Volume 182 Issue 6

We need a patient safety initiative that captures the imagination of politicians, professionals and the public Nearly 10 years have elapsed since the Journal published the ground-breaking Quality in Australian Health Care Study (QAHCS)1. With its disturbing findings, the study seared “patient safety” into the public’s psyche. The QAHCS methodology focused on the safety aspects of healthcare quality, without providing systematic data on other domains, such as access, efficiency and acceptability, and provided only some insight into effectiveness and appropriateness of care. The role of QAHCS was to estimate the size and nature of the problem of unsafe healthcare. . . . the absence of recent system-wide data on patient safety . . . makes a mockery of the tenets of continuous quality improvement. Now, 10 years on, most patients in our healthcare system do not suffer preventable harm, and receive good care. But it is still possible that up to 16% of hospitalised patients will suffer an adverse event: 50% of these events will be preventable and 10% of these preventable events will lead to permanent disability or death.1 Studies from the United Kingdom,2 Canada,3 Denmark,4 and France,5 using similar methodology to the QAHCS, indicate that Australian healthcare is no safer than that provided in these countries. The magnitude of the problem worldwide is reflected in the World Health Organization’s recent launch of the Patient Safety Alliance,6 which aims to improve patient safety in all 192 member nations. What has been achieved since the release of the QAHCS? In 2000, 5 years after the study’s release, the Australian Council for Safety and Quality in Health Care (ACSQHC) was formed to provide leadership in improving patient safety and quality through advice to all federal, state and territory health ministers. The ACSQHC has championed an extensive work program,7 including: developing an “open disclosure” standard for patients and their families when care processes go wrong; developing a national standard for credentialing and defining the scope of practice of medical practitioners; involving consumers in improving healthcare safety by producing the booklet Ten tips for safer health care: what everyone needs to know; establishing a national Centre for Research Excellence in Patient Safety; testing strategies to ensure safer medication use at the point of care by involving more than 100 healthcare facilities in the National Medication Safety Breakthrough Collaborative; introducing the “Ensuring correct patient, correct site, correct procedure protocol” to reduce “wrong site” or “wrong patient surgery” and launching a “high risk medication alert” on the use of concentrated potassium chloride solutions in hospitals. Furthermore, each state and territory has developed peak advisory bodies, and many elements of patient safety programs (eg, the reporting and investigation of serious incidents) have been incorporated into hospital practice in all states and territories. Professional bodies such as the Royal Australasian College of Physicians have strengthened activities for maintenance of their members’ professional standards,8 and hospitals and other healthcare facilities have formed committees and created departments to oversee patient safety activities. All this has involved considerable effort and resources. However, much of the investment has been in “top down” activities (in the form of policy or monitoring) rather than “bottom up” activities. This can result in a considerable gap between what patient safety strategies are supposed to have been implemented in the workplace and what strategies are actually in place. Instances of poor healthcare outcomes for individual patients, or adverse events involving particular hospitals, have rightly been highlighted in the media. The outcries reached deafening crescendos when perceived healthcare “scandals” in three Australian jurisdictions were revealed.9 This year, the NSW government’s Patient Safety and Clinical Quality Program released the “First report on incident management in the NSW public health system 2003–2004”10 452 incidents were reported that were regarded as “very high risk, can result in serious patient harm, and must be followed by immediate action . . .” This followed a similar report by the Victorian government in 2004.11 Ten years on can we confidently state that healthcare is safer for patients? Unfortunately, the answer is no. There is insufficient information at a state or national level to determine whether any or all of the efforts over the past 10 years have increased safety in our hospitals. It is regrettable that we have not measured the frequency of adverse events in Australia in a way that allows us to assess how we have fared since 1995; how we compare with other countries; and whether any of the initiatives described above have been effective in reducing patient harm. Given the truism we “manage what we measure”, the absence of recent system-wide data on patient safety seriously hinders our ability to manage the problem and make improvements. Its absence makes a mockery of the tenets of continuous quality improvement. We need a thorough understanding of the strengths and weaknesses of data derived from medical record audits, voluntary reporting systems, clinical indicators, and existing large datasets if we are to seriously tackle the size and nature of the problem, and determine whether a particular intervention or program has been successful in improving safety. This information gap is recognised in the 2005 national productivity report on government services.12 Despite all the developments in the last 10 years, and in the context of the current Australian Health Ministers’ review of the governance arrangements for safety and quality of healthcare,13 there are still four areas that require more action and greater urgency. Leadership — to provide clarity of vision and the will to change. As part of that leadership, we need an explicit and agreed goal, such as “to eliminate preventable patient harm from healthcare within 10 years”. A recent challenge from Don Berwick — the 100 000 lives campaign — is to avoid 100 000 preventable deaths in the United States between January 2005 and July 2006 and every year thereafter. The campaign aims to enlist thousands of hospitals across the US in a commitment to implement changes in care that have been proven to prevent avoidable deaths.14 Transparency — fears that open discussion will reduce patient trust in the healthcare system, leading to patients failing to present for care in a timely manner, seem to be unfounded.15 Measurement — to provide information about where to direct our improvement efforts and whether our interventions have been effective. Dependence on voluntary reporting systems will lead to a gross and inconsistent underestimate of the size of the problem. Improvement tools — there is a body of evidence on methodology for improvement projects at the local level, from the pioneering contributions of W Edwards Deming and Walter A Shewhart to the more recent Institute for Healthcare Improvement’s Breakthrough Collaborative methodology,16 which, through a collaborative learning model involving multiple organisations, helps health professionals to bring about breakthrough improvements in patient care outcomes. There has been a lack of appreciation that the use of tested methods increases the likelihood of success of a particular project. Hence, many efforts have not delivered their full potential, or discussion and learning have been prevented because successful efforts have not been publicised. The failure to successfully implement existing knowledge or policy is a worrying characteristic of healthcare systems,17 and demands greater rigour. Creating this capacity within our organisations is a major challenge to be addressed. The responsibility is on all of us — politicians, health administrators, clinicians and the public. Finally, the governance arrangements for transparency of performance of health service delivery, and the accountability for that performance at an individual, organisational, state and national level, need public negotiation and agreement. Currently, there seems to be an imbalance: much more attention is being paid to the accountability of individual healthcare providers than to improving healthcare safety at an organisational and whole-system level. Of equal importance is that the ACSQHC appears to have limited relevance to or influence on the daily lives of health professionals. It is sorely in need of an initiative that captures the imagination of politicians, professionals and the public.18 It could do no better than to emulate the US Institute of Medicine’s “Crossing the quality chasm” healthcare quality initiative19 by selecting a limited number of clinical conditions which have a high healthcare burden and resource use, and which clinicians agree are high priority. The task then is to apply the six aims for healthcare improvement to management of patients with these clinical conditions — their healthcare should be safe, effective, patient centred, timely, efficient, and equitable.18 Finally, the process must be driven from the bottom up. Alternatively, joining the Berwick challenge to save 100 000 lives by reducing unsafe healthcare could have a galvanising influence.14 The magnitude of the challenge of eliminating preventable patient harm is daunting, the progress slow, and the need for our efforts to be successful huge. A significant increase in resolve on the part of all Australians, regardless of their role in healthcare, is needed if we are to meet the challenge of eliminating preventable patient harm over the next 10 years.

