Volume 178 Issue 5

We have the tools to improve prescribing — the challenge is to use them Australia's place among the world leaders in the quality use of medicines is exemplified by its National Medicines Policy, the framework of which was put in place over 10 years ago.1 At the centre of the policy is the goal that medicines are used wisely — the Quality Use of Medicines (QUM) acronym has since become somewhat hackneyed and maybe the time is ripe to replace it by a less pretentious label. This issue of the Journal contains three reports that address issues related to QUM. Liaw and colleagues (page 203) examined doctors' perceptions of the Authority Prescribing system of the Pharmaceutical Benefits Scheme (PBS) and found (among other things) that doctors generally do not perceive the system as promoting QUM.2 South et al (page 207) describe how the use of laminated cards, which list guidelines for prescribing antibiotics for infections commonly seen in a paediatric hospital, significantly improved prescribing.3 Newby et al (page 210) found that computer-generated prescriptions for antibiotics in general practice are more likely than handwritten prescriptions to contain repeats, many of which are probably unnecessary.4 Each of these reports shows that, even a decade after the introduction of the National Medicines Policy, aspects of prescribing in Australia can be improved. Thus, it is timely to reflect on what we have been doing right, what we have not been doing right, and where there is still room for improvement. We have developed robust structures to promote QUM in Australia. For instance, Australian Prescriber commenced publication in 1975, and, despite a rather stormy career, continues to provide independent information on issues related to drug therapy. The first edition of Antibiotic Guidelines was published in 1978, and the Therapeutic Guidelines series now covers all the major therapeutic areas. The Australian medicines handbook was first published in 1998. An important initiative was the establishment in 1991 of the Pharmaceutical Health and Rational Use of Medicines (PHARM) Working Party (later Committee),5 which used its modest budget largely to fund projects studying QUM. This committee has been an important stimulus for QUM projects, rather like an "NHMRC" of drug prescribing. However, the committee did not have a mandate to fund ongoing programs. More recently, the National Prescribing Service (NPS) has been established. One of its major mandates is to put in place ongoing programs to improve prescribing, particularly of drugs listed on the PBS. Its continued funding depends on the demonstration of savings to the PBS. To date, the NPS appears to have largely managed to combine quality use with cheaper use, although it is the latter on which its survival depends. It has also managed its recent assimilation of Australian Prescriber in a mature manner. However, the NPS might have increasing difficulty in the future combining its cost-saving mandate with QUM, as this is not necessarily synonymous with cheaper use of medicines. There is also still an element of being "the new (rich) kid on the block", and the NPS has yet to define fully its relationship with established organisations involved with QUM in Australia, such as Therapeutic Guidelines (centred in Victoria), the Australian medicines handbook and the Drug and Therapeutic Information Service (DATIS) group (centred in South Australia), and State groups such as the NSW Therapeutic Assessment Group and the Victorian Drug Usage Advisory Committee. These have been some of the QUM successes, but what are the failures? Undoubtedly one has been the concentration of the Authority system of the PBS on cost saving rather than QUM. This was probably inevitable given that the accelerating expenditure on the PBS cannot be offset by savings elsewhere in healthcare. However, it is a failed opportunity as far as QUM is concerned. Another failure has been the continuing secrecy of the data submitted by pharmaceutical companies to the relevant advisory committees (such as the Pharmaceutical Benefits Advisory Committee [PBAC]) and on which the decisions on registration of drugs, their scheduling, and subsidisation by the PBS are based. Most of this information is not in the public domain, yet would greatly assist doctors and organisations in making good decisions about whether or when a drug should be used. In short, there is no good justification for this bureaucratic secrecy, and it undoubtedly hinders QUM in Australia. The recent putative moves to open PBAC deliberations to public scrutiny are to be welcomed. Another failure is the dependence of our drug evaluation system on fees paid by the pharmaceutical company applicants. It is a tribute to the professionalism of the evaluators that they appear to have largely retained their independence (but the secrecy surrounding the system does not allow for a definitive judgement). However, no regulatory system dependent on fees can ignore the interests of its payers, which are not necessarily the same as those of the Australian public, whom the regulatory system is supposed to serve. A further failure has been our inability to grasp the opportunities presented for QUM by the introduction of computerised prescribing. Unfortunately, this strategy seems to be following the same path as the introduction of computing into hospitals, where it was introduced very much as a management tool and not as a means of improving the quality of clinical care. So, where do we go next? First, the process to make bureaucracy more transparent should be vigorously pursued. Second, we should develop a national forum, for QUM issues. The NPS cannot provide that forum, as it has an overt cost-saving agenda, and its survival depends on it "blowing its own trumpet", sometimes at the expense of other bodies. Perhaps all the different organisations involved with QUM should form a QUM Society, and have national meetings to share results and experiences. Not only would that encourage cooperation rather than competition, it would also promote better recognition of the work of individuals involved in QUM. Most are in academic institutions, and QUM tends not to attract the research grants and publications that academia use to judge success. Third, we must quickly grasp the opportunities presented by computerised prescribing. Advertising must not be allowed to intrude into the prescribing process, automatic repeats for antibiotic prescriptions should not be allowed, and suitable incentives should be provided to ensure that decision support systems are embedded into prescribing software. Last, and most important, we should not rest on our laurels. Australia has done well, but QUM is a fragile flower, easily crushed by other forces, such as the economic imperative to support the pharmaceutical industry. My recent new experience in a country with far fewer resources than Australia has already taught me that much can be achieved with the wise use of resources (such as an essential drug list) I would previously have considered totally inadequate. We should not be in the thrall of the new — we already have the tools, and the challenge is to use them to maximum effect.

Robert F W Moulds PhD, FRACP

Needle/syringe programs have resulted in enormous savings in both lives and dollars Sixteen years after needle/syringe programs (NSPs) were first introduced in Australia, after a period of civil disobedience and amid intense controversy, the recent report Return on investment in needle and syringe programs in Australia1 has convincingly confirmed the effectiveness of NSPs in reducing HIV and hepatitis C virus (HCV) infection among injecting drug users. The report also draws attention to the program's low cost and high cost-effectiveness. Commissioned by the Commonwealth Department of Health and Ageing, the report summarises 778 years of data from 103 cities around the world. In cities that had ever had NSPs, there had been an average annual decrease in HIV prevalence of 18.6%, compared with an average annual increase of 8.1% in cities without such programs. Australia's NSPs were estimated to have cost Commonwealth and State governments $122 million by 2000, but the return on this investment was the prevention of an estimated 25 000 HIV and 21 000 HCV infections. By 2010, our NSPs will have prevented an estimated 4500 deaths from AIDS and 90 deaths from HCV. The savings to governments for HIV and HCV were estimated to be at least $2.4 billion (allowing for conventional government 5% annual discounting of future costs) or as much as $7.7 billion (without discounting). By any reckoning, this represents an enormous saving in both lives and dollars. In light of these outcomes, opposition to NSPs amounts to public health vandalism and financial recklessness with taxpayers' dollars. However, in spite of these gratifying health outcomes for investments in NSPs, the annual incidence of HCV in Australia continues to rise. Hepatitis C is a very common chronic infection in Australia. At least 80% of infected people have acquired HCV through injecting drug use. A recent report2 estimated that in Australia in 2001 there were about 210 000 people with HCV antibodies, of whom 53 000 had cleared their HCV infection, 151 000 were living with chronic HCV infection and 6500 were living with HCV cirrhosis. Furthermore, according to the report, despite the effectiveness of NSPs in reducing HCV incidence among injecting drug users (IDUs), there were 16 000 people exposed to HCV during 2001, representing a 45% increase on the estimated 11 000 incident HCV infections in 1997.3 The report also projected that the long-term sequelae of HCV infection, such as cirrhosis, liver failure and hepatocellular carcinoma, would all treble by 2020. These two reports1,2 raise several important questions. First, why have NSPs been so successful at limiting HIV infection among IDUs, but less effective in reducing HCV infection? One important reason for the apparent discrepancy is the greater infectiousness of HCV by blood–blood spread compared with HIV, and consequently its heightened transmission among IDUs. Another factor is the higher baseline HCV levels (of the order of 50%–70%) prevalent among IDUs when NSPs were introduced in Australia in the late 1980s.4 At that time, only one in 200 IDUs undergoing treatment in Sydney were infected with HIV.5 HIV appears to have entered IDU populations in Australia in the early 1980s, about 20 years after HCV.6 Second, why has HCV incidence continued to increase so rapidly in Australia throughout the 1980s and 1990s, despite early and vigorous implementation of NSPs? The answer appears to be a combination of the increase in the number of young people who inject drugs7 and the continued high incidence of HCV infection among IDUs, and in particular among young people who have recently started injecting drugs (around 20% of IDUs are infected with HCV within three years of commencing injecting).8 The heroin shortage in Australia beginning in 2000 may have interrupted the increase in the number of IDUs, but whether a shortage will persist is uncertain. It is too early to estimate the net costs and benefits of the heroin shortage, but one benefit has been the 25% drop in deaths from drug overdose between 1999 and 2000.9 Finally, what should be done? Alternative strategies that need to be considered (in combination with NSPs) include medically supervised injecting centres, drug law reform, a trial of medically supervised prescription of illicit drugs for treating refractory drug users, introduction of harm-minimisation strategies into prisons, and education programs to encourage people who do or might inject drugs to consider non-injecting routes of administration. Such strategies must be debated in the community and properly evaluated. As each new HCV infection is estimated to cost healthcare systems more than $10 000,10 such strategies make sound health and financial sense. Many IDUs ultimately abandon injecting illicit drugs — it is in everyone's interests that they are still healthy when they do so, to maximise the likelihood that they will lead normal and useful lives. With the recent confirmation of the effectiveness of NSPs in preventing HIV transmission, it is important that society continues to support these programs. This may appear self-evident, but closing down NSP centres is often politically popular, especially in marginal electorates in tight elections. We must not become complacent just because a feared epidemic of HIV among IDUs has not eventuated. There is no guarantee that it will not happen in the future, as has been seen in some other countries.11 Any loss of resolve in the commitment to NSPs increases the likelihood of an HIV epidemic among IDUs, with potentially disastrous consequences for other at-risk populations (such as female sex workers or Indigenous Australians) and thence for the wider community.

