaimed by the public and members of the medical and allied professions. He regarded this as his life's work. Richmond married Joan Davies in 1945 and had a very happy family life with his own six children and two adopted children. The medical tradition in his family is continued by three sons who have become outstanding doctors. Richmond had a lifelong interest in cricket and overseas travel. Although his last years were marred by periods of ill health, he never allowed these problems to affect his happy disposition and interest in his work and hobbies. Diagnosed with carcinoma of the colon, he faced his illness with fortitude and a positive attitude, seeing patients until the end. He died on 19 November 2001.

Ian S Collins FRACP FRCPE FRCP

Re "MJA Practice Essentials – Infectious diseases 3: Community-acquired pneumonia", by Johnson PDR, Irving LB and Turnidge JD, in the 1 April issue of the Journal (Med J Aust 2002; 176: 341-347). The authors would like to clarify an ambiguity in the text, after discussion with Professor Bart Currie (Director of Clinical Research, Tropical Medicine and International Health Unit, Menzies School of Health Research, Darwin, NT). On page 345, the last paragraph should read: "Tropical Australia: Patients in tropical Australia, particularly those with more severe pneumonia, may be infected with B. pseudomallei (melioidosis) or A. baumannii and thus may require different initial empirical therapy. Patients with CAP in risk classes III or IV who also have risk factors for these infections (eg, diabetes, chronic airways disease, high alcohol intake or renal disease) should receive initial therapy with regimens that include intravenous gentamicin plus ceftriaxone (2 g for adults). All patients in risk class V should receive regimens that include intravenous gentamicin plus meropenem, if available. The regimen needs to be further refined if one of these pathogens is identified.26" In addition, the last footnote to Box 6 on page 345 should be replaced with the following: "¶ In tropical Australia, melioidosis and Acinetobacter baumannii infection should be considered in all patients in risk class V and those with risk factors in risk classes III and IV." Antibiotic recommendations are under constant review because of emerging resistance and changes in epidemiology, and we remind clinicians to refer to the latest updates of Australian antibiotic guidelines when prescribing.

Paul DR Johnson PhD, FRACP · Lou B Irving FRACP, FRACGP · John D Turnidge FRACP, FRCPA

Breathing disorders in sleep. Walter T McNicholas and Eliot A Philipson. London: W B Saunders, 2002 (xii + 339 pp). ISBN 0 7020 2510 0. Sleep disorders are among the most prevalent problems in the Australian community, and compact, reliable sources of information on this topic are hard to find. There are good, large specialist textbooks on sleep medicine but no suitable short texts aimed at non-specialists. This book says that this is its market. Breathing disorders in sleep is, to a sleep specialist, a marvellous book and most sleep specialists will want it (although they might baulk at paying 70 cents a page). The authors are the leading lights in research into sleep-disordered breathing in both North America and the United Kingdom. Several chapters contain valuable new data, some previously unpublished results, and new presentations recalculated from the authors' raw data. Everywhere there are keen insights, some clinical and practical, some theoretical. The book's focus is narrower than its title implies — it is really about adult obstructive sleep apnoea. There are a few pages each on sleep apnoea in children, sleep in chronic obstructive airways disease and chest wall and neuromuscular disease, but specialists expecting a comprehensive reference on breathing during sleep will be disappointed. But is this the book non-specialists have been looking for? No! It looks like a book for non-specialists. A lot of attention has been paid to layout, and there are frequent “key points” boxes. Non-specialists could learn a lot by browsing through these key points boxes, and a good student text on obstructive sleep apnoea could be created from them. However, the book is essentially a collection of research reviews, which are excellent, but of little help to the non-specialist. For example, a reader wanting to know whether obstructive sleep apnoea causes vascular disease will find several detailed discussions of the evidence, but conflicting conclusions reached in different chapters. A lot of knowledge is assumed, and in some cases information is presented in such a technical way that most readers will be unable to make use of it. Clinicians who are used to systematic reviews and to thinking in terms of “absolute risk difference” and “number needed to treat” will be dissatisfied — by the management chapters in particular. Those interested in this book or in the politics of book pricing may like to note that amazon.com sells it new for US$99 or used for US$79, which (even with the shipping cost of US$7) makes it much cheaper than buying locally. Leslie G OlsonDepartment of Respiratory and Sleep Medicine John Hunter Hospital, Newcastle, NSW

