Volume 188 Issue 5

An integrated comprehensive approach to medication error is a national imperative Medication errors are among the most common incidents reported in public hospitals.1,2 This is not surprising, given that every admitted patient receives some medication. If medication is one of the hallmarks of treatment in our institutions, it, more than any part of our practice, should be made safer and, wherever possible, error-proof. In New South Wales public hospitals, the Incident Information Management System (IIMS) report for 2005–20063 included 17 367 medication incidents in which medication error was the primary cause of harm. In another 968 incidents, medication error was a secondary cause. Most incidents were notified from the services of general medicine or pharmacy, but all clinical services, including surgery, reported medication errors. The severity of most reported medication errors is minor. In the IIMS report, less than 0.3% of notified medication incidents in NSW were given a severity assessment code of 1 (SAC 1), compared with 0.8% SAC 2, 25.9% SAC 3 and 56.2% SAC 4 (SAC 1 = severe harm; SAC 4 = trivial or no harm). In this issue of the Journal, Nichols and colleagues4 examine medication errors and highlight the types and context of errors at Fremantle Hospital, Western Australia (→ Learning from error: identifying contributory causes of medication errors in an Australian hospital). Although the study was based on a small sample, its principal strength was that it examined not only the incident but also the environment, the team, the tasks being undertaken, and the individual circumstances of those “responsible” for the error. The study cohort was selected by pharmacists during regular ward rounds over a 6-month period. Fremantle Hospital participates in the Australian Incident Monitoring System and has patient safety committees. The Fremantle Hospital study did not give error rates, but the IIMS data3 suggest that the problem of medication errors is not small. We need to reinvigorate attempts to provide secure prescribing environments. Practitioners must be able to concentrate, without distraction, on the patients for whom they are prescribing. They must have adequate information on the indications for prescription, potential complications, contraindications and drug interactions of the prescribed medications. Nichols et al reported that 7/26 members of staff (27%) indicated there was lack of guidance from senior colleagues when they were prescribing unfamiliar medications, 8/26 (31%) were dealing with an unfamiliar patient when the error was made, and 5/26 (19%) were working in an unfamiliar ward! Hastily scribbled notes during a rushed ward round from a senior consultant who presupposes competencies to a newly posted intern are not a prescription for safety, but a recipe for error! Root-cause analysis data from NSW5 have shown that major factors leading to severe incidents (SAC 1) include deficiencies in policy (25%), communication (25%) and knowledge/competency (18%). These data are consistent with the study of Nichols et al, in which poorly defined policies or inadequate drug information were found to be a factor in 23% of medication errors. In the Fremantle Hospital experience, communication within the team was a factor in medication errors in 31% of incidents, and communication with others was also a factor in 31%. Various initiatives that may lessen the risk of medication errors in Australian hospitals require more evaluation. The National Inpatient Medication Chart,6 commissioned by the Australian Council on Safety and Quality in Health Care, is an important advance. All junior staff now know where to prescribe, how to look for and how to document medication. This evidence-based best practice initiative, led by the Safe Medication Practice Unit of Queensland Health, addresses key problems, such as the prescribing and dispensing of warfarin. It is important that the national initiative not be undermined as individual hospitals, units or clinicians make local modifications. Rather, local lessons must contribute to the national debate and the standard document should be improved by consensus. Standardised formats for multiple-drug protocols must also be developed. Many hospitals do not yet use electronic prescribing. The drug advice available to junior staff often consists of a dilapidated, torn and hard-to-find MIMS publication that is often many months out of date. Although MIMS is now available online in all public hospitals (except in South Australia), and NSW Health has a state licence for personal digital assistants (PDAs) for all staff, neither technology (online or PDA) is fully utilised in the public sector. Other electronic sources of drug information available include the “Therapeutic guidelines” series (http://www.tg.com.au/index.php?sectionid=97), the Australian medicines handbook (http://www.amh.net.au) and the Clinical Information Access Program (http://www.ciap.health.nsw.gov.au). Whatever the technology or software used, it is essential that teams develop, with hospital pharmacists, relevant orientation procedures, including information on medication usage, for new members of the team. Medication reconciliation7 (the formal process of obtaining a complete and accurate list of each patient’s current home medications and comparing the clinician’s admission, transfer or discharge orders with that list) and pharmaceutical review8 (the systematic appraisal of all aspects of a patient’s medication management to optimise patient outcomes) provide opportunities for minimising “slips and lapses”, but are not yet seriously “on the radar”. Multidisciplinary hospital drug committees could provide local champions for such programs, collect and evaluate data and develop the evidence base. These issues demand systematic attention from hospitals, administrators and clinicians. The NSW Therapeutic Advisory Group and the Clinical Excellence Commission (NSW) have adapted a Medication Safety Self-Assessment (MSSA) tool developed by the Institute for Safe Medication Practices (ISMP) in Canada and the United States for use in the Australian health care environment.9 A similar antithrombotics tool10 addresses the critical issues around the narrow therapeutic index of antithrombotic medicines. These tools, which are complementary to the Indicators for quality use of medicines in Australian hospitals,11 allow hospitals to assess their own performance and provide national information about safe medication use. Their effectiveness in reducing medication harm is yet to be proven in Australia. The ISMP MSSA tool was evaluated in the US12 in 2002 and again in 2004. Collaborating members did demonstrate continuing improvement in key elements of medication safety (Cohen MR, Vaida AJ. ISMP Medication Safety Self-Assessment — Australian version: experience in the United States. International video conference launch of MSSA. Sydney: ISMP, Feb 2007 [unpublished]). These and other tools could enable all clinicians to measure medication practice, monitor new protocols and minimise the types of slips, lapses and incidents reported in the study by Nichols and colleagues. An integrated comprehensive approach to medication error is a national imperative. We should not be afraid to compare and contrast systems, as long as designs allow an interface between core national and state platforms. Nichols and colleagues have given the problems of medication error human faces — both staff and patient. Only serious system-wide measurement and evidence-based change can return smiles to those faces!

Clifford F Hughes AO, FRACS, FACS, FACC

Excessive reliance on intraocular pressure to detect glaucoma leaves many affected patients undiagnosed and untreated; visualisation of the optic disc is a dying art that needs to be revived Intraocular pressure (IOP) is measured by tonometry. In our community, mean IOP is around 15 mmHg, with a normal range (mean ± 2 SD) regarded as 10–21 mmHg. This information is irrelevant to the diagnosis of glaucoma. Misconceptions about the importance of IOP in diagnosing and screening for glaucoma continue to result in unnecessary blindness in Australia from glaucomatous optic neuropathy. An aggressive realignment in our thinking is required. The classic diagnostic triad for glaucoma of raised IOP, arcuate visual field loss and optic nerve head cupping has been inverted. Glaucoma may now be defined as a characteristic, progressive, optic neuropathy showing optic disc cupping as a consequence of neural rim loss. It tends to produce arcuate visual field loss. It is frequently associated with an elevated IOP, but may be diagnosed at any IOP if there is characteristic optic disc and/or visual field damage. This damage indicates susceptibility of that optic nerve to a given IOP. Early work established a population mean IOP, with an about normal distribution.1 It is regrettable that this result came to be interpreted as indicating a “normal” (ie, safe) IOP for an individual patient, particularly as that report recognised that glaucoma could occur despite an IOP of less than 21 mmHg. In the Baltimore Eye Survey, more than 50% of patients with newly diagnosed glaucoma had a “normal” IOP on a single tonometry measurement.2 The term “normal pressure glaucoma” (NPG) has been coined for such eyes, and they may comprise a third to a half of all open-angle glaucoma cases.2,3 Conversely, there is a subset of the population that has IOP elevated above normal, yet does not have glaucoma. This status is labelled ocular hypertension. Detection of elevated IOP remains important at any time. The prevalence of glaucoma at successive levels of IOP greater than 21 mmHg rises exponentially.4 IOP is the single greatest risk factor for glaucoma, and its reduction is the cornerstone of all current treatment. Screening on the basis of IOP alone, however, clearly produces a high rate of potentially disastrous false negatives. Patients continue to undergo “eye-checks” and be reassured that they do not have glaucoma solely on the basis of an IOP measurement. This represents an inadequate standard of care. Visual field loss is no longer a sine qua non of diagnosis. In recognition that up to 40% of axons may be lost from the optic nerve before visual field loss is evident on standard automated perimetry,5 the term “preperimetric glaucoma” connotes this early disease. Rather than being a distinct entity, preperimetric glaucoma really indicates the inadequate sensitivity of this standard psychophysical test in detecting early glaucoma (as compared with its invaluable role in confirming and monitoring established disease). Early detection of disease can thus depend entirely on identifying optic disc cupping, notching or rim loss, and associated retinal nerve fibre layer defects, perhaps in the absence of raised IOP or visual field loss. Newer and more sensitive tests of specific visual processing such as frequency doubling perimetry or short wavelength automated perimetry may detect glaucoma earlier, and may thus shift the boundary in defining preperimetric glaucoma.6 We must also disabuse ourselves of any convenient dichotomy between chronic open-angle glaucoma and acute angle-closure “glaucoma”. (Acute primary angle closure [APAC] causes a painful, unilateral red eye with markedly elevated IOP: patients with APAC may not have optic disc cupping or visual field loss.) It is increasingly evident that a massive and untreated burden of chronic angle-closure glaucoma exists, particularly in Chinese and South-East Asian people,7 and therefore in our immigrant populations and their families. Glaucoma, whether open-angle or closed-angle, is an insidious disease — “the sneak thief of sight”. Its prevalence increases exponentially with age; progression is slow, painless and irreversible; visual acuity is affected only late; and symptoms of peripheral vision loss with mobility difficulties do not occur until gross levels of field constriction have developed. For all these reasons, affected patients tend not to present but instead need to be found. Prevention — or at least slowing — of further vision loss is possible with an effective range of medical, laser or surgical therapies directed at lowering IOP to an individualised target level (which may be considerably lower than 21 mmHg). The limitation to our preventing blindness in Australia is not so much a lack of therapies, but inadequate case detection. Awareness of the newer concepts in glaucoma has been variable among general practitioners, optometrists and even ophthalmologists. Glaucoma has a prevalence of around 3% in the population aged over 50 years, yet 50% of cases of glaucoma in Australia today remain undiagnosed.8 The Melbourne Visual Impairment Project provides a further indictment: of the patients whose glaucoma was detected during the survey and who had seen an eye-care practitioner in the preceding 12 months, nearly half (many of whom had established visual field defects) had not had their glaucoma diagnosed.9 Highly sensitive screening programs of the general population for glaucoma are, however, not cost-effective, producing low case yields and a high number of false positives.10 Despite a panoply of technological wizardry, there remains no device that in a single or screening test can identify early glaucoma with appropriate sensitivity and specificity. Local research is progressing with international collaborators to identify genetic loci responsible for glaucoma,11 but a blood test to identify those genetically at risk is not generally available. What is to be done? Ophthalmologists diagnose and manage glaucoma, but are referral-dependent and thus see a selected sample. The aim that every Australian aged over 40 years have a general eye examination by an eye-care practitioner remains an elusive goal, but such a strategy could detect glaucoma as well as other ocular abnormalities, particularly if glaucoma sufferers could be prompted to reveal their diagnosis to first-degree relatives. “More funding” is a mantra so tired as to engender indifference, but would certainly enable more targeted, resource-intensive testing.12 While the benefit of disease detection seems self-evident, legitimate public health arguments could be mounted that, as progression of glaucoma is slow, diagnosis and treatment of early disease (particularly in older patients with preperimetric glaucoma) is not justifiable. We must also be mindful of the burden of the diagnosis and treatment for the patient.13 Screening protocols would therefore be directed not to detecting early glaucoma per se, but rather to finding those with a greater lifetime risk of loss of functional vision (ie, advanced disease, younger age or higher IOP). In the absence of such a structured program, we are dependent on “opportunistic screening”. In this issue of the Journal, Zegers and colleagues present two clinical vignettes illustrating the importance of a family history of glaucoma,14 which is an excellent starting point in case detection (→ Primary open-angle glaucoma: the importance of family history and role of intraocular pressure). Glaucoma suspects can also be identified by general practitioners and optometrists prepared to examine the optic disc. For the former, ophthalmoscopy is a dying art that needs to be rejuvenated in training programs so that visualisation of the optic disc can resume its place in the routine medical check-up. Optometrists, on the other hand, are technologically equipped and trained to detect and diagnose eye disease, are frequently primary eye-care practitioners, and are numerous. The recent move by a vanguard of optometrists into therapeutics and comanagement remains politically vexed. Nonetheless, medical practitioners must accept and encourage the major contribution to glaucoma detection that many optometrists make. Vision loss from glaucoma is most often preventable. Current therapies are effective if the diagnosis is made early enough. Many treatable patients continue to lose visual field because case-detection strategies are haphazard, incomplete, or suffer from a lingering and inappropriate fixation on elevated IOP as the sole diagnostic criterion. The two simple tasks of asking for a family history of glaucoma and assessing the optic disc (with referral onward of patients with positive findings) represent opportunities to diminish the impact of the commonest preventable cause of irreversible blindness in Australia today. To heighten awareness of glaucoma, the first-ever World Glaucoma Day has been designated for 6 March 2008 (http://www.wgday.net). Glaucoma Australia provides patient and community education and support, and can be contacted at http://www.glaucoma.org.au.

