General medicine

Editorial Where has all our iodine gone? The possible re-emergence of iodine deficiency in Australia needs to be investigated in national surveys MJA 1999; 171: 455-456 Most countries in the world, including Australia, are signatories to the United Nations-sponsored "Declaration for the Survival, Protection and Development of Children", which states that "every child has the right to an adequate supply of iodine to ensure its normal development".1 One teaspoon of iodine is all a person requires in a lifetime, yet iodine deficiency at critical stages of development in fetal life and early childhood remains the world's single most important and preventable cause of mental retardation.2For the past three to four decades iodine deficiency has not been of significant concern in Australia (except in Tasmania); it was considered largely a problem of developing countries. That is what we thought until Gunton and colleagues give us a wake-up call with their article in this issue of the Journal 3. They found evidence of mild to moderate iodine deficiency in pregnant women, patients with diabetes and a small group of volunteers attending a Sydney teaching hospital. In their study, median urinary iodine concentrations ranged from 64 µg/L in the volunteers to 104 µg/L in pregnant women. The World Health Organization's standard for iodine-deficiency disorders in population surveys recommends that a median urinary iodine concentration above 100 µg/L is evidence against significant iodine deficiency in that population.4 Other population indicators of iodine deficiency, including total goitre rates in school-age children and serum thyrotropin (TSH) levels in the newborn, were not assessed in the Sydney study. The data of Gunton and colleagues indicate that the pregnant women they tested are ingesting less than half the recommended iodine intake in pregnancy of 200 µg/day. Although this study was not a national survey, and the sample size was small, the findings are alarming and raise concern that a major public health problem may be developing in the Australian community which could put future generations at risk of iodine-deficiency disorders. The key factor in the genesis of iodine-deficiency disorders is decreased production of thyroxine from the thyroid gland. While endemic goitre is the most easily recognised and best-known consequence of iodine deficiency, it is probably the least important. At critical periods in fetal development and in early childhood, biochemical hypothyroidism, due to iodine deficiency, results in a wide range of devastating and irreversible effects now known as iodine-deficiency disorders.5 More recently, we have come to appreciate that there is a general diminution in intelligence in iodine-deficient communities such that iodine deficiency is considered to be the commonest cause of preventable intellectual disability worldwide.2 Further, there is now very good evidence that a small decrease in serum free thyroxine level during pregnancy, either because of iodine deficiency or thyroid disease, is an important risk factor for impaired psychomotor development in infants.6,7 The recent demonstration of intellectual impairment in the children of American women who had mild hypothyroidism in pregnancy highlights the need for better detection and treatment of hypothyroidism in early pregnancy, irrespective of its cause.8 Tasmania is the only Australian State where regular surveillance of iodine nutrition is undertaken and records are maintained. Other data are available from the Australian Centre for Control of Iodine Deficiency Disorders (ACCIDD), located at Westmead Hospital, which has performed sporadic surveys of urinary iodine excretion levels in small samples of Australians for the past two decades. In 1992 we reported that the mean urinary iodine excretion level in Sydney residents was 180 µg/L, and over 200 µg/L in Tasmanian children.9 Since then, our sporadic surveys have shown a gradual but sustained decline in urinary iodine excretion levels in Sydney residents. We recently found similar results to those of Gunton et al 3 in a survey of primary schoolchildren from western Sydney who had a median urinary iodine concentration of 84 µg/L, and in 16% of whom the iodine concentration was less than 100 µg/L. Further, unpublished results we obtained in healthy pregnant women were also very similar to those of Gunton et al, indicating that widespread mild iodine deficiency threatens to affect the most vulnerable in our community. Why is our iodine intake decreasing in Australia? Gunton and colleagues implicate a combination of factors. Firstly, for over three decades, we have been dependent on iodine in milk contaminated by cleaning solutions used in the dairy industry; these solutions are gradually being replaced by others which leave less iodine in milk. Secondly, we seem to be using less iodised salt, through a combination of purchasing uniodised salt for domestic consumption, probably decreasing our salt consumption, and consuming most of our salt in processed foods, which, as far as we can ascertain, is uniodised. The problem is not unique to Australia, as similar downward trends in iodine intake have recently been noted in other developed countries such as the United States10 and New Zealand.11 What actions should be taken in response to these findings? Firstly, we need more information through a national survey of urinary iodine excretion and goitre rates to determine the status of iodine