Respiratory disease

John C Bridgman,* William F Heddle† * Cardiology Registrar, † Cardiologist, Flinders Medical Centre, Flinders Drive, Bedford Park, SA 5042. cameronbridgmanAThotmail.com To the Editor: A 50-year-old morbidly obese woman (weight, 183 kg; body mass index, 70 kg/m2) presented after 1 month of worsening dyspnoea. Risk factors for cardiovascular disease included hypertension, smoking and previous heavy alcohol consumption. She had left ventricular failure (thought to be due to diastolic dysfunction) and atrial fibrillation with rapid ventricular response. There was no evidence of infection or pulmonary embolism. A transthoracic echocardiogram showed normal systolic function, although the images were poor. Measurement of arterial blood gases showed a compensated respiratory acidosis (Paco2, 58 mmHg; Pao2, 76 mmHg; pH, 7.39; bicarbonate, 34 mmol/L; base excess, 8 mmol/L). Administration of intravenous digoxin, frusemide and heparin led to some symptomatic improvement. Cardiac monitoring showed atrial fibrillation, with ventricular rates of 120–170 beats/minute despite the digoxin treatment. Overnight, 70 pauses in heartbeat of up to 7 seconds were recorded (Box). The constellation of the nocturnal rhythm disturbance, hypercapnia and obesity suggested sleep disordered breathing as a unifying diagnosis. Further questioning revealed symptoms indicative of obstructive sleep apnoea. Polysomnography, performed that night, showed a respiratory disturbance index (number of apnoeic or hypopnoeic episodes per hour) of 130 (normal value, < 15). The longest apnoeic episode was recorded at 34 seconds. The average minimum oxygen saturation was 84% during non-REM (rapid eye movement) sleep and 64% during REM sleep. The lowest saturations reached during non-REM and REM sleep were 64% and 61%, respectively. These results suggested severe obstructive sleep apnoea.1 The following night, her condition improved with application via mask of continuous positive airway pressure (CPAP) at a level of 12 cm H2O using room air. Cardiac monitoring continued to show atrial fibrillation with high ventricular rates, but no pauses in heartbeat occurred. This allowed treatment with atenolol and digoxin to control the ventricular rate. At 6-week review, the patient was complying with home CPAP therapy and felt well. An electrocardiogram confirmed spontaneous reversion to sinus rhythm at 70 beats/minute. There is increasing evidence to suggest a link between obstructive sleep apnoea and atrial fibrillation.2 Obstructive sleep apnoea is also a risk factor for hypertension, coronary artery disease and heart failure, all of which are known to precipitate atrial fibrillation.3,4 Transient heartblock has been found in 10% of patients with obstructive sleep apnoea. Pauses of up to 2 seconds are a predictable physiological response to inspiratory airflow obstruction and hypoxia. These pauses are exacerbated by negative chronotropes. Studies have shown that bradycardia can be effectively abolished with mask CPAP therapy.5 The dramatic response to CPAP therapy in this patient suggests that sleep apnoea caused the significant nocturnal ventricular pauses and had a role in the aetiology of the atrial fibrillation. Overnight cardiac monitor trace, showing atrial fibrillation and a 7-second pause

John C Bridgman · William F Heddle

Susan F Hurley Associate Professor, School of Population Health, University of Melbourne; and Health Economics Consultant, Bainbridge Consultants, 532 Brunswick St, North Fitzroy, VIC 3068. susanhurleyATbainbridgeconsultants.com To the Editor: Previous analyses of costs to the Pharmaceutical Benefits Scheme and costs for stroke and acute myocardial infarction hospitalisations suggest that tobacco control programs are a good investment.1,2 To further highlight the economic benefits of reducing smoking rates, I estimated the hospitalisation costs attributable to cigarette smoking in Australia for 2001–2002 by applying aetiological fractions to hospitalisation data.3 Aetiological fractions were calculated using 2001 National Health Survey smoking prevalence data and relative risks of hospitalisation for current and former smokers, as previously calculated by English and colleagues through linkage of data from the Busselton health survey and the Western Australian Hospital Morbidity Data system.4 Counts of separations (hospitalisations), bed-days, and average costs for hospitalisations in Australia in 2001–2002, by sex and 5-year age category, were obtained from the Australian Institute of Health and Welfare. They had been sourced from the National Hospital Morbidity Database (http://www.aihw.gov.au/hospitals/nhm_database.cfm) and the National Hospital Cost Data Collection (http://www.health.gov.au/casemix), linked by the common variable “DRG4.2”. The results (Box) show that, in 2001–2002, almost 300 000 hospitalisations, costing $682 million, were attributable to cigarette smoking. English and colleagues estimated previously that, in 1992, 129 000 hospital separations and over 1.1 million bed-days were attributable to cigarette smoking.4 Although the proportion of the Australian population who are smokers has decreased since then, from 26% to 23% in 2001,5 cigarette smoking is still associated with substantial health care utilisation and costs. The actual costs are even greater than the $682 million per annum estimated by my analysis, as the following were not considered: hospitalisation costs for those aged 80 years and over; pharmaceutical costs (estimated at $126 million for cardiovascular drugs on the Pharmaceutical Benefits Scheme1); community care costs (such as general practitioner visits); and patient contributions to hospitalisation costs. In stark contrast to the $682 million spent on hospitalisations attributable to smoking, the Australian Government has committed an average of only $2 million per year over the last 10 years to tobacco harm minimisation programs.6 Hospitalisations, bed-days and costs attributable to cigarette smoking in Australia in 2001–2002* Hospitalisations Bed-days Costs† Proportion Number Proportion Number Proportion $ (millions) Men 7.6% 138 000 14.6% 891 000 7.6% $339 Women 8.6% 153 000 9.8% 581 000 8.6% $342 Total 8.1% 291 000 12.2% 1 472 000 8.1% $682 * For people aged 40–79 years. † Estimated costs are conservative, as they are based on average cost per hospitalisation for the total population. However, the higher proportion of bed-days than hospitalisations attributable to smoking suggests smokers tend to have longer stays and thus higher than average costs.

