Volume 178 Issue 10

Action plans are not a "quick fix", but only part of a care package requiring doctors' time and commitment Providing an individualised written asthma "action plan" is a particularly high-profile part of Step 6 of the Australian Asthma Management Plan: "Educate and review regularly". The idea of a written action plan is that the patient is given a set of rules by which to alter therapy, dependent on either peak expiratory flow monitoring or symptom levels. The implication is that an appropriate, early response to deterioration will prevent dangerous exacerbations and will generally improve health-related quality of life. Written action plans for asthma are perceived to be so important that they became one of the two Australian Council on Healthcare Standards Performance Indicators for quality assessment of acute respiratory medicine in Australian hospitals. However, the evidence — whether from research or from clinical practice — that written action plans, in themselves, are effective is equivocal. There are now a number of Cochrane Collaboration Airway Group systematic reviews that examine this area, but the outcomes are inconsistent. Gibson et al analysed up to 36 studies comparing self-management, education plus regular practitioner review against usual care.1,2 They found that active intervention significantly reduced hospitalisation, emergency room visits, unscheduled visits to the GP, days off work or school, nocturnal attacks of asthma, and quality of life, but that lung function was not altered. Self-management programs that involved a written action plan were more effective than those that did not, but regular doctor review seemed to be most important. Indeed, a review by Toelle et al failed to find consistent evidence that written plans, of themselves, have any effect on asthma control.3 Powell and Gibson found that optimising asthma control through adjustment of inhaled corticosteroid dose could be as well achieved by written guidelines for the patient as by seeing their doctor to adjust the dose.4 Somewhat paradoxically, there was evidence that removing regular doctor visits from a management plan was deleterious. Verbal and written instructions to patients seemed equally valuable: the intensity of education seemed to be more important than the format of the advice. But is the proof of the pudding in the eating? If so, ownership of written action plans seems to be falling in Australia although it was never particularly popular in the asthma community. A community sample in South Australia showed a fall from 42.3% in self-reported ownership of written plans in 1995 to 22.2% in 2001, as reported in this issue of the Journal (page 483).5 Furthermore, a large epidemiological study conducted recently in Melbourne also indicated a fall in written action plan use, albeit from an even lower base: in 1999 just 13.3% of Victorians with self-reported asthma had ever been given such a plan, compared with 19.9% in 1993.6 The current situation and available facts therefore raise more questions than they answer.7 Why is uptake of written action plans so disappointing? If written action plans work, why are they not more popular? What is their main purpose — is it to prevent exacerbations or to control day-to-day levels of disease activity? Studies have shown that written action plans are viewed positively by patients, but in practice, they modify their plans according to their own perceptions and experience of asthma.8 It is important that doctors realise this and give patients time to explore such issues and then incorporate them into an agreed plan. Indeed, the role of doctors is very important — their degree of empathy with patients and the amount of time they give to management issues have significant outcome effects in asthma.9 Presumably this "doctor effect" will extend to the uptake and usefulness of asthma action plans. What seems certain is that action plans cannot be used as a substitute for regular detailed review and comprehensive education of patients with asthma. Developing long-term relationships with their doctors, accompanied by being involved in discussion and decision making is important.9,10 Data suggest it is the "process" not the written action plan per se that is currently at fault. Complicating the delivery of asthma care is the poor training of doctors in creating or delivering care packages involving negotiated action plans. Indeed, the main reason for patients not having a written asthma action plan is that they are not given one by their doctor!8 Longitudinal studies are needed to evaluate the effects of enhancing physicians' "participatory decision making" style9 on outcomes of patients with asthma, especially in general practice, where most such patients are managed. This is particularly so in light of the year-old Commonwealth Government-funded national initiative for asthma management in the community, in which a 3+ visit plan in general practice11 provides a framework for optimising treatment and education. This plan includes a written action plan for patients with moderate-to-severe asthma. This needs to be rigorously assessed in routine clinical practice, as even the best ideas and most worthy initiatives from professional "enthusiasts" can be confounded through lack of sufficient time and commitment. Evidence shows that patients will not cooperate with any intervention that is less than fully backed by the time and authentic personal commitment of their doctors. Yet, in a pressurised fee-for-service system, it can be difficult to sustain interest and enthusiasm in the long term. In conclusion, the uptake of asthma action plans in Australia is disappointing, especially as we know they can be useful as part of the right package. Perhaps the management of chronic diseases like asthma needs different sorts of practitioners in a different professional and funding milieu. Yet another challenge for our beleaguered healthcare system?

E Haydn Walters MADM BCh FRACP · Julia AE Walters BM BCh · Richard Wood-Baker DM FRACP

Forewarned is forearmed Severe Acute Respiratory Syndrome (SARS) is now a global phenomenon, but it remains heavily clustered in mainland China, Hong Kong, Toronto, Singapore and Hanoi.1-5 The world is fearing a global pandemic, but it is not happening as initially predicted. Although there are some uncertainties regarding particular clusters of cases, such as the Amoy Garden Estate in Hong Kong (where about 300 people in one block of flats were affected), the primary mode of spread appears to be by infected droplets, and healthcare staff taking strict barrier precautions appear to be protected. There is some evidence that the virus is present in all body fluids, including faeces and urine, so taking precautions with waste disposal are also recommended. World Health Organization case definitions of severe acute respiratory syndrome (SARS) The WHO case definitions of SARS, revised as of 1 April 2003, for a suspected and a probable case of SARS: 6,7 A "suspected" case of SARS is a person presenting after 1 November 2002, who gives a history of high fever (> 38°C), and cough or breathing difficulty and one or more of the following exposures during the 10 days before the onset of symptoms — close contact with a person suspected of having SARS, or a history of travel to or residing in an affected area. A "probable" case of SARS pneumonia is a suspected case (as defined above), with radiographic evidence of infiltrates on chest x ray consistent with pneumonia or respiratory distress syndrome, or a suspect case with autopsy findings consistent with the pathology of respiratory distress syndrome, but without an identifiable cause. The World Health Organization case definitions of "suspected" and "probable" SARS are given in the Box. The clinical course of the disease follows a 2–16-day incubation period,4,5 with high fevers, chills, rigors and myalgia. In contrast to the WHO definition, respiratory symptoms are not prominent and many cases have presented with diarrhoea, abdominal pain and loss of appetite (unpublished observations). There are very few patients with abnormal findings on chest examination at presentation, but these changes develop in severe cases after admission to hospital.5 Laboratory tests typically show a reduced white cell and lymphocyte count, with a mild increase in the platelet count. Usually after 2–3 days of symptoms, x-ray changes become apparent. Typically, the changes are air-space consolidation, predominantly peripheral and often unifocal initially, but progressing over days to bilateral, multifocal changes. At around 7–10 days, about 20%–30% of cases deteriorate and require admission to an intensive care unit. Of these, about half require assisted ventilation. The overall mortality rate is 3%–5%, but may be higher in elderly people. Treatment has been largely empirical and usually has included an antiviral agent, such as ribavirin, and steroids.5 High-dose steroids have been effective in reducing fever and progression of x-ray changes, with the clinical response and radiological features suggesting bronchiolitis obliterans organising pneumonia as the possible underlying pathology.5,8 It is unclear whether any of these treatments alter the ultimate course of the disease. Intravenous administration of convalescent plasma has also been trialled, in the belief that antibodies may halt the progression of the disease,5 despite a theoretical risk of introducing another viral load. Currently, there are a number of possible aetiological candidates, with corona virus being the most likely;9-11 however, a metapneumovirus from the paramyxovirus group12 has also been suggested. Unfortunately, in our experience, field testing for the viruses has so far been unconvincing. It is unlikely that, in the short term, there will be a reliable diagnostic test or vaccine, although work is progressing at a rapid rate. In Australia, the response to SARS has been dichotomous — varying from panic that SARS will be another pandemic to complacency that this is another region's problem. It is likely that Australia will be less affected than countries with open land borders and crowded cities with poor hygiene control. However, the outbreak in Toronto shows that any Western city may have to manage such an outbreak.3 If this disease spreads in clusters rather than sweeps through communities, then the public-health response must be different. It is clear that hospitals and healthcare workers are particularly at risk. In Hong Kong, in the first weeks of the outbreak, 25% of patients with SARS were healthcare workers.5 The healthcare sector has to be particularly prepared, as this is most likely where a cluster will start. Revision of infection control, with meticulous attention to detail, is important. At the Prince of Wales Hospital, Hong Kong, it took three weeks to bring the secondary infections in staff down to near zero. Despite this experience, other hospitals in the region did not take heed, and many more staff in these hospitals became infected because of suboptimal infection control procedures. It is to be hoped that hospitals in Australia will learn from this experience. Screening potential cases of SARS is particularly difficult, as the signs and symptoms are vague and consistent with virtually any viral illness. Following up patients over a number of days is the only way of ascertaining whether they have SARS. The question of whether to admit all suspected cases to hospital is also an issue. If suspected cases are admitted, they may actually contract the disease in hospital. If they are discharged, they may infect their families and friends. In our recent experience of screening about 1000 people with suspected SARS, we uncovered over 100 confirmed SARS cases. We found that there was no secondary spread among the suspected cases followed at home with strict quarantine instructions. All people with confirmed SARS were admitted to hospital. Guidelines for screening high-risk contact and low-risk non-contact subjects have recently been published, although there are no good studies evaluating their utility or the quality of the supporting evidence.13 SARS will fundamentally change the interaction between primary healthcare workers and patients, in much the same way that AIDS changed the way we handle blood products, with universal precautions to protect ourselves from potential HIV infection. It is likely that, in the future, all healthcare providers in regions where SARS is endemic will use the standard droplet precautions of a mask, goggles, gown and gloves for all patient contact. SARS has the potential to totally disrupt the healthcare system of cities or states. Apart from the potential to use hundreds of general ward beds — a disaster in itself given the bed capacity of most Australian hospitals — the biggest threat is the need for intensive care unit (ICU) beds. If 20%–30% of cases required care in ICU, and a cluster of 200 cases occurred in Melbourne or Sydney, there would be little likelihood of finding 50 ICU beds at short notice. A further problem is that ICU staff are likely to contract the disease (unpublished data). If a number of staff contract the disease in an already overstretched ICU system, this may precipitate a fall in morale and staff departures. Furthermore, many nurses are of child-bearing age, and the antiviral agents and high-dose steroids used in the treatment of SARS are likely to be teratogenic. Health authorities need to think about their ability to provide "surge capacity" — not only in terms of ventilators, but also in terms of trained staff. This might include multiple-skills training for nurses and doctors working in non-intensive-care areas. Some healthcare epidemiologists have suggested that this disease is no more serious than the usual winter influenza outbreaks, and not nearly as serious as a new mutation of the influenza virus would be.14 The difference is that previously we have not seen a healthcare system paralysed for a period of months from the impact of one infectious agent. The annual reported death toll from influenza is mostly due to its impact on elderly people, who may die anyway. SARS puts young healthy people into ICU, and otherwise healthy people die. The death toll from SARS is undoubtedly higher in the elderly, and we have not yet seen what may eventuate if a SARS outbreak occurs in a retirement home. The sensible response of Australian health authorities is to remain on high alert, review infection control procedures within hospitals, develop contingency plans for a possible surge in demand for general and ICU beds, and develop an evidence-based approach to screening and quarantine procedures for potential cases.