Ross McL Wilson MB BS, FRACP, FJFICM · Martin B Van Der Weyden MD, FRACP, FRCPA

Using clinical trials to assess long-term drug safety is problematic; in Australia, simple data linkage based on Medicare numbers may provide useful monitoring information The era of pharmaceutical medicines began with the synthesis of acetylsalicylic acid (ASA) in the late 19th century. The reason for its synthesis was that natural salicylic acid was irritating to gastric mucosa, and the synthesised product less so. Subsequently, more potent non-steroidal anti-inflammatory drugs (NSAIDs) were introduced and, more recently, cyclooxygenase-2 (COX-2) inhibitors, also with a lesser risk of gastric irritation and bleeding. 1 The rapidly widespread and often prolonged use of these agents meant that even a small increase in the risk of a serious adverse event could be very significant in population health terms. This theoretical concern became a reality when rofecoxib (a COX-2 inhibitor) was found to confer an increased risk of cardiovascular disease — a risk uncovered in a trial to determine whether rofecoxib could prevent the recurrence of colorectal polyps. 2 Subsequently, the United States Food and Drug Administration has issued warnings on the cardiovascular safety of celecoxib and naproxen.3,4 More recent information links long-term use of celecoxib and short-term use of parecoxib and valdecoxib (though non-significantly for the latter two) with adverse cardiovascular events. 5,6 This is consistent with a class effect. Although the mechanism underlying the increased cardiovascular risk with COX-2 inhibitors is unknown, there is a biological rationale that might have predicted it and which, in retrospect, should have led to intense postmarketing surveillance of these inhibitors. The non-selective COX inhibitors (ASA and NSAIDs) inhibit platelet aggregation, whereas selective COX-2 inhibitors do not. 7 Selective COX-2 inhibitors may also be prothrombotic through prostacyclin, which has a markedly enhanced action in atherosclerosis.8 The widespread use of COX-2 inhibitors has been part of the historic trend from short-term use of drugs to treat acute conditions to prolonged use of drugs to treat symptoms and prevent disease. This change has brought to light shortcomings in the current methods of drug safety monitoring. In the past, the linchpin of postmarketing surveillance has been the spontaneous reporting system in which doctors, pharmacists and others report recognised adverse reactions to drugs. However, this mode of reporting is useful only for detecting narrow spectrums of adverse events, particularly those occurring soon after drug administration or those that have overt effects (eg, rash, hepatic inflammation or blood dyscrasia). This spontaneous reporting is particularly unsuitable for long-term monitoring of drug safety. These realities are poorly appreciated by healthcare professionals, who often assume that, in comparison with older drugs, a newly registered drug has superior short-term and long-term safety.9 However, the events with the COX-2 inhibitors, which follow on the heels of similar, unsuspected concerns about anti-arrhythmic therapy and hormone replacement therapy, has again highlighted the need for a more systematic approach to long-term safety monitoring of long-term drug therapy.10,11 The accepted gold standard for establishing the balance of long-term drug safety and efficacy is the controlled clinical trial. In 2005, it should not be possible for any long-term medicine to be approved without the security of a large-scale morbidity–mortality trial, or the commitment of the pharmaceutical industry to perform one as soon as practicable. Licensing should be conditional on these requirements being met, and the onus should be on regulators to make these changes in the interests of both the end-users and the pharmaceutical industry. However, even large-scale morbidity–mortality trials have their limitations. They are very costly to establish, and ethical considerations may preclude the use of placebos. Comparisons with other active drugs may be difficult to interpret, as illustrated by the comparison of rofecoxib and naproxen.1 Study inclusion criteria may lead to the exclusion of patients with comorbidity or polypharmacy, and yet these individuals are both more likely to be prescribed drugs and be at higher risk of adverse reactions. In addition, it has proven difficult to continue large-scale trials beyond 5–6 years, so adverse events with prolonged latency, such as malignancy, may not be identified. A solution to long-term drug safety monitoring might include observational epidemiology. Methods must be developed for early identification of users of new drugs and their subsequent disease history determined by data-linkage to various mortality and morbidity databases (such as hospital admissions, cancer and death registries). The inclusion of Medicare numbers on prescriptions in Australia provides a simple means for participation in these studies. An ongoing hurdle is the issue of confidentiality. We do not claim that data-linkage will provide a foolproof answer to drug safety issues. The future mortality and morbidity experiences of any cohort of drug recipients may be influenced by the underlying disease for which the drug has been prescribed. This makes it desirable to have one or more control groups (typically individuals receiving a different drug for the same disease) for comparison. Even if there are control groups, there may still be confounding by differences in indications or contraindications. Therefore, the gathering of linkage data is often relatively low grade, retrospective and useful mainly as a screen for further study if an unexpected finding arises. Such linkages were used in the US to bring into question the cardiovascular safety of rofecoxib before the VIGOR trial.12 Large linked databases are increasingly seen as the only reliable means of gaining the information necessary for monitoring long-term drug safety.13 Our unified healthcare system in Australia, with its standardised Medicare numbers and national databases, has the potential for providing Australia with a strategically important role in this crucial area of drug research.

Mark R Nelson PhD, FAFPHM · Andrew M Tonkin FRACP, MD · Flavia M Cicuttini PhD, FRACP · John J McNeil PhD, FRACP

The annual death toll from tuberculosis in the Indian Ocean region is 2–3 times higher than the toll from the recent tsunami A major earthquake measuring 8.9 on the Richter scale occurred off the west coast of Sumatra on 26 December 2004. 1 The quake even caused the earth to wobble in orbit. 2 The ensuing tsunami hit countries bordering the Indian Ocean. The estimated death toll exceeds 220 000. 1 The human and economic tragedy was evident to all, and national governments and international organisations have mounted an enormous relief effort. Coincidentally, seven of the tsunami-affected countries (India, Indonesia, Thailand, Bangladesh, Burma–Myanmar, Tanzania and Kenya) are among the 22 nations with the highest burdens of tuberculosis (TB). 3 Over three million new TB cases and 772 000 TB deaths occurred in these seven countries in the year 2000. 3 Similar annual statistics have been reported from these and other high-burden countries for more than 10 years. But the earth does not move! The human and economic toll is not appreciated, and an enormous global response is not mounted. The global TB situation is full of such paradoxes. It also highlights the global inequities in the distribution of healthcare services and other resources. 4 An estimated 8.3 million new TB cases and nearly 2 million TB deaths occurred worldwide in 2000. 3 Ninety-five percent of the TB cases and 98% of the deaths were in low-income countries. 4 Importantly, from Australia’s perspective, 60% of this global TB burden occurred in our neighbouring countries in South East Asia and the Western Pacific. 3 What is happening in low-income countries? In Africa, 38% of new adult TB cases in 2000 were in people who were HIV-positive. 4 HIV infection increases an individual’s susceptibility to infection and disease progression, and the increased burden of HIV-associated cases may increase TB transmission to those who are HIV-negative. HIV-related TB has swamped TB-control efforts in Africa, where case numbers increased 6.4% between 1997 and 2000. 3 Multidrug-resistant tuberculosis (MDR-TB), defined as Mycobacterium tuberculosis strains with resistance to at least isoniazid and rifampicin, is also perceived as a great threat to TB control. However, only an estimated 273 000 (3.2%) of new TB cases worldwide were multidrug resistant in 2000. 5 Mathematical modelling and other observations based on imperfect data suggest that MDR-TB strains are generally of lower reproductive fitness, and that MDR-TB will remain localised in foci such as the former Soviet Union. 5 Effective TB control in these MDR-TB-endemic foci may require additional measures, such as wider availability of drug-susceptibility testing and the use of second-line drugs under close expert supervision. 5 More mundane factors than MDR-TB are the real confounders of TB control in low-income countries. These factors include inadequate infrastructure (eg, roads, transport, electricity), weak primary healthcare systems, poor laboratory services, and insufficient engagement of private practitioners and other health providers in TB control. 6 A major impediment to TB control that must be highlighted is the lack of trained staff, particularly in HIV-endemic countries, where the epidemic has decimated the healthcare workforce. 6 What can be done in low-income countries? Effective TB control relies on halting transmission through the rapid detection and cure of infectious cases. International targets have been set to detect at least 70% of all new infectious cases and to cure at least 85% of those detected by 2005. 6 Attainment of these goals would result in a decline in TB incidence of 6%–7% per year. The World Health Organization (WHO) and the International Union Against Tuberculosis and Lung Disease have recommended and validated a policy package entitled DOTS to achieve these case detection and cure rates. The DOTS strategy contains five elements: government commitment, accurate diagnosis principally by sputum-smear microscopy, standardised short-course chemotherapy with direct observation of treatment, provision of reliable drug supplies, and systematic program monitoring. 6 Unfortunately, the WHO annual TB reports to 2003 suggest that the global targets for case detection and cure rates may not be met by 2005. Additional initiatives have been recommended, including increasing government stewardship of TB-control programs, engagement of private health practitioners in DOTS programs, and involvement of local community groups. 6 Tuberculosis and HIV-control programs in Africa and other HIV-prevalent areas must also be coordinated and integrated to achieve enhanced TB and HIV case-finding, to institute TB preventive treatment, and to establish interventions against HIV, such as antiretroviral treatment (which will also indirectly control TB). 6 High-income countries with a low incidence of TB, such as Australia, confront different challenges.7 The incidence of TB in Australia was 4.9 cases per 100 000 population in 2003, which is one of the lowest rates globally, and this incidence has remained stable since the mid-1980s.8 However, people born overseas and Indigenous Australians remain at increased risk of TB (with 9.9 and 8.5 cases per 100 000 population, respectively).8 Maintaining awareness about TB among the medical profession and governments is difficult when the overall TB incidence is so low.7 Undergraduate and postgraduate education programs must ensure that clinicians consider TB, particularly in patients from at-risk subgroups.7 Governments must continue funding specialist TB treatment services (including specially trained staff and reliable drug supplies).7 The TB services themselves must realign policies and procedures towards TB elimination, and consider innovative measures for controlling TB in the subgroups who remain at increased risk of TB.7 The National Tuberculosis Advisory Committee has addressed these issues and published a strategic plan that includes performance indicators for evaluating our national TB-control efforts.9 World TB Day on 24 March is a reminder to Australian doctors that TB is not a vanishing disease. Rather, a “tsunami of TB” occurs every year overseas. What can we do? At the clinical level, Australian doctors must “think TB” when seeing patients, particularly those from subgroups at risk of TB. Australia has laboratory and clinical expertise in TB which is being shared increasingly with our neighbouring countries. Finally, we must advocate for the Australian and other governments to provide funds for TB-control programs in our neighbouring countries, as has happened for the tsunami relief effort. Australia must do so for humanitarian reasons and for self-interest.