Susan F Hurley

Dx/Rx: lung cancer. Christopher G Azzoli. Massachusetts: Jones and Bartlett, 2006 (viii + 134 pp). ISBN 0 7637 2641 9. This small, single-author American text in pocket-book format provides a succinct but comprehensive overview of lung cancer including its epidemiology, diagnosis and treatment. There are also brief sections on mesothelioma and thymoma. Reflecting the author’s specialty, the content is heavily skewed towards medical oncology. Surgical and radiation oncology aspects are given limited coverage. The style and level of detail suggest that this book would be most useful for medical students and junior hospital doctors, or even lay consumers with some scientific background. The information is presented as dot points — hardly literature, but readable. A brief list of up-to-date key references is provided at the end of each chapter. In general, the information presented is accurate, although there are a few howlers: “Asbestos is ... used as inflammable building material”. “Anyone with a first degree relative with a smoking related cancer should not smoke cigarettes.” It is irritating to see myths perpetuated, such as “carcinoid tumours are highly resistant to chemotherapy and radiotherapy” and “large cell neuroendocrine tumours carry a poor prognosis compared with other types of non-small cell lung cancer”. What is the evidence for these statements? There are good practical hints on the management of complications of lung malignancy (these would be most useful for junior hospital doctors). There is, however, no mention of the use of lasers or stents for the treatment of major airway obstruction. So, in summary, a concise and contemporary overview, but too superficial for the practising clinician managing lung cancer. If the reader requires an evidence-based manual that contains statistics and treatment recommendations more relevant to Australian practice, I would suggest the NHMRC-endorsed Clinical practice guidelines for the prevention, diagnosis and management of lung cancer, recently published by the Australian Cancer Network. David L Ball Chair of Lung Service and Radiation Oncologist, Peter MacCallum Cancer Institute, Melbourne, VIC

David L Ball

A recent report outlines the good and the bad news about asthma Asthma is a common chronic condition among Australians, particularly children. In recent years, federal and state governments have responded to community and health professionals’ concerns by investing in strategies to improve asthma management.1 Coinciding with this, new pharmaceutical formulations have become available for managing asthma. The latest publication from the Australian Centre for Asthma Monitoring and the Australian Institute of Health and Welfare, Asthma in Australia 2005,2 provides a timely review of the good and the bad news about asthma over the past few years (Box). The prevalence of asthma is high in Australia compared with other countries,3 affecting 14%–16% of children and 10%–12% of adults. However, Asthma in Australia 2005 shows that, after a substantial rise in the number of children with asthma during the 1980s and early 1990s, this trend has reached a plateau. Although this pattern is consistent with observations in other countries, including Hong Kong, Switzerland and the United Kingdom,4 the reasons for this rise and subsequent plateau remain unknown. Nevertheless, the observation highlights the value of ongoing surveillance for asthma. Over the past 5–10 years, rates of general practitioner visits and hospitalisations for asthma have declined substantially. Furthermore, deaths due to asthma have fallen by more than 50% since the early 1990s. Despite these overall gains, there are important inequalities in the outcomes of asthma among Australians. Aboriginal and Torres Strait Islander people, particularly adults, have more asthma and higher rates of hospitalisation for asthma than other Australians. Adults living in rural or remote areas and people living in the most socioeconomically disadvantaged localities also have higher rates of hospitalisation for asthma. The reasons for these inequalities need exploring. The burden of GP consultations, emergency department visits and hospitalisations for asthma is highest among children and probably reflects their higher rate of disease exacerbations. At the beginning of school terms, particularly in February, rates of emergency department attendance for asthma are higher than usual and the episodes are more severe than usual among pre- and primary-school-age children. A similar return-to-school increase has been observed in other countries, and has been attributed to increased transmission of respiratory infections.5 This observation highlights the need to develop and test interventions to prevent exacerbations. Regular use of inhaled corticosteroids can reduce asthma symptoms and prevent severe episodes of worsening asthma.6,7 However, Asthma in Australia 2005 highlights evidence that inhaled corticosteroid therapy, the cornerstone of drug therapy for asthma, is not well targeted. Many people who would benefit from using them regularly are not doing so. Furthermore, most formulations are prescribed at the highest doses, in spite of evidence that many people with asthma can be well controlled, with fewer side effects, at lower doses of inhaled corticosteroids.8 This discrepancy with current evidence is further highlighted by the rapid market penetration of inhaled formulations that combine long-acting β-agonists with corticosteroids, a combination which achieves effective asthma control in most people with moderate to severe asthma with lower doses of inhaled corticosteroids.9 These combined formulations accounted for 64% of inhaled corticosteroids distributed in Australia in 2004. Hence, more work is needed to improve appropriate prescribing of inhaled corticosteroid therapy for people with asthma. The Asthma 3+ Visit Plan is an Australian Government initiative introduced to improve the quality of care for people with moderate to severe asthma by promoting structured care of asthma in general practice. However, it is estimated that only 14.1% of eligible people have used this program since its introduction in 2002. Respondents to a survey of GPs in Sydney indicated that the administrative complexity of the program acted as barrier to its uptake.10 Another cause for concern is the limited use of written asthma action plans. Despite evidence that these improve the outcomes of asthma,11 their use has decreased in recent years.12 Asthma in Australia 2005 shows that the outcomes of asthma in Australia are improving, but there is still a long way to go to ensure access to the best quality care for all Australians. We need to understand more about the barriers to effective care and the basis for inequalities in health outcomes for people with asthma.10,13 To investigate these issues, we need more detailed asthma-specific data at a population level, qualitative research in specific populations of health care users and providers, and randomised controlled trials of interventions designed to improve care and outcomes, particularly in disadvantaged groups. Major findings of the Asthma in Australia 2005 report Gains The rising trend in the prevalence of asthma among children during the 1980s and early 1990s has reached a plateau. Currently, 14%–16% of children and 10%–12% of adults have asthma. In 1990, there were 822 deaths attributed to asthma in Australia (5.6 per 100 000), whereas in 2003 there were 314 deaths (1.5 per 100 000). Hospitalisation rates for asthma have declined from 920 patient-days per 100 000 in 1993–94 to 419 patient-days per 100 000 in 2003–04. No gains Hospitalisation rates for asthma in 2002–03 were higher among: Aboriginal and Torres Strait Islander people compared with others in Australia (1003 v 418 patient-days per 100 000); Adults in rural and remote areas compared with adults in major cities and regional areas (728 v 331 patient-days per 100 000); and People with greater levels of socioeconomic disadvantage (528 patient-days per 100 000 in the most disadvantaged quintile v 309 patient-days per 100 000 in the most advantaged quintile). Only 34% of people with asthma aged 15 years and over are using inhaled corticosteroids, but 71% of inhaled corticosteroids are supplied in the highest dose formulations. In South Australia, the proportion of people with asthma who stated that they owned a written asthma action plan declined from 42% in 1995 to 22% in 2001.