Peter A Cameron MB BS, FACEM, MD · Timothy H Rainer MB BCh, FHKCEM, MD, FHKAM · Pieter De Villiers Smit MB ChB, FACEM

The findings of two major trials show that rhythm control is not necessarily superior to rate control There are two broad strategic options in managing recurrent or persistent atrial fibrillation (AF). They are: Rhythm control, in which treatment is directed toward restoring and maintaining sinus rhythm; and Rate control, in which AF is allowed to continue or recur unimpeded, and medications are given to control ventricular rate.1 It has been a widely held and natural assumption that rate control is inferior to rhythm control. Theoretically, the advantages of maintaining sinus rhythm should include fewer thromboembolic complications, reduced need for anticoagulation, and less cardiac failure. In short, fewer deaths and fewer symptoms. However, antiarrhythmic medications have only modest efficacy for preventing AF recurrences, both symptomatic and asymptomatic, so rate-controlling and anticoagulant drugs must also be used in many patients being treated primarily for rhythm control. Also, antiarrhythmic medications can have serious side effects, including life-threatening proarrhythmia and, in the case of the commonly used drug amiodarone, pulmonary fibrosis, thyroid dysfunction and hepatic toxicity. Until recently, few randomised trial data have been available to gauge the extent to which these practical deficiencies offset the potential benefits of rhythm control.2 Now, two major trials comparing the two treatment strategies have been published.3,4 The larger AFFIRM trial was conducted in North America, with all-cause mortality its primary endpoint.3 The smaller trial was conducted in the Netherlands, and had a composite primary endpoint which included heart failure, thromboembolism, bleeding, need for pacemaker implantation, death from cardiovascular causes, and other severe adverse effects of drugs.4 The primary finding in both trials was that rate control was not inferior to rhythm control, and that there were some trends towards superiority of rate control. In the AFFIRM trial, 5-year mortality was 21.3% for rate control versus 23.8% for rhythm control (P = 0.08). In the Dutch trial, the primary endpoint occurred in 17.2% (rate control) versus 22.6% (rhythm control), also narrowly failing to reach conventional significance. For the patient populations studied (minimally symptomatic; mean age, 69 ± 9 years; most with at least one prior episode of AF), these findings indicate that the benefits of the rhythm-control strategy do not, in general, outweigh the risks. What drugs were used? In AFFIRM, by physicians' choice, amiodarone was used in 38% of patients being treated for rhythm control initially, and in 63% at some time in the trial. Sotalol was used in 31% initially, and 41% at some time. Other drugs, including propafenone, procainamide, quinidine, flecainide, disopyramide, moricizine and dofetilide were each used in less than 10% of patients. In the Dutch trial, sotalol was used initially, but replaced (if AF recurred within six months) by propafenone or flecainide, and then, if necessary, by amiodarone. Warfarin treatment could be stopped at the physician's discretion when sinus rhythm had apparently been maintained for four weeks after cardioversion. The detailed outcomes quantify the impact of shortcomings of these antiarrhythmic agents. Sinus rhythm was present in 62.6% (AFFIRM) and 39% (Dutch), respectively, of patients being treated for rhythm control at the conclusion of the trials. The proportion of patients taking warfarin remained above 70% in the AFFIRM study, and above 86% in the Dutch trial. Most disappointingly, the strategy failed to reduce the rates of stroke, other thromboembolic complications, or haemorrhages compared with rate control (see Box). Of the 80 ischaemic strokes incurred in the AFFIRM trial's rhythm-control arm, 55% occurred after discontinuation of warfarin. A further 21% occurred during warfarin treatment, while patients' international normalised ratios (INR) were < 2.0. Only 31% had AF at the time of their stroke. These findings suggest that it may be unsafe to stop anticoagulation for AF patients treated with a rhythm-control strategy, unless there are no other risk factors for stroke (age > 60, previous stroke or transient ischaemic attack, hypertension, rheumatic valve disease, diabetes, cardiomyopathy, planned or recent cardioversion) and/or maintenance of sinus rhythm has been demonstrated not only by lack of symptoms, but also by appropriate ambulatory ("Holter") monitoring.1,5,6 The rate-control arms had significantly lower rates of severe adverse effects attributable to medications — effects such as torsade de pointes, resuscitated cardiac arrest due to bradycardia or pulseless electrical activity, and various non-cardiac adverse events (see Box). The incidence of congestive cardiac failure was non-significantly lower in the rate-control arms in both trials. In subgroup analyses of the AFFIRM trial, rate control had lower risk of death for patients older than 64 years, those without pre-existing congestive cardiac failure, and those with coronary artery disease. A trend in favour of rate control in patients with hypertension in the AFFIRM trial is supported by superiority (primary endpoint 17.3 % v 30.8% for rhythm control) in the corresponding subgroup analysis of the Dutch study. These two trials do not spell the end for electrical cardioversions and antiarrhythmic medications in the management of AF. They concentrated on older, high-risk patients, excluding or under-representing some subgroups of patients who experience AF, for example: patients considered unsuitable for one of the strategies (eg, those with hypertrophic cardiomyopathy, those too symptomatic in rate-controlled AF, or those at unacceptably high risk of bleeding with anticoagulation); and patients under 65 years of age and with no other risk factors for stroke or death. For many such patients, and for most patients' first episode of persistent AF, it remains appropriate to cardiovert once, with a level of anticoagulation appropriate to the patient's risk–benefit profile for some weeks or months, meanwhile treating any concomitant predisposing conditions (congestive heart failure, lung disease, etc), and then review. Many issues need to be considered when deciding and revising optimal treatment in an individual patient. In selected individuals, potentially curative non-pharmacological treatments (eg, pacing,7 catheter ablation,8,9 or maze operation10) may be appropriate. However, for patients represented in the AFFIRM and Dutch trials, a line in the sand has been redrawn. Rate control is safe and should not be considered inferior to rhythm control for minimally symptomatic patients in whom AF is considered likely to recur after cardioversion, particularly if they are older than 64, or have coronary artery disease or hypertension. Healthcare professionals should make assiduous efforts to help patients maintain their INR between 2.0 and 3.0 continuously, and to achieve adequate rate control (defined for the AFFIRM trial as resting rate ≤ 80 beats per minute, and either a 6-minute walk test with a rate ≤ 110, or a 24-hour Holter recording with average rate ≤ 100 and no individual rate more than 110% of the predicted maximum).11 Summary of the findings of two major studies examining rate control and rhythm control in atrial fibrillation AFFIRM3 Dutch study4 Number of participants 4060 522 Mean duration of follow-up 3.5 years 2.3 years Mean age at baseline 70 years 68 years Females 39% 36% Event Rate Rhythm Difference significant? (P ) Rate Rhythm Difference significant? Primary endpoint* 21.3% 23.8% No (0.08) 17.2% 22.6% No Congestive heart failure 2.1% 2.7% No (0.58) 3.5% 4.5% No Thromboembolism 5.5% 7.9% No Cerebral 5.5% 7.1% No (0.79) Other systemic 0.5% 0.4% No (0.62) Pulmonary 0.1% 0.5% No (0.16) Haemorrhage 4.7% 3.4% No Primary intracerebral 1.1% 1.3% No (0.73) Subdural or subarachnoid 0.8% 0.8% No (0.68) Non-central nervous system 7.7% 6.9% No (0.44) Severe adverse effects of drugs (other than anticoagulants) 0.8% 4.5% Yes Torsades des pointes 0.2% 0.8% Yes (0.007) Resuscitated cardiac arrest due to bradycardia or pulseless electrical activity < 0.1% 0.6% Yes (0.01) Pulmonary events† 1.7% 7.3% Yes (< 0.001) Gastrointestinal events† 2.1% 8.0% Yes (< 0.001) Bradycardia† 4.2% 6.0% Yes (0.001) Prolongation of corrected QT interval (> 520 ms)† 0.3% 1.9% Yes (< 0.001) Other adverse events† 14.0% 25.4% Yes (< 0.001) * All-cause mortality for the AFFIRM trial,3 and a composite primary endpoint which included heart failure, thromboembolism, bleeding, need for pacemaker implantation, death from cardiovascular causes, and other severe adverse effects of drugs for the Dutch trial.4 † Prompting discontinuation of a drug.

Michael J Kilborn FRACP, DPhil

Objectives: To assess trends in the prevalence of self-reported doctor-diagnosed asthma, associated asthma related morbidity, and the uptake of written asthma action plans in South Australia, 1990–2001.Design, setting and participants: Surveys by telephone interview of the South Australian population between 1990 and 2001, and interview of participants in their own homes by trained health interviewers.Main outcome measures: Asthma prevalence, percentage of patients with written action plans, and asthma associated morbidity.Results: The reported prevalence of doctor-diagnosed asthma has increased from 8% (95% CI, 6.4%–9.6%) in 1990 to 12.8% (95% CI, 11.4%–14.2%) in 2001. Morbidity, as measured by wakening at night (daily or weekly) and days lost from normal activities because of asthma, has remained constant over the decade. The percentage of patients with written asthma action plans increased to a peak of 42.3% (95% CI, 40.3%–44.3%) in 1995, but then declined to 22.2% (95% CI, 20.7%–23.7%) in 2001.Conclusions: The prevalence of asthma has increased while morbidity has remained constant, indicating that the burden of asthma has increased. The associated decline in the percentage of patients with asthma action plans in recent years is cause for concern.

David H Wilson PhD · Robert J Adams MD · Sarah L Appleton BSc · Graeme Hugo PhD · Janet Hiller PhD · Philip Ryan MD · Richard E Ruffin MD · David Wilkinson MD, PhD · Julianne Cheek PhD

Objective: To assess the effect of adding 1 mg dexamethasone to syringe drivers on the viability time of subcutaneous cannulation sites in palliative care patients.Design: Prospective, double-blind, randomised, controlled trial in which patients received half their daily infused medications plus 1 mg dexamethasone in 1 mL saline through one subcutaneous site (test site) and the other half of their medications plus 1 mL saline through another symmetrically placed site (control site).Participants and setting: Palliative care patients from the inpatient units at two hospices, recruited between 1999 and 2002.Main outcome measure: Difference in time that the test and control sites remained viable.Results: 38 patients consented and were randomised. Twenty did not complete the trial because their participation in the study finished before either site broke down. Eighteen patients either partially completed (at least one site broke down) or fully completed (both sites broke down) the trial. In these 18 patients, test sites lasted 3.6 days longer than control sites (95% CI, 1.5–5.8 days; P = 0.002). Twelve patients fully completed the trial. In this group, test sites lasted 3.9 days longer than control sites (95% CI, 0.6–7.2 days; P = 0.025).Conclusions: The addition of 1 mg dexamethasone to syringe drivers significantly extends the viability time of subcutaneous cannulation sites in palliative care patients.

Liz Reymond FRACGP, PhD · Pat Treston MPHC(Palliat Care), FAChPM · Margaret A Charles PhD, MAPS · Jan Bowman MPHC(Palliat Care), FAChPM

Objectives: To describe the short-term outcomes in Aboriginal children admitted to hospital with radiological alveolar lobar changes; and determine whether predischarge chest radiography can predict respiratory morbidity found at follow-up.Design, participants, setting: Prospective cohort study of Aboriginal children admitted to Alice Springs Hospital between October 2000 and April 2001 with alveolar lobar abnormalities (area of consolidation, ≥ 1 cm) on chest radiographs. Participants were to have a predischarge radiograph and be followed up for 12 months.Main outcome measures: Comorbidities, follow-up rate, and new respiratory disease found at follow-up.Results: Of 113 children hospitalised with radiological alveolar lobar changes, 109 were Aboriginal. Their median age was 1.8 years (range, 0.2 months–13.3 years), and 124 episodes were recorded. Comorbidities were common in these children (anaemia, 51.5%; suppurative otitis media, 37.3%). The follow-up rate one year after admission was 83.1% of episodes. New treatable chronic respiratory morbidity was found in 20 (25.6%) of the 78 children with completed follow-up. Predischarge chest radiographs were predictive of all chronic respiratory morbidity when they showed no or minimal resolution (0–20% resolution) (relative risk, 7.43; 95% CI, 2.07–26.60).Conclusions: Central Australian Aboriginal children admitted to hospital with alveolar changes on chest radiographs have a substantial burden of chronic respiratory illness, and should be clinically followed up for early detection and management of chronic respiratory morbidity. A predischarge radiograph is useful, and patients whose radiograph shows no or minimal resolution should have a follow-up x-ray film.

Anne B Chang MPHTM, PhD, FRACP · John P Masel MB BS, FRACR · Naomi C Boyce BNursing · Paul J Torzillo MB BS, FRACP, FFICM

Objective: To describe the levels of inflammation and vascular endothelial activation in an Aboriginal community, and the relationship of these factors to coronary heart disease (CHD) risk factors and markers of nutritional quality.Design and participants: A cross-sectional survey of 95 women and 76 men participating in a chronic-disease prevention program.Setting: A remote Aboriginal community in Western Australia in 1996.Main outcome measures: Concentrations of markers of inflammation (C-reactive protein [CRP]) and vascular endothelial activation (soluble E-selectin [sE-selectin]); presence of metabolic syndrome; concentrations of diet-derived antioxidants.Results: Participants exhibited very high plasma concentrations of CRP (mean, 5.4 mg/L; 95% CI, 4.6–6.3 mg/L) and sE-selectin (mean, 119 ng/mL; 95% CI, 111–128 ng/mL). Both CRP and sE-selectin concentrations were significantly higher in the presence of the metabolic syndrome. There were significant inverse linear relationships between concentrations of CRP and plasma concentrations of the antioxidants lycopene, β-carotene, cryptoxanthin and retinol. Even stronger inverse associations were evident between concentrations of sE-selectin and lycopene, β-carotene, cryptoxanthin and lutein.Conclusions: Vascular inflammation and endothelial activation may be important mediators of elevated CHD risk in Aboriginal people. Inadequate nutrition and physical inactivity may contribute to this process.