Ivan Bastian PhD, FRCPA

Identifying these reactions is a good start, now we must focus on managing and preventing them Australia’s voluntary reporting system for adverse drug reactions has one of the highest per capita reporting rates in the world. Reports to the Australian Adverse Drug Reactions Advisory Committee have played a significant international role in identifying previously unrecognised adverse drug reactions (ADRs), such as hepatitis with flucloxacillin and amoxycillin–clavulanic acid. However, in this issue of the Journal (page 267), Burgess and colleagues remind us that, although identifying ADRs is important, managing and preventing them are equally critical. Their study in Western Australia showed that the rate of ADRs associated with hospitalisations in people aged 60 years and over more than doubled between 1991 and 2002. South Australian data for all age groups showed a similar rise and correlated strongly with changes in medication use in the community.3 National data also show increases,3,4 although the correlation with medication use is less clear. As the Australian coding standards allow ADR codes to be applied to any diagnosis, not just the principal diagnosis,5 the WA data may represent all ADRs, not just those linked to admission or length of stay. Efforts to improve coding will have contributed to some of the observed rise as, for example, rates in SA increased in the year casemix funding was introduced. Increases in the number of hospital admissions over time will also have contributed, but the strong correlation with medication use in SA suggests an exposure effect. The rise in ADRs is not inevitable. The Quality in Australian Health Care Study estimated that 43% of adverse drug events were potentially preventable.6 Similarly, an Australian study of ADRs in oncology patients demonstrated that 48% of predictable ADRs were potentially preventable.7 The questions raised by Burgess et al’s study are: why are ADR rates rising and why have we been unable to prevent the rise, given the preventability estimates? Burgess et al suggest the rise represents a failure of the national strategies to improve the quality and safety of medicine use. There are many data available with which to dispute this claim. Over 100 performance indicators are used to routinely monitor the National Strategy for Quality Use of Medicines, with more than 85% of them demonstrating improvements over time and significant development of services and resources.4 The National Prescribing Service (NPS) has driven cultural change about quality prescribing in general practice, with more than 50% of general practitioners now voluntarily participating in initiatives to improve prescribing.8 Improvements in antibiotic, antidiabetic, analgesic and antihypertensive use have been seen, in keeping with NPS messages.8 The Safety and Quality Council are also driving cultural change, supporting the National Medication Safety Breakthrough Collaborative, which has worked with 100 hospitals and over 480 staff. This initiative is now focusing on disseminating knowledge of and sustaining successful practices. What the data on ADRs in hospitals indicate is our failure to focus on management strategies for ADRs as a specific topic within the national initiatives. Quality use of medicines and safety initiatives have generally focused on development of services, appropriate selection of medicines and error reduction. The focus for ADRs has remained predominantly on reporting and identification, with less emphasis on management. To improve ADR management, we must improve our information sources. Product and consumer information list ADRs but usually fail to provide management strategies. Incidence estimates in product information are based on the initial clinical trials and not easily updated when postmarketing surveillance is based on voluntary reporting. Information on the duration of side effects and consumer experience with medicines is also limited. Providing lists of ADRs does little to change behaviour; management strategies are required.9 The data-linkage studies now under way will enable better incidence data to be developed, as well as identify population groups most at risk of ADRs. The newly established consumer reporting service will also facilitate better understanding of consumer perspectives. This must be incorporated into information sources and supported by clear instruction on management. Detection of ADRs in routine clinical practice must also be improved, with more training needed in this area for health professionals. An Australian study of older people considered at high risk of medication misadventure found that 19% had had an ADR which had not been detected in routine clinical care, even though most were using multiple medicines, had comorbidities and were aged over 65 years.10 The other major requirement is to increase participation in services demonstrated to improve use of medicines and to help prevent ADRs. While consumer medicine information is now available for over 2000 products, it is not provided routinely and continues to be regarded negatively among some health professionals, despite consumer calls for information on side effects.11 Home-medication reviews involving general practitioners, pharmacists and patients have been shown to resolve or ameliorate ADRs in 56% of cases.12 However, the 26 000 home-medication reviews undertaken in 2003–200413 represented about 10% of the population likely to benefit from the service. Other multidisciplinary approaches such as clinical pharmacy, hospital discharge planning and case conferencing services have all been shown to reduce adverse drug events,3 but only 13 000 case conferences and 96 000 discharge-planning services were funded under Medicare’s Enhanced Primary Care packages in 2003–2004.14 The latter services account for 3% of hospital admissions involving overnight stays. These services are relatively new, which may contribute to the low uptake. However, their administrative requirements also need to be streamlined, as general practitioners have found them to be bureaucratic and onerous.15 In addition, trying to incorporate new services on top of existing practice may be adding to the burden and low uptake. It may be necessary to redesign general-practice systems to accommodate these new ways of working. Finally, we require a cultural and attitudinal change to the preventability of ADRs and to multidisciplinary practice. ADRs are often considered part of the price to be paid for the therapeutic benefit of medicines. The rise in ADRs despite preventability estimates suggests that we are currently paying too high a price. Preventing ADRs requires active participation by everyone.

Elizabeth E Roughead PhD

Objective: To examine trends in adverse drug reactions (ADRs) in people aged 60 years or over causing admission to or an extended stay in Western Australian hospitals between 1981 and 2002.Design and setting: Secondary data analysis of case series.Patients: 43 380 patients admitted to WA public and private hospitals with an (International Classification of Diseases) ICD external cause code for an ADR, identified by the population-based WA Hospital Morbidity Data System.Main outcome measures: Age-specific, age-standardised and drug-specific rates of ADR-related hospital stays.Results: The age-standardised rate of ADR-related hospital stays increased from 2.5 per 1000 person-years (py) in 1981 to 12.9 per 1000 py in 2002. The largest increases occurred in those aged 80 + years (tenfold in men and sevenfold in women). The most common drug group involved was cardiovascular agents (17.5%), while anticoagulants (7.5%), cytotoxics (7.4%) and antirheumatics (6.8%) were the more specific drug classes most often implicated. ADRs from the last three classes of drugs were still rising at the end of the study, whereas ADRs from corticosteroids and antihypertensives peaked in 1996 and from opioids in 2000.Conclusions: Increases in hospital admissions or extended lengths of stay due to ADRs in WA have continued despite programs to promote rational and safer use of medicines. The sharp increase in ADRs from anticoagulants warrants attention to revised clinical guidelines.

Christel L Burgess BHlthSc(Hons) · C D’Arcy J Holman MB BS, MPH, PhD · Anthony G Satti BEd

Objective: To evaluate the effect on depressive symptoms in cardiac patients of patient-specific advice to general practitioners regarding management of comorbid depression.Design and setting: A randomised controlled trial in four general hospitals in Adelaide, South Australia.Participants: Patients (n = 669) admitted to cardiology units for a range of cardiovascular conditions who were screened and assessed as being depressed according to the Center for Epidemiological Studies Depression Scale (CES-D).Intervention: Inpatient psychiatric review, followed by telephone case conferencing between specialist hospital staff and GPs to provide patient-specific information about the patient’s depression and its management, educational material, and ongoing clinical support.Main outcome measures: Level of depression severity at 12 months post-hospitalisation.Results: On the basis of intention to treat, intervention patients had lower rates of moderate to severe depression (CES-D ≥ 27) after 12 months (25% v 35%, relative risk, 0.72; 95% CI, 0.54–0.96, number needed to treat for benefit, 11). The intervention was most effective in preventing progression from mild depression to moderate to severe depression. The multidisciplinary telephone case conferencing was difficult to implement and, in a post hoc analysis, brief phone advice from a psychiatrist was found to be effective.Conclusions: Screening hospitalised cardiac patients for depression and providing targeted advice to their GPs reduces depression severity 12 months after hospitalisation.

Geoff Schrader PhD, FRANZCP · Frida Cheok PhD · Ann-Louise Hordacre PhD · Julie Marker GDPH · Victoria Wade FRANCGP, MPsych

Objective: To investigate whether Indigenous Australians with cancer have more advanced disease at diagnosis than other Australians, and whether late diagnosis explains lower Indigenous cancer survival rates.Design: Retrospective cohort study.Setting and participants: Indigenous and non-Indigenous people diagnosed with cancers of the colon and rectum, lung, breast or cervix and non-Hodgkin lymphoma in the Northern Territory of Australia in 1991–2000.Main outcome measures: SEER summary stage of cancer at diagnosis (local, regional or distant spread), cause-specific cancer survival rates and relative risk of cancer death.Results: Diagnosis with advanced disease (regional or distant spread) was more common for Indigenous people (70%; 95% CI, 62%–78%) than for non-Indigenous people (51%; 95% CI, 53%–59%) with cancers of the colon and rectum, breast, cervix and non-Hodgkin lymphoma, but for lung cancer the opposite was found (Indigenous, 56% [95% CI, 46%–65%] v non-Indigenous, 69% [95% CI, 64%–75%]). Stage-adjusted survival rates were lower for Indigenous people for each cancer site. With few exceptions, the relative risk of cancer death was higher for Indigenous people for each category of stage at diagnosis for each cancer site.Conclusions: Health services apparently could, and should, be performing better for Indigenous people with cancer in the Northern Territory, and probably elsewhere in Australia. This study has demonstrated that data from cancer registers, enhanced with data on stage at diagnosis, can be used to monitor health service performance for Indigenous Australians in the Northern Territory; similar data is available in other States, and could be used to monitor health service performance for Indigenous people throughout Australia.

John R Condon MPH, FAFPHM · Tony Barnes MSc · Bruce K Armstrong DPhil · Sid Selva-Nayagam FRACP · J Mark Elwood MD

A significant number of Australians are deficient in vitamin D — it is a fallacy that Australians receive adequate vitamin D from casual exposure to sunlight. People at high risk of vitamin D deficiency include elderly people (particularly those in residential care), people with skin conditions where avoidance of sunlight is advised, those with dark skin (particularly if veiled), and those with malabsorption. Exposure of hands, face and arms to one-third of a minimal erythemal dose (MED) of sunlight (the amount that produces a faint redness of skin) most days is recommended for adequate endogenous vitamin D synthesis. However, deliberate sun exposure between 10:00 and 14:00 in summer (11:00–15:00 daylight saving time) is not advised. If this sun exposure is not possible, then a vitamin D supplement of at least 400 IU (10 μg) per day is recommended. In vitamin D deficiency, supplementation with 3000–5000 IU ergocalciferol per day (Ostelin [Boots]; 3–5 capsules per day) for 6–12 weeks is recommended. Larger-dose preparations of ergocalciferol or cholecalciferol are available in New Zealand, Asia and the United States and would be useful in Australia to treat moderate to severe vitamin D deficiency states in the elderly and those with poor absorption; one or two annual intramuscular doses of 300 000 IU of cholecalciferol have been shown to reverse vitamin D deficiency states.