Guy B Marks MB BS, PhD, FRACP · Patricia K Correll MPH · Margaret Williamson MPH

Objectives: To ascertain what general practitioners’ priorities are for achieving optimal outcomes in people with asthma, and the barriers they face in delivering this care.Design: A qualitative study using the Nominal Group Technique (a highly structured meeting to gain information from experts about a particular issue) was conducted between August 2002 and September 2003. GPs in six discussion groups were asked “What do you think is needed to achieve best outcomes for asthma care?” To augment analysis of the discussion, sessions were taped and transcribed.Participants: Forty-nine GPs were recruited: 34 from metropolitan and 15 from rural areas.Results: All groups nominated asthma education for patients and continuing professional education for GPs as major priorities, but they also described educational and structural barriers to achieving these priorities. Other priorities were: medication adherence, facilitating regular patient review, negotiated treatment/management plans, making the correct diagnosis, increased remuneration and consultation time, and safer asthma medications and access to these. Health promotion initiatives and increased public awareness were also priorities. Spirometry was a significant cause of uncertainty. Overall, written asthma action plans were not considered a high priority.Conclusions: Remarkable consistency was found between GPs’ priorities for delivering best asthma care. Our study identified barriers to asthma guideline adherence, including accessible, relevant education for GPs, and structural, time and cost barriers GPs must overcome in providing asthma treatment and patient education.

Dianne P Goeman MA, DipSoc · Jo A Douglass MD, FRACP · Chris D Hogan MB BS, FRACGP · Rosalie A Aroni PhD · Michael J Abramson PhD, FRACP · Susan M Sawyer MD, FRACP · Kay Stewart PhD · Lena A Sanci MB BS, FRACGP, PhD