Mark J Walland MB BS, FRANZCO, FRACS

Gender is more than just a variable to be controlled for in statistical analyses Does ageing affect men and women equally? If not, how might differences affect research — and subsequently clinical practice? To answer this and related questions, the Mars and Venus: Does Gender Matter in Ageing? conference was convened by the University of Newcastle’s Research Centre for Gender, Health and Ageing, in association with the Australian Association of Gerontology and the Healthy Ageing Theme of the Australian Research Council/National Health and Medical Research Council (NHMRC) Research Network in Ageing Well.1 The 2-day conference, held in Newcastle in July 2007, featured longitudinal studies of ageing that have given specific attention to the health of men or the health of women, and introduced an NHMRC-funded initiative to link two of these studies. The conference also included a 1-day research workshop, sponsored by the Ageing Well Network, which involved researchers from longitudinal studies of ageing being conducted in Australia, and considered how such studies might take greater account of gender in their design and analysis. The conference attracted 85 participants from across Australia and overseas, who came together to consider ways in which the effects of ageing are unequal between men and women, and how these differences might be further exaggerated through interactions with socieconomic status and background. Conference overview: seeking balanced debateThe theme of the conference was set by Cherry Russell (School of Behavioural and Community Health Sciences, University of Sydney), who gave a keynote address, Ageing and the gender agenda: a critical reflection, which outlined gender differences in life expectancy, health, income, care needs, and level of social isolation, along with a discussion of gender biases in policy and service provision. Compared with men, women have more chronic illness and greater health service use at older ages; but they also live longer. Men have more fatal illness at younger ages.2 For instance, men have coronary artery disease earlier and have a higher death rate. Lung cancer is more common among men, who have had higher rates of smoking than women. Women have a higher incidence of musculoskeletal problems and a higher prevalence of incontinence, although these problems are also important for men. Although hip fracture also affects older men, the incidence increases at a later age and fewer men survive to the age of high risk. Women, therefore, dominate the clinical picture. Some health differences are related to biological sex; however, many differences are strongly linked to social influences of gender. These less obvious differences include environmental, occupational and behavioural risks, behaviour, and different adaptive techniques. There are also considerable differences in social roles and access to financial and social resources — which significantly affect the experience of ageing. Cherry Russell noted that there has been little balanced debate as to what the unequal effects of ageing for men and women mean and where they stem from. Debates about gender and ageing have focused on loss of men’s work roles, older women’s double disadvantage from age and gender inequality, and on a “paradigm of competitive suffering”. In contrast, this conference aimed for greater balance in considering how gender influences the health and wellbeing of men and women as they age. This theme was reflected in the proffered papers and workshops. Papers explored age and gender issues such as living arrangements; health and engagement for older men; gender bias in health service programs; retirement issues; and current research on gender differences, including results from the Household, Income and Labour Dynamics in Australia (HILDA) study and Melbourne Longitudinal Studies of Healthy Ageing (MELSHA). Workshop topics explored the needs of homosexual and transgender people, gender issues in dementia and sexuality in residential aged care, and the practicalities of conducting a large longitudinal study: the Australian Longitudinal Study on Women’s Health. Longitudinal studies: a focus on genderKeynote addresses throughout the conference featured longitudinal studies of older men and women. The Concord Health and Ageing in Men Project (CHAMP), presented by Bob Cumming (Centre for Research and Education on Ageing, School of Public Health, University of Sydney), involves 1705 men aged 70 years and over. Early findings from this study show a sharp increase in multiple falls, and declines in continence, cognitive function, and activities of daily living starting after the age of 80.3 The Florey Adelaide Male Ageing Study (FAMAS), presented by Gary Wittert (School of Medicine, University of Adelaide), focuses on chronic physical and psychological disease and reproductive and sexual health.4 Measures of testosterone show an age-associated increase in sex-hormone-binding globulin and a decrease in free testosterone, a change that may be adaptive rather than pathological. The Health in Men Study (HIMS), presented by Leon Flicker (Graduate Research School, University of Western Australia), involves 4262 men, and focuses on physical and psychosocial morbidity (including depression), health risks, weight and body mass index, cognition and mortality. One finding from this study has been the importance of health and lifestyle factors in determining cognitive function, even in advanced old age.5 Emily Banks (National Centre for Epidemiology and Population Health, Australian National University) provided an overview of the United Kingdom’s Million Women Study (MWS), which has shown increased risks of breast cancer,6 endometrial cancer,7 and ovarian cancer with use of hormone replacement therapy,8 and a protective effect on fracture.9 Annette Dobson (Division of Epidemiology and Social Medicine, University of Queensland) represented the Australian Longitudinal Study on Women’s Health (ALSWH), which has been running since 1996, and has investigated many factors affecting women’s health and ageing, particularly the influence of social context on health and health care use.10 Recent reports from this study emphasise the burden of illness associated with non-fatal conditions such as arthritis, the preventable burden of obesity, and safe levels of alcohol intake for older women.11 Leon Flicker, Annette Dobson and Julie Byles (Research Centre for Gender, Health and Ageing, University of Newcastle) also gave an overview of the recently funded Men, Women and Ageing Study, linking HIMS and ALSWH to generate cross-gender analyses. Additionally, Gita Mishra (University College, London) showed how gender interacts with effects of childhood socioeconomic status in determining early mortality in the 1946 British Birth Cohort. For example, a father’s occupation had a strong effect in women, but no significant effect in men. Studies of men and studies of womenWhat are the similarities and the differences?A workshop involving investigators from longitudinal studies and other researchers compared and contrasted issues, approaches and findings of longitudinal studies of men and women. Identified commonalities and differences between studies of men and women are shown in the Box. The main differences were conditions that could not be experienced by the opposite sex, such as hysterectomy for women and prostate disease for men. However, studies of men had a focus on testosterone and sexual function that was not mirrored by female equivalents. Studies of women measured oestrogen levels and sexual problems in relation to menopausal changes, not in relation to health in later life. Other differences were more subtle. For instance, while prostatism is a male issue, lower urinary tract symptoms are also experienced by women. It was agreed that more emphasis on these symptoms may be appropriate for studies involving women. As a general observation, studies involving men applied a biological framework, whereas studies of women applied a social model. For instance, caring has been emphasised in women’s studies but caring may be an equally important, although different, issue for men. Health after the death of a spouse has also been given greater emphasis in studies of women. Men are more likely to repartner, but this comparison is confounded by the construction of relationships, with men preferring to cohabit and women preferring to live apart from a new partner. Transport and mobility were also identified as major issues for women. This need may be experienced differently by men, for whom loss of a drivers licence may present more than a practical problem of “how to get around”, as it may also lead to depression and general decline. Cross-gender analyses: what are the opportunities?The workshops also explored how longitudinal studies of ageing can be analysed from a gendered perspective. It seems that almost any question on the ageing research agenda can be subjected to a gendered analysis. For instance, comparing genders: Which differences exist at a biological level, and which are socially determined? Does socioeconomic disadvantage have a differential effect on health? Does caring by men and women involve different activities and dimensions? What is the effect of ageing on sexual function, sensuality and spirituality? Is there a differential change in the importance of these outcomes with age? How do men and women engage with the health care system? Does health care need to become more gender-sensitive? Are there differences in diet and nutrition? Does nutrition have a differential effect on health outcomes according to gender? Are the predictors of survival and longevity different among women and men? For example, does comorbidity have a stronger effect in men? Do men and women have different health goals? If health is seen not as an end, but as a means to achieving life goals, then health will have different effects in men and women if their life goals are not the same. Gendered comparisons: simple or complex?However, gendered comparisons may not be as simple as stratifying variables by age and sex. Men and women may exhibit different levels of accuracy and reliability in reporting exposures and outcomes, and many measures have a strong gender bias. For instance, caring appears to have very different meanings and manifestations for men and women. Physical activity has a different nature, context, and inherent value. Even when the same measures can be used, different categorisations may be needed, especially if underlying distributions and associations vary by gender. Further, influences of gender may interact strongly with cognitive status, marital status and other socioeconomic factors. Cohort effects are also likely to be important, with changes in the social meaning of gender over time (for instance, disparities in education, employment, occupation, and assets have changed over the past century). The power that can be achieved by combining data from existing longitudinal studies, as will occur in the Men, Women and Ageing Study referred to above and in the Dynamic Analyses to Optimize Ageing (DYNOPTA) project led by Kaarin Anstey of the Australian National University, will allow robust statistical analysis of gender interactions and, in the case of DYNOPTA, the use of nested cohorts to control for cohort and geographical effects. Closing remarksJulie Byles and Hal Kendig (Faculty of Health Sciences, University of Sydney) noted that the discussion from the conference and the longitudinal studies workshop provided valuable insights into basic gender differences and will inform research for years to come. Sex and gender differences matter not only to the experience of ageing, but are also manifested in the design of the research projects which, to date, have shown a clear gender-specific focus. Participants agreed that gender is more than just a variable to be controlled for in statistical analyses — it needs to be understood within a social context and be included in all future analyses. In this way, we may achieve not only greater understanding but also greater benefits in future clinical practice. Commonalities and differences between studies of men and women identified at the workshop Commonalities Medication Obesity and weight Cardiovascular outcomes (heart attack, stroke) Health risks: smoking and alcohol Diabetes and the metabolic syndrome Falls Fracture and osteoporosis Hearing and vision Anxiety and depression Sleep Other medical history Quality of life Mobility and dependence Housing and neighbourhood Social support Health service availability, access and use Living arrangements and marital status Differences Men (Mars) Women (Venus) Testosterone levels Effects of hormone replacement therapy Hysterectomy Dementia and Alzheimer’s disease Sarcopenia (age-related muscle loss) Incontinence: urine flow Incontinence: leaking urine Lower urinary tract symptoms Dysuria Widowhood Caring Transport Prostate cancer Breast cancer Endometrial cancer Ovarian cancer Erectile dysfunction