Matthew G Law PhD · Robert G Batey MD FRACP FRCP

Academic pathology needs to be reinvigorated For well over a century, pathology has played a pivotal role in our understanding of disease. Its principles underpin many of our teachings in medicine and surgery, for, as Rudolf Virchow — the eminent 19th century pathologist and founder of modern pathology — so aptly observed, "Through the application of its doctrines ... it helps to deepen biological knowledge, and to light up still further that region of the unknown which still envelops the intimate structure of living matter".1 In short, an understanding of pathology is an essential prerequisite to an understanding of medicine. Against this background, it is of serious concern to the Royal College of Pathologists of Australasia that the role of pathology has been downgraded and marginalised with the ascendancy of problem-based learning in Australian medical schools.2,3 It is true that medical curricula over the previous half century placed too much emphasis on the basic sciences at the expense of the social and communicative aspects of medicine. However, as so often happens when changes are made, the pendulum has now swung too far the other way, to the detriment of pathology and anatomy. As Sir John Lilleyman, past President of the Royal College of Pathologists (UK), recently observed, "Current students are taught everything about grieving, but little about the causes of death".4 By its very nature, problem-based learning involves a multidisciplinary approach to clinical problems.2 Sometimes the facilitator for problem-based learning sessions is not a medical graduate. Furthermore, pathologists in academia are now in such short supply that those remaining have limited time to participate in these sessions. (In one Australian university with a faculty of medicine, there is only one half-time academic in pathology, and another university no longer has an independent department of pathology.) The end result is reduced exposure of medical students to pathologists and loss of invaluable mentoring. Consequently, more and more teaching is falling on already overburdened hospital pathologists and registrars-in-training. Furthermore, pathologists in private practice are reducing their teaching commitments because of heavy workloads. Anecdotal evidence suggests that the recruitment of medical graduates into a specialist discipline depends on a number of factors. These include the exposure to that discipline in the medical course and in postgraduate years 1 and 2, and the presence of role models in particular fields. Over the past half century, Australian pathology has been fortunate in having people of stature in academic positions. A recent Australian Medical Association study5 showed that lifestyle issues are becoming an increasingly important subject in career selection. With the currently decreasing staffing levels in academic departments of pathology and lack of formal rotations into pathology in the immediate postgraduate years, there is every likelihood that future recruitment of Australian graduates into pathology will be difficult. We are currently awaiting the report into the pathology workforce of the Australian Medical Workforce Advisory Committee. It will provide recommendations on the number of training positions needed in each State to satisfy future workforce requirements. What can be done to reverse the decline in pathology, particularly in academia? Firstly, the profile of pathology needs to be raised in the pre-university, medical, and general communities. To this end, the College introduced "Pathology Week" in 2002. It involved laboratory tours for secondary-school students, meetings with medical students in some universities, and a dinner bringing together pathologists and leaders in the business community. This year, "Pathology Week" will be held on 10–16 March. Part of the purpose of the Week is to raise the profile of pathology in the wider community: very few Australians know what a pathologist does, despite millions of pathology tests being performed each year. The College has also produced educational material for members of the public and for students contemplating a career in pathology. The Federal Government, through its Quality Use of Pathology Committee, is seriously considering providing financial support to create teaching modules for use in problem-based learning courses. The aim is to ensure that medical graduates of the future have some knowledge of the proper ordering of pathology tests in clinical practice. The Federal Government has also supported the production of a new edition of the Manual of use and interpretation of pathology tests6 for use by students and the profession. Both these initiatives, while most welcome, are unlikely to have medical graduates clamouring to choose a career in pathology. The Academic Advisory Committee of the College has prepared a core curriculum for use in medical schools, although advice from various Deans suggests that a surplus of curriculum content already exists. At the end of the day, the "committee sitters" usually win out in such exercises. Until such time as academic salaries in all branches of medicine become more realistic and aligned with other sectors in medicine, the future of academic pathology looks bleak. As New Zealand and the United Kingdom are experiencing similar shortages,4 there is little likelihood that academics can be recruited from those countries. In exchanges of correspondence with various Deans of medical schools, one has suggested that the College should do more to assist in the recruitment of pathologists to our universities. Perhaps it is time for governments and the private sector to put their support behind academic pathology to help resurrect the field of pathology and ensure it receives due recognition in the curricula of our medical schools.

David Weedon AO, MD FRCPA

Objective: To examine doctors' perceptions and attitudes to prescribing within the Authority Prescribing System (APS).Design and setting: Questionnaire survey of Australian doctors' responses to a number of statements and factorial vignettes, conducted between 1 May and 30 June 2001.Participants: A national random sample of 1200 doctors, stratified according to specialist/generalist, rural/urban and high/low prescriber: 669 (56%) responded.Main outcome measures: Self-reported perceptions of the APS and attitudes to prescribing within the APS.Results: 72% of doctors agreed that the APS makes effective medications available to the socioeconomically disadvantaged members of the Australian public and 50% agreed that it compromises patient privacy. Fewer agreed that authority indicators were based on the highest quality of evidence quality (40%) or medication safety (12%). Doctors placed more emphasis on the doctor–patient relationship than on the criteria for authority prescribing in their decisions about prescribing APS medications. Doctors who used computers to prescribe were more likely to agree that computers can improve the authority prescribing process.Conclusions: This study suggests that authority-required prescribing is not achieving the stated aims of the National Medicines Policy in reducing variability in prescribing. Strategies to improve the quality of prescribing must consider the professional and ethical conundrum associated with prescribing outside of PBS/APS approved use for clinical and patient-centred reasons.

Siaw-Teng Liaw PhD, FRACGP · Christopher M Pearce FRACGP, FACRRM, MFM · Patty Chondros MSc · Leone Piggford MB BS, FRACGP · Kay Jones MSW, PhD · Barry P McGrath PhD, MB BS

Objective: To evaluate changes in prescribing behaviour after distribution of antibiotic guidelines printed on a 9 × 6 cm laminated card suitable for clipping to a hospital identification badge.Intervention: Guidelines for appropriate antibiotic prescribing for 20 common and important paediatric infections were printed on a laminated 9 × 6 cm card suitable to clip to a hospital identification badge and distributed to all medical staff.Design: We collected data from medical records for three marker conditions (tonsillitis, pneumonia, and orbital/periorbital cellulitis) on samples of patients from the six-month periods either side of the month in which the cards were distributed. Prescribers were unaware of the study and investigators analysed the prescriptions without knowledge of the period in which they were written. Prescriptions were rated for appropriate choice of antibiotic and appropriate dose. Data were also collected on antibiotic costs.Main outcome measures: Proportion of cases in which antibiotic choice was appropriate; proportion of cases in which antibiotic dose was appropriate; annualised costs of third-generation cephalosporins.Results: For tonsillitis there was little change in prescribing practice after the cards were introduced. For pneumonia, cases with appropriate choice increased from 77% to 92% (P = 0.028) and cases with appropriate dose increased from 48% to 81% (P = 0.001). For orbital/periorbital cellulitis, cases with appropriate choice increased from 19% to 78% (P < 0.001) and cases with appropriate dose increased from 30% to 51% (P = 0.11). Annualised costs of third-generation cephalosporins were $193 245 pre-cards and $89 814 post-cards.Conclusion: The cards appeared to have a beneficial effect on prescribing practice for the three marker conditions. This simple intervention is likely to be cost-effective and useful in reducing inappropriate use of antibiotics.

Michael South FRACP, MD · Jenny Royle FRACP, MD · Michael Starr FRACP

Objectives: To examine whether the use of current prescribing software systems might raise rates of repeat prescribing, with a consequent increase in use of antibiotics in the community.Design and setting: A prospective audit of consecutive prescriptions for amoxycillin, cefaclor, roxithromycin and amoxycillin/clavulanate presented to community pharmacies in the Hunter region of New South Wales and a follow-up survey of people who received a repeat prescription, October to November 2000.Main outcome measures: The frequency of repeat prescription ordering on computer-generated and handwritten prescriptions; the proportion of people who filled their repeat prescription.Results: Data were collected for 1667 prescriptions presented to 35 pharmacies; 126 people who received repeat prescriptions completed the survey. The rate of repeat prescription ordering on computer-generated prescriptions was 69%, compared with 40% for handwritten prescriptions (odds ratio, 3.3; 95% CI, 2.6–4.2). Computer-generated repeat prescriptions were as likely to be filled as hand-written prescriptions (61% and 69%, respectively).Conclusions: The default settings on computerised prescribing packages result in a significant increase in the use of antibiotics. We estimate these settings result in about 500 000 additional prescriptions being filled annually in Australia for the four antibiotics in the study.