As I recently walked around Canberra’s Lake Burley Griffin in an air temperature of 5°C, I had plenty of time to contemplate the position statement on acute domiciliary oxygen therapy recently published in the Journal.1 I have fibrosing alveolitis and am awaiting a lung transplant. I am on domiciliary oxygen therapy 24 hours a day. There is much in the position statement to congratulate the authors on. They have rightly identified the importance for people like me of maintaining an increased level of fitness, which incorporates the use of ambulatory oxygen therapy to improve our prognosis. They have also identified contraindications for oxygen therapy, cited the appropriate levels of evidence as prescribed by the National Health and Medical Research Council, searched MEDLINE, and undoubtedly worked their way through the various committees of the Thoracic Society of Australia and New Zealand (TSANZ). What then is missing? The patients! Perhaps I am being unfair to the authors and perhaps there is a process within the TSANZ structure whereby consumers were consulted on the position statement, but this is not immediately evident. If consumers were partners in the development of this statement, it might have been possible to address its four glaring omissions: The issues of access to and equity of oxygen supplies across Australia; Portability and comfort; Assessment and review; and Quality of life. Access and equityWhile it is well known among respiratory and thoracic physicians that not all Australians have access to free or subsidised oxygen, it is not well known in the community. Different states and territories have differing rules for patients who are on oxygen therapy. Victoria, Tasmania, South Australia and Western Australia routinely provide free oxygen, based on clinical need, irrespective of the patient’s financial position. Queensland will generally provide the service if the patient is on a lung transplant waiting list, but otherwise its approach is similar to that in New South Wales, where all patients are vetted by a means test. The means test is particularly harsh, and patients must have a government Health Care Card. The Australian Capital Territory changed its rules from 1 July 2004 to bring it into line with Victoria, Tasmania, South Australia and Western Australia. Why is it that some people in Australia have access to free or subsidised oxygen supplies and others do not? I often hear health ministers, state and federal, boasting about the wonderful universal health system we have in Australia. Everyone pays their taxes and their Medicare levies — yet, at the whim of a postcode, some people do not have access to a basic supply such as oxygen. Another access and equity issue is whether the supply of oxygen is capped (ie, whether patients have access to unlimited supplies of cylinders per week or per month). While, for example, the ACT Health Minister recently explained that access would not be capped when the new system was introduced, in reality oxygen therapy is restricted by a contract. I am in the lucky position of being on a lung transplant list, and therefore my access is not capped. However, there are other (generally elderly) patients who are limited to small supplies of oxygen each month because their disease, prognosis or age precludes them from the opportunity of a lung transplant. A further difficulty is that there are currently only three lung transplant units in Australia (in New South Wales, Victoria and Queensland). I am required to attend a lung transplant unit interstate every 6–8 weeks, as are other patients. Some ACT patients have been told that, if they travel interstate, they will not have access to the ACT government-funded oxygen supply while they are travelling or staying interstate. The limited number of lung transplant units means that the chances of patients having to travel with oxygen are quite high. Yet, because they are travelling and not resident in the state with the lung transplant unit, they are required to pay for their own oxygen. There is surely a better way of managing all patients, irrespective of their state of residence. Portability and comfortThe position statement mentions a range of oxygen delivery modes. The most commonly used portable cylinder in Australia is the “C” cylinder, which weighs over 4 kg when full. This is far too heavy to allow me to maintain an independent lifestyle, and I have been able to obtain CFR (carbon fibre wrap) fibreglass cylinders, which weigh less than 4 kg when full and fit neatly into a backpack. I use one when out exercising and for most of my daily life. However, even the CFR cylinder is too heavy for the long walk around the Lake, especially on chilly days. Oxygen suppliers have rentable lightweight trolleys, but these are unstable on any surface other than a smooth surface. My husband has therefore redesigned a golf buggy (I hate golf anyway) so that my cylinder can fit neatly into that. The buggy’s wheel base is wide enough to allow it to cross all sorts of terrain. Stairs, however, are a problem. What a joy it would be to all Australians needing oxygen therapy to have access to lightweight, longlasting liquid oxygen systems that weighed less than gas cylinders and did not require constant visits to oxygen suppliers for refilling. Patients in the United States and now the United Kingdom (a new system was announced in June 2005) have access to liquid oxygen, but suppliers in Australia do not provide such a system. I am told that this is because clinicians do not want to prescribe liquid oxygen. While the position statement gives a thorough analysis of systems available, it might have been useful if some comment were made about what patients would prefer, as the inconvenience of the accoutrements available to enhance or prolong our lives makes the whole illness process much worse than it needs to be. Assessment and reviewThe position statement correctly suggests that patients should be reviewed within 1–2 months of beginning oxygen therapy, and thereafter at 12-monthly intervals. However, there is no mention of who should undertake these reviews. The logical assumption — and, indeed, good clinical practice — would be that thoracic/respiratory physicians would fulfil this role. However, recently in the ACT I was contacted by the oxygen supplier who has the government contract and told it was time for my respiratory review, which would be undertaken by the oxygen supplier! I have to wonder at the appropriateness of such an arrangement, in view of the following: Conflict of interest. It is in the oxygen supplier’s interest to increase sales of oxygen. Clinical governance. Oxygen suppliers are generally just that. They do not have a clinical governance structure in place to ensure that their ability to undertake clinical assessment is appropriate. Issues such as calibration of equipment and competence and currency of staff are also key concerns. As is privacy: I was told that my results would be passed on to the administration of my local health department, an organisation whose role does not include the maintenance of patient records. Repetitive assessment. All patients being prescribed oxygen are assessed by appropriate thoracic/respiratory physicians. Their lung function and other indicators are assessed at regular intervals. To incorporate another layer of review by an oxygen supplier is demeaning and disruptive to patients. Quality of lifeThe authors of the position statement touch briefly on quality-of-life issues, but seem to have little understanding of what quality of life means for people dependant on oxygen therapy. Rarely does a patient wish to remain confined to barracks, tied to an oxygen concentrator. Patients’ outlook on life is greatly enhanced by making some attempt to lead as normal a life as possible. In my own case, I am relatively young and it is essential that I maintain an active lifestyle to help me look after a young family and to ensure readiness for lung transplantation. Debilitating diseases such as fibrosing alveolitis and cystic fibrosis have a huge impact on family life. Regular and uncapped supply of an extremely basic commodity like oxygen goes some way towards alleviating the stress on families and individuals in coping with the psychosocial aspects of the disease. Issues and suggestionsOne might argue that the authors were trying to provide evidence-based guidelines for the clinical aspects of oxygen therapy — that they never claimed to be doing more than that, and wouldn’t presume to speak for patients or funding bodies. But is that good enough? Can the quality of life of patients (as they see it) and the appropriateness of reviews of their need for oxygen therapy really be irrelevant to their doctors? And there are other issues. I have met people who have struggled out of their vehicles, put their cigarettes out, and wheezed their way in to the “oxygen shop” for their free oxygen because they fulfil the requirements of the means test (while others, equally or more deserving, have to wait in line to pay for theirs). Does it seem right that patients who are not committed to improving their health outcomes should have ready access to such a scarce resource? Perhaps it is time for some of the tobacco tax to be put into funding oxygen supplies. While cigarette smoking does not cause all of the lung disease occurring in Australia, it is responsible for a large burden of disease and death, including death from lung cancer, chronic obstructive pulmonary disease and heart disease. It is also evident that the multilayered federal/state government arrangements for managing health care in Australia are totally inappropriate for managing something as basic as oxygen. Perhaps it is time for individual states and territories to relinquish the funds they are currently using for oxygen therapy and for the federal government to assume a management role, as they do with pharmaceuticals. This seems to me to be the only equitable way of allocating oxygen on the basis of need, rather than state of residence. Indeed, the United Kingdom has just introduced a centrally managed system for providing oxygen therapy, recognising the fragmented nature of the previous system. In common with other patients, I will no doubt shortly become an orthopaedic surgical patient as a result of an aching back due to carting around heavy oxygen cylinders. Although I have the lighter oxygen cylinders, they become quite heavy on my back and shoulders. Perhaps it is time for physicians to start advocating for the comfort of their patients through the medical colleges or the TSANZ. A shift towards liquid oxygen systems would be welcomed by many who have lung disease and require oxygen therapy. Surely it is also time for the medical colleges and/or the TSANZ to agree on some basic forms that physicians could use for prescribing and reviewing oxygen requirements. This would ensure that patient dignity and privacy issues were maintained. Quality-of-life issues for patients requiring oxygen therapy should also receive more than passing attention from clinicians. I am told that there is an extremely high number of patients awaiting lung transplantation who are also taking antidepressants. This is hardly surprising, given that such patients have so much of their independent lifestyle removed so quickly. Surely this issue should also be discussed when considering how best to provide domiciliary oxygen therapy. A final commentPatients (or consumers, as we are sometimes called) are central to the business of illness. They know a lot about their diseases. This is not to say that some are not ill informed. However, there is a vast wealth of knowledge and experience to be tapped in having patients as partners in the development of position statements such as the recent one on domiciliary oxygen therapy.1 The TSANZ’s position statement is a good, solid, clinical paper. It could have been a great, patient-friendly statement if the views of patients had been sought and incorporated.