Julie E Byles BMed, PhD · Matthew Carroll BA(Hons), PhD · and the Mars and Venus Writing Team

Suffering and healing in America: an American doctor’s view from outside. Raymond Downing. Oxford: Radcliffe Publishing, 2007 (xii + 126 pp). ISBN 978 1 84619 130 5. In an age of increasing disparity between the health systems of rich and poor countries, Suffering and healing in America offers an analysis of how America’s health system can learn from the achievements of those in more poorly funded settings. The author argues that health care in America risks the charge of hubris as it increasingly fails to address the needs of poorer members of the community. Furthermore, Western medicine has so raised the expectations of cure that it has contributed to the loss of capacity to cope with suffering when cure is not possible. He discusses the comparative notions of cure and healing and the evolving role of family medicine within the health care system. While many of the questions the author raises are undoubtedly serious challenges facing health care and therefore worthy of discussion, his subjective analysis rarely penetrates far below the surface of the more complex issues. The author makes heavy going of his cure versus healing discussion but never really mounts a clear argument. The way he uses anecdotes to illustrate certain points is reminiscent of parables, and too often they shed little light on the labyrinthine world of modern health care. The chapter on culture offers perhaps the most pertinent example of this, leaving the reader frustrated by the simplicity of the analysis. The title of the book is itself a curious example of the false trails the author follows: he spends more of the book discussing his experiences as a medical practitioner in Africa than America, and not all the comparisons he makes are relevant given the cultural, social and economic disparities between the two worlds. The repeated pattern of raising topical issues but then not really addressing them undermines the value of the book as anything more than a mildly interesting narrative.

Damien W Morgan

Objective: To study the clinical contexts contributing to harmful medication errors.Design, setting and participants: A qualitative study using semi-structured interviews was conducted between March and August 2005 at Fremantle Hospital, a 450-bed metropolitan teaching hospital. Twenty-six of 46 staff members (57%) identified by pharmacy staff as having contributed to a significant medication error were interviewed. Interviews were recorded and transcribed for thematic analysis.Results: Most errors were due to slips in attention that occurred during routine prescribing, dispensing or drug administration. Knowledge-based mistakes (eg, failure to follow a protocol) also contributed to prescribing errors. Errors were more likely to occur during tasks being carried out after hours by busy, distracted staff, often in relation to unfamiliar patients. Communication problems with senior staff and difficulty accessing appropriate drug dosing information contributed to knowledge-based prescribing errors. Several medical staff were unaware they had committed an error until their involvement with our study.Conclusions: Contextual factors that contributed to slips, lapses and knowledge-based mistakes in our sample are likely to be widespread in hospitals, and their impact on medication error may be substantial. Staff need training in how to recognise and deal with error-prone clinical situations. Safe prescribing practices (eg, the absolute requirement to acquire information before prescribing unfamiliar drugs) must be emphasised. Improved access to drug information at the point of prescribing, attention to communication barriers, and increasing staffing levels in particular areas are other potential strategies for reducing error.

Pamela Nichols PhD · Tandy-Sue Copeland DipPharm · Ian A Craib MB ChB, MRCP, FRACP · Paul Hopkins · David G Bruce BSc, MD, FRACP

Objective: To audit the accuracy of dose administration aid (DAA) packaging in regional aged care facilities (RACFs) within the boundaries of the Hunter Urban Division of General Practice.Design, participants and setting: Each participating RACF audited one DAA for each resident receiving medication between May and August 2006. Registered nurses compared the contents with the medication chart prepared by the general practitioner and recorded any discrepancies as incidents.Main outcome measures: Number of medication incidents in the provision of DAAs.Results: 297 incidents were detected from 6972 packs for 2480 residents (incident rate of 4.3% of packs and 12% of residents) from 42 participating RACFs. Reasons for incidents included medications missing from a pack (99 occasions), wrong medication dispensed (12), supply of the wrong strength (32), incorrect labelling (7), pharmacies supplying medication that had been ceased by the GP (37), incorrect dosage instructions (32), medications not delivered to the RACF (13).Conclusion: The rate of incidents in DAA packaging in RACFs was high. The error types included incorrect packaging, correct packaging but the DAA was no longer required, and operational problems. Recommendations for improvement include: continuing audit and analysis by RACFs; streamlining of communications among GPs, pharmacists and RACF staff; using electronic methods to chart, order and dispense medications; use of generic names as much as possible; development of guidelines for the supply of medication in DAAs.

Annette Carruthers MB BS(Hons), FRACGP, FAICD · Kialie Naughton · Gordon Mallarkey PhD

Objective: To examine mortality from all causes and from cardiovascular disease (CVD), and CVD hospitalisation rate for a decentralised Aboriginal community in the Northern Territory.Design and participants: For a community-based cohort of 296 people aged 15 years or older screened in 1995, we reviewed hospital and primary health care records and death certificates for the period up to December 2004 (2800 person-years of follow-up).Main outcome measures: Mortality from all causes and CVD, and hospitalisation with CVD coded as a primary cause of admission; comparison with prior trends (1988 to 1995) in CVD risk factor prevalence for the community, and with NT-specific Indigenous mortality and hospitalisation rates.Results: Mortality in the cohort was 964/100 000 person-years, significantly lower than that of the NT Indigenous population (standardised mortality ratio [SMR], 0.62; 95% CI, 0.42–0.89). CVD mortality was 358/100 000 person-years for people aged 25 years or older (SMR, 0.52; 95% CI, 0.23–1.02). Hospitalisation with CVD as a primary cause was 13/1000 person-years for the cohort, compared with 33/1000 person-years for the NT Indigenous population.Conclusion: Contributors to lower than expected morbidity and mortality are likely to include the nature of primary health care services, which provide regular outreach to outstation communities, as well as the decentralised mode of outstation living (with its attendant benefits for physical activity, diet and limited access to alcohol), and social factors, including connectedness to culture, family and land, and opportunities for self-determination.