David A Newby BPharm, PhD · Jayne L Fryer BMath, GradDipMedStats · David A Henry MB ChB, FRCP

Three children presented with adrenal crises, manifested by vomiting and hypoglycaemia, after protracted courses of high-dose inhaled corticosteroids for asthma. Significant dose reduction was possible in all three without loss of asthma control, emphasising the importance of back-titration to minimise dose. Parents of children taking high doses of inhaled corticosteroids should be alerted to the clinical features of adrenal insufficiency. If suspected, prompt medical assessment should be arranged, including serum glucose and cortisol measurement. The effectiveness of prophylactic inhaled corticosteroids (ICS) in childhood asthma is well established1 and these drugs are recommended as a safe, first-line preventive therapy.2-4 Dose-dependent biochemical adrenal suppression with ICS has been well documented,3-5 although, until recently, reports of frank adrenal insufficiency in children have been rare.6-9 We present the first documented Australian report of three children who presented with adrenal crises while being treated with ICS for asthma. Each had a history of an intercurrent illness during which they were unable to mount a stress-response rise in cortisol level. Clinical recordsPatient 1Presentation: A seven-year-old boy presented with hypoglycaemia associated with vomiting, abdominal pain and drowsiness preceded by two days of fever, rhinorrhoea and fatigue. He had had a previous episode of hyponatraemia and vomiting, but his blood glucose level was not documented at the time. Although he had been noted to have a cushingoid appearance in the past, he was normal on physical examination, his height and weight were on the 3rd percentile, and his growth velocity was normal. He was found to be hypoglycaemic and hyponatraemic, with a low serum cortisol level (Box 1). A short Synacthen test confirmed adrenal insufficiency (Box 2). Asthma history: The patient had a history of "poorly controlled" asthma, but his wheeze was minimal and not associated with increased work of breathing. He undertook normal physical activity and was rarely absent from school. Spirometry findings in the past had been normal. Medications: He was taking fluticasone propionate (1500 μg daily), nebulised budesonide (1000 μg daily till three weeks before presentation), salmeterol (50 μg twice daily), nebulised salbutamol (5 mg four times daily) and ipratropium (250 μg four times daily) and montelukast (5 mg daily). From the age of two years his ICS doses had been progressively increased and had been at these levels for 10 months before this presentation. He had received frequent doses of oral prednisolone from the age of four years, but had had none for the past eight months. Treatment and clinical course: Immediate treatment included a glucose bolus, fluid replacement and hydrocortisone. Ongoing treatment involved giving regular hydrocortisone while reducing the dose of ICS, with no deterioration of asthma control. Four months after his presentation he was taking 500 μg fluticasone daily and being weaned off hydrocortisone. Patient 2Presentation: A four-year-old boy was referred for investigation of two episodes of hypoglycaemia associated with vomiting and lethargy. There was a third episode of vomiting and lethargy; his blood glucose level was normal on this occasion (his mother had treated him with glucose before presentation at hospital). The patient was normal on physical examination, with height and weight between the 10th and 25th percentiles and with normal growth velocity. He was not cushingoid in appearance and had no abnormal pigmentation. Results of available baseline investigations during the hypoglycaemic episodes are shown in Box 1. A short Synacthen test confirmed secondary adrenal insufficiency (Box 2). Asthma history: The patient had had a history of episodic cough and wheeze since the age of four months, but had good exercise tolerance and minimal nocturnal symptoms between episodes. Past spirometry findings were normal. He had started taking ICS at 18 months of age, with progressively increasing doses in an attempt to control acute episodes. Medications: His medications were 1–2 puffs of 250 μg fluticasone propionate with 25 μg salmeterol (Seretide 250/25; Allen & Hanburys) twice daily (giving a daily fluticasone dose of 500–1000 μg), and salbutamol and ipratropium as required. He had never previously required oral steroids. Treatment and clinical course: With each hypoglycaemic episode he was treated with intravenous fluids, with good clinical response, but on one occasion he also received a short course of prednisolone for a "mild exacerbation of asthma". With the normoglycaemic episode he was treated with intravenous fluids and hydrocortisone for two days. After adrenal insufficiency was confirmed (Box 2), therapy with replacement hydrocortisone was commenced and he was weaned from his ICS dose. He currently takes 100 μg fluticasone and 4 mg montelukast daily, with no significant symptoms. He takes hydrocortisone as needed in times of stress, such as during infections. The patient was also subsequently found to have normal spirometry results, even during acute episodes of asthma. Patient 3Presentation: A 10-year-old boy presented after a hypoglycaemic seizure preceded by 24 hours of vomiting. He was normal on physical examination. His height was on the 90th percentile, weight between the 25th and 50th percentiles, and his growth velocity was normal. He was not of cushingoid appearance and had no abnormal pigmentation. He was found to have hypoglycaemia (Box 1), and hyponatraemia was also detected, but was possibly dilutional, as it was collected from the same intravenous cannula through which the dextrose bolus was given. A short Synacthen test confirmed secondary adrenal insufficiency (Box 2). Asthma history: The patient had a history of frequent episodic wheeze and breathlessness during early childhood, and had been admitted to a rural intensive care unit for asthma exacerbation at the age of five years. Past spirometry findings had been normal. He had been taking his current ICS dose for the previous two years, despite having no acute episodes of asthma or interval symptoms. Medications: He was taking Seretide 500/50 twice daily (giving 1000 μg fluticasone propionate daily) and salbutamol as needed. Treatment and clinical course: Therapy with replacement hydrocortisone was begun while the ICS dose was gradually decreased to two puffs of Seretide 50/25 twice daily (giving 200 μg fluticasone daily); hydrocortisone therapy was continued for four months and is now taken as stress cover for intercurrent illness. DiscussionOur case series further highlights the potential for the systemic activity of ICS to manifest as an acute adrenal crisis. These children, as well as patients in previously reported cases,6-9 all had biochemical evidence of adrenal insufficiency in the absence of other causes (normal long-chain fatty acids, excluding adrenoleukodystrophy, and normal adrenal antibodies, excluding autoimmune adrenalitis [Box 2]). The vomiting associated with hypoglycaemia seen in the three children has been previously described,6-9 as have seizures7-9 seen in our Patient 3. The hyponatraemia found in two of our patients is an unexpected feature, but mild hyponatraemia with normokalaemia has been documented in secondary adrenal insufficiency and postulated to be the result of inappropriate vasopressin secretion10 or subnormal aldosterone secretion in response to severe sodium restriction.11 Hydrocortisone has some mineralocorticoid action, and its use as sole replacement therapy was sufficient to restore electrolyte balance in these instances. While growth suppression was noted in one case series,6 and has been reported in association with asymptomatic adrenal suppression,12,13 it was not a feature in our patients, or in other reports.7,8 This suggests that adrenal suppression may manifest differently, perhaps related to differing patient susceptibility, or dose or duration of ICS use. Our patients and most children in previous reports6-9,12,13 were taking high doses of fluticasone. This may reflect current prescribing habits. While fluticasone may be more likely to cause severe adrenal suppression owing to its higher potency compared with other ICSs,7-9,12,13 all ICS medications have been shown to produce dose-dependent adrenal suppression in children.3-5 The low doses used in some reported cases6 again suggest varying patient susceptibility. Screening for asymptomatic adrenal insufficiency in children receiving high doses of ICS is problematic, particularly as abnormal results do not accurately predict clinically meaningful adrenal-axis suppression.4 Clinical indicators of systemic effects, such as poor growth or cushingoid features, were not seen in our patients or in previously reported cases.6-9 Results of tests such as 24-hour urinary free cortisol excretion and random serum or salivary cortisol levels are often indeterminate.14 Early-morning levels of serum or salivary cortisol which are at the high end of the normal range reassure that there is no serious adrenal suppression, but lower levels can be indeterminate.15 "Gold standard" tests, such as insulin-induced hypoglycaemia or metyrapone suppression, carry significant risks and are difficult to justify in this situation. The standard dose (250 μg) short Synacthen test is generally reliable, but may give false normal results in some instances where central hypothalamic–pituitary–adrenal-axis suppression predominates. The low-dose (0.5 μg/1.73 m2) short synacthen test has been proposed as being less prone to such errors,14 but abnormal test results do not always have clinical significance. A more pragmatic approach would be to warn the parents of children taking high dose ICS of the potential for adrenal suppression so that they seek medical advice during an intercurrent illness associated with unexpected lethargy, vomiting, abdominal pains or seizures. Such "non-respiratory" presentations warrant urgent assessment and tests for baseline blood glucose level (for hypoglycaemia) and serum cortisol level (which may be inappropriately low). Prompt recognition and treatment with hydrocortisone and intravenous fluids containing glucose may be life saving in the event of an adrenal crisis. In less acute presentations, suspected adrenal suppression warrants referral for endocrine assessment and adrenal testing, although there is considerable debate as to the best method for doing this.16,17 If significant adrenal suppression is evident by either a low cortisol level at the time of hypoglycaemia or an extremely low response to cortisol stimulation, then maintenance hydrocortisone should be used in the short term to facilitate safe weaning of the child from ICS. However, it is important to remember that some degree of adrenal suppression and risk of adrenal crisis may persist in such children if any steroid therapy continues, or for up to 12 months after steroid therapy is ceased. Two other important messages arise out of these case reports. Firstly, it is important to ensure that ICS therapy is appropriate for the child. The United Kingdom national survey indicated that around 20% of patients presenting with adrenal crisis were later shown not to have asthma.9 Other areas where ICS have no proven benefit are children presenting with recurrent cough18 or episodic viral wheeze.19 Secondly, in children with asthma receiving ICS therapy, it is important to minimise the dose by "back-titration" or by adding long-acting β-agonists (or both), as highlighted in recent guidelines.2,3 All our patients were taking more than 500 μg per day of fluticasone, which is currently the upper limit of the recommended dose for children.2 Further, significant dose reduction was possible without loss of asthma control, suggesting that these children were being overtreated. This report also serves to reinforce the recent guideline recommendation for specialist referral for children requiring high doses of ICS.2,3 1: Baseline investigations Daily dose of fluticasone propionate Blood glucose level (normal, > 3.5 mmol/L) Sodium level (normal, 135–145 mmol/L) Urinary sodium concentration (normal, < 20 mmol/L) Patient 1 1500 μg 1.3 mmol/L 130 mmol/L* 88 mmol/L Patient 2 (two episodes) 500–1000 μg 2.2 mmol/L < 1.2 mmol/L Not available 135 mmol/L Not available Not available Patient 3 1000 μg < 1.0 mmol/L 126 mmol/L† Not available * Specimen collected before glucose bolus. † Specimen collected after glucose bolus. 2: Adrenal investigations Stimulated cortisol level (normal, > 600 nmol/L) Adrenocorticotropic hormone level (normal, 2–10 pmol/L) Adrenal antibodies (normal, negative) Very long chain fatty acids (normal, negative) Patient 1 108 nmol/L* Not available Negative Negative Patient 2 44 nmol/L† < 1 pmol/L Negative Negative Patient 3 129 nmol/L† < 1 pmol/L Negative Negative * At time of presentation with hypoglycaemia (blood glucose level, 1.3 mmol/L). † During short Synacthen test (60 minutes after an injection of 250 μg Synacthen).