Working Group of the Australian and New Zealand Bone and Mineral Society, Endocrine Society of Australia and Osteoporosis Australia*

An elevated concentration of low-density-lipoprotein cholesterol (LDL-C) plays a causal role in the development of coronary heart disease and ischaemic stroke. Placebo-controlled intervention studies of statin drugs for lowering LDL-C provide clear evidence of cardiovascular disease prevention. LDL-C concentration below 2.5 mmol/L is an arbitrary goal, and recent trials support the benefit of achieving this goal, or even lower levels. Pharmacological treatment is warranted in patients with high absolute risk of future cardiovascular events. Effective monotherapy is available for predominant hypercholesterolaemia and predominant hypertriglyceridaemia, but combination therapy may be required for severe cases or in those with mixed hyperlipidaemia. Side-effects are infrequent and usually mild, but widespread use of lipid-modifying medication demands caution because of the possibility of muscle or liver dysfunction or drug interactions.

Leon A Simons MD, FRACP · David R Sullivan FRACP, FRCPA

Since 1996, an increasing proportion of federal government expenditure has been directed into Australia’s healthcare system via private health insurance (PHI) subsidies, in preference to Medicare and the direct funding of public health services. A central rationale for this policy shift is to increase the use of private hospital services and thereby reduce pressure on public inpatient facilities. However, the impact of this reform process on regional Australia has not been addressed. An analysis of previously unpublished Australian Bureau of Statistics data shows that regional Australians have substantially lower levels of private health fund membership. As a result, regional areas appear to be receiving substantially less federal government health funding, compared with cities, than if these funds were allocated on a per-capita basis. We postulate that the lower level of membership in regional areas is mainly due to the limited availability of private inpatient facilities, making PHI less attractive to rural Australians. We conclude that PHI as a vehicle for mainstream federal health financing has potential structural failures that disadvantage regional Australians.

Buddhima Lokuge MB BS, MPH · Thomas A Faunce LLB(Hons), BMed, PhD · Richard Denniss BCom(Hons), PhD

Death from mushroom poisoning in Australia is rare and usually due to liver failure produced by Amanita phalloides. We report a 53-year-old woman in Queensland who died from an acute muscarinic syndrome 10 hours after eating mushrooms belonging to the genus Rubinoboletus. To our knowledge, this is the first death in Australia caused by non-amatoxin-producing mushrooms. It highlights the need for awareness of non-amatoxin-producing mushrooms as potentially lethal. Reports of significant morbidity or mortality from mushroom ingestion in Australia have predominantly involved the “deathcap” mushroom (Amanita phalloides),1,2 which contains amatoxins that cause hepatic necrosis and often renal failure. Most of these reports have come from Victoria and the Australian Capital Territory.1,3 We report a death in Queensland after mushroom ingestion producing a severe muscarinic syndrome. The mushrooms involved were identified as Rubinoboletus sensu lato pro tempe, from the bolete group, which includes several species known to produce muscarine. Clinical recordA 53-year-old woman, originally from Switzerland, presented to a community hospital with a 2-hour history of headache, chest and abdominal pain, recurrent vomiting and profuse sweating. Symptoms began suddenly about an hour after she had eaten two large mushrooms which had been collected from bushland near her home and partly cooked. The mushrooms were growing near the base of trees, including both native and introduced species. The woman was previously well, with no significant medical history, and did not take prescribed or alternative medication. Her partner had eaten a small amount of the same mushrooms but rapidly vomited them. He had no toxicological sequelae. On presentation, 3 hours after eating the mushrooms, the patient was flushed, with profuse sweating, vomiting, diarrhoea and confusion (Glasgow Coma Score, E3 M5 V4 = 12/15). Her condition deteriorated rapidly. She developed hypotension (systolic blood pressure, 60 mmHg) and bradycardia (heart rate, 30 bpm). The Glasgow Coma Score fell to 5/15 (E1 M3 V1). Her pupils were constricted but equal and reactive to light. Arterial blood gas analysis revealed severe mixed metabolic and respiratory acidosis (pH, 6.7 [reference range {RR}, 7.35–7.45]; HCO3, 8 mmol/L [RR, 22–33 mmol/L]; Paco2, 55 mmHg [RR, 35–45 mmHg]; base excess, − 28 mmol/L [RR, − 3.0 to 3.0 mmol/L]; arterial lactate, 13 mmol/L [RR, < 1.3 mmol/L]). The patient was intubated and ventilated. Fluids were administered (3 L crystalloid and 2.5 L colloid), along with intravenous atropine (2 mg) and an adrenaline infusion. She was transferred to a tertiary hospital intensive care unit for further management. On arrival at the tertiary hospital, 7 hours after ingesting the mushrooms, she remained in shock, with mean arterial pressure of 40 mmHg and heart rate of 50 bpm. She was treated with high-dose adrenaline and noradrenaline infusions (up to 50 μg/min), further intravenous atropine (12 mg in boluses) and fluid loading (total 3 L colloid), intravenous sodium bicarbonate solution (100 mL, 8.4% solution), metaraminol (total, 20 mg), calcium chloride (200 mg total) and glucagon (6 mg total). Two doses of activated charcoal were given via a nasogastric tube an hour apart (total, 100 g). Despite maximal doses of inotrope infusions, the heart rate remained at 50 bpm and mean arterial pressure at less than 60 mmHg. Dialysis was begun in an attempt to correct the severe acidosis. However, after about an hour of dialysis and despite ongoing maximal supportive therapy, the patient developed asystole. Resuscitation was ceased 10 hours after mushroom ingestion. Autopsy was performed at the Queensland Health Scientific Services Forensic Pathology facility. External examination was unremarkable. Internal examination revealed small, bilateral, straw-coloured pleural effusions, bilateral diffuse pulmonary congestion and a small focus of acute pulmonary haemorrhage within the right lung. The liver had a pale cut-surface appearance, and histological examination revealed centrilobular congestion and collections of neutrophils within the sinusoids, but no associated hepatocellular necrosis. No underlying disease or other pathological findings were identified. Toxicological analysis of blood collected post mortem detected midazolam, lignocaine and atropine (used during intensive-care admission before death). Neither alcohol nor α-amanitin was detected. The patient’s partner provided samples of the remaining uncooked mushrooms, and further similar mushrooms were collected from the bushland for identification. They belonged to the bolete group and were identified in consultation with the Queensland Herbarium as Rubinoboletus sensu lato pro tempe (Box). DiscussionTo our knowledge, this is the first reported death in Australia from poisoning by a mushroom other than A. phalloides. This patient had many of the classical features of muscarinic poisoning, which is characterised by cholinergic-receptor agonist activity. Features include hypotension, bradycardia, vasodilation, bronchospasm, bronchorrhoea, headache and tremor secondary to the hypotension, excessive salivation, abdominal cramps, vomiting and watery diarrhoea. Urinary incontinence, confusion, miosis and impaired visual accommodation may also occur.4 Some muscarinic compounds have a more histaminic effect, with flushing, hypotension and bronchoconstriction.5 Muscarinic compounds are found in a number of species of mushrooms. These compounds are typically thermostable, with a quaternary configuration, and do not cross the blood–brain barrier. They therefore do not cause direct central neurotoxicity. As muscarine does not contain an ester linkage, it is not metabolised by plasma cholinesterase. Some muscarinic mushroom species produce mild, self-limiting symptoms, while others have severe parasympathomimetic effects, as seen in our patient. Most commonly implicated in severe cases of poisoning are Inocybe and Clitocybe spp.6 Boletus and Rubinoboletus spp. also belong to the group of muscarine-producing fungi, but a search of the English language literature has revealed no previous reports of severe toxicity or death caused by Rubinoboletus spp. Deaths from muscarinic mushroom poisoning have been reported in Europe, involving Inocybe and Clitocybe spp.5,6 Most were in children with cardiac or pulmonary disease. The lethal dose of muscarine for humans is not precisely known, with estimates ranging from 40 mg to 495 mg (the latter equivalent to 150 g of fresh Inocybe mushroom).2 Boletes, including the Rubinoboletus sp. implicated in this case, form mycorrhizal (symbiotic) relationships with trees, including hardwood species and conifers. Boletes appear similar to the gill fungi (such as the commonly grown Agaricus spp.) in having a cap and stalk. However, unlike the gill fungi, they carry their spores in tubes opening onto the underside of the cap rather than on radial gills. The underside of the cap thus appears covered in tiny pores, hence the common name “fleshy pore fungi”. Hepatotoxicity and hepatic necrosis are not typical of muscarinic poisoning. In our patient, the postmortem histopathological features of the liver were non-specific. In the absence of hepatocyte necrosis, an acute toxic hepatitis cannot be definitively diagnosed. The changes indicated a reactive process and may have been secondary to hypoperfusion, representing ischaemic injury as a pre-terminal event. Australian doctors need to be aware that some mushrooms contain substances that cause severe muscarinic symptoms, which may result in severe illness or death. There is little evidence for treatment strategies in mushroom poisoning, and the role of gastric decontamination is unclear. Atropine, a rational antidote, has been used successfully to treat less severe poisonings with muscarine-producing mushrooms.7 Mushroom implicated in a fatal ingestion Mushroom (Rubinoboletus sensu lato pro tempe) found at the same place as the ingested mushrooms and identified as similar by the partner of the deceased woman. (Photograph courtesy of Nigel Fechner, Queensland Herbarium, Brisbane, QLD.)