nutrition throughout Australia. Secondly, we need to educate the population and healthcare providers about the insidious and harmful effects of iodine deficiency, especially during pregnancy and early childhood. Finally, we must institute effective and sustainable means of iodine supplementation to our whole community through legislating for universal salt iodisation, so that all salt used for human and animal consumption in Australia is iodised. Iodising all edible salt will cost less than 10 cents per person annually. In the past this intervention has been viewed as politically unacceptable, but the debate was conducted with a view to eliminating endemic goitre without any real understanding of the often subtle, but devastating, consequences of impaired brain development. In the interim, every effort should be made to ensure every pregnant woman ingests an adequate amount of iodine to ensure her unborn child experiences normal mental development. Until we have educated the population as a whole about the risks of iodine deficiency and instituted mandatory iodisation of all salt for human and animal consumption, it may be prudent to recommend supplementary iodine for all pregnant women from the time of conception until weaning of the infant. Creswell J Eastman, AM Director, Institute of Clinical Pathology and Medical Research Westmead Hospital, Westmead, and Clinical Professor of Medicine University of Sydney, Sydney, NSW World Declaration on the survival, protection and development of children and a plan of action for implementing the world declaration on the survival, protection and development of children in the 1990s. New York: United Nations, 1990. World Health Organization. Progress towards the elimination of Iodine Deficiency Disorders (IDD). WHO/NHD/99.4. Geneva: WHO, 1999. Gunton JE, Hams G, Fiegert M, McElduff A. Iodine deficiency in ambulatory patients attending a Sydney teaching hospital: Is Australia truly iodine replete? Med J Aust 1999; 171: 467-470. World Health Organization. WHO, UNICEF, ICCIDD. Indicators for assessing iodine deficiency disorders and their control through salt iodisation. WHO/NUT/94.6. Geneva: WHO, 1994. Boyages SC. Clinical Review 49, Iodine deficiency disorders. J Clin Endocrinol Metab 1993; 77: 587-591. Pop VJ, Kuijpens JL, van Baar AL, et al. Low maternal free thyroxine concentrations during early pregnancy are associated with impaired psychomotor development in infancy. Clin Endocrinol 1999; 50: 149-155. Haddow JE, Palomaki GE, Allan WC, et al. Maternal thyroid deficiency during pregnancy and subsequent neurological development of the child. N Engl J Med 1999; 341: 549-555. Utiger RD. Maternal hypothyroidism and fetal development. N Engl J Med 1999; 341: 601-602. Eastman CJ. The status of iodine nutrition in Australia. In: Delange F, Dunn JT, Glinoer D, editors. Iodine deficiency in Europe -- a continuing concern. New York: Plenum Press, 1993: 133-139. Dunn JT. What's happening to our iodine? [editorial]. J Clin Endocrinol Metab 1998; 83: 3398-3400. Thomson CD, Colls AJ, Conaglen JV, et al. Iodine status of New Zealand residents as assessed by urinary iodide excretion and thyroid hormones. Br J Nutrition 1997; 78: 901-912.

Creswell J Eastman

Review Breast cancer screening and management A Patrick M Forrest and Elaine D C Anderson MJA 1999; 171: 479-484 Synopsis - Introduction - Why screen for breast cancer? - Evidence for screening - Screening programs - Breast self-examination - Familial breast cancer - Management of screen-detected breast cancer - The future -- specialised, multidisciplinary services - Acknowledgements - References - Authors' details - - More articles on Oncology Synopsis Mammographic screening to detect preclinical cancer was introduced when it was realised that once breast cancer became symptomatic it could not be cured regularly by local surgery, as early systemic dissemination had almost invariably occurred. Meta-analysis of randomised controlled trials of screened versus unscreened women has demonstrated a mortality benefit approaching 30% in screened women (> 50 years of age) seven to nine years from the start of the trials. The UK and Australian breast screening programs are compared. Differences in the design are largely a result of differences in the healthcare systems in the two countries. Breast self-examination, although still recommended by many Australian practitioners, is not an appropriate screening method, as it does not affect breast cancer death rates. About 5% of women have familial breast cancer (associated with mutations of BRCA1 or BRCA2). Women at high risk are screened at an earlier age and at more frequent intervals. Current best practice management of screen-detected breast cancer, including surgery, radiotherapy, assessment of the axilla, and systemic therapy, is summarised. Women with symptomatic breast disease ideally should be treated by a specialised multidisciplinary service, which can provide sophisticated diagnosis and treatment as well as supportive care. Introduction In 1987, the UK government initiated screening for breast cancer by a single medial-lateral oblique view of each breast every three years for all women aged 50-64 years.1 The breast screening program in Australia -- BreastScreen -- began in 1991 and provides two-view mammographic screening at two-year intervals, mainly for women aged 50-69 years.2 Why screen for breast cancer? Screening was introduced when long term follow-up studies showed that most women with