Anne E Cahill Lambert AM, MPubAdmin, BHA

We welcome the incisive comments from Cahill Lambert (page 472).1 The remit of our position statement2 was to update our previous evidence-based guidelines for the prescription of oxygen in Australia and New Zealand by reviewing the currently available literature. Informal consultation with consumers was made through the Australian Lung Foundation’s COPD (chronic obstructive pulmonary disease) Consultative Group, but no funding was available to seek broader community comment. Our position statement supports the use of ambulatory oxygen as part of continuous oxygen therapy in patients who fulfil criteria for long-term oxygen therapy — both to maximise the duration of normal blood oxygen concentrations and to maximise exercise capacity. Two of us (A J C, C F M) have been actively involved in research around the issue of quality of life of patients on long-term oxygen therapy.3-6 It has not yet been confirmed whether ambulatory oxygen is of significant benefit in this area.7,8 The unwieldiness of some of the currently available portable cylinders may counteract some of the potential gains of using ambulatory oxygen, but we have not been successful in securing the widespread use of liquid oxygen in Australia. It is yet to be demonstrated that the extra costs associated with a liquid oxygen system are balanced by greater benefits in useability (portability and comfort) and quality of life. Although we are keenly aware that there are major issues of equity and access to ambulatory oxygen therapy across Australia, as Cahill Lambert correctly asserts, discussing these issues was outside the parameters (and space constraints) of our position statement. While we may consider oxygen to be equivalent to a “drug” for the purposes of this discussion, oxygen, unlike pharmaceuticals, is not a federally-funded commodity but is provided on a state-by-state basis through programs such as the Victorian Aids and Equipment Program (except in the case of war veterans, who are funded through the Department of Veterans’ Affairs). Individual state funding arrangements have led to inequalities in the provision of this service. It is our understanding that New South Wales and Queensland do not currently supply portable oxygen to adults requiring long-term continuous oxygen therapy delivered by concentrator. However, Victoria, Tasmania, Western Australia and South Australia provide portable oxygen cylinders to such patients and to others who have demonstrable evidence of desat-uration on exertion and measurable benefit from portable oxygen therapy (in terms of improved exercise capacity or reduced breathlessness). There are caps on supply, with only a certain number of cylinders allowed per month in most instances. Capping, although understandable in fiscal terms, makes little sense to patients trying to maximise their exercise capacity (and quality of life) by exercising regularly with the help of ambulatory oxygen. We recommended in our position statement that patients requiring oxygen therapy should be assessed and reviewed on a regular basis. Although not explicitly stated in our position statement, we believe this review should be undertaken by the clinician managing the patient. We agree with Cahill Lambert that there is a potential conflict of interest in the review being conducted by the company supplying the oxygen. We support her call for more advocacy in this area, but assure her that we have personally been advocating for a fairer and more equitable system for many years. Patient advocacy groups, such as those run through the Australian Lung Foundation, as well as organisations such as the Thoracic Society of Australia and New Zealand clearly have an important role to play in ensuring that this issue makes its way onto the political agenda. We believe that further research is the key to providing more definitive answers to some of the more contentious questions around oxygen provision. Specific areas of research should include portable oxygen use in patients not requiring continuous oxygen therapy, nocturnal oxygen use in patients whose daytime resting arterial blood gas levels would preclude them from receiving continuous oxygen therapy, and the use of palliative oxygen therapy in non-hypoxaemic patients. A more extensive body of data in these areas would allow future updates of our position statement to provide higher levels of evidence, which we hope would translate into a more consistent approach to oxygen provision in Australia.