John L Pauli MB BS(Hons), BSc(Hons) · Carole L Foot MB BS(Hons), FACEM

Clinical record A 6-year-old girl presented to her general practitioner with a red left eye. She reported no pain or irritation, but did have difficulty seeing into the distance with blurring of vision in the affected eye. Associated with this symptom was the onset of neck stiffness with limitation in neck flexion and rotation. This had increased gradually over the preceding month and was most problematic in the morning. There were no associated fevers, rashes, gastrointestinal or genitourinary symptoms. She had been well in the past, was not taking any medications, and her vaccinations were up to date. Her elder sister had been diagnosed with juvenile idiopathic arthritis (JIA) at the age of 18 months, her mother had type 1 diabetes mellitus. A maternal aunt had been diagnosed with rheumatoid arthritis 4 years earlier. Examination revealed inflamed palpebral conjunctivae in the left eye, and mild restriction in the range of neck rotation and flexion. There were no other findings. The patient was diagnosed with conjunctivitis and intermittently prescribed chloramphenicol eye drops over 3 months. The neck discomfort continued over this period, despite physiotherapy. Ultrasonography of the neck showed no abnormalities apart from “unusual lymphadenopathy”. This finding prompted a referral to a paediatric oncologist who believed uveitis should be considered in light of the child’s family history of JIA. She was referred for an ophthalmologist’s opinion. At ophthalmological review, her vision was 6/7.5 in the right eye and 6/12 in the left eye. There was band keratopathy (see Box 1) present in the region of the visual axis and the pupil was adherent to the lens by posterior synechiae. The child’s vision continued to deteriorate to 6/24 in the left eye despite treatment with topical dexamethasone 0.1% and atropine 1%. She was referred to the rheumatology service. The rheumatologist found that the child had an elevated erythrocyte sedimentation rate of 43 mm/hour (normal range, 0–20 mm/hour), but the C-reactive protein concentration was within normal limits at 4 mg/L (normal range, 0–10 mg/L). The antinuclear antibody (ANA) titre was strongly positive at over 1:2560, and showed a homogenous pattern. The double-stranded DNA titre (Farr assay) was within normal limits at < 5 U/mL (normal range, < 11 U/mL). The extractable nuclear antigen screen was negative. Treatment with non-steroidal anti-inflammatory drugs resulted in little improvement, so therapy with oral prednisolone and pulse methylprednisolone was commenced. We saw her when she was admitted for the first of 3 methylprednisolone pulses (625 mg intravenously). Vision in the right eye was 6/9 and in the left it was 6/36. Topical medication was continued and the vision in the left eye improved modestly to 6/24. She was then discharged on topical treatment, and systemic treatment with 2.5 mg methotrexate weekly was commenced. This increased to 7.5 mg weekly over one month. At the most recent review, conducted at the time of the final dose of intravenous methylprednisolone, the vision was stable at 6/6, the intraocular pressure was within normal limits and the anterior chamber appeared quiet, the band keratopathy had partially resolved, but the posterior synechiae remained. The neck symptoms had resolved. Uveitis associated with JIA can have an insidious onset, and is often asymptomatic before sight-threatening complications develop. It is an inflammatory condition of the eye, involving the uveal tract,1 and is frequently not seen until a thorough slit lamp examination is performed. Without a slit lamp one may see an inflamed eye with ciliary injection, and the iris may appear adherent to the lens (Box 2). Anterior uveitis is the most common form of childhood uveitis.2 Anatomically, the inflammation involves the iris and the anterior part of the ciliary body. This form of uveitis is the type most commonly associated with JIA. Less common causes of anterior uveitis include herpetic uveitis, Behçet’s disease and Fuch’s heterochromic iridocyclitis.2 The insidious course and difficulty of diagnosis in preverbal children paves the way for the development of sight-threatening complications. Over time, even low-grade inflammation can lead to cataract, glaucoma, maculopathy and the band keratopathy which was demonstrated in this child. Over 75% of eyes affected by JIA-associated uveitis can develop one or more complications.2 Lessons from practice Uveitis is associated with sight-threatening complications. These complications may have an insidious onset and may initially be asymptomatic. Children with juvenile idiopathic arthritis often have active inflammation without any symptoms and should therefore have ophthalmic screening, as early treatment can be sight-saving. Any person presenting with a persistent red eye and blurred vision should trigger suspicion of a sinister disorder, such as uveitis or acute glaucoma. Early referral to an ophthalmologist for these conditions is imperative. The risk of these complications developing heralds the need to be acutely aware of the signs, and to institute and maintain screening programs for children with JIA. Children with JIA who are at a high risk of developing uveitis, that is, those who have pauciarticular arthritis and a positive titre for antinuclear antibody (ANA) at a young age, need slit lamp examination by an ophthalmologist at 3–4 month intervals. Children with JIA who are assessed to be at a low risk of developing uveitis (ie, those who have a negative ANA titre with systemic disease of more than 4 years duration) should be seen at 12-month intervals.3 The development of uveitis in children with JIA is not uncommon, and a child presenting with unilateral red eye must raise the suspicion of uveitis. However, even in the absence of a red eye, children with JIA may develop ocular inflammation, which, if not detected, can proceed to permanent visual loss. Ophthalmic advice should therefore be sought sooner rather than later. The left eye of our patient with arrows indicating the band keratopathy found at initial review. 2 The eye of another patient with arrows (large) showing the ciliary injection typical of acute anterior uveitis Smaller arrows show areas of the iris adherent to the lens (posterior synechiae).

Shane R Durkin MB BS(Hons) · Theresa M Casey MB BS, GDPH, FRANZCO

A child with atopy produces IgE antibodies after exposure to common environmental allergens. The atopic diseases (eczema, asthma and rhinoconjunctivitis) are clinical syndromes each defined by a group of symptoms and signs. Not all children with atopy will have atopic disease or develop symptoms after exposure to an allergen. Both genetic and environmental factors determine the development of atopic disease. The presence of specific IgE antibodies to environmental allergens is determined with skin prick or radioallergosorbent testing in children with atopy. Test results should be interpreted in the context of the clinical history and further investigations (eg, allergen avoidance or challenge). Management of atopic disease is frequently symptomatic, but it is important to avoid identified allergen triggers. Immunotherapy may be considered in selected school-age children with severe rhinoconjunctivitis. Preventing atopic disease in high-risk infants and hindering progression of disease in children with established disease are the areas of active research.

Michael S Gold MD, FCP, FRACP · Andrew S Kemp PhD, FRACP

Robert J Menz General Practitioner, East Adelaide Healthcare, 296 Payneham Road, Payneham, SA 5070. robert.menzATeahc.com.au To the Editor: “Texting” tendinitis (resulting from excessive sending of text messages via mobile phone) has not been reported in Australia, although a recent article in the Adelaide Advertiser reported a case in Italy. 1 A 13-year-old girl presented to me in mid-January with an acutely tender swelling in the mid-radial aspect of her right forearm. It had been present for about 2 days. There was no history of trauma, or recalled change of activity. Further enquiry revealed that she had been given a mobile phone in December and that the associated plan allowed $100 credit that had to be used between 5 January and 4 February. This equates to nearly 300 SMS messages, or 10 a day, if all available credit were used for sending text messages (although, in this case, some of the credit had been used in making calls). The phone and plan also allowed up to 760 characters per message, instead of the usual 160. The patient had been using only her right thumb to press the keypad, and was using “traditional” rather than “predictive” text input (ie, creating the message one letter at a time, rather than using the mobile’s interpretative software to reduce the number of keystrokes). Examination of the patient’s forearm revealed a firm, tender swelling in the dorsi-radial aspect of the mid-forearm (presumably involving the abductor or extensor pollicis longus muscle). There was pain with resisted thumb and wrist dorsiflexion. A presumptive diagnosis of “texting” tendinitis was made. The condition settled rapidly with explanation and reassurance, rest, application of naproxen gel twice daily for 2 days, and use of both hands to operate the keypad. To my knowledge, this is the first report of this condition in Australia, although other unusual overuse injuries of the hand have been described with Nintendo playing. 2 Perhaps the manufacturers of mobile phones should include health warnings of the risk of overuse injury as part of product labelling.