Leslie G Olson

Struan Sutherland, an Australian pioneer in medical research on envenomation and an expert on the management of envenomated victims, died on 11 January 2002. As Head of Immunology Research at the Commonwealth Serum Laboratories (CSL), he was the force behind the development of the antivenom to the Sydney funnel-web spider. Born in Sydney on 17 June 1936, Struan was raised in Bendigo and educated at Bendigo High School. He graduated in medicine from the University of Melbourne in 1960, and from 1962 to 1965 served as a Surgeon-Lieutenant in the Royal Australian Navy. Struan started work at CSL in 1966, and in the following year was appointed foundation Head of Immunology Research, a position he held for 28 years. His interest in venoms was sparked in 1967 by the deaths of a young soldier bitten by a blue-ringed octopus and of a child bitten by a Sydney funnel-web spider. He renewed research into finding a spider antivenom, but it was not until 1980 that the research team finally succeeded. This was a remarkable scientific achievement — many others had tried and failed in this endeavour. Struan also developed techniques that have made the medical management of envenomation in Australia the best in the world. He invented the pressure-immobilisation technique of first-aid, which revolutionised the management of snakebite world-wide. He also developed a snake venom detection kit that enabled doctors in Australia and Papua New Guinea to determine which snake antivenom should be administered to a victim. In recognition of his achievements, he was awarded the AMA Prize for Medical Research in 1977 and the James Cook Medal of the Royal Society of NSW in 1984. Struan was a prolific author, publishing over 300 scientific articles and book chapters. His book Australian animal toxins was the standard medical textbook on envenomation, and he co-authored other books, including the best-selling Venomous creatures of Australia. Struan served the medical profession and the public selflessly. He was always available to give advice at any time of day or night on management of envenomated victims. He was dedicated and passionate about things that mattered, and prepared to fight for a principle. His departure from CSL in 1994 was precipitated by the closing of the antivenom research program when the organisation was privatised. His outspoken view that antivenom research should continue and that the public good was more important than profitability led to many heated clashes with management. After leaving CSL, with the help of Professor Jim Angus he established the Australian Venom Research Unit within the Department of Pharmacology at the University of Melbourne. Struan was a generous, kind person. He married three times, and was devoted to his children and grandchildren. Visitors to his home would be plied with produce from his hydroponic garden, another of his passions. His autobiography, A venomous life, tells the story of his life with characteristic candour and dry wit. A variant of Parkinson's disease eventually slowed him down, but, although confined to home, he continued writing. Struan was honoured posthumously in the 2002 Australia Day awards as an Officer of the Order of Australia.

James Tibballs MD MBA FANZCA

Protecting islet cells A monoclonal antibody treatment shows promise for the management of type 1 diabetes. Researchers in the United States gave 12 of 24 newly diagnosed diabetics in whom antibodies were detected a 14-day course of anti-CD3 monoclonal antibody. A year later, when most of the control patients showed a marked diminution in insulin production, nine of the 12 patients in the intervention group had maintained, or even improved, their baseline level of insulin production. The treatment also resulted in significant decreases in both HbA1c levels and requirements for exogenous insulin. N Engl J Med 2002; 346: 1692-1698 Tackling the burden According to the evidence so far, screening for depression in primary care is worthwhile. A review prepared for the US Preventive Services Task Force considered 14 randomised trials. Feedback of screening results to the doctor generally increased the recognition of depression, especially major depression, by a factor of two or three. Whether screening resulted in better patient outcomes was less clear. However, when the results of seven trials were combined, it appeared that screening had facilitated a 9% increase in the proportion of patients achieving remission at six months. The authors note that two recent trials of screening for depression, followed by integrated support for treatment, suggest that such programs can produce cost-effectiveness ratios similar to screening mammography or the treatment of mild to moderate hypertension. Ann Intern Med 2002; 136: 765-776 I stay dry with a little help from my friends Australian researchers have shown that a simple intervention can decrease urinary incontinence after childbirth. A randomised controlled trial1 targeted women at risk of urinary incontinence (those with large babies or who had required assisted vaginal delivery). A physiotherapist visited each of the 348 women in the intervention group the day after delivery, providing information, training in pelvic floor exercises, aids to compliance and a special booklet, with a follow-up visit at eight weeks. Three months after delivery, women in the intervention group were more likely than controls to be doing their exercises at least three times a week (84% v 58%), less likely to report any symptoms of incontinence (31% v 38%), and less likely to report severe incontinence (10% v 17%). Meanwhile, Canadian research demonstrates the efficacy of "nurse continence advisers".2 Researchers used advertising to recruit 421 men and women with urinary incontinence. Patients in the treatment group each received an individually tailored program of lifestyle and behavioural interventions, including a follow-up appointment every four weeks. After six months, incontinence episodes and pad use were virtually halved in the treatment group, compared with minimal improvement in the control group. 1. BMJ 2002; 324: 1241-1246 2. CMAJ 2002; 166: 1267-1273 Important tip from MRFIT A follow-up study of the Multiple Risk Factor Intervention Trial (MRFIT) confirms that both systolic and diastolic blood pressure predict cardiovascular risk. In this US study initiated in the early 1970s, 34 2815 men aged 35 to 57 years had their blood pressure recorded. For this analysis, they were divided into two groups, according to their age at MRFIT screening (35–44 and 45–57). Over 22 years of follow-up, 25 721 men died of cardiovascular disease. Higher mortality was associated with elevation of both systolic and diastolic blood pressure. In the men aged 45–57 years at baseline with high normal blood pressure or hypertension, a high systolic and low diastolic blood pressure (and consequent high pulse pressure) was also associated with greater cardiovascular disease risk, and may be a marker for end-organ damage. JAMA 2002; 287: 2677-2683 Risk of clots Another review, performed for the US Preventive Services Task Force, quantifies the association between postmenopausal oestrogen replacement therapy (ORT) and venous thromboembolism.1 The baseline risk in the 12 studies included was 1.3 thromboembolic events per 10 000 women per year. A further 1.5 events could be expected in women taking ORT. The increase in risk was greatest in the first year of taking ORT (relative risk, 3.49). The link between long-haul flights and venous thromboembolism is more difficult to measure. Participants in a meeting convened by the World Health Organization in 2001 considered the available evidence (from case reports, case–control studies and observational studies), concluding that a link probably exists, but that it is not quantifiable owing to a lack of data.2 1. Ann Intern Med 2002; 136: 680-690 2. Bull World Health Organ 2002; 80: 4