Kevin G Rowley PhD · Kerin O’Dea PhD, AO · Ian Anderson MB BS, FAFPHM, PhD · Robyn McDermott FAFPHM, MPH, PhD · Karmananda Saraswati MB BS, FAMAC · Ricky Tilmouth · Iris Roberts EN · Joseph Fitz · Zaimin Wang PhD · Alicia Jenkins MD, FRACP · James D Best MD, FRACP, FRCPath · Zhiqiang Wang PhD · Alex Brown BMed, MPH, FCSANZ

Donough O’Brien was born on 24 June 1911 in Dublin, Ireland. He was brought up on the family’s country estate in County Limerick and later won scholarships to Bromsgrove School in England and to Trinity College Dublin, where he began a medical course in 1929. He graduated top of his year, with first class honours, in 1934. In 1939, he gained Fellowship of the Royal College of Surgeons (Ireland) and was awarded the Surgical Travelling Prize. At the outbreak of war in the same year, he joined the British Army and spent 7 years as a surgeon in Scotland, Iraq, Egypt, Malta and Sicily. Early in the war, as a Duty Officer at Drymen in Scotland, he admitted and treated a “Captain Horn” for an injured ankle. It quickly transpired that the “captain”, who had flown a plane from Germany and landed in Glasgow, was in fact Rudolf Hess, who had come to the United Kingdom to try to negotiate a peace settlement with Winston Churchill. Donough had married his first wife Pamela in 1941, and his daughter Caroline was born in 1943, but the marriage did not survive his years away on active service. After the war, he undertook postgraduate study in orthopaedics, then spent 2 years in Tanganyika. He later married Lucy Stafford, and in 1951 they emigrated to Scottsdale in Tasmania, where he worked as Superintendent at the Soldiers’ Memorial Hospital. A few years later, with their two sons Bart and Ken, they moved to Burnie, where he worked as Superintendent at the North Western General Hospital. For some years, as the only surgeon on the north-west coast, he was constantly “on call”, but, as the staff and work at the hospital gradually expanded, he had more opportunity to develop his wide range of non-medical skills and interests. Donough and Lucy were allotted a derelict house belonging to the hospital, with an overgrown garden on a steep hillside. Together they restored the garden, which became a place of beauty and solace. As active members of the Burnie Arts Council and the Coastal Arts Group, they shared their garden with writers, artists and actors, and were constant and delightful hosts to their wide circle of devoted friends. Both he and Lucy were artists themselves, Lucy also being a poet. Donough was a skilled sailor, giving much time to the Burnie Yacht Club. There would always be a boat or two under repair in his shed. His passion for sailing was shared with his son Ken, who is now a sailmaker in Adelaide. Retiring from the hospital in Burnie at the age of 65, Donough practised rehabilitation medicine for a further 10 years. In 1976, he was awarded Membership of the General Division of the Order of Australia for services to the community. He and his wife later moved to Adelaide to be near their family, after Lucy had undergone a series of unsuccessful operations for a hip condition. Lucy died in 2005, and Donough died two years later, on 2 August 2007, of heart failure. He is survived by his three children. Donough will be remembered as a fine surgeon, an accomplished artist, writer, sportsman, a loving husband and father, and an inspiration to all whose lives were enriched by his skills and by the warmth of his care and friendship.

Mary L Kille

Autism spectrum disorders (ASDs) are severe developmental conditions that require specialised intervention and lifelong support. Recent increases in ASD prevalence have prompted new initiatives in Western Australia to improve the consistency of assessments and to more accurately monitor diagnostic trends within the population. WA has implemented statewide guidelines for the assessment of ASDs, has developed an open forum for clinicians to discuss issues relating to the assessment process, and supports a statewide register of newly diagnosed cases. These initiatives have led to improved consistency across assessments, allowed analysis of diagnoses over time, and promoted cohesiveness among autism assessors. These strategies potentially provide an alternative model for other states and territories that wish to strengthen and assimilate ASD assessments.

Emma J Glasson BPsych, BSc(Hons), PhD · Sarah MacDermott BAppSc, MA · Glenys Dixon BPsych, MPsych(Clin) · Hugh Cook AM, MB BS, FRANZCP · Peter Chauvel MPH, FAFRM, FRACP · Alana Maley-Berg BPsych · John Wray MB BS, FRACP

Objective: To assess the outcomes for chronic dialysis patients requiring admission to an intensive care unit (ICU) or high dependency unit (HDU).Design: Retrospective audit of prospectively collected data from local and national databases.Setting: The ICU and HDU at a tertiary referral hospital.Participants: 70 chronic dialysis patients admitted between 2001 and 2006.Main outcome measures: Unit and hospital mortality, recurrent admission patterns and median survival after discharge from hospital.Results: For patients’ last admissions, mortality in the ICU or HDU was 17% and in hospital was 29%. The 12 deaths in the ICU or HDU occurred a median of 18 hours (range, 3–203 hours) after admission, reflecting the severity of their underlying illness. The independent predictors of death in hospital were age and the number of non-renal organ systems failing. Patients with pulmonary oedema had a lower risk of death than patients admitted for other reasons. Although 21 patients accounted for 55 of 104 admissions (53%), recurrent admissions to the ICU or HDU generally occurred during different hospital admissions. They were not associated with a higher risk of death in hospital. Patients discharged home had a median survival of 2.25 years, and a median survival of 3.5 years from starting dialysis. The median survival for patients on dialysis in Australia in general is 4.5 years (Australia and New Zealand Dialysis and Transplant Registry).Conclusion: Dialysis patients discharged home after an ICU or HDU admission have survival similar to that of Australian dialysis patients generally.

Sivagnanavel Senthuran FRCA, FJFICM · Hiran Bandeshe BSc, BEng(Biomed) · Dwarakanathan Ranganathan FRCP, FRACP · Robert Boots PhD, FRACP, FJFICM

Paracetamol is involved in a large proportion of accidental paediatric exposures and deliberate self-poisoning cases, although subsequent hepatic failure and death are both uncommon outcomes. The optimal management of most patients with paracetamol overdose is usually straightforward. However, several differing nomograms and varying recommendations regarding potential risk factors for hepatic injury introduce complexity. In order to reconcile management advice with current Australasian clinical toxicology practice, revised guidelines have been developed by a panel of clinical toxicologists consulting to the poisons information centres in Australia and New Zealand using a workshop and consultative process. This article summarises the rationale for the recommendations made in these new guidelines.

Frank F S Daly MB BS, FACEM · John S Fountain MB ChB · Lindsay Murray MB BS, FACEM · Andis Graudins MB BS, PhD, FACEM, FACMT · Nicholas A Buckley MD, FRACP

Results from recently published clinical trials provide additional information to be considered in the choice of therapies in the management of acute coronary syndromes. This addendum summarises the important findings and their implications for recommended practice. This addendum supplements the recommendations outlined in the National Heart Foundation of Australia/Cardiac Society of Australia and New Zealand “Guidelines for the management of acute coronary syndromes 2006”.1 Results from recently published clinical trials provide additional information to be considered in the choice of therapies in the management of acute coronary syndromes. This new evidence provides additional information that strengthens the recommendations in the guidelines or provides alternatives to current recommended practice that should be considered based on the circumstances of the individual patient and setting. The specific implications of this new evidence on recommended practice are highlighted in the “Implications of the findings” sections of this addendum. Reperfusion and revascularisation for ST-segment-elevation myocardial infarctionImportant findingsThe REACT (Rescue Angioplasty versus Conservative Treatment or Repeat Thrombolysis) study,2 MERLIN (Middlesbrough Early Revascularisation to Limit Infarction) study and a recent meta-analysis3 have demonstrated a decrease in the composite endpoints of death, re-infarction, stroke and heart failure with rescue percutaneous coronary intervention (PCI). The OAT (Occluded Artery Trial)4 trial showed no reduction in death, re-infarction or heart failure during 4 years of follow-up in stable patients with occlusion of the infarct-related artery 3 to 28 days after myocardial infarction who underwent routine PCI. Implications of the findings (Guidelines page S19)Rescue PCIThe evidence for rescue PCI has strengthened since the development of the 2006 guidelines. Patients who receive fibrinolytic therapy and have not reperfused by 90 minutes should be considered for rescue PCI, which optimally should be performed within 12 hours. Transfer between facilities may be necessary to achieve this, and systems need to be in place to facilitate transfer of appropriate patients. If it is not possible for transfer within the 12-hour window, then transfer can be delayed if the patient is asymptomatic. RevascularisationPatients in whom the infarct-related artery is completely occluded do not benefit from re-opening the artery routinely if this occurs more than 24 hours after the initial event. If patients are symptomatic, revascularisation may be considered. Antiplatelet and antithrombin therapyRecent evidence, while providing additional information on outcomes for individual agents, does not provide conclusive evidence of the superiority of one agent over another, nor of one combination of therapies over another. The risks and benefits of these therapies and strategies should be evaluated individually in each patient. Important findingsThe EXTRACT (Enoxaparin and Thrombolysis Reperfusion for Acute Myocardial Infarction Treatment) trial5 demonstrated that, in patients receiving fibrinolysis for ST-segment-elevation myocardial infarction (STEMI), the use of enoxaparin (a low molecular weight heparin; 30 mg intravenous bolus followed by 1 mg/kg every 12 hours in patients younger than 75 years, omission of the bolus but 0.75 mg/kg every 12 hours in patients aged 75 years or older) results in less re-infarction than the use of unfractionated heparin, but is associated with an increase in episodes of major bleeding. The OASIS-6 (Sixth Organization for the Assessment of Strategies for Ischemic Syndromes) trial6 demonstrated that fondaparinux in comparison to no heparin or unfractionated heparin reduces mortality and produces less bleeding in patients with STEMI. Patients treated with fondaparinux who went on to PCI required additional heparin to reduce catheter thrombosis. The OASIS-5 (Fifth Organization to Assess Strategies in Acute Ischemic Syndromes) study7 and the ACUITY (Acute Catheterization and Urgent Intervention Triage Strategy) study8 on the treatment of non-ST-segment-elevation acute coronary syndromes (NSTEACS) demonstrated non-inferiority of two new agents, fondaparinux and bivalirudin, in the treatment of patients with NSTEACS when compared with “standard” antithrombin therapy, but with a significant reduction in major bleeding. The OASIS-5 study demonstrated non-inferiority of fondaparinux (2.5 mg daily) compared with enoxaparin (1 mg/kg twice daily) at the composite clinical endpoint, but reduced the rate of major bleeding at 9 days and reduced total mortality at 30 days and at 6 months. The ACUITY study demonstrated non-inferiority at a composite ischaemic endpoint, but a reduction in the rate of major bleeding and an improvement in the net clinical outcome endpoint when comparing bivalirudin with a glycoprotein IIb/IIIa (GP IIb/IIIa) inhibitor with standard treatment with unfractionated heparin or enoxaparin. The ISAR-REACT 2 (Second Intracoronary Stenting and Antithrombotic Regimen: Rapid Early Action for Coronary Treatment) study9 demonstrated that GP IIb/IIIa inhibition with abciximab administered among heparin-treated NSTEACS patients undergoing PCI and being pretreated with clopidogrel 600 mg, at least 2 hours before intervention, reduces rates of death, myocardial infarction or urgent target vessel revascularisation at 30 days, driven largely by the reduction in myocardial infarction. Following further analysis, it appeared that all of this benefit was evident among the troponin-positive patients. The ACUITY Timing trial10 demonstrated that “in-lab” initiation use of GP IIb/IIIa inhibitors (abciximab or eptifibatide) just before PCI compared with routine “upstream” use (for a median time of 4 hours before intervention with tirofiban or eptifibatide) in high-risk NSTEACS patients could be associated with a 25% increase in ischaemic events, but is associated with a reduced rate of major bleeding. Implications of the findingsAntithrombin therapy for acute STEMI (Guidelines page S14)Enoxaparin and fondaparinux are appropriate antithrombin agents and may be considered for use in patients with STEMI. Antithrombin therapy for NSTEACS (Guidelines page S22)Fondaparinux and bivalirudin, both currently not licensed for upstream therapy of NSTEACS, may be preferable alternatives to standard therapy with unfractionated heparin or low molecular weight heparin with a GP IIb/IIIa inhibitor for patients with high-risk NSTEACS, particularly where there is an increased risk of bleeding. The selection of the most appropriate upstream therapy may best be determined for any individual patient from their risk of ischaemia versus bleeding. Fondaparinux may be particularly useful in patients for whom invasive management is significantly delayed or those not suitable for invasive management. Bivalirudin has the advantage of monotherapy for both upstream and procedural administration at the time of PCI, and therefore may be particularly useful in patients planning to have an early invasive intervention. Antiplatelet therapy for NSTEACS (Guidelines pages S21–S22)GP IIb/IIIa inhibition with abciximab reduces adverse cardiac events in biomarker-positive NSTEACS patients undergoing PCI who have been pretreated with clopidogrel. Pretreatment with high-dose clopidogrel is not an adequate alternative to abciximab among biomarker-positive NSTEACS patients. A deferred in-lab initiation approach to the use of intravenous GP IIb/IIIa inhibitors (particularly with abciximab) may be preferable to short-term (median 4 hours) upstream administration in patients presenting with high-risk NSTEACS.