Joseph S Macdessi MB BS, DCH · Peter P van Asperen MD, FRACP · Tabitha L Randell MB ChB, MRCP, MRCPCH · Kim C Donaghue MB BS, PhD, FRACP · Geoffrey R Ambler MD, FRACP · Craig M Mellis MD, MPH, FRACP

Objective: To systematically review randomised controlled trials (RCTs) of computer-generated medication reminders or feedback directed to healthcare providers or patients.Data sources: Extensive computerised and manual literature searches identified 76 English-language reports of RCTs reported before 1 January 2002. Searches were conducted between June 1998 and April 2002.Study selection: 26 papers making 29 comparisons (two papers reported on multiple interventions) of computer-supported medication management to a control group.Data extraction: The quality of the RCTs was systematically assessed and scored independently by two reviewers. Rates of compliance with (potential) reminders for the control and intervention groups were extracted.Data synthesis: Heterogeneity of studies prevented a meta-analysis. Where possible, rates were calculated using the intention-to-treat principle. The comparisons were grouped into five areas. Reminders to providers in outpatient settings: six of 12 comparisons demonstrated positive effects (relative rates [RRs: intervention rates/control rates], 1.0 to 42.0). Provider feedback in outpatient settings: five of seven comparisons showed improved clinician behaviour (RRs, 1.0 to 2.5). Combined reminders and feedback in outpatient settings: the single comparison found no improvement. Reminders to providers in inpatient settings: three of five comparisons showed improvements (RRs, 1.0 to 2.1). Patient-directed reminders: two of four comparisons showed improvements in patient compliance.Conclusion: Reminders are more effective than feedback in modifying physician behaviour related to medication management. Patient-directed reminders can improve medication adherence.

John W Bennett MB BS FRACGP · Paul P Glasziou MB BS PhD

Objective: To define the evidence for doses of inhaled corticosteroids in asthma and describe this in clinically meaningful, evidence-based terms.Data source: Cochrane Database of Systematic Reviews.Study selection and data extraction: We identified systematic reviews of randomised controlled trials of dosing of inhaled corticosteroids in asthma. Data on efficacy and safety of different doses were extracted from meta-analyses and summarised as the number needed to treat (NNT) and number needed to harm (NNH).Data synthesis: Inhaled corticosteroids were highly efficacious, with a relatively flat dose–response curve. Three patients needed to be treated with fluticasone 100 μg daily to prevent worsening asthma (NNT 3), and for fluticasone 1000 μg the NNT was 2.1 patients. The dose–response curve for side effects was steep. For a dose of fluticasone 100 μg, oral candidiasis developed in one of every 90 subjects treated (NNH 90). In contrast, the NNH for fluticasone 1000 μg and 2000 μg daily were 23 and 6, respectively.Conclusion: Level 1 evidence supports the use of low-dose inhaled corticosteroids in asthma. Clinicians should review doses of inhaled corticosteroids used for treating patients with asthma.