Robert J Menz

Lourdes I St George,* Daniel Lin† * Obstetrician and Gynaecologist, Suite 4, 36 Belmore Street, Burwood, NSW 2134. † Paediatrician, Westmead Private Hospital, Westmead, NSW. lourdesstgeorgeATbigpond.com To the Editor: A 33-year-old woman, who had borne five children and had had previous caesarean sections, presented in her eighth pregnancy with worsening malabsorption after biliopancreatic diversion for morbid obesity, performed 3 years earlier. Before surgery, she had weighed about 130 kg (height,161 cm; body mass index [BMI], 46 kg/m2); she had gradually reduced her weight to 67 kg. Her surgery had created intestinal malabsorption resulting from the intestinal bypass and from dietary restriction because of gastroplasty. The physiological stress associated with pregnancy worsened her anaemia from protein and vitamin deficiencies, especially fat-soluble vitamins and calcium. She required frequent hospitalisation for intravenous fluids to compensate for dehydration from vomiting and diarrhoea. She was taking oral iron, folate, vitamin D, a calcium supplement, vitamin B12, and having vitamin K injections. Her total weight gain in pregnancy was poor (from 71 kg to 74 kg). At 32 weeks she presented with premature labour and a persistent low fetal baseline heart rate of 90 beats per minute and an unstable lie. She had an emergency caesarean section and delivered a baby boy with a birth weight of 2095 g (average for gestational age). Apgar scores were 7 and 8 at 1 and 5 minutes, respectively; the baby required ventilation for hyaline membrane disease and phototherapy for jaundice, although his blood profile was normal. His clinical course thereafter was uneventful. Obesity (BMI > 30 kg/m2), has become the epidemic of the 21st century, with one in two Australian women being overweight or obese. 1 Morbid obesity (BMI > 40kg/m2) is associated with a 6–12-fold increase in mortality.2 A multifaceted approach is essential for treatment in all patients with obesity, but unfortunately, medical treatment mostly produces short-term weight loss. Thus, bariatric surgery is being performed more frequently. Biliopancreatic diversion has two components: a limited gastrectomy results in reduction of oral intake, inducing weight loss, especially during the first postoperative year; and the construction of a long limb Roux-en-Y anastomosis with a short common “alimentary” channel of 50 cm length, which maintains weight loss long term. Scopinaro, who pioneered this technique, has published long-term results reporting 72% excess body weight loss maintained for 18 years.3 He documented 239 pregnancies in 1136 patients who had undergone biliopancreatic diversion, 25% of whom had been infertile before the operation. During pregnancy, 20% required parenteral nutrition and had fetuses that were small for gestation age. The women had a mean weight gain of 6 kg during their pregnancies, and 80 % delivered babies at term with a mean birth weight of 2.8 kg. 4 From the patient’s perspective, the great advantage of biliopancreatic diversion is the ability to eat a normal diet and still achieve excellent, long-term weight loss. The most serious potential complication is protein malnutrition, with a need to take supplemental calcium and vitamins, particularly vitamin D, lifelong. Because of this potential for significant complications, patients who have had biliopancreatic diversion require lifelong follow-up and pregnancy should be avoided. Ideally this operation should be performed in women who have completed their childbearing.

Lourdes I St George · Daniel Lin

Alexandra A Bennett,* Jo-anne E Brien,† Peter S Macdonald‡ * PhD Candidate, † Professor of Clinical Pharmacy, University of Sydney, Sydney, NSW (address for correspondence: Therapeutics Centre, St Vincent's Hospital, Darlinghurst, NSW 2010); ‡ Associate Professor of Medicine, and Cardiologist, St Vincent's Hospital, Sydney, NSW. sashabATpharm.usyd.edu.au To the Editor: We wish to add our perspective to the article by Phillips et al. 1 Needs identified by GPs included education about the effectiveness and target dosing of angiotensin-converting enzyme (ACE) inhibitors and β-blockers, and improved communication. We wish to highlight the potential roles hospital and community pharmacists have in supporting GPs caring for patients with heart failure. It is expected that by 2010 there will be at least 25 patients with heart failure per GP and 100 per community pharmacy in Australia. A recent review of 100 patients with heart failure discharged from St Vincent’s Hospital (SVH) in New South Wales showed they were taking an average of 9.5 regular medications, two-thirds of which were cardiac medications. 2 Their average age was 70.5 years. They had an average of 7.3 diagnoses, including ischaemic heart disease, atrial fibrillation and osteoarthritis. They were commonly taking amiodarone, warfarin and digoxin. Six per cent of patients had taken cyclooxygenase-2 (COX-2) inhibitors before they were admitted to hospital. 2 While rates of ACE inhibitor (or angiotensin-II-receptor antagonist) and β-blocker use at discharge were high in patients with systolic dysfunction (84% and 65%, respectively), only a minority of patients were taking target doses (27% and 15%, respectively). This highlights the need for good communication between healthcare providers. Discharge letters are often illegible and do not necessarily prioritise issues or detail future management, such as stating whose responsibility it is to up-titrate the dose of ACE inhibitor or β-blocker. Electronic entry of medical information, including e-prescribing (currently being trialled in some hospitals), may assist. Some patients have typed medication cards from a pharmacist on discharge. However, this is not routine practice. Ideally, all patients should receive such cards with supporting information. Copies of this information should be provided for the GP and pharmacist. Such a system would support Australian Pharmaceutical Advisory Council guidelines for continuity of care. Since 2002, a pharmacist has consulted with patients in the SVH Heart Failure Clinic regarding medication and lifestyle issues. Problems identified are referred to the treating cardiologist. A pilot study of this service showed high patient satisfaction (T Hargraves, Pharmacist, St Vincent’s Hospital, personal communication). Such a service could also be provided by community pharmacists, perhaps linked to home medicines review. A pharmacist is also employed by the community multidisciplinary heart failure service based at SVH. These positions support patients and their carers as well as healthcare providers, including GPs, community and hospital pharmacists and nurses. Evidence for such roles for pharmacists is supported by US and UK data. 3 We propose that designs for future models of care for patients with heart failure should incorporate pharmacists.

Alexandra A Bennett · Jo-anne E Brien · Peter S Macdonald

Matthew J Bragg,* Paul Middleton* * Emergency Physician, Prince of Wales Hospital, Barker St, Randwick, NSW 2031. braggmATsesahs.nsw.gov.au To the Editor: We read with interest the case reported by Williamson and colleagues of an adult survivor of near-drowning complicated by cardiorespiratory arrest. 1 This is a remarkable account of survival with near-intact neurological recovery from what was a very bleak initial clinical scenario, and the pre-hospital and hospital personnel responsible for his resuscitation should be congratulated for their efforts. However, the authors’ use of therapeutic hypothermia in this case does not necessarily support their contention that “controlled hypothermia . . . should be used in near-drowned patients who have spontaneous circulation but remain comatose”. As presented, the case illustrates the benefit of supportive care in general, and the use of appropriate controlled ventilation in particular. As the authors noted, “gentle hyperventilation to ‘blow off’ excess CO2” corrected the hypercapnia and acidosis. The graphs of arterial pH, lactate level and Pco2 presented in the report show a linear improvement in all three indices after controlled ventilation, before hypothermia measures were begun. Indeed, the commencement of hypothermia had no discernible impact on these trends. While there is some evidence in the literature for the use of controlled hypothermia after cardiac arrest,2 there is no direct evidence of its benefit for victims of near-drowning. We do not feel that controlled hypothermia can currently be recommended as standard of care for near-drowning on the basis of this single case report.

Matthew J Bragg · Paul Middleton

Jonathan P Williamson,* Stan Braude† * Intensive Care and Respiratory Registrar, † Intensivist, Department of Respiratory and Critical Care, Manly District Hospital, Darcy Road, Manly, NSW 2095. JonowilliamsonATozemail.com.au In reply: We agree that our patient’s survival from the near-drowning incident was primarily attributable to the initial and subsequent supportive care. Clearly, the contribution of hypothermia to his survival cannot be quantified from one case. However, previous studies have shown that the use of controlled hypothermia in comatose survivors of out-of-hospital cardiac arrest improved survival with good outcome. 1,2 These studies did not focus on drowning victims — a study in this group would be extremely difficult — but had neurological recovery in patients with anoxic brain injury as principal outcome. In this sense, it can be argued that the aetiology of the brain anoxia is not in itself important. The Amsterdam World Congress on Drowning in 2002 recommended the use of controlled hypothermia in the comatose near-drowned patient. 3 This is a relatively simple procedure (albeit labour intensive) and is becoming the standard of care in many hospitals for out-of-hospital cardiac arrest. In these hospitals, its routine use in the near-drowned patient would not be difficult. Given the evidence so far accumulated in its favour, and the lack of adverse effects if undertaken correctly, it seems justified to seriously consider its use in the near-drowned patient. We therefore argue that the ventilation and supportive care of our patient aided his physiological recovery, while the neurological recovery was at least partly due to the hypothermia.

Jonathan P Williamson · Stan Braude

Andrew Firestone Psychiatrist, 30 Burke Road, East Malvern, VIC 3145. afireATtpg.com.au To the Editor: The drug company-funded article Diabetes, psychotic disorders and antipsychotic therapy: a consensus statement by Lambert and Chapman1 tests some ethical boundaries. Firstly, although categorised as a position statement, it does not express the position of any professional body. The cumbersome title was probably inspired by a recent landmark review of the same topic.2 But there, the American Diabetes Association (ADA), with others, recommended that prescribers bear in mind the strong association of olanzapine and clozapine with diabetes when choosing an antipsychotic drug. The MJA article does not dispute the ADA data, which rate a brief mention. But — and here is the second, more serious, ethical issue — the key ADA recommendation, that the varying diabetogenic potential of antipsychotic drugs should be a factor to consider when choosing an antipsychotic drug, is not mentioned at all. Instead, the article appears to be trying to use the weight of an impressive consultation process to influence prescribers to ignore the present state of knowledge. One cannot take issue with the Australian recommendations, which echo those of an important North American 2002 conference.3 But the funding source means that the omission of the ADA recommendations is an ethical problem: one must question why they have been omitted. To end on a positive note, the Australian recommendation for a prospective comparison trial of antipsychotic drugs for weight gain and diabetes is certainly a good one. It is high time that a university took this up —and published the results without drug company assistance.

Andrew Firestone

Timothy J R Lambert,* Leon H Chapman† * Director, OPEN (Office for Psychiatric Evaluation and Educational NewMedia), Department of Psychiatry, University of Melbourne, 7th Floor, Charles Connibere Building, Royal Melbourne Hospital, Melbourne, VIC 3050; † Diabetologist, International Diabetes Institute, Melbourne, VIC. lamberttATunimelb.edu.au In reply: Our article did not ignore the relative diabetic potential of various antipsychotic drugs. We wrote “clozapine and olanzapine are associated with greater weight gain and a higher occurrence of diabetes and dyslipidaemia than risperidone and quetiapine”, and so on.1 However, the article was not aimed to influence prescribing habits, but rather to alert health professionals to the relative metabolic risks both inherent in people with psychosis and arising from treatment with antipsychotic drugs in general, and the consequent need for constant assessment. The article tried to emphasise the need to balance risk versus benefit. We also tried to underline the need to effectively treat the illness (ie, the psychosis) with the most appropriate agent. Ignoring this would be akin to not using corticosteroids in severe asthma for fear of metabolic consequences. Finally, the article is a pointer to the full consensus statement, which is available on the Internet at www.psychiatry.unimelb.edu.au/open/diabetes_consensus/ and may be downloaded without charge.