Constantine N Aroney MD, FRACP · Philip Aylward PhD, FRACP, FCSANZ · Derek P Chew MB BS, MPH, FRACP · Nancy Huang MB BS, DipRACOG, MPH · Anne-Maree Kelly MD BS, MClinED, FACEM · Harvey White DSc, FRACP, FCSANZ · Michelle Wilson BHSc

Probiotics consist of yeast or bacteria, especially lactic acid bacteria. They are available as capsules, powder, fermented milks or yoghurts. Probiotics exhibit strain-specific differences in their resistance to acid and bile, ability to colonise the gastrointestinal tract, clinical efficacy, and benefits to the health of the host. There is level I evidence for the use of probiotics in treating acute infectious diarrhoea and preventing antibiotic-associated diarrhoea, with Lactobacillus rhamnosus GG and Saccharomyces boulardii having the most evidence to support their use for these conditions. There is level II evidence that S. boulardii combined with high-dose vancomycin is more effective than the antibiotic alone in preventing recurrent Clostridium difficile diarrhoea. There is level I evidence that probiotics prevent traveller’s diarrhoea. There is level I evidence for use of the high-potency probiotic VSL#3 in preventing pouchitis, and level II evidence for this agent in preventing relapse in patients with ulcerative colitis. Probiotics are generally regarded as safe and well tolerated. Some probiotics may be contraindicated in patients who are immunocompromised or have severe underlying illness, as they have been reported to cause fungaemia and bacteraemia.

Mimi Pham MB BS · Daniel A Lemberg FRACP · Andrew S Day MD, FRACP

Same time, another place An 8-year-old boy with marasmus presented with poor vision. His right eye had a staphyloma and his left eye a leukoma. He was totally blind in the right eye. His visual acuity in the left eye was only perception of light. Corneal transplantation for his left eye has been planned. The right eye will be enucleated and an ocular prosthesis implanted. Five years earlier, the child was admitted for treatment of kwashiorkor with associated bilateral keratomalacia due to vitamin A deficiency. These ocular sequelae of vitamin A deficiency could have been prevented by its timely supplementation. CommentaryAlthough it is no longer common in Australian Aboriginal communities, malnutrition still occurs in isolated areas. In Australia, keratomalacia of the degree shown here would be exceptional.1 In Africa and parts of south Asia, however, such causes of blindness are not uncommon, particularly among refugees from war and civil strife, where community structure is destroyed, immunisation rates (especially for measles) are low, and malnutrition is common. These circumstances are unfortunately still occurring, exacerbated by climate change, protracted drought and disruption of the normal seasonal cycles of agricultural production. Vitamin A deficiency is common even without kwashiorkor or marasmus, and keratomalacia can be precipitated by an outbreak of measles or acute diarrhoeal disease if vitamin A levels are low. Although blindness in children is far less common than in adults, blind children tend to be blind for longer and have less access to education, and are then less able to contribute to the community and the economy. Such a serious disorder can be avoided entirely by using one of the simplest and most cost-effective public health interventions: vitamin A supplementation. Vision 2020: the Right to Sight (the global initiative of the World Health Organization and the International Agency for the Prevention of Blindness to eliminate avoidable blindness and vision impairment by 2020) prioritises such devastating but needless causes of blindness. This has, through surveillance, advocacy and direct action, led to such sequelae becoming very rare in politically stable countries.

Sunil Karande · Sujit Jagtap · Richard T Le Mesurier

A woman with acute poisoning from extended-release paracetamol presented at 14.5 hours post-ingestion. The paracetamol’s absorption phase and elimination half-life appeared prolonged, with peak blood concentration occurring at 20 hours post-ingestion, requiring an extended course of intravenous N-acetylcysteine. Current treatment recommendations, based on experience with a different formulation in the United States, may not be appropriate for the Australian formulation. Clinical recordA 25-year-old woman, weighing 54 kg and with no other medical conditions, ingested 96 extended-release paracetamol tablets with suicidal intent (total dose, 64 g [1185 mg/kg]). Onset of nausea and intermittent vomiting occurred after a couple of hours, and about 9 hours later she reported the exposure to relatives. The woman was taken to a regional hospital, from where she was transferred to a tertiary hospital for management, arriving 14.5 hours post-ingestion. She was given antiemetics, and an intravenous N-acetylcysteine infusion was immediately commenced (standard regimen: 150 mg/kg over 60 min, then 50 mg/kg over 4 h, then 100 mg/kg over 16 h). A blood sample collected on admission for laboratory analyses showed a paracetamol concentration of 2235 μmol/L. As this concentration is above the treatment line on the Rumack–Matthew nomogram (Box, A), the N-acetylcysteine infusion was continued. Given the limited available data on the pharmacokinetics of extended-release preparations in overdose, blood samples were obtained about every 6 hours to guide treatment. Changes in the blood paracetamol concentration during the patient’s stay are shown in the Box. The maximum concentration (2487 μmol/L) occurred at about 20 hours post-ingestion, and the apparent elimination phase appeared biphasic on visual inspection (Box, B). The apparent elimination half-life was 9 hours between 20 and 34 hours post-ingestion, decreasing to 5 hours between 34 and 48 hours post-ingestion, suggesting that absorption was ongoing during this time. With the exception of intermittent nausea and vomiting, the patient remained clinically well. After 48 hours, the paracetamol concentration had decreased to a non-toxic (therapeutic) concentration and results of liver function tests were normal. The N-acetylcysteine infusion was ceased, and the patient was transferred to a mental health unit. Despite the large paracetamol ingestion and delayed initiation of N-acetylcysteine, no biochemical evidence of hepatotoxicity or other markers of significant toxicity were observed during admission. Mild coagulopathy was noted at 48 hours post-ingestion (prothrombin time, 19 s [reference range (RR), 9–15 s]; international normalised ratio, 1.7 [RR, 0.8–1.2]; activated partial thromboplastin time, 37 s [RR, 23–34 s]; fibrinogen, 1.3 g/L [RR, 1.5–4.0 g/L]), which is not expected to be significant in this clinical setting.1 A mild increase in total bilirubin level (peak, 28 μmol/L [RR, 2–20 μmol/L]) was also noted, but other liver function test results remained within reference ranges. DiscussionIngestion of paracetamol is one of the most common causes of acute intentional self-poisoning in Australia. Management is well described, and includes consideration of gastrointestinal decontamination and administration of intravenous N-acetylcysteine. The decision to administer N-acetylcysteine is based primarily on the plasma concentration of paracetamol and time of poisoning in relation to the treatment line on the Rumack–Matthew nomogram. Blood paracetamol concen-trations are obtained 4 or more hours after ingestion of immediate-release paracetamol preparations because absorption is largely complete by this time. Patients with a paracetamol concentration above the treatment line should be treated with this antidote, while those with a level below the line do not require treatment.2 N-acetylcysteine is administered as a 20-hour intravenous infusion in the majority of patients. These treatment guidelines reflect clinical experience with the standard immediate-release formulation of paracetamol, with or without coformulants such as codeine or dextropropoxyphene. An extended-release formulation of paracetamol was recently marketed in Australia under three proprietary labels. Each tablet contains 665 mg paracetamol; 31% of the dose is released immediately, while the remaining 69% is released over 6–8 hours at therapeutic doses.3 To determine whether N-acetylcysteine is required in an acute overdose of an extended-release formulation, the manufacturer recommends obtaining an initial paracetamol concentration either on admission or at 4 hours post-ingestion. If this concentration is below the treatment line on the nomogram, a repeat concentration should be determined 4–6 hours later. A 20-hour infusion of N-acetylcysteine is recommended if either concentration is above the treatment line.3 This approach to risk assessment is similar to that recommended for a different extended-release preparation marketed in the United States (650 mg paracetamol; 50% released immediately).4 In volunteer studies of simulated overdose with this US formulation (75 mg/kg orally), the time of peak concentration was similar to the immediate-release formulation, occurring within 4 hours.5,6 However, a study of simulated acute overdose in volunteers using the Australian product (mean dose, 73 mg/kg) found that the absorption phase is prolonged — compared with the standard immediate-release formulation, the time until the maximum concentration occurred was delayed for the extended-release formulation (0.94 v 2.83 hours).7 These differences in absorption kinetics between the Australian and US formulations might influence treatment guidelines. Reported cases of acute overdose with the US formulation have noted that the peak concentration may actually occur up to 12 hours post-ingestion, suggesting that the pharmacokinetics of extended-release paracetamol change substantially in acute overdose.8-12 To our knowledge, no cases of acute poisoning with the Australian formulation of extended-release paracetamol have previously been reported. It is therefore not known whether the current recommendations for treatment are appropriate. Absorption may be sufficiently prolonged in acute overdose of extended-release paracetamol that the peak plasma concentration occurs around 20 hours post-ingestion. In this patient’s case, the only data point earlier than this was at 14.5 hours, when the concentration was already extremely high (Box). Given the amount ingested, it seems likely that at least one of the blood samples that the manufacturer recommends obtaining within 8–10 hours of ingestion would have prompted treatment with N-acetylcysteine. However, due to the lack of data during this period for our patient, this cannot be confirmed. Of importance in this case is the prolonged apparent elimination half-life of paracetamol, such that the concentration remained elevated for 48 hours post-ingestion. This required the N-acetylcysteine infusion to be administered beyond the usual 20-hour protocol that is recommended by the manufacturer and used for immediate-release preparations. The duration of N-acetylcysteine infusion in this patient was guided by the serial blood samples taken about every 6 hours. In the absence of more informative pharmacokinetic data, it seems reasonable that serial blood samples (every 6–12 hours) should be obtained from patients presenting with ingestion of the extended-release formulation, to guide duration of treatment. The absorption kinetics observed in this patient suggest that the ingested tablets formed an aggregate (a pharmacobezoar) in the gut from which absorption is very slow. Therefore, administration of activated charcoal and, potentially, whole bowel irrigation might be considered, even in cases of delayed presentation.13 On the basis of this case, the treatment of acute poisoning with the extended-release formulation of paracetamol differs from recommendations developed for the immediate-release formulation. While it appears reasonable to continue to use the Rumack–Matthew nomogram for determining which patients require N-acetylcysteine, more than one blood sample may be required to confirm that an exposure is non-toxic. Intravenous N-acetylcysteine infusion can be initiated according to the standard regimen, and should be continued until the paracetamol concentration has decreased to a therapeutic level (less than 120 μmol/L or 20 mg/L) if the transaminase concentrations remain normal. If the transaminase levels are rising, N-acetylcysteine should be continued. This can be determined by blood samples taken every 6–12 hours, depending on the time of day, location of the patient, laboratory services available, and compliance of the patient. If the infusion is required for longer than 20 hours, this should be done by continuing the final phase of the regimen (ie, N-acetylcysteine 100 mg/kg bodyweight in 1000 mL of 5% dextrose over 16 hours) until a therapeutic paracetamol concentration is achieved. More experience in the management of acute poisoning with the extended-release formulation of paracetamol is required to better determine the optimal treatment. Linear (A) and logarithmic (B) paracetamol concentration–time profiles after ingestion of extended-release paracetamol, with reference to the treatment line on the Rumack–Matthew nomogram t1/2 = apparent elimination half-life (determined using non-linear regression with a monophasic decay, with GraphPad Prism, version 4.03 for Windows [GraphPad Software, San Diego, Calif, USA]).