Christine F McDonald MB BS, FRACP, PhD · Alan J Crockett PSM, MPH · Iven H Young PhD, FRACP

Heather Cleland Director, Burns Unit, The Alfred Hospital, Commercial Road, Prahran, VIC 3181. burnsunitATalfred.org.au To the Editor: While mention is made in the recent position statement1 of the inappropriateness of home oxygen use in association with continued smoking, I wish to highlight the fact that the dangers of this activity — and indeed of any open flame in proximity to oxygen delivery units — constitutes significantly more than a theoretical hazard. In the past 4 months, the Victorian Adult Burns Service at The Alfred Hospital, Melbourne, has admitted two patients with severe burns sustained in fires caused by smoking in association with domiciliary oxygen use. Both these patients died of their burn injuries, and the cases have been reported to the coroner. I am aware of at least one other fatality that occurred under similar circumstances in the same time period in Victoria. If patients or people living with them continue to smoke, oxygen therapy should be withdrawn. I also suggest that the position statement should emphasise the need for adequate and regular domiciliary assessments of people using this therapy and the importance of ongoing education about the dangers of oxygen use in association with any open flame.

Heather Cleland

Anthony Proust was born in Sydney on 23 February 1924 and graduated in medicine from the University of Sydney in 1948. After doing his residency at the Royal Prince Alfred Hospital, he studied and worked overseas from 1950 to 1953, first at Winnipeg General Hospital and the Manitoba Sanatorium in Canada, then at Johns Hopkins Hospital in Baltimore, and finally in Edinburgh and London. In 1953 he gained membership of both the London and Edinburgh colleges of physicians. As a well trained general physician with expertise in thoracic medicine and diabetes mellitus, Tony moved to Canberra in 1954. He first practised medicine in a partnership and later entered full-time consultant practice. Tony’s expertise in tuberculosis and lung disease led to an invitation to become foundation Director of Tuberculosis for the Australian Capital Territory and Director of the Canberra Chest Clinic, a position he held from 1967 until his retirement in 1985. He was elected Fellow of the Royal College of Physicians (Edinburgh) (1971), the Royal Australasian College of Physicians (1978) and the Royal College of Physicians (London) (1981). One of Tony’s major contributions to medical research was as coordinator of the Australian Rifampicin Trial (published in 1971 and 1972), a trial that led to the drug becoming the mainstay of antituberculosis treatment, which it remains to this day. In 1984, he founded a medical periodical, the Australian Tuberculosis Newsletter, a publication that remains alive and well. He was a longstanding member of both the Thoracic Society of Australia and New Zealand and the Australian Society of the History of Medicine. Tony’s reputation also extended outside Australia. In 1981, Sr Mary Aquinas invited him to work with her at the world famous Ruttonjee Hospital for tuberculosis in Hong Kong. In 1991, St John’s Medical College, Bangalore, appointed him Visiting Professor of Medicine. Tony’s interest in diabetes continued, and his passion for the history of medicine grew with age. His History of tuberculosis in Australia, New Zealand and Papua New Guinea was published in 1991, and his final book, A companion of the history of medicine in Australia 1788–1939, appeared in 2003. He was contemplating another work, on medical women in Australia, when his last illness, cryptogenic fibrosing alveolitis, overtook him on 16 May 2005. He is remembered by his wife Moya, their five children and eight grandchildren. -->

John Thompson FRACP, FRCPE, FCCP

Objective: To determine whether community management of mild to moderate community-acquired pneumonia (CAP) is as effective and acceptable as standard hospital management of CAP.Design: Randomised controlled trial.Setting: Christchurch, New Zealand, primary and secondary care.Participants: 55 patients presenting or referred to the emergency department at Christchurch Hospital with mild to moderately severe pneumonia, assessed using a validated pneumonia severity assessment score, from July 2002 to October 2003.Interventions: Hospital treatment as usual or comprehensive care in the home delivered by primary care teams.Main outcome measures: Primary: days to discharge, days on intravenous (IV) antibiotics, patient-rated symptom scores. Secondary: health status measured using level of functioning at 2 and 6 weeks, patient satisfaction.Results: The median number of days to discharge was higher in the home care group (4 days; range, 1–14) than in the hospital groups (2 days; range, 0–10; P = 0.004). There was no difference in the number of days on IV antibiotics or on subsequent oral antibiotics. Patient-rated symptom scores at 2 and 6 weeks, median change in symptom severity from baseline to 6 weeks, and general functioning at 2 and 6 weeks did not differ between the groups. Patients in both groups were satisfied with their treatment, with a clear preference for community treatment (P < 0.001).Conclusions: Mild to moderately severe CAP can be managed effectively in the community by primary care teams. This model of comprehensive care at home can be implemented by primary care teams with suitable funding structures.