Timothy J R Lambert · Leon H Chapman

Marc M Cohen Professor of Complementary Medicine, School of Health Sciences, RMIT University, PO Box 71, Bundoora, VIC 3083; and President, Australasian Integrative Medicine Association. marc.cohenATrmit.edu.au To the Editor: I read Constable’s article1 on age-related macular degeneration with interest, but was surprised at its somewhat guarded advice on nutritional supplementation and the fact that it gave only passing reference to uncontrolled studies of the carotenoids lutein and zeaxanthin and failed to mention a number of controlled studies that have recently shed light on the potential for these nutrients to influence the progression of age-related macular degeneration (ARMD). Lutein and its isomer, zeaxanthin, are deposited in the macula, where they make up the macular pigments and act as a blue-light filter to protect the underlying tissues from phototoxic damage, as well as providing antioxidant activity. Lutein was not available in supplement form at the time of conducting the Age-Related Eye Disease Study (AREDS).2 However, the more recent Lutein Antioxidant Supplementation Trial (LAST), a double-masked, placebo-controlled, randomised trial of lutein and antioxidant supplementation in people with ARMD, demonstrated that taking 10 mg lutein daily, with or without additional nutrients, improved visual function.3 Interestingly, lutein supplementation was also found to improve vision in a small, randomised, placebo-controlled study of people with cataracts. It was suggested that these improvements were due to improved macular function and increased macular pigment density.4 Furthermore, a recent study showed that lutein supplementation results in increased macular pigment density in both normal and ARMD patients.5 Lutein occurs naturally in foods such as eggs, spinach, romaine (cos) lettuce, broccoli, zucchini, corn, peas and Brussels sprouts. Although lutein is readily absorbed from foods and dietary supplements, surveys indicate that average lutein intake may be below levels that are associated with disease prevention.6 Toxicology studies have established that lutein is generally safe, with potential for use as a supplement in foods and beverages.6 While advice on smoking cessation and increasing fruit and vegetable intake is useful for a wide range of conditions, including ARMD, Constable’s statement that “antioxidant supplements should be recommended if a fresh diet is impractical and if retinal signs of progression are present”1 appears overly cautious. In light of recent findings on the potential benefits of antioxidants such as lutein, and the low cost and minimal risks associated with supplementation compared with the potentially devastating consequences of blindness from ARMD, it may be prudent to make more general recommendations on nutritional supplements, rather than waiting until signs of retinal progression are evident.

Marc M Cohen

Ian J Constable Director, Lions Eye Institute, Centre for Ophthalmology and Visual Science, University of Western Australia, 2 Verdun Street, Nedlands, WA 6009. ijcATcyllene.uwa.edu.au In reply: While the published literature on dietary supplementation with the antioxidants lutein and zeaxanthin is highly encouraging, it does not yet pass the requisite standards for public endorsement provided by large-scale, independent, evidence-based medical trials. The controlled (“LAST”) trial of lutein1 cited by Cohen consisted of just 91 patients divided into three subgroups including the placebo group, who were followed for only 1 year. The measurement of visual improvement on a Snellen chart would not be accepted as “gold standard” evidence by major granting agencies and regulatory affairs bodies, who demand the higher discrimination of a logarithmic visual acuity chart. Moreover, the data were not derived from multicentre trials and independently assessed. It is instructive to compare the methodology of the LAST trial with that of the ARED Study,2 which involved 11 centres, 3640 patients and an average follow-up of 6.3 years. For these reasons, although I mentioned lutein in an encouraging fashion, I did not endorse it to the same extent as vitamin C, vitamin E and zinc supplements. The other reasons for giving limited recommendation of antioxidant supplements at this stage relate to the fact that it is not yet clear to what extent supplements would be beneficial over and above a diet targeted to provide these antioxidants in plentiful supply. It may yet be shown that a nutritious diet — with emphasis on brightly coloured and leafy vegetables, fresh fruits, nuts and fish, coupled with reduced processed vegetable oils (except olive oil) — can, alone, provide substantial protection. While the supplements are generally deemed to be safe, they are not without occasional serious side-effects and have not been followed long term. Richer, one of the authors of the lutein study, 1 acknowledges commercial relationships with the supplement suppliers, and states that the study requires greater numbers and long-term follow-up to be confirmed. Cohen cited a second article3 that refers to a 2-year study of cataract, in which a mere 17 patients were allocated to three subgroups including the placebo group. It is not usual practice to quote conclusions from such a small, and therefore potentially unreliable, trial design. Cohen is right to point to lutein and possibly zeaxanthin supplements as an encouraging possibility for preventing blindness from macular degeneration, and I hope the evident enthusiasm and rapid marketing of lutein proves justified in the long run by forthcoming major trials.

Ian J Constable

Kenneth Wong Surgical Registrar, Gosford Hospital, Holden Street, Gosford, NSW 2250. kennethwoATyahoo.com To the Editor: I am writing to offer a registrar’s perspective on the constructive comments by Lack and Cartmill on registrar–intern interactions.1 The same comments would be equally applicable to consultant–registrar interactions. The current strict hierarchical, “militaristic” structure of the hospital system, with a “top down” approach to performance assessment (which, in turn, influences career prospects), is conducive to neglect of junior colleagues, as they are often the most expendable cogs in the wheel. In my experience, the two key selection criteria for hospital appointments and career advancement — namely, impressing senior colleagues and passing postgraduate examinations — bear little correlation to the ability to supervise or instruct junior staff. Training in human resource management is not part of any undergraduate or postgraduate medical curriculum. Yet, negative junior–senior staff interactions can potentially compromise patient safety, as junior colleagues, acting only as acolytes in the professor’s entourage, are not empowered to actively contribute to patient care. So, what are the solutions? A formal circular feedback system that has “teeth” would be a start. Incorporating regular evaluations of senior staff by junior staff as part of the hospital’s quality assurance program and as a condition of continued employment may be effective in identifying those who are unsuitable for supervising junior colleagues. Simple educational measures may alleviate some of the difficulties experienced by interns as highlighted by Lack and Cartmill.1 For example, the difficulties of contacting surgical registrars “hidden” in the operating theatre are cited as a cause of intern distress. But operating theatres are not located on a distant planet beyond feasible means of contact. Most operating theatres are equipped with telephones and are located centrally within the hospital. Educating the intern to telephone through to the operating theatre or possibly even venture inside should enable resumption of contact with even the most evasive surgical registrar. Finally, published guidelines detailing acceptable behaviours and responsibilities towards junior colleagues may benefit senior staff who may not have had appropriate senior role models themselves. Having a junior colleague attached to one’s team is not an assumed right that comes with consultant or registrar status. It is a distinct privilege that carries distinct obligations. Failure to respect these obligations should precipitate removal of this privilege.

Kenneth Wong

Jeanette I Nordon Retired, 42 Milroy Avenue, Kensington, NSW 2033. To the Editor: I spent a lot of my working life treating patients in an area with an ageing population. I am now elderly and I hear many of my peers complaining bitterly about their doctors. Even if they have a serious illness they are often told, “What can you expect at your age?”. This unhelpful attitude does nothing to alleviate the patients’ concerns. Often, after some questioning, it may be apparent that these patients have some conditions that are eminently treatable and, without this questioning, may be missed. With the advances in medicine and surgery, the proportion of elderly people in our population is increasing. “He or she has had a good innings” was a comment that I heard doctors make in the past. But, doctors change their tune as they age, and these platitudes are much less frequently used! So, in spite of the fact that we are living much longer, with new joints, new transplanted organs, new patent coronary arteries, better means of treating neoplasms, and more exotic investigations to make more exact diagnoses, we must still address our patients in a civil manner, and remember that often the older methods of diagnosis are still important. And don’t let us forget that doctors also get old.

Jeanette I Nordon

CorrectionRe: “Bilateral acute angle closure caused by supraciliary effusions associated with venlafaxine intake” by de Guzman M H P, Thiagalingam S, Ong P Y and Goldberg I in the 7 February 2005 issue of the Journal (Med J Aust 2005; 182: 121-123). In the second paragraph of the “Clinical record”, the number “3” appears, instead of a multiplication symbol, in two places. The second sentence should read “Spectacle correction revealed compound hypermetropic astigmatism (right eye, +1.00 + 1.50 × 75°; left eye, +1.75 + 2.25 × 110°).” In the same article, the initial capital letter (“V”) of the first paragraph after the clinical record box is missing: the first word should be “Venlafaxine”. Similarly, in the article by Ng C V T [page 120] in the same issue, the initial capital letter (“M”) is missing: the first word of the first paragraph should be “Myasthenia”. The html and pdf versions of these articles were correct when published online.