Darren M Roberts MB BS · Nicholas A Buckley MD, FRACP

Clinical records Patient 1 In March 2005, a 58-year-old man was referred by his general practitioner for evaluation of a central scotoma with macular sparing in his right eye of 6 weeks’ duration, noticed during reading as a sort of shadow following his point of fixation. He had had no previous ophthalmic complaints and had worn spectacles to correct moderate myopia since the age of 12 years. His health was excellent; he was on no medication and had never had a surgical procedure. Both parents had lost vision from glaucoma. For this reason, his intraocular pressure (IOP) was monitored by his brother, an optician. Over 4 years, repeated IOP measurements of under 22 mmHg had been obtained by non-contact tonometry in both eyes. On examination, visual acuity was 6/6 in both eyes. IOPs of 38 mmHg in the right eye and 30 mmHg in the left eye were obtained by applanation tonometry. A non-contact method yielded pressures of 28 mmHg in the right eye and 22 mmHg in the left eye. Further examination showed open anterior chamber angles and a myopic optic nerve head which was pathologically cupped on the right side and “suspicious looking”, with elongated vertical cupping on the left (Figure A). Later, automated visual field testing showed a large central defect in the right eye, almost reaching the point of fixation (Figure B). The left eye was normal. Therapy with eye drops (timolol/dorzolamide fixed combination, twice daily) was started, which stabilised the pressure at around 10 mmHg in both eyes. The patient’s brother, who had never consulted an ophthalmologist, was advised to do so. He showed no signs of glaucoma. Patient 2 A 69-year-old man presented in June 2005 with slowly deteriorating vision over several years. For the previous 2 months, he complained of bumping into objects in his path. He had never experienced eye pain and had been healthy all his life. His mother, whom he had accompanied to the GP and ophthalmologist for many years, had eventually become blind from glaucoma when very elderly. His sister went blind from glaucoma at the age of 65 years. Twenty-five years earlier, the patient had been seen by an ophthalmologist who saw no signs of glaucoma during a routine examination. The patient claimed that he had never been told to have regular eye checks for glaucoma, and had not done so. On examination, visual acuity was light perception in the right eye and hand movements at 2 m in the left eye. IOPs by applanation tonometry were 53 mmHg for the right eye and 49 mmHg for the left eye. Gonioscopy showed open anterior chamber angles. Both optic nerve heads were completely cupped (Figure C). Visual field examination showed no vision in the right eye and a temporal island of vision in the left eye (Figure D). In an attempt to preserve his remaining vision, medical therapy (timolol/dorzolamide fixed combination, twice daily and latanoprost, daily) was instituted, which stabilised pressures at below 18 mmHg in both eyes. He has noticed no further decline in vision since presentation. The two cases we present here are good examples of how the diagnosis of glaucoma is often missed because of lack of history-taking and/or insufficient clinical examination. Glaucoma is the second leading cause of blindness worldwide;1 nevertheless, knowledge of this disease is poor among the general population as well as among health professionals.2 Primary open-angle glaucoma (POAG) is a chronic and progressive optic neuropathy that causes visual field loss, eventually leading to complete blindness. It can be present for a long time before patients have symptoms. About half of those affected with glaucoma are not aware they have the disease.3 While the most important risk factor for POAG is elevated intraocular pressure (IOP), pressure is only one component of a constellation of findings that define POAG. Glaucoma is a specific optic neuropathy, characterised by optic nerve head cupping and usually associated with (arcuate) visual field loss. Glaucoma may be associated with elevated IOP, but can be diagnosed irrespective of the IOP, so IOP is no longer considered part of the diagnosis. Established risk factors for POAG (besides elevated IOP) are higher age, African ethnicity, a positive family history, thinner corneal thickness, and myopia.1 Diagnostic clues include gonioscopy (visualisation of the drainage angle), characteristic changes in the optic nerve head (cupping — elongation of the optic cup in a vertical direction, as result of, typically inferior, notching of the neuroretinal rim that will be the first sign of POAG), and characteristic (mostly midperipheral) defects on visual field testing. To date, the only effective evidence-based treatment for glaucoma is decreasing IOP;4 any local or systemic risk factors should also be addressed. Lessons from practice All primary care doctors should ask their patients about a family history of primary open-angle glaucoma (POAG), which is an important risk factor for this disease. Patients with POAG should be told to alert their first-degree relatives to the need for an adequate glaucoma screening. “No visual symptoms” does not equal “no POAG”, as visual field defects occur mainly at advanced stages of the disease. Pain is seldom a symptom in POAG (it is associated with acute angle closure glaucoma). About a third of patients with POAG have so-called “normal tension glaucoma”; this will not be detected by measuring intraocular pressure alone. Examining the optic disc is much more important for a correct diagnosis of POAG than measuring intraocular pressure. It is critical to note that symptoms occur late in POAG. If a diagnosis is based only on symptoms, advanced irreversible vision loss is likely. Patients with POAG need to be identified early, which requires a high level of suspicion, adequate screening and prompt referral. In many countries, primary eye care is provided by general practitioners and eye specialists. In others, this role is fulfilled by optometrists. Unfortunately, many health care workers, including (in our experience) even some ophthalmologists, only look at IOP when considering glaucoma as a diagnosis, as in our Patient 1. Over a third of patients with glaucoma have an IOP within the average range (10–21 mmHg).5 They have “normal tension glaucoma” in which, despite an IOP that is not elevated beyond the arbitrary upper limit of 21 mmHg, the optic nerve can show pathological cupping, and the visual field examination can show characteristic defects. These patients will easily be missed if diagnosis is based on IOP. Moreover, some health care workers tend to use non-contact tonometry to measure IOP. Such tonometry tends to underestimate the true pressure, which is more accurately measured with a Goldmann applanation tonometer (Haag–Streit International, Koeniz, Switzerland).6 We emphasise that examination of the optic disc is much more important for a correct diagnosis of POAG than IOP. However, measuring IOP remains important, as our Patient 2 would have been diagnosed by screening IOP alone. We also emphasise that pain is seldom a symptom of POAG. Pain is a feature of acute angle closure glaucoma, in which the IOP reaches very high levels in a very short time because of acute blockage of the drainage angle; this is not a feature of POAG. Family history played an important role in both our patients and should have been investigated during history-taking. First-degree relatives of patients with POAG have a risk about 10 times greater than for people with no family history of glaucoma.7 However, relatives are often unaware of their risk, sometimes even decades after treatment is initiated in their family.8 Patients with primary glaucoma should be advised to alert relatives to the need for adequate glaucoma screening and follow-up. We believe awareness of POAG among the general population (as well as among health care professionals) is poor at best. To increase awareness in the general population, primary care health professionals in particular need a better understanding of this disease. We believe that asking about a family history of glaucoma as a part of an ophthalmic history, or as part of a general medical history, should be routine in all new patients. First-degree relatives of patients with POAG should be advised to be screened by an ophthalmologist or optometrist. Depending on ophthalmic findings, age and other risk factors, first-degree relatives should have a full ocular evaluation on a regular basis (eg, every 2 or 3 years, or more frequently if findings are equivocal). This simple step, and a timely referral can prevent much disability and associated cost for individual patients and the community.