Kevin Rowley BAppSci PhD · Jacob Cohen BSc · Alicia J Jenkins FRACP FRCP · David O'Neal MB BS, MD, FRACP · James D Best FRACP FRCPath · Karen Z Walker PhD MND · Qing Su MSc PhD · Kerin O'Dea BSc PhD

No Australian Indigenous doctor has previously chosen a surgical career Medical training is an arduous task in optimal circumstances. When also confronted by myriad social issues, the task can be quite daunting. I hail from the Worimi mob, located north of Newcastle in the Port Stephens area, and I am currently in my first year of advanced training in otolaryngology, head and neck surgery. I am extremely fortunate in the support I have been given, to help me make the most of the opportunities afforded to me. However, despite the support, there have been many difficulties, and here I will attempt to outline some of my experiences as my career has unfolded. From an early age, I was interested in the field of health. My mother comes from a solid family of 12, and I was lucky enough to grow up among what I call my nuclear family — this includes all of my mother's family and a plethora of cousins. My mother, as the eldest in her family, didn't have the opportunity to finish secondary school; rather, she was given the task of helping to raise her siblings in very poor socioeconomic circumstances. The demands and stress imposed on our family are not new to most Aboriginal families, who confront these on a daily basis. Despite my mother's situation and lack of opportunity, her determination allowed her to successfully attain registered nursing qualifications. With the myriad health problems that face us, and the reluctance of Aboriginal people to seek medical help, it was very common to see family and friends seek help from mum. Naturally, as a curious child, I was always keen to assist in a range of basic first aid. The greatest reward was seeing the appreciation and smiles that came with improvement in their wellbeing. It wasn't until I was older that I questioned why my family would seek help from mum and not from the medical system. More intriguing was why it seemed to be Indigenous people, and not my non-Indigenous counterparts, who frequently were afflicted. With my twin sisters who led the way. It is only now that I can discuss with my sisters the humorous side of our upbringing and how it has affected us. Simple things like bed arrangements, and our desire to have our own bed instead of sharing it with our cousins; the wish to have a doona instead of a bundle of crocheted blankets; and the longed-for luxury of an indoor toilet or simple heating for the house in the winter months. By no means am I trying to embellish a hard-luck story, but, rather, to illustrate the closeness and appreciation of family life that I experienced. The greatest quality that I have gained from this experience is to be humble and non-judgemental. My acceptance into university created a "mixing pot" of emotions. On the one hand I was elated — fancy me, going to university to study medicine! Of course, to enter the health profession had long been an ambition, but it had been an unlikely prospect, particularly as I was actively discouraged from pursuing tertiary education, both covertly and overtly, by people who thought the idea of a Koori studying medicine was incredible. There was also pressure to get a job to help bring in money, rather than create an extra financial burden by going to university — tertiary education is a daunting expense for already strained family finances. Apart from two very recent exceptions, none of my family had finished Year 12, and anything beyond that was a far cry from their world. What I did have on my side were my amazing twin sisters. They had always shown the way by example, and have given me so much encouragement. They both completed Year 12, and both were accepted into medicine at Sydney University. In fact, they were the first Indigenous medical graduates from the oldest university in Australia. Now, for this to occur first in the 90s is a modern-day example of institutionalised inequality. Their acceptance into medicine also cast some doubts on my medical career, as there was resentment from the non-Indigenous community, even though my sisters' academic merit spoke for itself. To counter this, they gained strength from a belief in themselves and the big smiles of pride emanating from our community. In my final year of high school, I was without my sisters' physical presence for the first time. But their words of encouragement and pride in me had strengthened my determination to succeed. I was still fortunate to have the support of my mother, who always believed in all of us. It is easy, in retrospect, to realise why she saw our education as such a high priority, particularly when you hear of the battles she went through at a similar age. She always kept me grounded in reality and enlightened me on the journey ahead, but, most importantly, she impressed on me, and instilled in me, pride in our heritage. No one would ever take that away. Many instances of institutionalised racism occurred — unless you are on the receiving end, you often don't see it. It can be as subtle as being the only black face in a sea of white faces; to schoolyard taunts; to double standard treatment (eg, being checked when purchasing items on a credit card as a "routine" security check); to hearing other people speak slightingly of your family; and to hearing media stories denigrating your culture. But my mother never wavered in her support for our culture, and explained the importance of our ancestry. My mixed emotions included intimidation — the medical culture was a daunting thought. I was leaving my comfort zone. I had felt the emptiness at home when my sisters ventured to medical school, but now I was to follow. As I was not accepted at Sydney University, I could not follow exactly in their footsteps. I entered the medical course at the University of New South Wales (UNSW), and, initially, it took me quite a while to settle in. Today, as an ENT registrar. It was hard to leave the friends I had grown up with, who accepted me for who I was and what I represented. They knew my background and my family, and I considered them to be family. I envisaged medical students as all upper class, private school boarders, with no idea about the realities of life as I knew them. I thought my colleagues would be my opposites: had never left the city, had never met a Koori, had their own rooms, owned cars, and had always been comfortable financially. I also wondered how my lecturers and seniors would treat me. Needless to say, entering university was terrifying. Leaving my family behind was extremely difficult. As a Koori, family is extremely important to me — looking after cousins, big family gatherings, and being able to support one another in difficult times. I really wanted them all to move with me. I was terrified of becoming an "outer" in the family; to be rejected for following what, until recently, was a non-Indigenous career path; to lose my identity that I had finally grasped (from teenage years); to become lost in the system; and to fail (when my sisters had led the way and the community had high expectations). I am happy to say all my fears were ill founded, and studying at UNSW was a delight. It is true it took me a while to adjust. The new social surroundings were initially difficult, but I was fortunate enough to reside at a university college, and met many new people and formed long-lasting, inspirational friendships. This also gave me an avenue for meeting people outside the medical course, so I could appreciate the diversity of opportunities the university had to offer. The university environment is dynamic as well as diverse, and I strongly feel that being immersed in this ambience was equilibrating. I learnt a great deal from other people's experiences, as they learnt from mine. I acquired a better understanding of other cultures and how other people lived. This provided a great opportunity to learn to treat different people. I have made wonderful friendships with the very people I was initially afraid of, and I soon realised that the majority of medical students are pleasant and open. Sure, there were a lot of mixed impressions, and ignorance sometimes reared its ugly head. But, talking to other Indigenous medical students made me realise that my experience was not unique, and the strength that had been instilled in me helped me to rise above any adversity. I also realised the magnitude of help and assistance that was available to students, and that most lecturers were readily available and willing to help. Although I had become comfortable among my new friends, I felt alone in my studies. I realised this when a dear Aboriginal friend transferred from another university halfway through my training. Instantly, I didn't feel alone any more. It was a feeling of someone else understanding my predicament without having to explain it myself. Newcastle University had always had strength in numbers of Indigenous students, and at Sydney University my sisters had each other. This inspired the instigation of a premedical program at UNSW for Indigenous students wanting to study medicine. I was passionate about creating an environment that supported, rather than discouraged, the aspirations of Indigenous students, while at the same time not creating unrealistic dreams. A small group of us set about formalising a program. We received lots of strong support, mixed with a small amount of resistance. Rallying the support of the Faculty, making a presentation at a medical deans' conference and providing a realistic business plan were all worthwhile and achievable. My graduation highlighted the pride of my family. A strong family contingent attended my graduation, many of whom had never set foot in a university. In their words, it "charmed" them to attend and be part of it. And, in many ways, it was their graduation — my accomplishment is a testament to my family, my mother, my community and my ancestors and to the incredible fight they have endured, and the struggle that we as a race continue to endure. This aspect was really brought home to me when, as an intern, I first treated an Indigenous patient. My worst fear was upsetting the elder, as being able to treat Indigenous patients was my reason for being there. After a thorough history and examination, the patient began to cry. My heart sank and I felt I had failed. My smile proudly appeared again when she explained that her tears were tears of joy, as she never thought she would ever be treated by an Indigenous doctor. The importance of professional equality hit home, and it reaffirmed my desire to give back to my community. Residency was hard work, but fun and rewarding. It seems, though, no matter what you go through, you always come across poorly managed Indigenous patients. What surprised me most was that their first contact with a medical institution seemed to have a profound effect on how these patients responded, not medically, but rather in their compliance and willingness to attend follow-up. I continued to come across racism, but again it was more institutionalised. For example, there was the reaction and misunderstanding of medical staff when confronted by an Indigenous patient, at the same time claiming they were not racist — their actions obviously stated otherwise and they didn't have the insight to recognise their inbuilt perceptions and prejudice. I decided to pursue a career in surgery because it appealed to me and suited my persona. I was fortunate to have the great benefit of support from my surgical mentors at St Vincent's Hospital, although the surgical exams were my toughest exams to date! The major difference was being able to create a suitable study environment, and the greater appreciation of my desire to better equip myself for my future role. Although my mentors were wonderful, again I felt isolated, given that no Australian Indigenous doctor had previously chosen a surgical career. This is understandable, given the demands of surgical training and the small number of Indigenous doctors Australia has, as yet, produced. I passed my surgical primary examination and have gained great experience in general surgery. With the Third World status of ear disease in Indigenous Australians, I had always had a desire to pursue a career in ENT. After gaining some experience in ENT, I realised the scope of the specialty beyond ear disease, and the great professional opportunities available. I am back where my passion originated, but now I am on the professional side. The understanding and support from the otolaryngology community has been overwhelming. As I embark on my advanced training, it seems almost surreal to be where I am now, and I am even more proud of my culture.

Kelvin M Kong MB BS, BSc

How to heal the festering sore of Indigenous health? In Australia, Indigenous health remains a blot on the nation's collective consciousness. There has been little, if any, improvement in the last quarter of a century.1 Although an association between health and socioeconomic status has been described in many different societies, in Australia we seem to avoid taking this connection into account when considering Indigenous health. The First Nation's people of Australia still do not have the same access to housing, education and employment as those who are relative newcomers; thus, it should not be surprising that their health status is worse. Senator Aden Ridgeway, in his address to the United Nations Human Rights Commission,2 summarised the root of this problem as: Non-Indigenous Australians are keen to embrace the rhetoric of reconciliation, so long as it doesn't require them to take effective action to share the country's abundant resources and political power. Most are not prepared to make any significant adjustments in how they live their lives or how they see their future. Few are prepared to really look within themselves to challenge their beliefs and values, for fear of what they might find and for fear of what they think they might lose. So, what might it be that non-Indigenous Australians are so fearful of finding? Possibly, that the entire basis of land ownership in Australia, and therefore our economy, is based on the lie of Terra Nullius — that is, that no one owned the land claimed by others.3 And, what might non-Indigenous Australians be so fearful of losing? All their benefits, including health benefits, that they may have derived from this lie. At a recent National Health Summit in Sydney (held at Merchant Court Hotel, Sydney, 18–19 February 2003; hosted by Terrapinn), speakers outlined Australia's achievements in health, most notably that we can boast the second highest longevity among OECD countries. But little of what was said had any bearing on Indigenous health — it was almost as though Indigenous health had to be annexed so that the mood could remain positive. However, it is neither moral nor ethical for Australia to continue to ignore the deplorable state of Indigenous health. For too long, too many of the issues have been relegated to the too-hard basket. The festering sore of Indigenous health will not go away by ignoring it, but rather needs direct action — the active promotion of opportunities for Indigenous Australians in mainstream professions and services, health or otherwise. The medical profession has long recognised its social contract to Indigenous Australians, and we can easily start to fulfil this contract by attending to our own backyard. For proportionate racial representation in the medical profession in Australia, we should have about 1260 Indigenous doctors; however, there are no more than 55. All have graduated since 1983 and more than half from the one medical school. Had the other nine medical schools made the same effort to recruit and train Indigenous doctors, we would now be much closer to the racial equity goal of 1260 doctors. The presence of Indigenous Australians within the student body of our medical schools does more than just help to meet a target. It enriches the profession and enables other medical students to access something of the Indigenous experience — many Indigenous medical students and doctors have been the first Indigenous Australians that our non-Indigenous colleagues have met. The presence of Indigenous Australians in our medical schools also keeps the focus on Indigenous health active and honest. And it can provide a shining example and model for other professions who should recruit, support and graduate Indigenous students. In fact, it is important for our Indigenous students in primary and secondary school to see that all professions are accessible and supportive, so they can confidently consider tertiary education as a reality rather than a fanciful dream. Many of our medical postgraduate clinical colleges are already seeking to actively recruit Indigenous doctors into their training programs; we will also need to see the introduction of compulsory Indigenous health curricula into each of the postgraduate training programs. Beyond incorporating Indigenous health and health workers into our ranks, we need to actively encourage appropriate access to health services. For example, as a profession we need to call for the introduction of a Medicare safety net that will make a discernible improvement to the health status of Indigenous Australians. Real gains in Indigenous health are attainable by incorporating Indigenous health provision (albeit with additional benefit or consideration) into our mainstream delivery of health services, rather than, or at least in addition to, setting up more and more services specifically for Indigenous Australians. Beyond healthcare delivery, more of our profession should consider taking leadership in issues related to sovereignty and treaty, and ensure that satisfactory access to housing, education and employment is pursued. What benefit can Australia expect to receive from such a radical change in approach? As Senator Ridgeway said, much of Australia may avoid self-examination for fear of what will be found and what will be lost. This apparent milieu of fear is a poor legacy to leave to future generations of Australians. In confronting these issues, we can offer a better future for our nation and bring healing to the festering sore that is Australia's Black history (and health). The medical fraternity can play a leading role in this process — after all, healing is the prime concern of our profession.