Dee A Richards MB ChB, DPH(Dist) · Les J Toop MD, MRCGP, FRNZCGP · Michael J Epton MRCP, FRACP, PhD · G Ian Town MB ChB, FRACP, DM · Robin D Dawson MB ChB, MRCGP, DCH · Michael C Hlavac MB ChB, FRACP · Graham R B McGeoch MB ChB, FRNZCGP · Simon M H Wynn-Thomas BM BS, MRCGP, FRNZCGP · Paul D Abernethy BA(Psych), RN · Anja M Werno MD, FRCPA

Objective: To examine the effects of asbestos exposure and tobacco smoking on the level and rate of change of the diffusing capacity of the lung for carbon monoxide (Dlco).Design and participants: A cohort study of 934 people (including both mine workers and town residents) exposed to crocidolite (blue asbestos) at the asbestos mines and in the town of Wittenoom, Western Australia, between 1943 and 1966. Dlco measurements were taken during a follow-up period from 1992 to 2002.Main outcome measures: Baseline levels of Dlco and change in levels over time.Results: 2980 Dlco measurements were done on 934 people (of whom 818 were men and 724 were workers) who underwent a median of 2 (range, 1–17) measurements during the follow-up period. Radiographic asbestosis at baseline and asbestos exposure at a younger age were associated with lower Dlco values. The average rate of decline in Dlco was 0.33 (95% CI, 0.31–0.35) units per year, plus an additional decrement of 0.22 (95% CI, 0.12–0.32) units per year if the participant had radiographic asbestosis at the beginning of the follow-up period. Compared with never-smokers, current smokers and ex-smokers had lower Dlco at baseline, but smoking status did not affect the change in Dlco during the follow-up period.Conclusions: Our results confirm a continuous deleterious effect of crocidolite on Dlco, especially on people with asbestosis. Smoking was associated with lower Dlco levels, but was not a significant predictor of rate of change in Dlco. Smoking status did not affect the relationships between crocidolite exposure and the level or rate of change of Dlco in this population.

Helman S Alfonso PhD · Lin Fritschi PhD · Nicholas H de Klerk PhD · Nola Olsen MSc · Jan Sleith MSc · Arthur (Bill) W Musk PhD, FRACP

To the Editor: The clinical update on venous thromboembolism by Lee and colleagues advises that “Ventilation perfusion (V/Q) isotope scanning reliably establishes the diagnosis of PE [pulmonary embolism] if the V/Q features suggest a high probability of PE . . .”.1 Although this is probably true for patients with intermediate or high pretest probability, a discordant result (low pretest probability and high probability V/Q) should be regarded with suspicion. From the original PIOPED data, high probability V/Q was predictive of angiographically confirmed PE in 80% of patients,2 which drops to 56% by Bayesian analysis if the pretest probability is low. False positive results may be due to previous PE or unrelated parenchymal lung disease. There is significant potential morbidity associated with a false positive result for PE, both from the acute anticoagulation and for future presentations with PE-type symptoms, where PE will be accorded a higher probability because of the previous documented diagnosis. As Lee and colleagues also state, D-dimer testing must be combined with an estimate of pretest probability to be useful. They advocate excluding PE on the basis of low pretest probability and negative D-dimer result. However, a negative D-dimer result (rapid enzyme-linked immunosorbent assay [ELISA] type) may be used to exclude PE in intermediate as well as low probability patients.3 This is dependent on the type of assay available as well as the local PE prevalence, and local guidelines should therefore be developed.

Matthew J Bragg

To the Editor: I read with interest the article by Lee et al regarding the investigation and treatment of pulmonary embolism (PE).1 The investigation of patients presenting with PE as a diagnostic possibility is of great interest to emergency physicians, and such presentations are a daily occurrence in emergency departments around the country. Unfortunately, only a small amount of text is devoted to describing the relative merits of ventilation perfusion (V/Q) scanning and computed tomography pulmonary angiography (CTPA), and no guidance is provided as to which is the test of choice when both are available. The British Thoracic Society has recommended CTPA as the lung imaging modality of first choice for patients presenting with non-massive PE.2 There is a large and increasing body of evidence that CTPA provides superior specificity to V/Q scanning in the detection of PE. CTPA also provides the opportunity of establishing diagnoses other than PE and, in addition, a negative multi-slice CTPA is of sufficient sensitivity to enable the withholding of anticoagulation.3 It is also my experience that CTPA is easier to obtain out of hours, compared with V/Q scanning. The authors state that V/Q scanning “reliably establishes the diagnosis of PE if the V/Q scan features suggest a high probability of PE . . .”.1 Unfortunately, this statement is incorrect. It is essential that V/Q scan results be interpreted in the light of the patient’s clinical probability for PE. In the PIOPED study, only 56% of patients with high probability V/Q scan reports had pulmonary embolism if the pretest probability was low.4 No mention is made of the special situation of pregnant women presenting with pleuritic pain, or which lung imaging test is considered “safest” for both mother and baby. Although the risks of PE are generally agreed to be increased in pregnancy, it is my experience that pregnant women are extremely reluctant to undergo any form of diagnostic investigation that exposes the fetus to radiation. The Wells criteria have been validated for the assessment of PE in emergency department patients only, and provide a means for clinicians with little experience to make an accurate assessment of an individual patient’s clinical probability of PE.5 Once initiated, clinical assessment of the patient with possible PE is straightforward. The key question facing emergency physicians is this: is there a group of patients that have such low probability for PE that no investigation at all is required?