Richard H C Zegers MD · Erik F Reinders MD · Marc D de Smet MD, PhD

To the Editor: In their report of a child with peanut allergy who developed sunflower seed allergy, Hsu and Katelaris caution against marketing claims of “safe alternatives” in allergic children.1 Their report also raises practical issues for those advising the parents of a child with food allergy: what is the risk of a new allergy developing; should a child with peanut or tree nut allergy avoid similar foods as well; and will food avoidance prevent new allergy from developing? The natural history of peanut and tree nut allergy is for polysensitisation to develop over time. One study demonstrated that, in children younger than 2 years with peanut or tree nut allergy, 19% were sensitised and 2% were clinically reactive to more than one nut.2 By the age of 14 years, the percentages had risen to 72% and 47%, respectively. This has led to people with peanut or tree nut allergy being advised to avoid all nuts and seeds.2 Strategies commonly advised to reduce the risk of allergy developing are to avoid food allergens and to delay the introduction of allergenic foods until the age of 2 years, but evidence to support their effectiveness is limited,3 particularly for preventing food allergy.4 While studies in infants at high risk of allergic disease have reported an increased risk of eczema with early introduction of solids (before the age of 3–4 months),3 and a protective effect against asthma and eczema with the avoidance of environmental and food allergens in the first 6 months of life,4 a recent systematic review found “no strong evidence to support the association between early solid feeding and the development of persistent asthma, persistent food allergy, allergic rhinitis, or animal dander”.5 Furthermore, there is currently no evidence that avoidance strategies applied beyond 6 months of age are effective for allergy prevention, and provisional evidence that such strategies might actually promote sensitisation and food allergy rather than tolerance.6 So how should we advise patients? The peanut and tree nut avoidance strategies advised will be largely dictated by: choking hazards in infants; the risks of cross-contamination in commercially prepared foods; and the potential for confusion in young children (and caregivers) trying to differentiate one “nut” product from another. Regarding the risk of developing new food allergy, we should advise patients that: new allergies may develop with time; this risk is unpredictable; we have little evidence to recommend avoidance beyond the age of 6 months as an effective preventive strategy; and parents should not be optimistic (given the current state of knowledge) that such strategies will prevent new sensitisation once food allergy has developed.

Mimi Tang · Raymond J Mullins

To the Editor: The case reports presented by Gunja et al1 are a serious concern from many perspectives. The health authorities should be commended for their rapid risk assessment and alerting the community, which led to the immediate withdrawal and recall of the toy beads from the marketplace. However, the question needs to be asked: Could this situation have been prevented, and if so, how? There are many toys in Australia that potentially pose risks to children. These can include physical dangers, such as the size of toys, with risk of choking, to toxicological dangers, as we have seen with Bindeez toy beads (containing 1,4-butanediol), and psychological and social concerns, such as the effects of sexually provocative toys on young girls and “aggressive” toys (which may encourage violence) on young boys. More research is required to test the psychological influence of such toys on children. The evidence should be used in the development of guidelines for safer toys. At present, toy manufacturers in Australia must adhere to the Australian Toy Standard (AS/NZ 8124), established by Standards Australia.2 Toys are monitored and regulated mostly by the state governments. While the manufacturers are expected to adhere to these standards, they are in fact voluntary standards and self-regulated, and many toys can enter and be sold in Australia without meeting these standards. When a consumer or state government inspector is concerned about the safety of a toy, or if it violates the regulation, they may contact one of the state offices of fair trading, which have the power to remove the toy from the marketplace. This is essentially a post-hoc auditing system and plays an important role in safety, but action is essentially taken after a problem is detected, such as is the case with the Bindeez toys. In view of potential concerns, I believe what we need in Australia are stronger regulations and guidelines that we can provide to manufacturers to help produce safer toys. Our efforts should be towards preventing any potential harm by strengthening existing regulations, establishing consistent national and international standards for all imported toys, providing more resources for the verification and testing procedures and more expertise and wider consumer input into the safety and suitability of the types of toys permissible in Australia. We have a duty to protect and safeguard our children from both psychological and physical dangers.

Vicki Kotsirilos

To the Editor: Australia, like many other nations, is experiencing an epidemic of overweight and obesity. The most recent National Health Survey reported that 62% of men and 45% of women were overweight or obese.1 Among numerous associated concerns is the cost burden of obesity-related illnesses on individuals, the community and the health system. Among the 45–54-years age group (the stage at which osteoarthritis becomes a significant health problem), we calculated the population attributable risk (PAR) for osteoarthritis associated with obesity to be 25% for men and 22% for women, using a relative risk (RR) of 2.4 and obesity estimates of 23.3% for men and 20.1% for women. In terms of major health sequelae of the epidemic, this is second only to obesity-related type 2 diabetes (RR, 3.2; PAR, 34% for men, 31% for women). Some obese patients will have multiple obesity-related comorbidities. In 2005 in Australia, 2551 national hospital separations among people aged 45–54 years were for obesity-related osteoarthritis.2 Using data from the three most recent National Health Surveys, we projected the likely prevalence of obesity among 45–54-year-old Australians in 20251,3,4 and then estimated future hospital separations and direct health system expenditure, using costing information supplied by the Australian Institute of Health and Welfare.2 We project that in 2025, if Australians born between 1971 and 1980 maintain their current rate of weight gain, the proportion of obese 45–54-year olds will rise to 38.8% of men and 32.2% of women. The estimated number of hospital separations for obesity-related osteoarthritis will increase to 4216. The direct health system cost (in current dollars) will rise to $44.4 million, from an estimated $25.5 million in 2005. The 45–54-year-old population comprises a considerable proportion of the workforce, and obesity-related illness impacts on absenteeism5 as well as individuals’ and families’ quality of life. As the current generation of young adults ages, a trend toward increasing illness arising from high levels of obesity is likely, unless health and government policy initiatives to prevent weight gain are given higher priority.

Margaret A Allman-Farinelli · Robert J Aitken · Lesley A King · Adrian E Bauman

To the Editor: I write in response to two articles published recently in the Journal.1,2 Both propose that substitution of doctors with paramedical professionals is reasonable. I disagree. I think it is imperative that before doctors decide to only see the “fun” patients, we had better be sure we want to surrender our status in the health care system. In the report by Oldmeadow and colleagues,1 as a result of workload constraints, the proposition is made to have physiotherapists run and manage an orthopaedic clinic. By the patient-to-doctor ratio in the study, the average load per week for each doctor was four new and five old patients in a 3-hour clinic. Perhaps readers will compare that load with their own. The study’s outcomes are a cause for concern. Recommendations for management and treatment by two physiotherapists were compared with those of an orthopaedic surgeon. If the surgeon’s opinion is deemed to be correct, then over 25% of the patients who attended these clinics would have been treated incorrectly. In addition, 13% of the physiotherapists’ assessments were not only wrong, but the management plans did not include referral to the surgeon. Remember, this was a highly artificial, simplified clinic treating a limited range of conditions. Consider what the error rate would be in an open clinic with no restrictions on the patients to be seen. In the same issue of the Journal, Smith and Baird proposed that radiographers are qualified in some way to read images.2 While radiographers are skilled technicians, in no way would their interpretive skill be equal to that of a general practitioner, radiologist, or consultant in any other specialty. We should not lower standards for the sole reason of speed of access. I would advocate focusing on consolidating the education of GPs, and so empower them as a group. GPs with special interests could equally act as the gatekeepers to clinics. It is unfair to foist the decisions on care, which are our duty, onto other professionals who are not as extensively trained as we. The job of a surgeon is not to operate on patients. It is rather to organise the care of patients who have a problem in the area of our specialty.

Jeffery M Peereboom

In reply: Peereboom appears to ignore reality. Recent news media1 gave an insight into the state of radiological services at some Sydney teaching hospitals. Thousands of images have never been seen by a radiologist. Yet, all of those images were seen by radiographers, who also saw the patients. I am frequently asked by doctors for my opinion about radiographs. At times, I volunteer my opinion to junior doctors and general practitoners. Thirty years of experience tells me that, if I don’t, they miss abnormalities, delaying treatment and decreasing the quality of care. Peereboom will have worked with radiographers capable of accurately interpreting radiographs. Today, many Australian radiography students have tertiary entrance scores in the 90s. Arguably, the only reason we cannot teach them to formally give their opinion on radiographs is because of a professional boundary drawn in the sand in the 1920s.2 However, the sand is shifting under the health care system. I have the greatest respect for radiologists’ knowledge, skills and intellectual capacity. However, an advanced practice role for radiographers is not just about respect. It is a human resource issue. Knowing that the current service model is antiquated, do we wish to limit the potential of both radiographers and radiologists in the future?

Tony N Smith

To the Editor: We read with interest the recent article by Oldmeadow and colleagues.1 Patients on waiting lists have long waits and poor quality of life,2 and we are currently piloting a similar model for assessment of patients referred for orthopaedic opinion for hip and knee arthroplasty.3 In keeping with other authors, the article by Oldmeadow and colleagues provides encouraging data to support role substitution. However, we suggest that important issues need to be addressed before wide-scale adoption and expansion of the model. More information is needed about the proportion of all referred patients eligible for the physiotherapist assessment, and the cost–benefit figures for “avoided” orthopaedic consultations. It is quite difficult to evaluate the outcomes given the exclusion criteria, which are common comorbidities in these settings. While the κ statistic implies concordance between two physiotherapists and one surgeon, the disagreement was still about one patient in four. Of course, this level of disagreement may also be found between surgeons. However, for a new health intervention, such discordance needs to be understood within an appropriate evaluation framework. What level of diagnostic error are consumers prepared to accept from any health care provider? The article reports five episodes of disagreement between the physiotherapists and the surgeon, where the need for surgery, medical treatment or further imaging was missed; this represents 13.2% of patient assessments (were there multiple missed opinions in individual cases?). The fact that a patient refused surgery is irrelevant if that decision was not identified a priori before surgical referral. Every consumer has the right to accept or reject recommendations about care based on the best available information about potential benefits and harms. An important role of specialist medical providers is that of diagnostician, particularly when there are multiple or complex conditions. Changes to the management of common musculoskeletal conditions should not reduce opportunities for expert input when required. Waiting times for many patients are clinically and ethically unacceptable and we agree new service delivery models are necessary. We suggest that: professional groups work together to develop agreed evidence-based protocols for triage, assessment, investigation and management of common musculoskeletal conditions; funding providers and health care organisations develop and evaluate new models of care, including their cost-effectiveness, and provide appropriate training and monitoring to ensure role redefinition is associated with maintenance of equal or better quality and safety of care; and a musculoskeletal clinical network be developed to support these objectives.