Louis G Peachey BMed, FACRRM

A 43-year-old woman taking warfarin for past venous thrombosis presented with 4 days of flu-like symptoms and deterioration in level of consciousness. Computed tomography suggested subarachnoid haemorrhage, and magnetic resonance imaging showed widespread cerebral infarcts. However, these seemed out of proportion to the amount of haemorrhage, and lumbar puncture revealed meningitis caused by Streptococcus pneumoniae. Computed tomography (CT) is a vital investigation in acute medicine, but CT appearances may occasionally be misleading, as illustrated here. Clinical recordPresentation (Day 0): A 43-year-old woman was admitted to the emergency department (ED) in June 2002 with deterioration in her level of consciousness. She had a 4-day history of non-specific flu-like symptoms. On the day of admission, her husband had noted her to be lucid at 09: 00 but found her semi-comatose when he returned home at 14: 30. She had a past history of venous thrombosis, thought to be secondary to the presence of anticardiolipin antibody and lupus inhibitor, for which she took warfarin. She used topical and parenteral corticosteroids to control severe eczema, was a non-smoker and did not take the oral contraceptive pill. On examination, her score on the Glasgow Coma Scale (GCS) was 7/15. Pupils were equal and reactive, and no definite signs of meningism could be elicited. Respiratory rate was 24 breaths/min, with oxygen saturation of 99% on supplemental oxygen, 15 L/min via a Hudson mask. Tympanic temperature was 40.8°C, blood pressure 168/92 mmHg and pulse rate 128 bpm in sinus rhythm. Serum blood glucose level was 7.8 mmol/L (reference range [RR], 3.6–5.8 mmol/L), white cell count was 18.6 x 109/L (RR, 4.2–11.0 x 109/L), with toxic changes on the blood film, and platelet count was 357 x 109/L (RR, 150–460 x 109/L). The international normalised ratio (INR) was 1.8 (RR, 0.8–1.3), with normal values for fibrinogen and fibrin cross degra-dation products, and activated partial thromboplastin time. C-reactive protein level was raised at 402 mg/L (RR, 0–10 mg/L). Other laboratory results, including renal function, were within the reference ranges. In the ED, the patient underwent tracheal intubation because of her low GCS score, and was subsequently sedated with morphine and midazolam. Blood was taken for culture, and intravenous ceftriaxone (2 g daily) was begun. Chest radiography showed segmental right upper-lobe consolidation. Non-contrast CT of the brain was performed during her transfer to the intensive care unit (ICU). This was reported as showing subarachnoid haemorrhage, with increased density in the subarachnoid space, particularly within the basal cisterns (Box A). A neurosurgeon was consulted, and subarachnoid haemorrhage with aspiration pneumonia was diagnosed. The differential diagnosis of meningitis was thought less likely because of the CT appearance. A nimodipine infusion was begun, and cerebral angiography was planned. Her high INR was normalised with 4 units of fresh frozen plasma. Day 1: At 06: 00 the next morning, the patient's pupils became unequal and non-reactive. This was thought secondary to either vasospasm or a re-bleed. Urgent repeat contrast CT at 07: 00 showed a parietal infarct, but no further bleeding or signs of raised intracranial pressure. The hyperdensity in the basal cisterns was less apparent, but there was subtle hyperdensity within the subarachnoid space, around the cerebral sulci near the vertex. On subsequent review, the amount of haemorrhage suggested by the cranial CT scans appeared insufficient to account for the patient's clinical condition. Diffusion-weighted magnetic resonance imaging (MRI) at 13: 30 showed multiple acute cerebral infarcts in the territories of the right middle and posterior cerebral arteries, as well as in the watershed zone between the middle and anterior cerebral arteries (Box B). There was no abnormal enhancement of the leptomeninges to suggest infectious meningitis, and, in particular, no basal leptomeningal enhancement to suggest granulomatous meningitis (Box B). In the absence of abnormal leptomeningeal enhancement, the presence of increased signal within the subarachnoid space was thought to be due to subarachnoid haemorrhage (Box B). Magnetic resonance angiogram and venogram showed no aneurysm or dural venous sinus thrombosis. Appearances were again thought most likely to represent primary subarachnoid haemorrhage, with acute cerebral infarction secondary to vasospasm. However, meningitis with secondary cerebral infarction was raised as a differential diagnosis, and lumbar puncture was recommended. Lumbar puncture was subsequently performed after correction of residual coagulopathy, and revealed an opening pressure > 35 cmH2O, a white blood cell count in cerebrospinal fluid (CSF) of 1510 x 106/L (all polymorphs), red blood cell count of 160 x 106/L (decreasing on subsequent tubes, with xanthochromia not detected), and protein level of 2291 mg/L (RR, 150–450 mg/L). Gram-positive diplococci were visible on Gram stain, and the CSF was positive for pneumococcal antigen. Blood taken on admission subsequently grew Streptococcus pneumoniae. After consultation with the infectious diseases team, we changed the antibiotic regimen to intravenous ceftriaxone (2 g) and vancomycin (1 g) twice daily. The diagnosis was revised to primary pneumococcal pneumonia with secondary pneumococcal meningitis. Course: After 11 days' treatment in the ICU, the patient was transferred to a ward. On Day 13, she developed a large pulmonary embolus confirmed by CT angiogram and was readmitted to the ICU for respiratory support. She recovered and subsequently resumed anticoagulation therapy with heparin and warfarin. She was discharged back to the ward on Day 18. At review a month later: She was undergoing rehabilitation, and was lucid and able to move with a frame, but remained blind in both eyes. DiscussionCranial CT scanning is a vital diagnostic tool in patients presenting with acute alteration in level of consciousness. Our case posed a diagnostic difficulty because of the unusual appearance on initial brain imaging. The initial CT scan showed increased density in the subarachnoid space, which is mostly caused by subarachnoid haemorrhage. Based on the imaging findings alone, the most likely diagnosis was therefore felt to be subarachnoid haemorrhage with secondary vasospasm causing cerebral infarction. However, there seemed to be a disparity between the amount of subarachnoid blood and the patient's clinical condition. This was reinforced by MRI, which showed extensive infarction in different vascular territories. This degree of infarction secondary to vasospasm would be unusual without widespread haemorrhage or thick focal clot, which were not seen. Additionally, vasospasm secondary to subarachnoid haemorrhage tends to peak 4–12 days later, while our patient showed signs of neurological deterioration less than 24 hours after admission. Cerebral infarction has been well reported in bacterial meningitis in both adults2,3 and children,4,5 and is thought to result from an intense inflammatory response in the cerebral vasculature. It is particularly noted in pneumococcal meningitis. Although pneumococcal meningitis was not diagnosed initially in our patient, broad spectrum antimicrobials, to which the organism was fully sensitive, were fortuitously begun on admission. The delay in ascertaining the correct diagnosis created a dilemma about subsequent anticoagulation, which probably could have been recommenced earlier. Increased density in the subarachnoid space on CT has been described in tuberculous meningitis.6-8 However, this was unlikely in our patient — the condition is still uncommon in the Western world, and contrast enhancement of the basal leptomeninges (a sign of granulomatous meningitis) was absent. Increased density in the subarachnoid space has also been reported in anoxic encephalopathy,9 but our patient had no history of hypoxia or prolonged ischaemia. In addition, although the acute infarcts were within regions of the brain susceptible to acute hypoxic injury, they were all within the right cerebral hemisphere. With a global insult such as hypoxia, bilateral lesions would be expected. To our knowledge, there has previously been only one English-language article describing a patient with acute purulent meningitis mimicking subarachnoid haemorrhage on CT scan.10 Presumably this appearance is caused by the high protein concentration of the purulent exudate in pyogenic meningitis, as noted in our case. Although this is uncommon, we present this case to alert both radiologists and clinicians to the presence of this atypical appearance on imaging and to highlight the need for careful evaluation of such patients. The case also illustrates that results of investigations should not be interpreted in isolation from the clinical picture. We suggest that lumbar puncture should be performed if the clinical presentation is atypical or not in keeping with the radiological findings. Brain imaging in a patient with pneumococcal meningitis A: Computed tomography (CT) on Day 0 Non-contrast CT scan, showing increased density within the basal cisterns (arrow A) and along the sylvian fissures bilaterally (arrow B), suggesting subarachnoid haemorrhage. B: Magnetic resonance imaging (MRI) on Day 1 Diffusion-weighted MRI scan showing multiple foci of increased signal intensity in the anterior part of the right thalamus, posterior right temporal lobe and right occipital lobe. Increased signal intensity was also seen in the right frontal and parietal lobes (not shown). This appearance was consistent with multiple acute infarcts in the territories of the right middle and posterior cerebral arteries. Not shown: Multiple small acute infarcts were also seen in the watershed zone in the centrum semi-ovale between the territories of the right middle and anterior cerebral arteries. Gadolinium-enhanced T1-weighted MRI scan showing no abnormal enhancement of the leptomeninges, including the basal leptomeninges. This suggests no evidence of a granulomatous meningitis. Not shown: Increased signal intensity was seen within the subarachnoid space overlying the cerebral sulci of both cerebral hemispheres on the FLAIR sequence (a T2-weighted sequence that nullifies the signal from cerebrospinal fluid [CSF], improving detection of lesions within the subarachnoid space and brain parenchyma1). This is a non-specific finding in a wide range of conditions, principally subarachnoid haemorrhage and meningitis. In our patient, the absence of leptomeningeal enhancement on the post-contrast images favoured a diagnosis of subarachnoid haemorrhage.