Heather Powell RN, MMedSci (ClinEpid) · Peter G Gibson MB BS, FRACP

1: Clinical definition of adult male or female sexual assault6 a) Penetration of the vulva (beyond the labia majora) and/or anus by a penis or any other object, and/or penetration of the mouth by a penis and b) Without the consent of the person A United States meta-analysis estimates that 13% of women and 3% of men worldwide may be raped at some time during their lives.1 New Zealand and Australian data suggest similar findings,2 ranging from 4.6%3 to 11.3%4 in different populations. Although reliable incidence figures are impossible to estimate given considerable barriers to reporting,4 sexual assault presents, often unexpectedly, to healthcare providers working in diverse areas.5 Practitioners may feel sexual assault is challenging to manage, but it is simple when broken into components — emotional, physical and medicolegal. Here we provide a framework for non-forensic medical management of recent adult sexual assault. Box 1 gives a clinical definition, broader than that used in Australian law. DisclosureVictims are reluctant to disclose that they have been sexually assaulted for many reasons, including fear of police, not being believed or retribution, as well as guilt and a desire to forget the event. However, they may present for medical care because of concerns about pregnancy, sexually transmissible infections (STIs), or injury.7 They may present with post-traumatic stress, depressive symptoms,8 alcohol or substance misuse or self-harm.9 To encourage disclosure it is necessary to ask directly about the possibility of sexual assault. 2: Asking about sexual assault Have you ever been forced to have sex you didn't want? Have you ever had sex forced on you? Have you ever been sexually assaulted? Most victims of reported sexual assault are women; men are also assaulted, but are less likely to disclose.10 Although people of all ages and cultures are vulnerable, prisoners,11 adolescents, injecting drug users, the elderly, those who experienced sexual assault as children, and people with mental or physical disabilities are at particular risk.12 A recent survey of sexual health clinics in Australia and New Zealand found that staff were more likely to ask about sexual assault if their workplace encouraged it.13 It also identified patient distress, time constraints and lack of expertise in managing a positive response as barriers to asking. However, nearly all of the patients in the survey reported they did not mind being asked about sexual assault.13 A recent Sydney survey linked sexual assault firmly with the words "forced" and "non-consent" (L Dayan, Director, Sexual Health Services, Royal North Shore Hospital, Sydney, personal communication). Suggestions on how to ask about sexual assault are shown in Box 2. ManagementWhen responding to a disclosure of sexual assault, it is important to: ensure privacy, safety and adequate time for the victim; acknowledge their courage in speaking out; accept the victim's story in a non-judgemental way — it is the role of police to investigate story veracity; explain that reactions to rape, such as shock, arousal, anxiety and fear are normal, emphasising that the victim is not to blame; and understand that the aim of management is to return control to the victim by enabling them to make choices about reporting, counselling and medical therapy (see Box 3). Further action is defined by whether the victim decides to make a formal complaint. Most jurisdictions require that the first person who hears an allegation of sexual assault must give evidence if the complaint comes to trial, so document the exact words used, even if the victim is referred for forensic management. HistoryAssess any injuries and ongoing safety and support. Emergency accommodation may be needed if the victim's home is not safe. A brief history of when and where the assault took place, who put what where, and contraception or condom use will inform immediate treatment. Ask whether the victim wants to report the assault to the police. Early referral to a sexual assault service assists forensic testing. A forensic assessment involves careful documentation of injuries and testing for the presence of foreign DNA; the findings are compiled in a court medicolegal report. Even if the victim is unsure about wanting to report the assault, if there is any possibility of a complaint being made forensic assessment will preserve evidence in case a formal report is made to police at a later date. Ask about the possibility of drug-assisted rape, which is becoming increasingly common worldwide.14 Early forensic referral may facilitate detection of commonly used drugs (eg, flunitrazepam, ketamine) in the victim's blood or urine. Testing must be performed in a police laboratory to preserve continuity of court evidence. If the patient keeps a spot urine specimen, this can be handed directly to the police. ExaminationA thorough general and genital examination should be performed and any injuries documented. Although most sexual assault services use speculums for examining women, this depends on both the woman (comfort versus her need to know all is normal) and the practitioner (expertise and requirement for testing), and should be discussed with the woman before examination. Similarly, the use of a proctoscope may be required. Victims are often afraid that there has been genital damage which will make it obvious to others that they have been raped. Feedback that everything looks normal, as is usually the case,15 can be very reassuring. InvestigationTests for forensic purposes, sexually transmissible infections and pregnancy are performed according to need. If a woman is being transferred to a sexual assault service for forensic assessment after unprotected vaginal rape, the initial dose of the emergency contraceptive pill should be given first. Forensics: If the victim is willing for the police to be involved, he or she should be referred immediately to an expert sexual assault service for forensic assessment (a list is provided at the end of this article). If a victim is undecided about reporting the assault, forensic specimens may be stored while a formal complaint is considered. DNA evidence left on or in the body of a victim, particularly in moist areas, degrades quickly over 2–10 days.16,17 Therefore, forensic assessments need to be made as soon as possible, but within 10 days of an assault. If proceeding to a forensic assessment, advise victims not to shower (or to clean their teeth or rinse their mouths if the assault was oral), and ensure all clothes worn during the assault remain unwashed. As DNA evidence degrades quickly if moist, ask the victim to store underclothes worn during the assault in paper (not plastic) bags. In remote areas, timely expert forensic assessment is difficult. Most sexual assault services provide 24-hour phone assistance by doctors experienced in forensic medicine to discuss assessment. After discussion, some practitioners in remote areas may decide to perform forensic assessments, but this can be a difficult decision, as the practitioner may later be required to give evidence in court. Sexual assault services in Western Australia suggest a compromise solution that entails wiping the victim's vulval and/or anal area with sterile gauze, air-drying it, putting it into a labelled sterile container and handing it directly to local police for forensic testing before the victim's transfer for forensic assessment.18 Pregnancy risk: Depending on the victim's contraceptive and menstrual history, testing urine or serum might be useful to direct therapy and follow-up. Sexually transmissible infections: Baseline testing of sexual assault victims for sexually transmissible infections (STIs) in Australia varies with local clinical practice. In some Queensland sexual assault services serum is held in case STI testing is requested or required later (M Mobbs, Visiting Medical Officer, Brisbane Sexual Assault Service, personal communication). Baseline testing usually occurs in sexual assault services and communities with known high STI risk. As victims of sexual assault have higher rates of STIs compared with the general population,19 opportunistic screening is worthwhile if follow-up can be organised. Under Australian law, a rape victim's sexual history is inadmissible in court and this includes any history of STI. Thus, possible court prejudice is not a reason to withhold testing. See Box 4 for screening test recommendations. Note PAP smears are not generally included. The HIV/STI status of the perpetrator is usually unknown. In the absence of any better indicators, ethnicity or culture is sometimes used as a proxy for HIV/STI risk. The purpose of this judgement of risk is not to vilify minority groups, but to assess the victim's risk of infection on the basis of often very limited information about the perpetrator. Treatment recommendations alter for victims assaulted by anyone thought to be from a high risk group (see Box 5). The National HIV/AIDS Strategy states that community prevalence of HIV and STIs is higher in certain groups, including African and South-East Asian people, homosexual and bisexual men, and injecting drug users.21 Rates of STI are high in northern Australia, including in Indigenous communities,22,23 while HIV prevalence is higher in inner Sydney than elsewhere in Australia.24 As the risk of sexual transmission of hepatitis C virus (HCV) is low,25 tests are usually only performed in high risk situations (eg, assault with bleeding injuries, or assault by known HCV-positive assailant). Although the risk of HIV from one act of unprotected intercourse is very small, if the assault was penetrative unprotected vaginal or anal rape victims should be advised to use condoms until follow-up testing at three months. Most victims are concerned about HIV risk, even though they may not admit it.7 The vast majority will not require HIV prophylaxis, as the risk of transmission from an HIV-positive assailant is very small (see Box 6) and the chance that the perpetrator was HIV positive far smaller. Specific therapyCounsellingSexual assault is a frightening and sometimes life-threatening violent experience and counselling should be offered to all. Even if victims do not wish to attend counselling, it is important that they know where they can go for help, as memories can surface later (eg, at first childbirth) and can impair future functioning.27 Family and partners may also require counselling, or referral may be needed for domestic violence issues. Safety after rape can require moving house if the rapist lives with the victim, or knows where he or she lives. Emergency housing may be needed, as may other forms of immediate support, such as certificates for absence from work and support letters for school. Emergency contraceptionIf the assault was unprotected vaginal rape, or if there was any possibility that this occurred (eg, victim lost consciousness, was intoxicated or is unsure), then emergency contraception can be offered up to three, and possibly up to five, days after the assault.28 The progesterone-only regimen is recommended over the Yuzpe method because it is more effective with fewer side effects. Give the first dose as soon as possible, as efficacy halves with each 12-hour interval after the assault.29 Progesterone-only method: 750 μg levonorgestrel orally; repeat 12 hours later. A 750 μg tablet (Postinor-2, Schering Pty Ltd) is now available in Australia, or 25 30-μg tablets (Microval, Wyeth Australia Pty Ltd; or Microlut, Schering Pty Ltd) can be used for each dose. Yuzpe method: 100 μg oestradiol orally; repeat 12 hours later. Use two 50-μg oestrogen-containing combined oral contraceptive tablets for each dose. This regimen should only be used if the progesterone-only method is not tolerated or unavailable. Sexually transmitted infectionsFor unprotected vaginal or anal assault, victims are offered single-dose prophylaxis with azithromycin for chlamydia (see Box 5). They are also offered prophylactic hepatitis B vaccine if likely to be non-immune. Treatment varies according to community prevalence of STIs and perceived individual risk. In tropical areas of Australia, or if the perpetrator is considered at high risk of being infected, prophylaxis may also be added for gonorrhoea, occasionally syphilis, and passive vaccination with hepatitis B immune globulin30 may also be given if the recipient is not immune. For victims at high risk of having acquired HIV infection (eg, rape by someone from an area of high HIV prevalence), urgent phone consultation with an infectious diseases or sexual health physician about post-exposure prophylaxis for HIV is recommended (see Box 7). ReviewIt is notoriously difficult to get victims back for follow-up.31 The review program suggested (Box 4) is a guide only and should be tailored to suit individual patients. At the very least, an appointment is recommended at two weeks for discussing test results, further testing (eg, pregnancy), review of coping, and assessment of healing. Follow-up serological tests should be performed at three months for HIV, hepatitis B virus and syphilis. Reviews are a good opportunity to assess the need for counselling if this has not already been organised. Before the victim leaves, give written instructions for taking medications and review appointments, and include counselling service phone numbers. Victims may be intoxicated, shocked or tired and are unlikely to remember verbal medical instructions. SummaryManagement of acute adult sexual assault may appear daunting, but when viewed in its component parts is not difficult. Review by a sympathetic, non-judgemental practitioner can play an important role in helping victims regain control of their lives. Australia-wide resources Websites Comprehensive listing of services available in Australia and New Zealand, both updated 2002. Australia: http://www.acshp.org.au/sexual_health/assault.htm New Zealand: http://www.dsac.org.nz Major State and Territory resource phone numbers for sexual assault services The following lists only one major service for each Australian State or Territory, as these services will refer to other local services as appropriate. Australian Capital Territory Forensic and Medical Sexual Assault Care BH 02 6244 2184/3058 Canberra Rape Crisis Centre 02 6247 2525* Queensland Brisbane Sexual Assault Service 07 3636 5206* Toll free 1800 010 120* Government Medical Office (forensic regional services) 07 3405 5755* Tasmania Sexual Assault Support Service Hobart BH 03 6231 1811 AH 03 6231 1817* New South Wales Eastern and Central Sexual Assault Service, Sydney BH 02 9515 3680 AH 02 9515 6111* (ask for sexual assault counsellor) South Australia http://www.wch.sa.gov.au/yarrow/index.html Yarrow Place, Adelaide BH 08 8226 8777 AH 08 8226 8787* Toll free 1800 817 421 Western Australia Sexual Assault Resource Centre, Perth 08 9340 1820/1830 08 9340 1828* Toll free 1800 199 888* Northern Territory Darwin Sexual Assault Referral Centre 08 8922 7156* Victoria Victorian Institute of Forensic Medicine 03 9684 4444* * Denotes 24-hour contact number. 3: Guide for sexual assault care * Usually includes medical care; check with local service. † See resources section at end of article. ‡ Some rural/remote general practitioners perform forensic assessments after consultation with a sexual assault service. STI = sexually transmitted infection. 4: Baseline screening recommendations for sexually transmitted infections Infection Test Site (take according to history) HIV HIV antibody Blood Hepatitis B Hepatitis B surface antigen (HbsAg), core antibody (anti-HBc) and surface antibody (anti-HBs) Blood Syphilis Rapid plasma reagin (RPR) + treponema pallidum haemagglutination assay (TPHA) Blood Chlamydia Polymerase chain reaction Endocervical swab, first-void urine or high vaginal swab Gonorrhoea Polymerase chain reaction or microscopy, culture and sensitivity (M,C&S) Endocervical swab, first-void urine, rectal swab* or throat swab* Trichomonas Microscopy, culture and sensitivity (M,C&S) High vaginal swab * M,C&S only, as PCR is not validated for these sites. 5: Suggested prophylaxis for sexually transmitted infections (treatment for high risk is bolded) STI Treatment Chlamydia Azithromycin (1 g orally) Hepatitis B Hepatitis B vaccine (1 mL intramuscularly) For high risk add: Hepatitis B immune globulin (400 IU intramuscularly*) Gonorrhoea (only if high risk) Ceftriaxone (250 mg intramuscularly) OR, where local gonococcal sensitivities permit: 20 Ciprofloxacin (500 mg orally) OR Amoxycillin (3 g orally) and probenecid (1 g orally) Syphilis (if high risk) Benzathine penicillin (1.8 g intramuscularly) HIV (if high risk) Phone local infectious diseases or sexual health physician urgently Other STIs Consult local infectious diseases or sexual health physician * Available from Commonwealth Serum Laboratories. STI = Sexually transmitted infection. 6: HIV transmission risk per unprotected act of intercourse with an HIV-positive person*26 Type of intercourse Risk per 1000 acts Receptive anal 1–30 in 1000 Receptive vaginal 1–2 in 1000 Insertive vaginal 1 in 1000 Insertive anal 3–9 in 1000 * For comparison, the risk of acquiring HIV infection from using a shared HIV-contaminated needle is 667 in 1000, and from a needlestick injury to healthcare workers is about 4–8 in 1000. 7: Suggested review program 2–3 days: Assess injury healing if relevant 2 weeks: Test results, pregnancy testing, healing, coping Follow-up testing: Chlamydia, gonorrhoea, trichomonas (depending on local practice and whether previous treatment was given) 3 months: Follow-up serological tests for HIV, hepatitis B virus, syphilis 6 months: Follow-up serological test for hepatitis C virus if a test was performed initially

Jacqueline K Mein,*† MB BS, FACSHP, MAE · Cheryn M Palmer,† BMed, MMed, FACSHP · Meon Carol Shand,* MB ChB, FRNZCGP, FACSHP · David J Templeton,*† MB ChB, DipVen · Vanita Parek,* MB ChB, FACSHP, DRANZCOG, DipVenDFFP · Margaret Mobbs,*† MB ChB, DipVen, Visiting Medical Officer. · Kay Haig,* MB BS, FACSHP · Sarah E Huffam MB BS, FRACP · Lyndall Young MB BS, DFFP

People with dementia usually experience behavioural and psychological symptoms of dementia (BPSD) during the course of their illness. Currently, in Australia, there is a lack of comprehensive planning for managing and preventing BPSD, and the resources required for optimal care are inadequate and unevenly distributed. We propose a seven-tiered model of service delivery based on severity and prevalence of BPSD, ranging from no dementia through tiers of increasingly severe behavioural disturbance to the propensity for extreme violence in a small number of individuals. Each tier is associated with a different model of intervention. People with dementia may move up or down between tiers depending on their condition, their care and the intervention provided. Lower-level interventions may prevent the need for the more intensive interventions needed when disturbance becomes more severe.