Caroline A Brand · Richard H Osborne · Ian P Wicks · Richard N de Steiger

In reply: The proportion of patients who, after being referred to specialist orthopaedic surgeons by general practitioners, are then listed for surgery, is around 20%–30%.1-3 In our trial, the diagnostic and management concordance between the physiotherapists and surgeon for this group was very high. It was also high for the 63% for whom evidence-based physiotherapy was appropriate. Management discordance occurred when surgical treatments that are controversial, and variously used by surgeons (as noted by Brand and colleagues), were recommended. It is important to note that the 74% agreement between the surgeon and physiotherapists in our trial was achieved under research conditions, with the physiotherapists screening independently. We suggest that the physiotherapist clinic be co-located with that of the surgeons, to facilitate further investigations, enhance the pathway to surgery and manage safety concerns. The advantages of a physiotherapist screening clinic are in (i) triaging out from waiting to see a surgeon, patients predicted to benefit from non-surgical interventions (including those not willing to consider surgery at the time) and (ii) triaging patients in to the appropriate non-surgical care. We agree that patients with degenerative, osteoarthritic conditions, for whom joint replacement surgery may be the eventual treatment, will be best managed through multidisciplinary care.

Leonie B Oldmeadow · Harvinda S Bedi · Hugh T Burch · Jenni S Smith · Edmund S Leahy · Miron Goldwasser

To the Editor: The concerns expressed by Byard and colleagues about “safe-sleeping messages”1 are based on the assumption that bed-sharing (mother and baby sleeping on the same bed surface) is intrinsically dangerous. While some case–control studies have shown increased mortality for young (but not older) bed-sharing babies of non-smoking mothers, more detailed studies have found excess risk only among parents affected by alcohol, extreme overtiredness, overcrowded housing, or where the sleeping environment was unsuitable, including prone or side sleeping, heavy bedding, waterbeds and sofas.2 Epidemiological studies support the safety of bed-sharing. For example, in Hong Kong and mainland China, bed-sharing is very common, but rates of unexpected infant death are extremely low. This implicates aspects of Western lifestyle and sleeping practices — including the V-shaped pillows (tri-pillows) highlighted by Byard et al, other suffocation and entrapment hazards, and maternal smoking — rather than bed-sharing per se. Bed-sharing is also the evolutionary norm, providing many opportunities for “mutual regulation” of maternal–infant physiology, including body temperature, sleep cycle and breastfeeding.3 Modern bed-sharing mothers may appreciate the more restful sleep and easier breastfeeding. Overnight sleep laboratory studies of bed-sharing and solitary-sleeping mother–baby pairs show that bed-sharing mothers are very aware of their baby’s presence, even in deep sleep, and move to avoid overlaying. Bed-sharing babies breastfeed more frequently, but with equivalent total sleep for mother and baby.3 Researchers note the rarity of unsafe prone positions among breastfeeding, bed-sharing infants.3 Other studies have shown increased rates and duration of breastfeeding among bed-sharing mothers and infants.4 For these reasons, bed-sharing has become more popular in Western cultures, with an Australian survey in 2000 finding around 40% of young babies bed-sharing for at least part of the night.5 As with other aspects of care, it is our duty as health professionals to discuss the risks, benefits and practicalities of bed-sharing so that parents can make an informed and safe choice. The Royal Australasian College of Physicians comments, “Co-sleeping or bed-sharing is common and associated with increased breastfeeding rates, longer and more restful sleep, and a protective posture and synchrony of mother with baby . . . All parents should be informed about how to safely co-sleep with their infants”.6 Safe bed-sharing recommendations are available from websites such as the UNICEF UK Baby Friendly Initiative.7

Sarah J Buckley

In reply: Our position on bed-sharing was not based on the assumption that it is intrinsically dangerous, but that there is an increased risk of mortality for bed-sharing babies of “parents affected by alcohol, extreme overtiredness, overcrowded housing, or where the sleeping environment was unsuitable” (to quote Buckley). These risk factors were not mentioned by the telephone health advice line quoted in our letter,1 which rather commented that mortality in bed-sharing babies was such a rare event that the caller should not worry about it — little consolation if a fatality occurred. We agree completely that parents need to be able to “make an informed and safe choice”, but this also requires informing them of potential dangers — which did not happen. Also, we do not agree that mothers are always aware of the presence of their babies, as reports of accidental suffocation during breastfeeding in bed clearly demonstrate.2,3 An informed decision is made when all the information has been provided, not just information that supports a particular point of view. Curiously, Buckley’s final point is to recommend a website for safe bed-sharing advice4 that states quite clearly (with italics): “the safest place for a baby to sleep is in a cot by your bed”. We concur.

Roger W Byard · Glenda Cains · Helen Noblet · Maxine Weber

To the Editor: Since graduating from medical school in 2004, I have dutifully read the Medical Journal of Australia. I was initially intrigued to read sporadic letters to the Editor in which authors, when commenting on current issues in medical education and clinical practice, referred to what happened “in our day”. Topics have included anatomy (eg, dissections), Latin and Greek lessons, teaching methods and hours worked. At times, I feel that the new generation of doctors, of which I am a part, must justify how we can work as medical professionals given our presumed inadequate knowledge. I believe that the skills I learned while at university have enabled me to successfully manage patients who not only have complex medical problems treated with numerous medications, but often require more support to be provided when at home. My training has taught me to solve problems and resource answers using multiple modalities and resources, at the same time keeping abreast of rapidly evolving medical theories and treatments. I do so while also facing the current economic challenges of rising insurance premiums, housing costs, and concerns about global warming. I did not learn Greek or Latin at school, but I did learn to touch type, design a database and formulate a spreadsheet. In my day, when electronic interfaces involved with patient care are changing rapidly, these skills have greatly enabled me for work in the 21st century.

Sara L Barnes MB BS

A modern chimera An Australian paediatric liver transplant recipient has created world news by taking on the immune system of her organ donor. The female patient, now aged 15 years, suffered acute fulminant hepatitis after a non-specific viral illness at 9 years of age for which liver transplant was performed. The postoperative course was complicated by acute biliary obstruction, profound lymphopaenia, haemolytic anaemia, and cytomegalovirus (CMV) infection. Over the following 12 months, clinicians were surprised to discover that the recipient’s immune system appeared to have undergone complete haemopoietic chimerism, resulting in tolerance of the liver allograft. The recipient has taken on the blood type of the donor and lost antibody responses to measles and mumps, against which she had been previously immunised. All immunosuppressive therapy has since been withdrawn and the patient remains well, with no evidence of graft-versus-host disease and normal liver function. The authors comment that the profound lymphopaenia experienced by the child and the immunosuppressive effects of therapy, in combination with the early CMV infection, may have contributed to the engraftment of donor cells. N Engl J Med 2008; 358: 369-374 Big headaches for small people Treating childhood migraine can be difficult, but it appears that only a few medications are effective, according to the results of a meta-analysis of randomised controlled trials. Canadian researchers analysed the findings from 11 clinical trials including over 3000 participants. The trials assessed the effects of paracetamol, ibuprofen, sumatriptan, zolmitriptan, rizatriptan, and dihydroergotamine. Only ibuprofen and sumatriptan showed statistically significant pain relief and relief from headache in paediatric migraine patients. The researchers suggest a trial of ibuprofen prior to sumatriptan in the management of acute paediatric migraine. J Paediatr Child Health 2008; 44: 3-9 Antipsychotics for aggression Although a common practice, there seems to be little evidence supporting the use of antipsychotic drugs in the management of aggression in patients with intellectual disability, say British and Australian researchers. In a randomised controlled trial, 86 patients with aggressive challenging behaviour were randomly allocated to three groups, each receiving haloperidol, risperidone, or a placebo for 26 weeks. Outcome measures included change in aggressive and aberrant behaviour, quality of life, and the feelings of the carer responsible for the person treated. Assessments were made at 4, 12, and 26 weeks after randomisation. Aggression decreased substantially in all three treatment groups by 4 weeks, with the placebo group showing the greatest change. There was no difference between the treatments in relation to the other outcome measures. The authors comment that although antipsychotic drugs may have some place in the treatment of people with intellectual disability, it appears that routine prescription of such medications early in the treatment of aggressive challenging behaviour is not warranted. Lancet 2008; 371: 57-63 An aspirin a day... Some people appear to be “resistant” to aspirin; their platelets are not affected in the same way as those who benefit from therapy. People with a resistance to the effects of aspirin appear to be at a greater risk of cardiovascular morbidity than those who are sensitive to aspirin, according to the results of a systematic review and meta-analysis. Using mainly studies in which compliance with aspirin therapy was confirmed, Canadian researchers conducted a meta-analysis of results to determine the effect of aspirin resistance on cardiovascular events. In total, 28% of the 2930 patients studied were reported as aspirin resistant; these people were at a greater risk of a cardiovascular-related event, a new cerebrovascular event, or death. The authors comment that the lack of an acceptable platelet-related assay of aspirin resistance hinders research into the phenomenon. BMJ 2008; 336: 195-198 Vitamin E for older people Keeping older people active and independent is a common goal of clinicians and public health officials alike. There is little evidence of the effect of poor nutrition on physical function and the role of nutrition in the disablement process. An Italian study has set out to asses the effects of serum micronutrients on physical function in older people and has come up with some interesting results. The 3-year longitudinal study included 698 people aged 65 years or older living in the community in Tuscany, Italy. Serum micronutrients including vitamins E, B and D, iron, and folate were measured. To assess function, researchers used the Short Physical Performance Battery, a standardised measure of the aetiology and progression of functional decline and disability. A low concentration of vitamin E appeared to be associated with a subsequent decline in physical function. The researchers suggest that vitamin E, acting as a lipid-soluble antioxidant, plays a role by neutralising free radicals and minimising oxidative damage to tissues. JAMA 2008; 299: 308-315

Tanya Grassi