Taposh Chatterjee MB BS · John R Gowardman FRACP, FJFICM · Tony D Goh FRANZCR

The care of a dying person requires qualities of a medical practitioner that do not sit neatly within the prevailing medical paradigm. "Don't just do something, sit there!" This twist on a well known adage was coined by the American social psychologist Richard Kalish,1 and at the time was directed to those whose task it was to care for the sick and dying. It is a novel, but pointed, statement that stresses the importance of being really present for people who are suffering, and truly hearing their pain. The statement may not have been made with the medical profession specifically in mind, but it is nonetheless as pertinent to doctors as it is to anyone involved in caring for the sick. For doctors, the challenge implicit in the statement is that patients, particularly those with a life-threatening illness, may not be well served by a model of care that concentrates on diagnostic and therapeutic interventions.2 Indeed, the threat of death creates needs that can never be met by attending to the physical domain alone. Pain relief and meticulous attention to troublesome symptoms certainly go a long way towards restoring comfort and dignity, but emotional and existential issues need to be approached in a more holistic way — one in which honesty, empathy, authenticity and the ability to communicate feature high on the list of qualities required of the doctor. "The physician is only the servant of nature, not her master" –Paracelsus (1493 – 1541) The emphasis in medicine over the past 50 years or more has been on cure, or at least on what can be done technically and pharmacologically. With the increasing number of tests and treatments now available, the tendency to intervene has reached a point where it is hard to imagine how we, as practitioners, could function in anything other than this model — a model described by Moskowitz as a "medical juggernaut driven by a logic of its own, one less focused on human suffering and dignity than on the struggle to maintain vital functions".3 As a young physician in the early 1970s, I vividly remember an elderly general practitioner reflecting on his 60 years in practice. It was both fascinating and enlightening to hear someone talk about the care of patients at a time when there were no antibiotics or specific treatment for chronic illnesses such as asthma, diabetes mellitus and hypertension. It was a time when morphine, mercurial diuretics, digitalis leaf, tourniquets and venesection were the only interventions available for heart failure, and treatment for most conditions was guided by clinical judgement rather than "numbers" and x-rays. By present-day standards, this doctor had little in the way of a medical armamentarium. But, although he may have been helpless to influence the course of many illnesses, he did not consider himself to be helpless. He comforted the sick, sat with them and their families during difficult times, and was a trusted and reassuring presence in the face of death. He may have had little to offer medically, but what struck me was that I, with my newly acquired specialist ticket and accompanying bag of tricks, felt more uncomfortable and helpless than he when faced with a dying patient. Times have changed, and many of the illnesses that claimed lives in the early part of the 20th century are now preventable, curable or more easily palliated. For many patients we have succeeded in postponing death and have hopefully improved the quality of their life. But have we improved the care of those who cannot be cured? Are we as skilled as my GP colleague in comforting and communicating with the sick and dying, or are we distracted by unnecessary tests and futile treatments that threaten to engage us in a form of subterfuge that serves only to conceal a sense of helplessness, while adding considerably to a patient's distress? In a retrospective study of 100 deaths at an Australian hospital, Middlewood et al4 noted that 74 of the patients were considered by the attending medical team to be dying, and "do not resuscitate" (DNR) orders were completed for 88 patients. Despite this, 78 were subjected to one or more tests after the DNR order, 67 received antibiotics, and 88 were given intravenous fluids. At the time of death, 27 of the patients were still receiving antibiotics and 49 had a drip in situ. Although most of the patients were thought to be dying, the approach to care did not appear to reflect this, or if so, only very late in the course of the illness. Similar outcomes were found in a study of 200 deaths within a large medical centre in the United States.5 In this study, comfort-care (palliative-care) plans were completed in just 46% of the patients and, once again, this occurred late in the admission, even though most patients had been identified as dying and DNR orders were completed well beforehand. In a report entitled Pursuing a peaceful death, Callahan6 intimated that the medicalisation of death has made the prospects of "dying well" more of a hope than an expectation. "Death", he says, "is now harder to predict, more difficult to manage, the source of more and more moral dilemmas and nasty choices, and spiritually more productive of anguish, ambivalence and uncertainty". Callahan is not making excuses for clinicians, nor is he suggesting a return to the days when death was more predictable simply because there was little that could be done to prevent it. Rather, he implores that we, individually and collectively, look at the way we care for the dying and reflect on whether our actions contribute to patients not dying well. He urges us to see death not as a failure of medical treatment but as one of the most important times in a person's life — a time that calls for respect rather than interference. It is a time when attention to suffering is more important than the maintenance of physiological function. We physicians can help patients die with comfort and dignity by withholding or withdrawing treatment that is clearly futile. Such a decision is never easy, and circumstances pertinent to each patient can make this more difficult. Our honesty, authenticity, and the way we impart information can effectively bridge such difficulties and allow the patient, his or her family, and the attending team to refocus on the broader issues. To inform a patient that he or she is dying is painful and traumatic, but it is not made any easier by deferring or avoiding the subject altogether. Our honesty only confirms what most dying people already suspect. If we ignore the truth, we deceive ourselves as well as our patients and deprive them and their families of the opportunity to say goodbye and prepare for death.7 Grahame Jones, writing about an illness that ultimately claimed his life, said, "let the healthy talk of illness; let the sick talk of more important things".8 Care modelled around tests and futile attempts at cure only succeeds in maintaining a focus on illness. This may be comforting to the clinician, but it effectively robs the dying patient of the opportunity to talk about the "more important things". In the many public talks that she has given in the past, Elisabeth Kubler-Ross, author of On death and dying,9 often spoke about a member of the hospital staff whom dying patients would invariably seek out when they needed comfort or someone to talk to. This person was not a doctor, nurse, social worker or counsellor. She was the cleaner, and, when asked by Kubler-Ross why she was so sought after, her reply was simple but direct. "Death", she said, "is an old friend". This woman had seen a lot of death, not just in the hospital but also within her own family, and, like the elderly GP who had so impressed me, was not afraid to journey with people as they were dying. Neither she nor the GP relished the task, but neither sought to abandon their responsibility during the difficult and sometimes frightening time leading up to death. Both are excellent role models and demonstrate the important role we can play in helping patients prepare for death. If we are able to do this, we not only play an important part in their healing but also heal a part of us that may be uncomfortable with death.

Michael Barbato MB BS, FRACP

The work of Daniel Kahneman shows that there is much more to clinical decision-making than the weight of numbers The research on the psychology of decision-making by Daniel Kahneman (joint Nobel Prize Winner in Economic Sciences, 2002) is apposite to clinical practice. In parallel with Herbert Simon1 (winner of the same prize in 1978), Kahneman linked behavioural sciences with decision-making in economics. Intriguingly, experts in the dry science of economics are slowly becoming aware that human choices are not based on numbers alone. In conducting studies of decision-making, Kahneman found people's choices often differed from those that would be expected based on numerical probabilities alone. He examined the influence on the decision-making process of risk perception, risk-avoiding and risk-seeking behaviour, aversion to loss, distortion by hindsight, lack of statistical awareness, framing of choices, previous memories, and worries about the future.2 In the sphere of clinical medicine, teasing apart the factors that influence choices is necessary if we are to understand what goes through the minds of both doctors and patients. In life-and-death situations, survival overrides all other factors, and choices are based on the highest chance of survival. But Kahneman (with his colleague Amos Tversky) showed that, when the likely outcomes are less momentous, human factors can weigh more heavily than probabilities. In some situations, for example, the threat of a loss has a greater impact on choices than the chance of an equivalent gain.3 Patients may be "loss-averse" in avoiding losing something important, such as their independence or their right to stay in their own home. In other situations, patients are not necessarily "risk-averse" — they may be willing to "take a chance on it" if the anticipated gain is large. Clinicians and patients accept high risks with low probabilities of success (say, in radical head-and-neck surgery for cancer) when the payoff from success is high.4 Such behaviour parallels chasing jackpots and buying lottery tickets "against the odds". Quite apart from any health or financial motive, risk-taking has its own psychological payoff, which adolescent males relish.5 Losses disturb us emotionally, as we agonise retrospectively over whether they could have been avoided ("if only . . ."). We regret losses that flow from actions we have taken, such as buying shares that drop in value, more than from actions we could have taken but didn't, like not buying shares that rose in value. Clinicians use many devices (eg, prophylactic antibiotics and anticoagulants) to reduce the threat of possible therapeutic loss from complications of treatment. They protect themselves from the threat, the regret and the losses from litigation by adopting defensive medicine and medical insurance. Humans don't think probabilistically, especially at the upper and lower ends of the probability scale. For example, we are unable to meaningfully assess differences between 1% and 5%, or between 90% and 95%, in weighing our decisions. Kahneman and Tversky also showed that humans usually weight low probabilities too high and high probabilities too low relative to certainty. People tend to categorise some factors in "either/or" terms (say, that vaccination is either "safe" or "dangerous"), without incorporating any numerical likelihood in their choice. Another factor that can bias risk perception is fear and "imaginability" of a disaster. If you fall out of a boat, you may react dramatically to your fear of being attacked by a shark, even though you know the probability is extremely low. Kahneman was Professor of Psychology at Princeton University, where John von Neumann and Oskar Morgenstern had developed "expected utility theory" in 1944. This theory of decision-making, incorporating all the outcomes and consequences of a decision, provided mathematical frameworks for "game theory", which underpinned strategic thinking during the Cold War.6 This quantification of risks, costs and benefits of medical decisions is still used in healthcare today, but may lack credibility with patients, who are expected to assign a number, or betting odds, to the relative benefit of an outcome of treatment they haven't yet experienced. Rather than measuring outcomes, Kahneman and Tversky shifted the focus to measuring change — the gains and losses each individual experiences. Gains and losses have personal meanings to each of us, and are not objective, calculable units. Patients have difficulty assessing the value of a hypothetical treatment outcome, but they understand the known and the familiar. They don't wish to lose what is predictable and comfortable in their lives for the sake of a potential gain that they are unable to visualise. The relative importance of gains and losses was further demonstrated when Kahneman and Tversky tested the effects on decision-making of how questions were "framed". Phrasing a question around the concept of "saving lives" shifted choices towards risk-taking; the same probabilities phrased around "lives lost" induced risk-averse choices.7 Both patients' and doctors' perceptions of risk shifted according to how the choice between alternatives was phrased. Kahneman's belief that numerical probabilities are the correct determinants of decision-making was one side of a "clinical versus statistical" war within the psychology of decision-making. Jeremy Bentham's utilitarian rule of the "greatest happiness for the greatest number" claimed that numbers from group data should override individual factors — his presumption that group data are "right" disregarded individual differences and contexts. This issue also arises in the practice of evidence-based medicine. Management based on group outcomes may take precedence over management that is tailored to the patient's motivations and circumstances as well as the disease. Choice based on numerical probability works if only one outcome variable is being counted (say, survival after coronary artery bypass). But the situation becomes more complicated if the choice must incorporate multiple outcome variables, such as recurrence rate, complications, cost, return-to-work issues or level of anxiety. The complex interaction between other significant factors such as age, comorbidity, drug sensitivities, rehabilitation resources, coping skills and family support can swamp single-factor numerical logic, for better or for worse. Decision-making is not truly "rational" (and is ethically doubtful) when numerical variables are considered to the exclusion of all others. In this context, we must acknowledge that, in our discussions with patients, we often use vaguely quantitative terms, such as "frequent", "likely", "common", "rare" and "possible". These approximations honestly reflect the real world of partial knowledge within which decisions are made. If clinicians don't use, and don't know, the predictive probabilities that shape their therapeutic decisions for each patient, attempts to weigh significant numerical variables against one another to reach a decision may be no more than pseudo-accuracy. We need to develop a little "science of the individual" that can weight all the human and medical factors at play, together with a calculus for clinical judgement that guides the parties to a decision most likely to optimise the chosen outcomes. A Nobel Prize may be waiting for the clinical researcher who cuts a sound and workable path through these complexities of the real world!