Henry Brodaty AO, MD, FRACP, FRANZCP · Brian M Draper MB BS (Hons), MD, FRANZCP · Lee-Fay Low BSc (Hons) (Psych)

Clinical questionA physiotherapist at Monash Medical Centre wanted to know the most effective physiotherapy treatments for lymphoedema following treatment for breast cancer. Search questionPeople undergoing physiotherapy for lymphoedema formed the patient group of interest. Clinical outcomes were reduction or prevention of lymphoedema. A randomised controlled trial comparing physiotherapy treatment to no treatment, placebo, or other conservative treatment would be the most appropriate study design. SearchThe search term "lymph(o)edema" was combined with the general treatment search terms "physical therapy", "physiotherapy", "conservative treatment", "non-invasive treatment" and the more specific treatment terms "complex physical therapy", "compression sleeve/bandaging/garment", "manual lymphatic drainage", "mechanical compression" to identify all English-language controlled trials, meta-analyses and systematic reviews published between January 1970 and August 2000. We electronically searched the Cochrane Library, Best Evidence, MEDLINE, Cumulative Index of Nursing and Allied Health Library (CINAHL), Current Contents and the Physiotherapy Evidence Database (PEDro). We also searched the websites of 12 relevant health organisations, including the National Guidelines Clearinghouse, National Breast Cancer Centre, and Agency for Healthcare Research and Quality. Summary of findingsOur search identified two systematic reviews,1,2 and five randomised controlled trials3-7 and one non-randomised controlled trial8 published subsequently to, or not included in, the systematic reviews. There are few well-designed randomised controlled trials that examine the effectiveness of physical therapies for lymphoedema. The two identified systematic reviews1,2 included uncontrolled studies with methodological problems, and their conclusions cannot be confidently endorsed. Furthermore, as no single validated and widely acceptable outcome measure is available, comparison of results across trials or pooling of results in a meta-analysis is not appropriate. Some conclusions can be drawn by examining the controlled studies included in the systematic reviews, and the subsequently published randomised3,4 and non-randomised8 controlled trials. While there is some evidence that compression garments reduce limb swelling, the addition of other modalities, including multilayer bandaging,4 manual lymphatic drainage,3,8 pneumatic pumps or electrical stimulation,1 does not provide additional benefit. However, one randomised controlled trial found that compression sleeves provided only short term benefit (over four weeks),6 while the remaining randomised controlled trials reported that compression was no more effective than manual lymphatic drainage7 or no active treatment5 to reduce lymphoedema. The randomised controlled trials of Dini et al5 and Hornsby6 illustrate the importance of appropriate control groups. Both reported that adherence to skin-care guidelines and other self-care protocols reduces lymphoedema as effectively as the addition of active treatment. Although the International Society of Lymphology9 recommends complex physical therapy (skin hygiene, lymph drainage, bandaging, and exercises in treatment and maintenance phases) as the initial treatment for lymphoedema, we found no rigorous evidence to support this. OutcomeSubsequently published evidence-based clinical practice guidelines10 support our findings, namely that compression garments are of some but limited value, although they are as effective as other, more resource-intensive methods. Other physical therapies, such as complex physical therapy, pneumatic pumps, rigorous massage and compression bandaging, require further rigorous evaluation before recommendations about their use can be made. These recommendations were incorporated into a lymphoedema service for women in south-east Melbourne.

Renea V Johnston PhD · Jeremy N Anderson MD, FRANZCP · Barbara L Walker BAppSci(Phty), GradDipHealthAdmin

Evaluation of patients for rehabilitation after musculoskeletal injury involves identifying, grading and assessing the injury and its impact on the patient's normal activities. Management is guided by a multidisciplinary team, comprising the patient, doctor and physical therapist, with other health professionals recruited as required. Parallel interventions involving the various team members are specified in a customised management plan. The key component of the plan is active mobilisation utilising strengthening, flexibility and endurance exercise programs. Passive physical treatments (heat, ice, and manual therapy), as well as drug therapy and psychological interventions, are used as adjunctive therapy. Biomechanical devices or techniques (eg, orthotic devices) may also be helpful. Coexisting conditions such as depression and drug dependence are treated at the same time as the injury. Effective team communication, simulated environmental testing and, for those employed, contact with the employer facilitate a staged return to normal living, sports and occupational activities.

Series Editors:

To the Editor: It has been known for a long time that washing soda (crystalline sodium carbonate) is effective for removing fluid from joint effusions. The crystals are simply wrapped in a tea towel, crushed with a rolling pin and wrapped around the joint overnight. In the morning the sodium carbonate is rock solid and the joint effusion has markedly improved. I was discussing with one my patients her problem of gross upper-limb lymphoedema after surgery and radiotherapy for breast cancer to the axilla. She went home and made an appropriate pack of sodium carbonate, which she wears overnight. She can now use her arm throughout the day. Obviously, the lymph fluid reaccumulates because her lymphatic system is well and truly obstructed. This patient spoke to several other patients in the Day Centre at the Monash Medical Centre, who tried this in addition to other exercises for lymphoedema, and they have found it to be extraordinarily effective. One woman had gross oedema of her hand, which rendered it useless: she simply immersed her hand in a solution of sodium carbonate and thus dialysed the fluid from her hand. Thereafter she could use her hand for 12 hours before significant amounts of fluid reaccumulated. While this is obviously not the perfect solution to lymphoedema in patients with breast cancer, anything that may help them is worth noting. Perhaps a suitable linen device could be made which would cover the whole arm at night. Evidence for the use of this simple dialysis treatment is currently anecdotal. It might be appropriate to design a clinical trial to determine whether this method has potential in treating this extremely troublesome form of lymphoedema.

Graeme N Brodie

To the Editor: Although liver flukes (genus, Fasciola) are parasites of livestock, human infection is a significant global health problem,1 albeit seldom seen in Australia.2 Infected livestock contaminate waterways with parasite eggs, leading to infection of snails that shed metacercariae on to vegetation, such as watercress.1,3,4 Adult parasites reside in and damage the bile ducts.1,3 Liver flukes could cause disease if introduced into the food chain.1 We report the first case in Australia of liver fluke infection (fasciolosis) in a patient with no history of farm or livestock contact. She probably acquired the disease from eating watercress purchased at a Melbourne market four to five months before symptom onset. Computed tomography of the liver in a woman with fasciolosis Low density lesions (arrowed) following intrahepatic ductal branches in the right lobe of the liver were consistent with Fasciola parasites causing biliary obstruction. A 35-year-old woman presented in August 1998 with fever and right upper quadrant abdominal pain. Blood examination showed eosinophilia (2.5 x 109/L; reference range [RR], < 0.6 x 109/L]). Liver function tests gave normal results apart from elevated serum aspartate aminotransferase levels of 48 U/L (RR < 41 U/L). Abdominal computed tomography showed multiple low density lesions in the right lobe of the liver, with diameter up to 3 cm (Box). A fine needle aspirate showed no evidence of malignancy. Blood tests four weeks later revealed increasing eosinophilia (3.5 x 109/L) and worsening liver function (serum levels: alanine aminotransferase, 163 U/L [RR, 7–56 U/L]; alkaline phosphatase, 126 U/L [RR, 30–120 U/L]; γ-glutamyl transferase, 98 U/L [RR, 5–45 U/L]). A parasitic infection was suspected, but four faecal samples and serological tests for hydatids, Schistosoma, Strongyloides and Entamoeba spp. were negative. Coprological diagnosis of fasciolosis can be problematic, as eggs may be released intermittently and in small numbers, especially in low-intensity infection.1 Enzyme-linked immunosorbent assay (ELISA) using Fasciola hepatica antigen, performed at Westmead Hospital, Sydney, was borderline positive. However, ELISA for IgG4 antibodies against recombinant F. hepatica cathepsin L5 antigen, performed at Monash University, Melbourne, was strongly positive. The patient was treated with two doses of triclabendazole (12 mg/kg body weight per dose) on successive days in October 1998. Abdominal pain subsided within two weeks, her appetite was restored, and eosinophil count and liver function normalised within four weeks. Computed tomography two months after treatment showed a reduction in size of the liver lesions. The patient remained well six months later. This case demonstrates that fasciolosis may present to urban medical practitioners in Australia. Ingestion of watercress is an important clue to the aetiology.2 Serological diagnosis is possible before eggs appear in faeces using a new specific ELISA test that detects the IgG4 response to cathepsin L antigen.5

Andrew J Hughes · Terry W Spithill · Rebecca E Smith · Craig S Boutlis · Paul DR Johnson