Paul M Bailey

John W Eikelboom,* Graeme J Hankey,† Wai Khoon Ho,‡ Cindy H Lee§ * Haematologist, Thrombosis Service, McMaster University, HHS General Divison, 237 Barton Street East, Hamilton, ON L8L2X2, Canada; † Neurologist, ‡ Fellow in Haematology, § Senior Registrar in Haematology, Royal Perth Hospital, Perth, WA. eikelbj@mcmaster.ca In reply: Pulmonary embolism (PE) remains a complex diagnosis despite the availability of validated prediction models and D-dimer testing to direct the need for diagnostic imaging. We agree with Bailey that the ability to exclude the diagnosis of PE on clinical grounds in patients with a low pretest probability is highly desirable. Unfortunately, clinical features lack sensitivity and specificity for the diagnosis of PE, and clinical prediction models, laboratory investigations, and diagnostic imaging are likely to remain an integral part of the clinical work-up. As suggested by Bragg, it may be possible to simplify the diagnostic approach by using a highly sensitive D-dimer assay, and simplified pretest probability models have been proposed. However, this may come at a cost of reduced specificity,1 which leads to unnecessary diagnostic imaging studies and thus limits the clinical utility of these approaches. Further improvements in the diagnostic approach to PE are clearly needed. There are emerging data demonstrating the accuracy of computed tomography pulmonary angiography (CTPA) for the diagnosis of PE. However, CTPA has limitations (a large contrast load, high radiation dose, and lack of sensitivity of first generation scanners for small thrombi2), some of which are evident in the recently published validation study referred to by Bailey:3 25% of screened patients with suspected PE were not eligible for this study because of renal impairment, a contraindication to CT, or other reasons. The diagnostic algorithm that we provided in our review suggests that either ventilation perfusion (V/Q) scanning or CTPA can be used for patients with suspected PE who require diagnostic imaging,2 with the choice determined by patient factors and availability. The diagnosis of PE during pregnancy is challenging because of concerns about radiation exposure and uncertainty about whether CTPA or V/Q delivers more radiation to the fetus.4 Furthermore, clinical decision rules have not been validated in pregnancy. However, recommendations from experts and professional bodies suggest that V/Q scanning can be used in combination with compression ultrasound to establish or exclude the diagnosis of PE during pregnancy in most cases with minimal fetal radiation exposure.5,6 The comments by Bailey and Bragg concerning the interpretation of high probability V/Q scan results highlight the pitfalls of performing diagnostic imaging without considering the patient’s pretest probability of PE. Although a high probability V/Q scan is diagnostic in patients with a moderate or high pretest probability of PE (prevalence of disease ≥ 90%), the prevalence of disease is only about 50% in those with a low pretest probability.7,8 Therefore, V/Q scanning should not be performed in patients with a low pretest probability unless the D-dimer test is positive. In this situation the algorithm for moderate or high pretest probability should be followed,2 and a high probability scan reliably establishes the diagnosis.

John W Eikelboom · Graeme J Hankey · Wai Khoon Ho · Cindy H Lee

Re: “Adult domiciliary oxygen therapy. Position statement of the Thoracic Society of Australia and New Zealand”, by Christine F McDonald, Alan J Crockett and Iven H Young, in the 20 June issue of the Journal (Med J Aust 2005; 182: 621-626). In the section on “Nocturnal oxygen therapy”, the hypoxaemia selection criterion for the study by Chaouat et al (reference 19) on page 623 (column 1) should read “Pao2 56–69 mmHg (7.4–9.2 kPa)” rather than “Pao2 56–59 mmHg (7.4–7.8 kPa)”. The html and pdf versions of the article published online were corrected on 28 June.

Christine F McDonald · Alan J Crockett · Iven H Young

Asthma can occur in any age group from the very young to the very old. However, evidence suggests that a broad range of complicating factors and comorbidities specific to the ageing population frequently confound the accurate diagnosis and treatment of older Australians with asthma. In response to such evidence, the Asthma Foundations of Australia, in partnership with the Macquarie Bank, hosted a Colloquium focusing on “Asthma ...

Christopher Pyne MP

The statistics behind asthma will be known to almost everyone reading this report. A disease affecting 2.2 million Australians, it reaches across all age groups. One in six children of primary-school age has asthma, while, at the other end of the spectrum, chronic asthma affects up to 10% of people aged over 65. In recent years, the figures have improved, but the incidence of asthma in ...

David Clarke AO

When Australia’s first Asthma Foundation was started in 1962, the body of knowledge about asthma was minimal. At best, asthma was thought to be related to allergies, and at worst it was considered to be the consequence of overprotective mothers. It became clear to the founding mothers of the Asthma Foundation that medical and scientific research was essential in order to establish a body of ...

Peter Adamson

Asthma and airway diseases are a significant problem for older Australians. They cause a large burden of illness in the community, and in primary care settings they present particular problems for diagnosis and management. Despite this, much of what we now know and do for asthma in older Australians is based on studies conducted in young people with asthma, and these findings may be of ...

Peter G Gibson MB BS, FRACP · Richard E Ruffin MB BS, FRACP, MD

What we need to knowWhat we need to do

Guy B Marks PhD, FRACP · Leanne M Poulos BMedSc(Hons)

What we need to knowWhat we need to do

Alan L James MB BS, FRACP, MD · Matthew W Knuiman BSc, PhD · Helen C Bartholomew BSc, GradDipComp · Arthur (Bill) W Musk MB BS, FRACP, PhD

What we need to knowWhat we need to do

David H Wilson PhD · Sarah L Appleton BSc · Robert J Adams MD · Richard E Ruffin MD

What we need to knowWhat we need to do

Michael J Abramson PhD, FRACP

What we need to knowWhat we need to do

Dianne P Goeman MA, GradDipSoc · Jo A Douglass MD, FRACP

What we need to knowWhat we need to do

Norbert Berend AM, MD, FRACP