Ken Cox MA, MS, FRACS

This is the first time I have felt threatened by the work that I do It begins on Tuesday afternoon, 11 March, with another bothersome call from hospital administration. They want to take over our Emergency Department (ED) observation ward because the Department of Medicine has a couple of doctors who feel ill. They think that this illness may be contagious to other staff and patients, so a ward with a separate entrance and separate air-conditioning would be ideal. I make them aware that this action would severely hamper operations within the ED and that they should manage these doctors the same way we have treated the five ED doctors who, at the moment, have some viral illness: send them home. My answer to their request: no way. A short time later, the Professor of Medicine and the hospital's CEO visit my office — a very unusual event. They say they are very concerned because not just two but up to eight medical staff and a number of nurses are febrile and feel unwell. Being a pragmatic ED doctor, I point out that we have to make sure that this illness isn't just one of the many benign URTIs we see at this time of the year. After all, about 20% of our ED attendances relate to URTIs. So, we all agree to callback 40 medical and nursing staff and have them examined that evening. If it turns out they are suffering from some unusual disease, I will be more than happy to hand over the observation ward. I go home at 7 pm in the certain knowledge that I will have a relaxed evening with my family and will turn up to work tomorrow to greet a red-faced professor, apologising profusely for trying to disrupt our emergency service. But, at 9 pm, I take a call from the medical team: they have screened the first few patients and all have high fevers and pneumonic change on chest x ray. Within hours, 20 staff are patients in the observation ward, not desperately unwell but a little anxious about what will happen next. An over-reaction?The following day, we held a meeting of all the chiefs of clinical services to discuss what we should do next. Among many of the senior people, there was a fair degree of scepticism and more than a suggestion that we were over-reacting to this mystery illness. Could it just be that influenza or mycoplasma infection was affecting a disproportionate number of our staff? An over-reaction to the usual round of spring respiratory infections? We had heard of an outbreak of atypical pneumonia in Guangzhou, but the reports were that this was now under control, although rumours suggested otherwise. Certainly, the features of the illness were typical of the reports of severe acute respiratory syndrome (SARS) in Vietnam. We decided to work on the assumption that all three of the illness clusters were related in some way. The ED staff who had been away from work with a "viral illness" were assumed to have the same disease. Despite their protests that it was just another minor illness, they were forced to come in and be admitted to hospital. More medical and nursing staff became ill, as did patients from the same hospital ward. A number of senior staff refused to come into hospital until they became very ill; this resulted in the spread of the infection to their families. Early scareDespite treatment, the condition of all the patients seemed to deteriorate over the first few days. It was not clear whether anyone was going to improve. Only five days after the illness first became apparent in our hospital, I was facing the real prospect that a member of my own staff would die. One of my residents, gravely sick, now required intensive care; even with 100% oxygen, he could not maintain adequate arterial oxygen saturations. I prepared myself for his death and let my other staff know that it was likely that he would die. Overnight, he was given high-dose steroids; he improved marginally. By some miracle, his condition continued to improve and he survived. However, at this stage of the outbreak, eight other staff from my ED, as well as over 50 other healthcare workers, were still patients in hospital. This illness looked like it could eventually involve all the hospital staff; potentially, any or all of us could end up in the ICU. Empirical experienceMedical treatment was largely empirical because the causative agent responsible for the illness was unknown to us. Patients were initially treated with oseltamivir and broad-spectrum antibiotics to cover all likely known pathogens. Ribavirin and steroids were used, but there was no way of knowing whether this was altering the basic course of the disease. With experience, it became apparent that high-dose steroids had a major impact in halting deterioration late in the illness. Managing an illness that you know little about, under the scrutiny of your colleagues (as your patients), is very difficult. The pressures on all medical units and ancillary staff were enormous. The whole medical department was involved in treating the patients, and the number of staff affected grew steadily to more than 150. After considerable negotiation with the health authorities, normal operations within the hospital were suspended. Fortunately, there was a high degree of altruism and cooperation among the medical staff; all departments contributed to both staffing (in a high-risk situation) and to the overall management of this disaster. There were daily meetings of chiefs of services and forums for regular staff. Daily, factually accurate updates were posted electronically. It was simply incredible to see staff turning up to work each day despite the fact that, in the first two weeks of this experience, each day about four or five more staff members would succumb to the illness. From Day 1, all staff wore masks and gowns but we were still getting breakthrough cases. With meticulous attention to infection control, watched over by infection control "police" in each ward, we were able to reduce this occurrence to near zero. Like a stakeoutAt a personal level, this is the first time I have felt threatened by the work that I do. Perhaps, it's a similar experience to that of a policeman on his first "stakeout", when he realises he might get shot. As a doctor, you know you are potentially vulnerable to the getting of all sorts of illnesses, but rarely a devastating, life-threatening one. I was worried about going home in case I would infect my family. When I did get home, I felt physically exhausted and emotionally drained, and didn't really want to talk to anyone. I would not and could not touch my wife or children for fear of giving them the disease. I slept in a separate bedroom; I ate separately. Clothes and fomites were washed separately and chlorine bleach was everywhere. My youngest boy developed a nervous twitch as he was told tales of the disease and harassed to wash his hands and wear a mask. Some of my colleagues began sleeping in their offices, refusing to go to their homes at all for fear of infecting their families. It wasn't a situation I could go on living with. My wife and I decided it would be easier for all of us if my family returned to Australia. A couple of weeks after they left, I realised how isolated I had become outside of my work setting. No one wanted to come near me for fear of getting the disease; any social encounters became uncomfortable. Even in the carpark, people would skirt around me to avoid close contact. There was little time off work, anyway, because of the constant meetings and service commitments occasioned by the outbreak. By strange coincidence, news of the Iraqi war was being broadcast continuously on television. Disturbing as the images of this war were, I realised that the battle we were fighting here might well have a more long-lasting, devastating impact. Missing the pointWhen I spoke with friends in Australia, I was struck by how little they had heard about the outbreak in the first weeks and how little preparation authorities seemed to have undertaken. Some "armchair experts" were even saying that it was irrelevant to Australia, just another "beat-up". In their minds, influenza was much more important. I tried to remember the last time influenza had put 250 healthcare workers into hospital, with 20% of them in an ICU. I tried to remember the last time all the ICU beds in a city had been filled by influenza cases. As far as I was concerned, these "experts" had clearly missed the point. Also, initially there seemed to be a high degree of misinformation about the symptoms, signs and mode of spread of this disease. In general, the only definite symptom was fever. In the early stages of the illness, cough, rhinitis and other URTI symptoms were actually less prevalent in the SARS group than in other patients. I believe that information being promulgated by WHO and the Centers for Disease Control and Prevention (CDC) was, in some instances, inaccurate and at other times misleading. For example, early enthusiasm surrounding diagnostic tests proved misplaced when we found only a 10% positivity rate. I felt compelled to make time for some radio and television interviews to raise awareness of SARS. Late warningsIn Hong Kong itself, I believe the authorities were initially very keen to keep the public "in the dark". This was followed by an attempt to blame the hospital (and staff) for allowing the disease to spread. Initially, for fear of creating pandemonium, no moves were made to educate the public about preventive measures. We tried, through official channels, to get these messages out; unfortunately, most officials seemed to me to be more concerned with protecting the economy and preventing panic than containing disease. Unfortunately, this response seems to have been the typical one in some other jurisdictions as well. Although the Hong Kong government has since adopted widespread public health measures, at time of writing it still maintains that there is no crisis. I do not agree; there is no obvious end in sight. More and more of the public are becoming infected. There is a high likelihood that more healthcare workers will be struck down. It is distinctly possible that if the numbers of affected patients continue to rise the whole public health system may collapse. The most likely pressure point will be the intensive care setting: with over 100 cases already requiring intensive care, it is inevitable that untrained staff will have to manage critically ill patients. Also, hospitals will have to "triage" patients, allocating intensive care beds and technology to those most likely to benefit before those with a lesser or low chance of survival. Today, despite my concerns for the community, my personal fear has receded. I feel more capable of managing this threat than I did in my first fortnight's experience of it. Although I am not 100% sure of the cause of this illness (despite the confident reports from scientists), I do understand something about its course and how to control its spread, at least within the hospital. I know that most people will survive the disease. However, I remain extremely frustrated that others are not learning the lessons that we have learnt regarding the need for stringent infection control. Most medical staff think they know about infection control and how to manage a crisis, and are unwilling to take advice. As a result of this attitude, and despite direct knowledge of our experience, I believe that about 20 staff at another hospital in Hong Kong have contracted the disease. As a healthcare worker, the likelihood of contracting an infectious disease that will kill you is usually quite small. When a new, mysterious illness smites down a whole hospital and its workers, it hits at the heart of the health system.

Peter A Cameron MB BS, FACEM, MD

Patient care in the "new genetics" era encompasses not only the diagnosis of a genetic condition or risk, but also managing the psychosocial, familial and ethical sequelae. Partnerships between the medical professional and expert clinical genetics services, support groups, registries and genetics education services provide a framework for this management. More than 750 Australian support groups assist individuals and families with genetic conditions through contact with peers, information and education resources for patients and professionals, practical advice about coping and advocacy.

Kristine K Barlow-Stewart · Clara L Gaff

To the Editor: Chlamydial infection is the most common bacterial sexually transmitted infection in Victoria and Australia, and notifications are increasing significantly. Most chlamydial infections are asymptomatic and, if untreated, lead to significant morbidity.1 The direct costs of these infections to the Australian healthcare system have been estimated at $90–$160 million annually.2 Chlamydial infection has been implicated in as many as 50% of cases of infertility.3 Widespread screening is cost effective and reduces both the prevalence of infection and the rate of complications.4 Screening is recommended in a number of countries and in the recently released Victorian Chlamydia Strategy.2 To determine if there has been an increase in the proportion of women tested for chlamydial infection who are asymptomatic in Victoria, we analysed notification and enhanced surveillance data. Since 1997, the Department of Human Services has collected enhanced surveillance data using a standard questionnaire distributed by laboratories to clinicians. The forms record information on risk factors and the reason for testing. Data from the Health Insurance Commission were obtained to provide an indication of trends in testing through Medicare. The number of notifications almost doubled between 1997 and 2001, from 2059 to 3977 notifications (Box). In 2001, enhanced surveillance data were available on 2300 notifications (58%). Symptomatic presentation remained the major reason for testing (53%), with no significant change in the proportion tested for this reason since 1997. However, when data for the two sexes were analysed separately, the proportion of men who were symptomatic fell significantly between 1997 and 2001, from 77% to 65% (P = 0.02), while there was no change in the proportion of women who were symptomatic — 42% in 1997 and 41% in 2001 (P = 0.35) (Box). From 1997 to 2001, the number of positive chlamydial tests notified relative to the number of tests conducted has remained constant (9.7%, 8.8%, 11.8%, 11.5% and 9.8% in consecutive years, respectively), despite the increase in number of tests performed. However, even if all tests had been performed in the 20–30-year-old age group, they would represent only 10% of the population in that age group tested each year. Our data suggest that the reasons for testing over the past 5 years have not changed, and, in particular, that there has been no change in the proportion of women tested who are asymptomatic. Chlamydial infection meets the World Health Organization criteria for a screening program,5 and screening for this infection is cost effective.4 Although chlamydial infections are a significant public health concern for women, targeted screening is not occurring widely. Chlamydia notifications and enhanced surveillance data for Victoria, 1997–2001 1997 1998 1999 2000 2001 Male Female Male Female Male Female Male Female Male Female Number of notifications 788 1271 948 1542 1181 1761 1328 1915 1631 2346 Number with enhanced surveillance data 484 782 619 954 735 968 858 1037 992 1308 Reasons for testing* Symptomatic 76.9% 42.3% 75.8% 46.0% 73.9% 44.1% 68.6% 39.4% 64.9% 41.1% STI Screen 7.2% 25.4% 6.5% 25.6% 9.0% 26.3% 9.8% 27.2% 12.3% 27.2% Asymptomatic contact 13.8% 15.5% 16.2% 17.5% 15.8% 18.7% 18.1% 16.9% 18.9% 17.4% Abnormal examination 0.2% 3.2% 0.6% 3.8% 0.7% 4.0% 0.2% 1.6% 0.8% 2.3% Pre-termination screen 0 9.3% 0 5.5% 0 5.6% 0 5.6% 0 3.7% Other/not stated 1.9% 4.3% 0.9% 1.7% 0.6% 1.2% 3.2% 9.3% 3.1% 8.4% Total notifications 2059 2490 2942 3243 3977 STI = sexually transmitted infection. * Mutually exclusive choices presented to clinicians in the surveillance questionnaire.

Megan L Counahan · Jane S Hocking · Christopher K Fairley

To the Editor: We describe six cases of amoebic appendicitis, encountered during a 15-month period in the Pathology Department of the Royal Darwin Hospital. The patients were all Indigenous Australians and four of them came from remote communities. The average age was 24 years and five of the six were men. They all presented with abdominal pain, fever and right iliac fossa tenderness for up to 6 days. The clinical notes did not indicate the presence of pre-existing dysentery, and no faecal examination was undertaken. Recovery following appendicectomy was uneventful in all the cases. No further follow-up is available. The aetiology was established histo-logically, as no distinctive clinical or macroscopic features were noted. The appendices showed extensive coagulative necrosis of the mucosa, submucosa and muscularis propria and invasion of the wall by variable numbers of amoebae with ingested blood cells. Inflammation secondary to perforation was evident in the serosa and the mesoappendix, but no significant inflammation was seen in the inner layers of the wall (Box). Coagulative necrosis of the appendiceal wall was seen in all the cases. In fact, in some of the cases the diagnosis was suspected on seeing this distinctive coagulative necrosis and the amoebae were only found later. Thus, we believe this type of necrosis, which has not been previously emphasised in the literature, to be characteristic of the condition. Amoebiasis is rare in a developed country like Australia. The infection is generally acquired during travel to endemic parts of the world. However, case reports of invasive amoebiasis in Indigenous Australians who have not travelled outside Australia have been previously reported.1,2 Immigration, immunosuppression and poor sanitation are other settings in which amoebiasis can be seen.3 The finding of six cases of amoebic appendicitis in Indigenous Australians in the Northern Territory in a 15-month period is significant, as appendicitis is a very rare manifestation of the disease. McCarthy et al, in a recent MJA article,2 highlight the potential public health significance of endemic invasive amoebiasis because of its high transmissibility in settings where hygiene may be suboptimal. We agree with this and believe in selective screening and appropriate treatment of at-risk contacts of the patients, as prolonged latency between infection and disease is well documented.3 Cross-section of appendix Cross-section of appendix with coagulative mural necrosis and secondary serosal inflammation (haematoxylin and eosin [H&E] original 1×). Numerous amoebae in clear spaces, some with ingested blood cells, are seen in the insert (H&E original 40×).