To the Editor: Collins and colleagues1 reported a case of bacteraemic community-acquired MRSA (CAMRSA) infection that they believed to be the first reported in Australia. One of us (G N) published a reference to a case of septicaemia and osteomyelitis in Brisbane caused by CAMRSA in 2000.2 This severe case occurred in a previously healthy 16-year-old boy with no risk factors for MRSA infection who, after prolonged ventilatory and inotropic support and vancomycin therapy, required a long period of rehabilitation. A further two cases of septicaemia occurred in Ipswich and will soon be published as part of a study of CAMRSA conducted in 2000–2001.3 We recently encountered another case involving a previously well 23-year-old man who presented to the emergency department with a large abscess on his upper lip and extensive cellulitis of the surrounding face and neck, and with left-sided pleuritic chest pain and associated fevers and rigors. The patient denied previous antibiotic use or contact with healthcare facilities at any time in the past. There was no history of injecting drug use or trauma. Staphylococcus aureus was isolated from blood cultures, and resistance to oxacillin and susceptibility to erythromycin, clindamycin, tetracycline, gentamicin, ciprofloxacin, fusidic acid, rifampicin, and vancomycin was shown. Specimens from operative debridement of the facial abscess yielded S. aureus with the same susceptibility pattern. Chest x-rays showed extensive consolidation of the left lower lobe and an associated loculated pleural effusion. Clinical, radiological, and echocardiographic evaluations did not reveal another focus of infection. The patient was treated with intravenous vancomycin for three weeks followed by oral clindamycin, with complete clinical resolution. It is now clear that CAMRSA infection may result in severe, life-threatening sepsis. The possibility of pneumonia associated with CAMRSA is of particular concern. A 1999 report from Minnesota and North Dakota documented four deaths in children from CAMRSA, including two with necrotising pneumonia.4 A further two fatal cases of necrotising pneumonia caused by CAMRSA were recently reported from France.5 The strains involved in all of these cases carry the gene for Panton-Valentine (P-V) leukocidin, a staphylococcal toxin that has been shown to be strongly associated with cases of severe superficial abscesses and necrotising pneumonia.6 As the strain of CAMRSA most commonly encountered in Eastern Australia also carries the P-V leukocidin gene (Professor J Etienne, Faculty of Medicine, Claude Bernard Lyon 1 University, personal communication), doctors should be aware of the possibility of severe community-acquired pneumonia caused by this organism.

Graeme R Nimmo · E Geoffrey Playford

To the Editor: Kuchar et al1 describe a patient who received an implantable defibrillator discharge after a single ingestion of loratadine. We are concerned that their conclusion — that this patient "probably" had drug-induced torsade de pointes — is incorrect. Review of the intracardiac electrograms from this patient (shown in Box 2 of their article) with known monomorphic ventricular tachycardia (VT; shown in their Box 1) shows a relatively fixed rate of the VT without the large variations in cycle length consistent with torsade de pointes. While there are no established guidelines for determining torsade de pointes based on intracardiac electrograms, it is clear that during monomorphic VT electrocardiograms can show variability in amplitude and orientation. Consistent with the early stages of monomorphic VT,2 the first three electrograms have a different orientation compared with the remaining electrograms, which are largely similar. Unfortunately, as the transition from supraventricular rhythm to tachycardia was not shown, it cannot be ascertained whether the tachycardia began with a pause-dependent mechanism, an important criterion to help diagnose torsade de pointes.3 Given that this patient's implantable defibrillator intracardiac electrograms do not show a continually changing electrogram pattern, that the cycle length is relatively constant, and that there is a lack of documented QT prolongation, there is no evidence of the patient's arrhythmia being torsade de pointes. Incidentally, it is unclear whether these electrograms were recorded before (as specified in the discussion) or after defibrillator discharge (title of Box 2). It is well documented that a defibrillator discharge can have significant effects on the recording of intraventricular electrograms. Most likely, this patient, with documented pre-existing monomorphic VT (their Box 1[b]), had an episode of VT (not torsade de pointes) appropriately treated by the implanted defibrillator, probably having no direct relationship with loratadine. Notably, their Box 3 shows torsade de pointes in another patient, not receiving loratadine. In summary, Kuchar et al1 correctly state that there have been no documented episodes of torsade de pointes after ingestion of loratadine. Similarly, their report does not appear to document an episode of torsade de pointes.

Philip T Sager · Enrico P Veltri

In reply: We agree that there are no guidelines defining torsade de pointes based on intracardiac electrograms, but there are several reasons why the likelihood of torsade de pointes (as opposed to any other arrhythmia) in our patient is high. The electrogram shows the arrhythmia just before delivery of direct current shock, this being about 30 minutes after the patient took her first ever dose of loratadine. There are marked variations in electrogram morphology, despite minimal variation in RR interval, in a short strip of recording in this patient with documented QT prolongation. Further, she had no history of monomorphic ventricular tachycardia, no inducible monomorphic ventricular tachycardia at electrophysiologic examination, and no evidence of structural heart disease. Neither was a mechanism for supraventricular arrhythmia identified. The absence of initiating beats showing pause-dependence is unfortunate, but this is not provided by the generation of device implanted in this patient. Hence, we believe the word "probable" is an apt description for the observation made.

Dennis L Kuchar · Bruce D Walker · Charles W Thorburn

To the Editor: We welcome Ring and Brown's editorial comment1 on the Public Report Card 2002 No More Excuses,2 produced by the Australian Medical Association's Task Force on Indigenous Health. We hope that drawing attention to the poor outcomes of Indigenous Australians will catalyse Federal and State governments to take action, particularly as international comparisons demonstrate the likelihood of success. Australia's poor performance in relation to its Indigenous people is a complex phenomenon, involving political, sociocultural and historical factors, as well as health factors. Levels of ill health among Indigenous communities in post-colonial Australia, Canada and New Zealand are particularly disturbing from a global health perspective, as they persist despite the relative affluence and excellent health status enjoyed by the general population in these nations. One of the difficulties in assessing progress is the lack of high-quality data for comparative purposes. The types of indicators of Indigenous health in common use in Australia, Canada and New Zealand range from central indicators (such as the age-standardised rate ratios for Aboriginal people) to secondary indicators (such as change in the prevalence and incidence of chronic diseases, like diabetes, in Aboriginal communities). It would be useful to develop additional indicators that more closely reflect Aboriginal community knowledge models and values.3 Existing indicators emphasise outcomes rather than opportunities for early intervention, such as early childhood development and youth resilience. Finally, there need to be greater attempts to explore how to use and compare international experiences to help Indigenous people most effectively. The Memorandum of Understanding between the Canadian Institutes of Health Research, the Medical Research Council of Australia, and the Health Research Council of New Zealand may provide a framework for international collaboration.4

Paul Bauert · Elizabeth McMaugh · Carmel M Martin · Janet K Smylie

To the Editor: Our recent study of patients' priorities for asthma care1,2 provides additional evidence supporting the concerns of Wilson and Robertson in their editorial questioning the possible overuse of inhaled corticosteroids.3 We have reported a qualitative study of 62 individuals who presented to an emergency department at either a central city, suburban or rural hospital, in which we explored individuals' perceptions about their asthma, its care and the impact of asthma on their lives.1,2 We also asked participants to complete a questionnaire on the use of medications and sought to amplify this information by further probing the use of medications in our qualitative data collection. Of the 82% of participants in our study currently using inhaled corticosteroid medication (51), 30% (16) were taking 1000 μg of fluticasone or equivalent daily and another 19% (10) were taking more than 1500 μg or equivalent. Current product information for fluticasone suggests a maximum dose of 1000 μg twice daily, whereas National Asthma Council (NACA) guidelines recommend that 500 μg fluticasone or equivalent daily may be the upper limit of useful effect.4,5 We also asked patients how long their medication lasted. Eleven (18%) stated that inhaled corticosteroid devices lasted three weeks or less. Use above recommended doses did not only occur for inhaled corticosteroids, but also for symptom controller medications. Twenty-four (35%) of the 31 (50%) patients receiving this medication reported that a device lasted three weeks or less, indicating use above usual recommended doses. Most patients in our study voiced concerns about the cost of asthma and drug side effects; some adjusted their medication use to manage these issues.1 In such individuals, high use or overuse of preventive and controller medication would increase both costs and side effects, partly explaining these patients' concerns. Doctors may be overprescribing inhaled corticosteroid medication because there is a discrepancy between dosages recorded in published drug information and newer recommendations for optimal inhaled corticosteroid dose.4,5 Our findings show that, in some patients, the risks associated with the use of inhaled corticosteroids are likely to be compounded by using them at higher doses than those recommended. Doctors need to be aware of this in managing patients with asthma who have severe symptoms, in whom overuse, rather than underuse, is likely to be a problem.

Dianne P Goeman · Susan M Sawyer · Michael J Abramson · Kay Stewart · Francis C K Thien · Rosalie A Aroni · Jo A Douglass

To the Editor: Halasz and Vance1 are correct to point out that there is a diversity of causes that can contribute to a child exhibiting symptoms of attention-deficit hyperactivity disorder (ADHD), as defined in the Diagnostic and statistical manual of mental disorders (DSM-IV).2 In their article, they describe a child who meets the DSM-IV criteria for diagnosis of ADHD and in addition has been affected by environmental factors including poor bonding (due to maternal depression), domestic violence and parental separation. The child also exhibits developmental disability, as exemplified by delayed language development. The message is that, by explaining his symptoms in terms of his early experiences and his developmental disability, a diagnosis of ADHD can be excluded. Children with ADHD frequently come from families with disharmonious parental relationships. This may be associated with ADHD in one of the parents, perhaps the violent father in the case described. As clinicians our aim is to ameliorate symptoms as promptly and effectively as possible, and I am frequently impressed by the dramatic improvement that stimulant medication can make to a child's functioning both at school and within the family, with follow-on improvements in mood and self-esteem. Behavioural interventions and family therapy are important adjuncts to medication, but families such as the one described can be difficult to work with and this can limit the effectiveness of such interventions. A carefully monitored one-month trial of stimulant medication, with behavioural rating scales completed by the class teacher, may be appropriate in cases such as the one described. On the other hand, to deny a child a trial of stimulant medication on the basis of adverse early experiences and developmental disability may be to keep from the child the treatment that would help most.