Maria Hannah Pia de Guzman MD, DPBO · Sureka Thiagalingam MPH, MB ChB · Poh Yan Ong MD, MS · Ivan Goldberg MB BS, FRANZCO, FRACS

David Ogilvie White was born in Canberra on 30 August 1931 and died on 7 November 2004 after an 11-year battle with primary biliary cirrhosis. David was Professor of Microbiology at the University of Melbourne from 1967 to 1994. He held various high-level appointments at the university, including Head of the Department of Microbiology, Dean of Research and Graduate Studies, Chairman of the Academic Board, and Pro-Vice-Chancellor. David graduated in medicine from the University of Sydney in 1954 and completed a PhD on influenza virus at the Australian National University in 1958. He was an outstanding teacher of undergraduate students, and was recognised by the University of Melbourne and the Australian Society for Microbiology, each of which has named an annual excellence-in-teaching award in his honour. David’s ability as a mentor for research students and staff was exemplary. He supervised numerous BSc Honours and PhD students and a series of outstanding postdoctoral fellows, with whom he coauthored more than 100 original research papers. In 1992, he was made an Officer of the Order of Australia for “service to education, particularly in the field of microbiology”. David authored six major books on virology, including coauthorship with Frank Fenner of Medical virology, a classic text that is used in medical schools throughout the world. He was an editor of the journal Archives of Virology from 1985 to 1994, and served on the editorial boards of several other international journals. David also held positions on many national and international committees, including Foundation President of the Cell Biology Society of Australia, President of the Australian Society for Microbiology, and Foundation Member of the Commonwealth AIDS Research Grants Committee. David had lifelong interests in ornithology, exploration and wilderness, and was a life member of the Australian Conservation Foundation and the Bird Observers Club of Australia. He was Grand Master of the Australian Bridge Federation, several times Victorian bridge champion, and an Australian pairs champion. Despite his remarkable achievements, David was an extraordinarily humble and self-effacing person. Throughout his life, he voluntarily took on an enormous workload, not for self-aggrandisement or personal gain, but in the firm belief that he could make a difference. Those who were privileged to know him will remember his warm, constant and lively friendship. David is survived by his wife, Marjorie, and their three daughters, Alison, Merran and Rosalind.

Roy M Robins-Browne · Michael J Studdert

Marijuana and madness. David Castle and Robin Murray (editors). Cambridge: Cambridge University Press, 2004 (xvi + 218 pp). ISBN 0 521 81940 7 The relationship between marijuana use and mental illness is a hotly debated topic. Tabloid headlines refer to “supergrass” causing schizophrenia, while alternative lifestyle enthusiasts claim medicinal properties for marijuana. Social conservatives argue it is a pernicious drug that leads to harder drug use, while social progressives use its ubiquity to argue that much of the harm associated with its use comes from its criminalised status. A book that cuts through the polemic and takes a scientific view is most welcome. Castle and Murray are widely published psychiatrists (from Australia and the United Kingdom, respectively). They have assembled 13 chapters, prepared by international experts, examining the links between cannabis use and mental illness, especially psychosis. The book opens with an exploration of exogenous cannabinoids and the endogenous cannabinoid system in the brain. It goes on to explore the links between cannabis use and psychosis, with particular emphasis on schizophrenia. There are also chapters discussing depression and anxiety disorders allegedly associated with marijuana use, and whether there is a specific cannabis psychosis. Two groups explore research linking the endogenous cannabinoid system and schizophrenia. The book closes with contributions of immediate clinical relevance. These examine the motives that sustain cannabis misuse in individuals with psychosis, some strategies for addressing cannabis abuse in this population, and the residual cognitive effects of long-term cannabis use. Despite the dedication “to Francis Ames, whose belief in the potential medical and environmental benefits of marijuana was never obscured by the smoke of political rhetoric”, a balanced approach is taken to the subject. The text is densely written and heavily referenced. A great deal of attention is paid to the careful methodologies and their limitations. The conclusions drawn by each group are understandably cautious. I found this an interesting compilation of research covering a poorly understood area of great clinical relevance. Doctors who work in this field could update themselves on a large body of research by reading this book. With cannabis use continuing to rise and the causes of schizophrenia continuing to elude us, I am sure this will be an expanding field. Joshua D Geffen Psychiatrist, Brisbane, QLD

Joshua D Geffen

Medicines out of control? Antidepressants and the conspiracy of goodwill. Charles Medawar and Anita Hardon. Amsterdam: Aksant Academic Press, 2004 (x + 258 pp) ISBN 90 5260 134 8 When Charles Medawar, a professional consumer advocate in the UK specialising in medicines policy and drug safety issues, first made The antidepressant web available on his Social audit website in 1998, the kinds of concerns he was expressing about antidepressants were very much on the fringe. In 2004, with the publication of Medicines out of control?, the mainstream has moved significantly towards Medawar’s stance. Together with Ralph Nader, Medawar began his career as a consumer advocate in the United States some 30 years ago, and experience has taught him the need for persistence and assertiveness in challenging the prevailing view in psychiatry. Recent scientific publications have largely vindicated his claims that the newer antidepressant drugs cause dependence and suicidal behaviour, and have poor efficacy; that the pharmaceutical industry is in the business of disease promotion; and that much “expert opinion” is compromised. He and his coauthor, Anita Hardon, an anthropologist, begin with a historical overview of psychotropic medications. They describe a recurrent pattern of new “wonder drugs” first hailed as the answer to mental illness, or to addiction, and eventually discarded as ineffectual, habit-forming, or frankly dangerous. The focus then shifts to the newer antidepressants, and the authors discuss the problems of patients who become dependent on the medication; the manipulation by the pharmaceutical industry of the public perception of the need for antidepressants; and the way in which regulatory authorities have failed public health. Medawar was instrumental in drawing attention to the real and significant adverse effects of these newer antidepressants, paroxetine in particular, and for this he deserves praise. One quibble is that he does not always show the same level of healthy scepticism to some of the reports of the apparent side effects of these drugs as he does to their apparent benefits — their capacity to be a “nocebo” does not get as much attention as their placebo qualities. Jon N JureidiniHead, Department of Psychological Medicine Women’s and Children’s Hospital, Adelaide, SA

Coxib class effect? The cardiovascular complications of cyclo-oxygenase-2 (COX-2) inhibitors appear to be a class effect, according to Dr Jeffrey Drazen, Editor-in-Chief of The New England Journal of Medicine (NEJM). Drazen was commenting on three research articles published on the NEJM website that report cardiovascular toxicity data for not only rofecoxib but also celecoxib, and valdecoxib and its intravenous prodrug, parecoxib. The data came from trials designed to test the efficacy of these agents for a variety of indications rather than associated risks. Data for celecoxib came from the Adenoma Prevention with Celecoxib study, a randomised, controlled trial involving 2035 patients in which celecoxib at a dose of 400 mg twice daily was associated with more than a tripling of the risk of cardiovascular events; 200 mg twice daily more than doubled the risk. US experts, who also commented on these results, say we know that COX-2 inhibitors inhibit the production of prostacyclin and favour vasoconstriction, which may increase the risk of cardiovascular events, including myocardial infarction, stroke, hypertension and heart failure. However, we lack adequate information to make confident statements about the exact levels of risk for each COX-2 inhibitor, the time course of the risk during therapy, and the population of patients, if any, in whom the benefits of therapy might exceed the risks. Drazen said it was reasonable to ask whether the use of COX-2 inhibitors can now be justified, given that there are well-established options for the treatment of all the approved indications for these drugs. www.nejm.org Stroke: early discharge Early supported discharge of some stroke patients for rehabilitation at home can offer benefits for both the patient and the healthcare system, say international authors. They conducted a meta-analysis of data from 11 randomised trials from six countries, including Australia, which compared early supported discharge after stroke with conventional care. Patients who received an early supported discharge service were at reduced risk of death and of dependency, experienced fewer adverse outcomes and had improved scores for activities of daily living. The hospital stay for these patients was about 8 days shorter. The greatest benefits were seen in patients with mild to moderate disability. Lancet 2005; 365: 501-506 Broken heart syndrome US researchers have begun to unravel the mystery surrounding cases of profound but reversible left ventricular dysfunction that have occurred after sudden emotional stress. They studied 19 patients with this presentation, finding much higher levels of plasma catecholamines (ie, adrenaline, noradenaline and dopamine levels), neuronal metabolites and neuropeptides than in patients with Killip class III myocardial infarction. The researchers suggested that exaggerated sympathetic stimulation could be central to the cause of this "broken heart syndrome". They proposed microvascular spasm and direct myocyte injury as potential mechanisms of myocardial stunning. N Engl J Med 2005; 352: 539-548 Missing in practice Ever-increasing amounts of individual clinical information now seem necessary for the daily practice of medicine, say US experts.1 They suggested that patients could serve as a safety buffer in improving the communication of this data between different healthcare providers. For example, patients should be encouraged to keep a medication list and be provided with a synopsis of past hospitalisation and procedures that they can take with them to hospital emergency departments and consultants. The experts were commenting on a US survey that found that at least one piece of clinical information (such as a lab report or a letter) was missing from the medical record of nearly 1 in 7 of more than 1500 patient consultations conducted in a general practice setting.2 Doctors were spending valuable consultation time searching, often unsuccessfully, for missing pieces that could affect quality of care. Missing information was frequently reported to be located outside the practice, and the disjointed nature of healthcare delivery and privacy issues were considered to be factors contributing to the problem. 1. JAMA 2005; 293: 617-619 2. JAMA 2005; 293: 565-571 Keep on trying In 1990, a 29-year-old patient with unexplained sub-fertility whose partner had moderate oligospermia embarked on a series of cycles of assisted reproductive technology (ART). 12 years later, in 2001, and after 37 cycles of ART and 26 embryo transfers in 22 attempts, a pregnancy was achieved and the couple took home a healthy male infant. The Australian authors of this case report say that this patient’s experience is in line with previous reports of in vitro fertilisation, which show that, in general, success depends on multiple attempts. Aust N Z J Obstet Gynaecol 2004; 44: 580-582 Dr Ann Gregory, MJA