Ibrahim M Zardawi · Joseph S Kattampallil · Jurgen W Rode

To the Editor: Murray et al recently suggested that after an initial screening urinalysis, routine urinalysis could be eliminated from antenatal care without adverse outcomes for women.1 Their conclusions are based on a prospective observational study of 1000 women, 26 of whom developed pre-eclampsia, with 6/24 (25%) developing new proteinuria before the onset of hypertension. We have concerns about the authors' claims, which, we believe, are not justified by their findings. Pre-eclampsia remains a major cause of maternal and perinatal mortality.2 A study of 26 cases of pre-eclampsia is clearly underpowered to evaluate important morbidity and mortality outcomes. Therefore, one must place great emphasis on potentially undetected cases of pre-eclampsia, such as those that repeatedly appear as examples of substandard care in the Report on confidential inquiries into maternal deaths in the United Kingdom.3 That the initial screening urinalysis detected only 2/26 (8%) women who subsequently developed pre-eclampsia is no surprise. In contrast, routine urinalysis at antenatal visits detected 25% of cases of pre-eclampsia before the onset of hypertension. In the UK, this would amount to 4500 women per annum. The detection of proteinuria provokes further antenatal visits earlier than would normally be planned, facilitating early detection and management of pre-eclampsia. Intervals of 2–4 weeks between visits are usual in the early part of the third trimester when the risks to mother and fetus of severe early onset pre-eclampsia are greatest.4 By eliminating routine urinalysis from antenatal care, a quarter of affected women are potentially exposed to the risk of ongoing undetected pre-eclampsia for up to four weeks. Murray et al suggest that most women would be detected by risk assessment at the initial visit. While there are known risk factors for pre-eclampsia, the largest group who develop pre-eclampsia are primigravid women with no previous history of note. In addition, there are no reliable studies to justify this claim of Murray et al. Recent randomised controlled trials have suggested that the frequency of antenatal visits could be reduced without demonstrating harmful effects.5 None of these trials, however, have the power to demonstrate safety. Even the recent large World Health Organization trial involving 24 526 women6 would have required 490 000 women for 80% power, and 649 910 women for 90% power, to exclude the 40% increase in maternal mortality actually observed with reduced antenatal care. Changes in well-tried methods of antenatal care need to be assessed with more stringency before it is concluded that they are safe.

Deirdre J Murphy · Christopher W Redman

In reply: We agree with Murphy and Redman that pre-eclampsia remains an important disorder and a major cause of maternal and perinatal mortality. However, we disagree with their interpretation of our data. Murphy and Redman allege that, by eliminating routine urinalysis, a quarter of cases of pre-eclampsia may remain undetected for up to four weeks. As we pointed out in our article,1 three of the six women who developed dipstick proteinuria before they developed pre-eclampsia were already considered "at risk" for pre-eclampsia — two because of multiple pregnancies and one with a history of prior pre-eclampsia. These women would, in our practice, continue to have routine urine tests during their pregnancies. The argument is then whether it is justifiable to undertake repeated urinalysis in almost 1000 women to detect three who have dipstick proteinuria, but no other warning signs before the onset of their hypertension. In practice, we would have had to increase antenatal clinic visits for 338 women with dipstick proteinuria (most of whom will have had false-positive results2) to detect these three women with proteinuria before they developed pre-eclampsia. It is already our normal practice for women to have antenatal visits every second week in their third trimester. Therefore, it is just as likely that their blood pressure changes would have been detected by our routine surveillance as by the knowledge that they had dipstick proteinuria. We did acknowledge clearly in our discussion that our study had a potential for type II error and that the best approach is a randomised controlled trial of outcomes between those who do and do not have continued urinalyses during pregnancy. None of this belittles the importance of pre-eclampsia, nor the need for us to separate women considered at "low risk" from those considered "at risk" for pre-eclampsia on the basis of well recognised risk factors. The latter group should never be considered among those in whom routine urinalysis can be omitted.

Mark A Brown · Caroline S E Homer · Gregory K Davis · George Mangos

To the Editor: As practitioners in a community-controlled Aboriginal and Torres Strait Islander primary healthcare centre, striving to better meet the healthcare needs of our community, we would like to offer some thoughts on a recent article by Coory et al.1 In reporting on cervical cancer screening participation rates in Indigenous communities in Queensland, Coory et al identified the communities but did not inform them that the study was being conducted. We feel that such an approach is unhelpful and reflects a paternalistic attitude. The accompanying editorial2 rightly drew attention to the lack of direct consultation with the communities involved and the consequences of this in terms of future interventions. Without a true partnership with the women and their communities, the authors were unable to do more than imply that participation rates were better in centres with a primary-healthcare approach to screening. Information about the types of services and choice of Pap smear providers available in each community, in addition to the Pap smear screening participation rate, would be of great interest. It would, in part, answer the question the authors themselves posed about the role of primary healthcare in improving Pap smear participation rates. Already scarce funds could then be committed to improving access to quality primary healthcare rather than to conducting further trials. A further factor, which was not explored in either the study or the editorial, was health promotion. The cornerstone of health promotion in the Indigenous community remains the "kit-video" model, comprising posters, leaflets and a video. In contrast, mainstream health promotion often involves expensive multimedia campaigns promoted by national celebrities. Such campaigns have been shown to increase Pap smear screening in the wider community.3,4 To date, these campaigns have rarely had an Indigenous focus, and it might be argued that a consequence of this is the low Pap smear participation rate documented by Coory et al. In our experience,5 the Indigenous community does respond to culturally appropriate holistic primary healthcare. The study by Coory et al demonstrates a lack of commitment, collaboration and innovation — essential features for the delivery of quality primary healthcare — that is all too common in the current approach to Indigenous health.

Katie S Panaretto · Sarah Larkins · Vivienne Manessis

In reply: Black has argued that the role of evidence in policy development is to create concern and set agendas.1 This was the aim of our article. Although there has been a national, organised approach to preventing cervical cancer since 1991, our study found that screening rates for Indigenous women still lag well behind those of non-Indigenous women. Workers in Indigenous health might have suspected as much, but valid data have not previously been available for a wide geographical area. As Murray and Lopez point out, the lack of good data on a health issue is often taken to mean that the problem is not important.2 We agree that the development of effective programs should be done in consultation and partnership with Indigenous communities. However, there is an additional need to influence decision-makers and budget-holders at national, State and regional levels. An evidence base that identified effective interventions would facilitate this process. Such evidence need not come from randomised controlled trials. On the other hand, case reports of successful interventions in a single community that cannot be sustained when key personnel leave are not very persuasive. It is also useful to demonstrate that the situation is not hopeless. The encouraging finding from our study was that the participation rate in cervical cancer screening was more than 50% in three of the 13 communities studied.

Michael D Coory · Patricia S Fagan · Jennifer M Muller · Nathan AM Dunn

To the Editor: The beyondblue guidelines for treating depression in primary care by Ellis and Smith1 are intended to assist both healthcare professionals and consumers. While they provide several helpful indications, they also include some misleading suggestions. The authors state that drug treatment of depression should continue for at least one year for a first episode of depression, and at least two years for repeated episodes or when there are other risk factors for relapse. However, no background literature is cited in support of this statement, and indeed would be difficult to find. Maintenance pharmacotherapy has been advocated as an effective tool for reducing relapses and recurrences in major depression.2 A number of studies have shown the superiority of antidepressant drugs (mostly tricyclics) compared with placebo in protecting the patient from relapse. Duration of drug treatment, however, did not seem to affect long-term prognosis once treatment with the drug was discontinued. In clinical terms this means that, whether you treat a depressed patient for three months or three years, it does not matter when you stop therapy with the drug. In fact, after recovery from an index episode of major depression, risk of postdiscontinuation relapse was nearly significantly greater after longer treatment (ρ = 0.37; P = 0.052).3 Further, Ellis and Smith1 fail to mention a vexing clinical problem in maintenance antidepressant treatment: the return of depressive symptoms.3 Dose increase is likely to entail only a temporary solution to the problem, which may occur in up to 57% of patients. However, there is a promising alternative. Treatment of depression by pharmacological means is likely to leave substantial residual symptoms.4 Residual symptoms hinder lasting recovery and are one of the strongest risk factors for relapse. In randomised controlled trials, cognitive behavioural treatment of residual symptoms was found to significantly improve long-term outcome of recurrent depression and to allow discontinuation of drug therapy.4 Preventing recurrence in major depression cannot simply be based on prolonging ongoing pharmacological treatment. The belief that a longer course of treatment will result in a more favourable outcome after discontinuation of antidepressant drug therapy is not supported by research evidence.5 Active collaboration with the patient (in choosing a treatment option, in lifestyle modification, in seeking treatment again when needed) is a crucial, and yet neglected, variable. It can lead to a more rational use of antidepressant drugs and to therapeutic efforts of more enduring quality than those prevailing today.

Giovanni A Fava · Chiara Ruini · Eliana Tossani

In reply: Fava observes that duration of treatment with an antidepressant does not affect the subsequent rate of relapse. Indeed, it would be unexpected if it did; medication only works while it is being taken. He then states that the duration of antidepressant treatment is immaterial. However, Figure 1 of the reference he quotes1 indicates that, for at least 54 months after the index episode, continuing medication provides greater protection against relapse than early discontinuation. This argues strongly for the beneficial effects of continuing antidepressant therapy for a significant period after recovery. The duration of this period depends on the number of previous episodes of depression and is a compromise between the benefits of effective prophylaxis and the burden of treatment. He also refers to a study of "tolerance" to 20 mg fluoxetine.2 Of patients who responded to treatment, 31.4% relapsed while on maintenance treatment. Of these, 57% responded to an increase to 40 mg fluoxetine and remained well for six months. He appears to have interpreted these data differently. I agree that treating depression involves more than prescribing. The beyondblue guidelines promote active collaboration with the depressed person in addressing key issues in their lives and a focus on relapse prevention.3 Cognitive behavioural therapy is one strategy for achieving this.

Pete M Ellis

To the Editor: Van Der Weyden has commented on the World Health Organization's Utopian definition of "health", first promulgated in 1948.1 In 1973, I addressed this matter in a speech to the All Nations Club in Sydney, and again in 1980 when presenting a paper to The Hope Foundation (a large charitable health organisation in the United States). For what it is worth, my suggested definition of "health" was: Health is a high level of physical, mental and social comfort appropriate to the age of the person concerned and attainable within the economic constraints of the particular environment. It seems we have some agreement, and I would like to see the WHO again consider definition!