Alison Poulton

In reply: We believe the core symptoms of attention-deficit hyperactivity disorder (ADHD) in children reflect a behavioural "final common pathway" of developmental risk factors,1 which can include transgenerational associations of core symptoms, as Poulton notes. Current scientific evidence suggests both genetic and environmental contributions, such as verbal and visuospatial executive dysfunction2 and/or early patterns of attachment deficits.3 Increased levels of parental psychopathology, associated with (in the child) deficiencies in problem solving, affect regulation, emotional communication and secure attachment, may contribute to the child's symptoms. For this reason, we advocate that medical management be based on a thorough assessment, to ensure that appropriate psychological interventions (eg, parent and teacher management training) are offered alongside psychostimulant medication. In a recent speech at a scientific meeting of the Faculty of Child and Adolescent Psychiatry, Dr A Mawdsley, a distinguished child psychiatrist, expressed his belief that "prescribing medication in the absence of a careful emotional state assessment is inferior medical practice". He went even further to state that "prescribing medication in the absence of a behavioural modification program should be considered medical negligence".

George Halasz · Alasdair LA Vance

To the Editor: I wish to draw attention to a draconian anomaly in the National Health Act 1953 (Cwlth). All GPs encounter patients "shopping" for narcotics and/or tranquillisers. The Doctor Shopper phone line (which enabled GPs to rapidly obtain information from the Health Insurance Commission to identify non-genuine patients) was a boon in guiding GPs' management of such situations. Concern over the new private sector amendments to the Privacy Act 1988 (Cwlth) led to an examination of the legal standing of the Doctor Shopper phone line, and it has now been cancelled. Concerned GPs are now limited to requesting that a "patient" sign a voluntary release of their Pharmaceutical Benefits Scheme record. This tells the "patient" that they have been rumbled, and they move on to the next practice on their list. If they have signed the Privacy Release Form, then the GP will receive a printout of the drugs they have received under the Pharmaceutical Benefits Scheme in the previous six months. This is accompanied by a letter informing the doctor that he or she "cannot make a record of, divulge or communicate to any person, any information with respect to the affairs of the person whose information has been released. To do so attracts a penalty of $5000 and/or imprisonment for a period not exceeding two years". So, under the provisions of the National Health Act (subsection 135A), even putting this information in the medical records of a multidoctor practice would appear to be illegal. It is clearly illegal to warn other doctors outside the practice. There is no corresponding legislation which affects doctor shoppers. So the "right-doers" can finish up in jail, while the "wrong-doers" can, with impunity, continue to play their dissembling, time-consuming, and sometimes harassing, games.

Max Kamien

Counseling the Alzheimer's caregiver: a resource for health care professionals. Mary S Mittelman, Cynthia Epstein and Alicia Pierzchala. Chicago: AMA Press, 2002 (vii + 346pp). ISBN 1579472621. This is an excellent book for staff, researchers or policy makers whose business it is to assist people with dementia and their families. The book amply lives up to its subtitle — it is the best practical guide I have seen for workers in the field, who often struggle to support dementia caregivers through the myriad problems they have to face. Theoretical topics are vividly brought to life with clinical vignettes, and the book is well written and easy to navigate, with a short index that I could not fault. There is plenty of advice about most problems likely to be encountered during the long ‘career’ of someone with dementia — from early diagnosis to death. There is a guide for staff to assess caregiver needs, covering topics such as changes in relationship roles, unsafe driving, problem behaviours and the need for services such as nursing home care. Other family members are included in the approach advocated by the authors, and there is an emphasis on empowering caregivers and their families to solve future problems, with support from the professional counsellor when necessary. The breadth of approach is illustrated by interesting topics such as “the caregiver’s role in hospital”. Here, caregivers are advised how to deal with hospital staff in a tactful manner while negotiating the hazards of a hospital stay. These authors, from the United States, advocate a thorough approach to caregiver support that surely is rarely achieved in Australia or, for that matter, in most of the world. They prescribe a number of education and counselling sessions with the caregiver alone, then with the caregiver and other family members. Caregivers can access a counsellor at any time to deal with new problems. In a landmark clinical trial, this expensive-sounding program led to improved caregiver wellbeing and impressive delays in subsequent admissions to nursing homes. Although economic studies have not yet appeared, this program may well be cost-effective. It is somewhat sobering to ponder on the enormous gap between what is possible to help dementia sufferers and their families and what actually occurs in Australia, where dementia care remains fragmented and crisis driven. Nevertheless, the book provides adequate detail to assist policy makers, and the practical guidance should prove invaluable to all involved in dementia care. I strongly recommend it. David G BruceProfessor Department of Community and Geriatric Medicine Fremantle Hospital, Fremantle, WA

David G Bruce

Clinical sports medicine (2nd edition). Peter D Brukner and Karim Khan. Sydney: McGraw-Hill, 2001 (xxix + 918pp). ISBN 0 074 71108 3. This is the second edition of a highly successful local textbook that has sold over 40,000 copies worldwide. It is a staple recommended text for physiotherapists, sports medicine registrars and general practitioners in Australia and is also very popular in the USA and UK. It would be a particularly good reference text for orthopaedic surgeons who are experts in the major types of bone and joint pathology, but who would like information on the common types of sports injury that do not commonly present to hospital orthopaedic departments (eg, iliotibial band syndrome of the knee in runners; concussion; chronic groin pain; menstrual disorders in female athletes). Two major improvements have been made in the second edition. All chapters are now fully referenced, although most of the text remains easy to read. In addition, many chapters now have contributing authors who are international experts in their particular subject areas (eg, Ben Kibler on shoulder pain, Tim Noakes on exercising in the heat). Peter Brukner is an adjunct Associate Professor at the Centre for Sports Medicine Research and Education, University of Melbourne, and has vast experience as a team physician in athletics and Australian football. Karim Khan is an expatriate working as an Assistant Professor at the University of British Columbia, Vancouver, Canada, and a leading researcher in tendon injuries and bone health. John W OrchardSports physicianKensington, NSW Order this book

John W Orchard

Nothing but trouble Men are more likely than women to have health problems at most times in life, so the recent finding that male babies are born through more complicated labours than females should come as no surprise. Researchers analysed data from over 8000 births at the National Maternity Hospital in Dublin, Ireland, between 1997 and 2001. Among babies born to primigravid mothers after spontaneous labours, male infants were more likely than females to require oxytocin augmentation, fetal blood sampling, and forceps or caesarean section delivery. After adjustment for confounding factors such as birthweight, duration of labour and the use of epidural anaesthesia (all greater for boys), a strong association between sex, birthweight, duration of labour and mode of delivery remained. The big “hole” in the study was the lack of data on head circumference (also greater in boys than girls). However, the researchers did not believe this factor would fully account for the differences. BMJ 2003; 326: 137 Upping the ante Parents who fear that their marijuana-smoking teenagers may end up as drug addicts may have cause for their anxieties, if Australian twins are any example. Over 4000 twin pairs are enrolled in the Australian Twin Registry. Born between 1964 and 1971, their median age was 30 years when interviewed between 1996 and 2000. Three hundred and eleven of the 2765 twin pairs who were available for interview were termed discordant for early cannabis use (ie, one twin had used cannabis before the age of 17, the other had not). Early cannabis users were two to five times more likely than their co-twins to use a range of other drugs, and had higher rates of dependence on illicit drugs (including cannabis [OR, 1.96], stimulants [OR, 3.98] and opioids [3.67]) and alcohol (OR, 1.85). These results held when re-analysed to exclude the 77 pairs in which one twin had never used cannabis, and after controlling for multiple environmental risk factors. JAMA 2003; 289: 427-433 The back-happy tap stand Low back pain is a big problem in rural Tibet, say Australian researchers, who are also working on potential solutions. In 1999 they used two-stage random cluster sampling to survey 499 adults from 19 Tibetan villages. The point prevalence of low back pain, at 34.1%, was much higher than expected, and the 12-month prevalence was 41.9%. The researchers went on to determine precipitants of the pain (collecting water, harvesting, carrying heavy objects etc) and to observe that activities carried out at ground level, such as sweeping, washing and lifting, were often done with a flexed lumbar spine and little bending of the knees. Locally applicable back care programs are now being introduced, and waist-high tap stands are replacing the original, ground-level stands in many villages. Lancet 2003; 361: 225-226 Lost property Researchers in the United States have examined malpractice claims to determine some of the factors at play when surgeons inadvertently leave surgical paraphernalia inside patients. Reviewing the records of the Controlled Risk Insurance Company (insurer of a third of Massachusetts physicians) between 1985 and 2001, the researchers identified 54 patients with retained surgical sponges or instruments. One patient died from complications of the retained foreign body, and 37 required reoperation. Comparing each patient with four controls who had undergone the same operation during the same six-month period, three significant risk factors emerged: emergency operation (risk ratio [RR] 8.8), an unexpected change in the operation (RR 4.1), and increasing body mass index in the patient (RR 1.1/unit increment). N Engl J Med 2003; 348: 229-235 Ageists or realists The United States National Institutes of Health consensus guidelines for women with breast cancer recommend chemotherapy based on tumour size and the presence of positive nodes, but in the “real world” it seems that patient age is also a factor. According to the New Mexico Tumour Registry, among 5101 women diagnosed with breast cancer between 1991 and 1997, the overall rates of chemotherapy use were 11% for women with stage 1 cancer, 47% for stage 2 and 68% for stage 3A. Regardless of tumour stage, chemotherapy use declined significantly with age; for example, in women with node-positive and hormone-receptor positive tumours (n=1030) the percentage receiving chemotherapy was 87% for women aged