Keith S Jones

In reply: I thank Sir Keith for his pragmatic proposal. The concept of health has individual and societal connotations. At its most basic level, it is the avoidance of pain and suffering. More broadly, it is a basic human resource for the pursuit of life's goals.1 But, as argued by Lewis and Leeder, "health is a good to be pursued, but not an absolute one" for the "functioning of social institutions does not require perfectly healthy citizenry, nor does the individual have to be perfectly healthy to take part in social life."2 As such the perfect definition of health espoused by the WHO is Utopian and removed from reality. It is, as poignantly captured by René Dubos, the "mirage of health", as "complete freedom . . . from disease is but a dream remembered from imaginings of a Garden of Eden."3

Martin B Van Der Weyden

To the Editor: The editorial by Cameron and Campbell on access block is an excellent summary of the causes and potential solutions to access block.1 The effects of overcrowding in the emergency department (ED) have been previously reported, including risks to patient safety, prolonged pain and suffering, and decreased clinical productivity and effectiveness.2 Access to emergency care is impaired. The fundamental problem is that while demand has increased, the capacity of the system has decreased.3 This is best exemplified by the significant reduction in hospital bed numbers. Healthcare in Western societies has been through a period of severe economic rationalisation, resulting in closure of thousands of beds in the acute hospital system. For example, in the United States, the number of medical and surgical beds declined by 18% in the period 1994–1999. From 1990 to 1999, attendances at EDs increased 15%. There have also been many aged care beds closed or changed to community-based facilities.4 It has been suggested that the problem is "a badly flawed approach to financing health care that values profits over patients."5 Spare bed capacity is essential for the effective management of emergency admissions. At least one study has found that if hospital bed occupancy rates exceed 85%, then bed crises occur.6 In fact, the Guinness Book of World Records now has a category for longest wait on a hospital trolley!7 The official record currently stands at 77 hours 30 minutes, although anecdotes report longer times. It is paradoxical that other departments within a hospital cannot exceed 100% occupancy, and yet the ED, which may contain some of the most seriously ill or injured, is allowed to exceed the safe level of 100% occupancy. The ED has always been available to help if all else fails in the healthcare system. That basic tenet is now being challenged, and the general public may no longer be able to rely on EDs for quality and timely emergency care, placing the safety of people at risk.8 In addition, Derlet has stated that should there be a major infectious disease epidemic or national catastrophe, EDs and hospitals could not accommodate the demand, undoubtedly leading to increased suffering and excess mortality.3 For all patients, increasing the capacity of the hospitals across the system (viz beds) would really make a difference.

Daniel M Fatovich

To the Editor: The series of articles concerning access block1 indicates that access block is a major health issue in this country. It is remarkable that, despite all these efforts to avoid admissions and reduce inpatient length of stay, only a few occasions of brief success at reducing ambulance diversions were described, and only one case of reducing access block (Royal Melbourne Hospital). We contend that it is now time to increase available beds. In several cases, the association between worsening access block and closure of beds was noted (Australian Capital Territory, Queen Elizabeth Hospital, Royal Perth Hospital). Available data show a steady reduction in hospital beds per thousand population in Australia, from 3.3 in 1995–96 to 2.8 in 1999–2000,2 a decrease of more than 11%. Keeping inpatient occupancy below a threshold percentage is important to controlling access block.3,4 Reducing occupancy by increasing available beds is the logical recommendation.

Peter A Roberts · Paul A Cunningham

To the Editor: I was interested in the letter by Marks et al,1 indicating that the efforts of over-worked medical staff in emergency departments to introduce patients to local general practitioners had been largely unsuccessful. A few years ago I noted the success with which this problem was handled by the emergency department management at Huddinge University Hospital in Stockholm. All patients were charged 60 krone at triage. Those who sat in the waiting room were confronted by two large electronic signs. The first listed the waiting time for the 10 most common GP-type ailments. The second listed 10 local GPs, where the consultation fee was then 50 krone, with the offer to refund their initial payment if they chose to take their business elsewhere. I was told that this was the very successful first of eight "barriers" between the emergency department door and the intensive care unit. Since the middle of last century, Sweden has been held up as a model provider of an egalitarian and "free" healthcare service. Perhaps our country could benefit from the revisions and improvements that the Swedes have made over recent decades.

Peter J Burke

On 11 September 2002, at the age of 45, Tim McArdle was killed in a road accident while cycling. Tim was the third of seven children, a son of the late Frank McArdle, formerly a general practitioner in Ballarat, Victoria, and mother Patricia, a nurse and nurse educator. Born on 30 September 1956 in Ballarat, he was educated at Villa Maria and St Patrick's College, Ballarat. Tim was an outgoing, humorous and playful person who loved people. From an early age, his many talents and formidable intellectual qualities were evident. He gained a place at Monash University Medical School in 1974 and completed the medical course with seemingly effortless ease, graduating among the top 10 students in his year. Tim worked at Prince Henry's Hospital, Melbourne, the Royal Children's Hospital and the Queen Victoria Medical Centre, where he obtained a diploma in obstetrics and gynaecology. He then spent a year in Cohuna, in northern Victoria, working in a typical rural general practice, before returning to Melbourne to run the Moorabbin Hospital Emergency Department for a year. In 1987, Tim was invited to Warragul, in south-eastern Victoria, where he decided to join an established practice because of the congeniality of the colleagues and the "grass tennis courts". It was in Warragul that his medical and personal skills blossomed and he developed a love for the local community. He had the good fortune to enter a happy and thriving medical practice, working with colleagues with whom he established wonderful personal and professional friendships. Tim's own practice focused on maternal and child health, but over the years he branched out into other areas. Tim's interest in community medicine inspired him to write a weekly local newspaper column on health issues for 15 years, under the by-line of "Dr Kev". In more recent years, he chaired a regular session on health issues on ABC Regional Radio. In 2000, he spent five weeks as a volunteer medical practitioner in East Timor. Tim loved sport, including tennis, golf, cross-country skiing and horse-racing, which for him were a source of relaxation and comradeship. He was also a natural musician and inveterate performer. He supported himself at university playing piano in restaurants and bars, and later played for 12 years with a group of medical friends in a local Warragul band called "The Fabulous Beatroots". Tim appeared particularly happy and content in the company of his partner Robyn during the last year before his death. His sudden and tragic death leaves a huge gap in rural medical services and is an enduring loss to his mother, siblings and many friends.

Peter McArdle

Re: Injecting drug use in Australia: needle/syringe programs prove their worth, but hepatitis C still on the increase, by Law MG and Batey RG in the 3 March 2003 issue of the Journal (Med J Aust 2003; 178: 197-198). Dr Batey's position was incorrectly given as Director, Gastroenterology Department, John Hunter Hospital. His position is Clinical Chair, Division of Medicine, John Hunter Hospital. The html and pdf versions of the article on the website were corrected on 12 May 2003.

Matthew G Law PhD · Robert G Batey MD FRACP FRCP

Re: Fatal intravenous misuse of transdermal fentanyl (Med J Aust 2002; 177: 552-553) by Mark D Reeves and Corinne J Ginifer. In Box 2A (page 553), the computed tomography scan of the brain was not the correct image. The correct image is given below. The html and pdf versions of this article were corrected on the website on 12 May 2003. A: Brain — arrows indicate areas of low attenuation in basal ganglia.

Mark D Reeves MB BS, FANZCA · Corinne J Ginifer MB BS, FACEM

In early 1919, before the full force of the influenza pandemic was felt in Australia, there were doubts expressed in the Journal about the veracity and balance of media reports. The profession has to thank you [the Journal] for your dignified protest against the hysteria and exaggeration which has distinguished the press of Sydney in connexion with the present epidemic. I believe in those three millions dead in India about as much as I believe in the three millions who accompanied Xerxes over the Hellespont. Both numbers simply signify Oriental historians' and American journalists' ideas of a large number, and are incredible. And when the Herald says outright that this is the most terrible visitation that has ever attacked mankind, and that it has killed more people than the war, one wonders whether one is awake or dreaming. Journalists ought to read history. I wonder is there a single one in Sydney who has ever read a detailed account of the Black Death; and yet that was the turning point of history and the source of almost all the troubles which afflict society to-day. There is no doubt that it was to a large extent the ordinary bubonic plague . . . . . . We have so long been certain that no other disease but the plague could have caused such a catastrophe that we cannot bear to think that there may possibly be another. Was it pneumonic plague? . . . It does seem to me quite possible that at the time of the Black Death there was for the first and only time in history a combination of the plague and the strange disorder which is now knocking at our doors. Hence the unparalleled mortality. But that does not justify us in calling this disorder by the dreadful name of plague. . . . . . . the Oriental plague . . . rendered cities almost uninhabitable for thousands of years, till about 1700, when man conquered that dreadful enemy without his knowing how he had done it. He began to lock up his foodstuffs and his stores of grain; he built his houses better; perhaps he became cleaner in his habits; in other words, he kept the rat at a distance, and, without the rat, . . . you can have no plague. The story of the plague is the most dreadful in all that narration of the crimes, follies and misfortunes of mankind which Gibbon called history. It has slain uncalculable millions; during the Middle Ages it was the unquestioned Captain of the Men of Death; it was probably almost the normal cause of death for centuries; no man can even venture to guess at what the world might have been had there been no plague. And yet our hysterical journalists apply that name of awful omen to the comparatively harmless disease which we have so far kept at bay. . . . But once more I wish to emphasize the hysterical folly of fixing the dreadful name of plague on to this influenza. Let us thank our God that we shall never more be subject to that terror of the human race. C MacLaurin FRCS, Sydney Med J Aust 1919; 1: 71-72

Sex in Australia Not everyone has sex: about 3 in 100 men and women in Australia aged between 16 and 59 have never had sex, and around one in 10 will not have had a sexual partner in the last year. These statistics are just a few of an orgy of initial findings reported from the Australian Study of Health and Relationships. The study was a quantitative survey conducted by a multidisciplinary research team; it covers a broad range of sexual and reproductive experience, including masturbation, sexual difficulties and commercial sex. Interviews with over 20 000 individuals were conducted between 1999 and 2002. More detailed reports from the study are expected. Aust N Z J Public Health 2003; 27: 103-256 Before 'fore' When it comes to sports-related ocular injuries in North America, golfing injuries of the eye rank third, behind ice hockey and air gun injuries. New Zealand authors have reported a series of 11 serious cases of golf-related ocular trauma seen at two tertiary hospitals. Four of the injuries were caused by golf clubs and occurred only in children who were playing with other children. Of the seven injuries due to golf balls, three occurred in spectators. The authors recommended supervision for children and, for adults, the wearing of protective polycarbonate lenses, which can be incorporated into sunglasses or prescription lenses. Clin Exp Ophthalmology 2003; 31: 110-113 Stonehenge and the vulva Canadian theorists have likened the layout of the ancient and mysterious Stonehenge to the anatomy of the human vulva. The outer stone circle would correspond with the labia majora as the altar stone would to the clitoris. By extending the analogy, they say the henge could represent, symbolically, the opening by which Earth Mother gave birth to the plants and animals on which the peoples of the time so depended – ie, via its empty geometric centre (the birth canal). J R Soc Med 2003; 96: 94-98 Prevent cancer, lose weight A prospective study of a cohort of 900 000 adults in the US has found that increased body weight is associated with increased death rates for all cancers combined and for cancer at many specific sites. Study subjects were cancer-free at enrolment. By the end of follow-up 16 years later, 57 145 deaths from cancer had occurred. Compared with men and women of normal weight, the risk of dying from cancer in those with a body mass index of at least 40 was 52% higher for men and 62% higher for women. In both men and women, a higher body mass index was also linked to increasingly higher rates of death due to non-Hodgkin's lymphoma, multiple myeloma and to cancer of the oesophagus, colon, rectum, liver, gallbladder, pancreas and kidney. N Engl J Med 2003; 348: 1625-1638 Hip protection . . . or not? The Amsterdam Hip Protector Study a randomised controlled (but not blinded) trial of 561 institutionalised elderly people at high risk of hip fracture has found that the hip protector studied was not effective in preventing hip fractures. Also, four of the 18 people in the intervention group who went on to fracture a hip did so while wearing protectors. The study researchers pointed out that theirs is the fourth of 11 published randomised controlled trials to report a negative finding; further, none of the four were considered in a Cochrane review of the matter. JAMA 2003; 289: 1957-1962 How SARS was contained A mass voluntary quarantine of over 5000 people was one of many steps undertaken by a 419-bed community hospital in Toronto that helped in the successful containment of an outbreak of severe acute respiratory syndrome (SARS) in that institution. The index case had been transferred from another hospital for urgent haemodialysis on 16 March 2003; a diagnosis of probable SARS was reached on 28 March 2003, after the patient had spent 13 days in the intensive care unit. In the interim, no specific respiratory isolation precautions were used and potential unprotected exposure of other patients and staff occurred. Because of uncertainty about SARS infectivity at the time, the public health measures taken included the quarantine of 1800 hospital staff, 225 physicians, as well as volunteers, patients and all visitors to the hospital in the period between admission and diagnosis of the index case; a screening questionnaire for all those entering the hospital; wearing of gowns, gloves and N95 masks by all staff and visitors to the hospital; cessation of many of the hospital's clinical services; and the development of a self-contained SARS Assessment and Treatment Unit. The outbreak was limited to 15 others: the patient's wife, three other patients, a hospital visitor and 10 staff, mainly nurses. CMAJ 2003; 168(11): Online-1-6