symptomatic breast cancer could not be cured by local surgery.3,4 Breast cancer was not a slowly progressive, locoregional disease; early systemic dissemination with the formation of distant micrometastases was the rule. Proof of this has now come from unequivocal evidence that systemic treatment, either by anti-oestrogens or chemotherapy, significantly prolongs survival in women with symptomatic disease.5-7Mammographic screening can detect cancer of the breast in its preclinical phase (ie, before it is palpable). The success of screening depends in part on the size of the tumour and whether the cancer has spread to the axillary lymph nodes, but the tumour's biological aggressiveness also needs to be taken into account. The excision of small tumours which are markedly undifferentiated may save lives in the short term, but it is the detection of small tumours while still of favourable grade which is likely to confer the greatest long term benefit. Evidence for screening Evidence that mammographic screening reduces mortality comes from randomised trials comparing mortality from breast cancer of women invited to be screened with women without any intervention. Recent meta-analyses have demonstrated a mortality benefit approaching 30% in women over 50 years of age seven to nine years from the start of the trials.8,9 In the 70% of women who accepted the invitation, mortality reduction is obviously larger. The 14-year follow-up of one of these six randomised trials,10 initiated in Edinburgh in 1978 and including over 22 000 women, indicated a reduction in breast cancer deaths of 21% (relative risk [RR], 0.79; 95% CI, 0.60-1.02), which bordered on significance. As patients diagnosed with breast cancer after the conclusion of the trial (when both study and control groups were eligible for screening) could not have influenced the mortality rate, a further analysis was performed with patients censored 10 years after entry. The 29% mortality reduction was significant (RR, 0.71; 95% CI, 0.53-0.95), and this mortality advantage was no less in women 45-50 years of age than in older women.10 Screening programs In the NHS Breast Screening Programme in the United Kingdom, the need for quality at every stage of the screening process has been emphasised, and national coordinators and regional advisory committees publish annual reports which include regularly revised targets against which performance can be measured (Boxes 1 and 2).11Australia's program, BreastScreen, which began in 1991, has a different design and less standardisation than in the UK program, largely because Australian general practitioners and surgeons work as independent providers. Women aged 50-69 years are eligible for two-yearly screening, but younger women, 40-50 years, and those over 70 years are screened on request. Women in the target group are invited to take part by direct mailouts based on the electoral roll, and 1996-1997 compliance rates were 52.2%.2 Two-view mammography is used, and double reading of mammograms is mandatory. However, the experience of radiologists reading mammograms, the protocols for assessment of screen-detected lesions, and arrangements for surgical biopsies and their pathological interpretation vary greatly between clinics and between States and Territories. National evaluation is only now under way. Breast self-examination Breast self-examination (BSE) can detect symptomatic breast cancer at an earlier stage, but it does not appear to influence mortality. A recent American Cancer Society study compared 177 602 women who practised BSE during the preceding 13 years with 272 554 women who did not, and found similar breast cancer death rates in the two groups.12 The UK Trial of Early Detection of Breast Cancer (TEDBC)13 involved 300 000 women in eight health districts, two with mammographic screening centres, two where BSE was taught by trained nurses, and four where neither form of intervention was available. At 16 years the relative risk of death from breast cancer in women attending the two screening clinics was reduced by 27% (RR, 0.73; 95% CI, 0.63-0.84), but there was no risk reduction in the two BSE centres (RR, 0.99; 95% CI, 0.87-1.12). Three randomised trials to evaluate the effect of BSE on breast cancer mortality are under way in St Petersburg and Moscow,14 and Shanghai.15 Preliminary results of the Shanghai study, which included over 250 000 women, found a similar incidence and an identical number of breast cancer deaths among BSE subjects and controls.15 BSE has greatly increased biopsy rates, with the number of benign lesions detected in the BSE group being twice those of the controls.15 These findings indicate that women should be aware of their breasts as part of general body awareness and seek medical help when their breasts look or feel abnormal, but the promotion of regular BSE is not justified. Familial breast cancer Some 20% of women with breast cancer report a "family history", but only about 5% are truly familial cancers, with the proportion being greater in women under 45 years at diagnosis (Box 3). Management of screen-detected breast cancer A recent audit of 500 screen-detected invasive cancers treated in Scottish hospitals found that 75% were under 1 cm in size and 70% node negative.30 Mastectomy is not necessarily the best treatment for such cancers; some surgeons believe that local excision alone is appropriate. However, the results of five randomised trials show a high local relapse rate if radiotherapy is not also given (Box 4).31-35 After nine years of follow-up in the US National Surgical Adjuvant Breast Project B-06 (NSABP B-06) trial, the relapse rate reached 43%.36 As these trials included tumours of 2.5-4 cm in size, the need for radiotherapy in small (< 1 cm) tumours of low grade and special histological type is unknown. Some surgeons believe that if tamoxifen is given after local excision radiotherapy can be avoided. The Scottish Conservation Trial, in which all 585 patients were prescribed adjuvant systemic therapy (tamoxifen or CMF [cyclophosphamide-methotrexate-5-fluorouracil]) appropriate to the oestrogen-receptor status of the tumour, indicated that this was not so.35 After six years of follow-up, locoregional relapse rates in the non-irradiated group were 24.5%, compared with 5.8% in those irradiated. This does not mean that no patients can safely be treated by local excision alone, but that more precise methods of selection are required before this can be recommended. A number of factors affect relapse rates after local excision and radiotherapy. These include tumour size, the extent of an in-situ component and histological grade. However, the need for complete excision with "clear margins" overrides other considerations, and it is essential that surgeons ensure accurate margin assessment. Biopsy of the excision cavity (cavity shavings) is reported to increase the accuracy of margin assessment.37 The axilla Some surgeons still perform complete dissection of the axilla for all invasive breast cancers; others advise routine radical radiotherapy. Neither approach is logical; an uninvolved axilla needs no treatment. Trials in Edinburgh have shown that sampling fewer axillary nodes (four nodes) provides adequate information on axillary node status, but, as this requires exposure of the axilla under general anaesthesia, it is appropriate only if radiotherapy is the preferred treatment for the involved axilla.38-40For staging the axilla, sentinel node biopsy is under intensive study. The sentinel node or nodes, the first node to which lymph drains from the tumour, can be marked by injecting blue dye or a radioactive marker around the breast tumour.41,42 With the former, visualisation of the axillary contents is necessary, but a radioactive marker allows precise identification of the sentinel node in the operating room with a hand-held gamma probe. The node can be removed with minimal disturbance to other tissues. Some surgeons advocate immediate examination by frozen section, and, if the sentinel node is shown to be involved, a full axillary dissection can proceed. However, frozen section examination is less accurate for node assessment,43 and histopathological examination of the suspected node is preferred practice. If the node can be identified by radionuclear scanning, it can be removed under local anaesthesia before final treatment is planned. Cytokeratin immunostaining improves the accuracy of detection of metastases, but is not appropriate for peroperative assessment. Many surgeons are already practising sentinel node biopsy, but, as recently stressed, the definition of a best method and its evaluation under controlled conditions is required before sentinel node biopsy can be regarded as an acceptable alternative to axillary sampling or clearance.44,45 Systemic therapy Despite evidence that ovarian ablation, tamoxifen and chemotherapy appropriate to the oestrogen-receptor status of the tumour increases this benefit, most surgeons do not advise adjuvant systemic therapy in small node-negative tumours.5-7 Yet, a small proportion of these are still aggressive and cause rapid death. There is a need for tumour markers which can predict likely outcomes for these small tumours; in the meantime, histological grade (as used in the Nottingham Prognostic Index), oestrogen-receptor status and possibly expression of C-erb B2 (HER-2) are the only markers routinely available.46The Nottingham Prognostic Index,47 which combines the size and histological grade of the tumour with the status of the axillary lymph nodes, has been validated in several studies as a reliable prognostic indicator in symptomatic breast cancer.48This Index has also been applied to predict mortality differences in the UK randomised trial of frequency of screening,49 but in a recent study of its application to the Edinburgh randomised trial of screening we have found that the inclusion of more detailed discrimination of size and also of histological type improves prediction in screen-detected cancers (Dr T J Anderson, Pathologist, Department of Pathology, University of Edinburgh, personal communication). Ductal carcinoma in situ (DCIS) Mammographic screening detects an increased number of cases of DCIS,11 but the natural history of the disease is not well understood. In an extensive review of 11 760 excisional breast biopsies performed for accepted benign conditions, 28 DCIS were identified for which a 24-year follow-up was available.50 Invasive breast cancer developed in nine of the 28 patients (32%). However, all were of favourable (non-comedo) type and had been excised, although the completeness of the excision was unknown. These figures may underestimate the true risk in those with more aggressive comedo-type of disease, but it is clear that there is a need for effective treatment. Some surgeons still advocate mastectomy as the only means of guaranteeing cure, but this can no longer be regarded as best practice for other than extensive disease. In Europe, local excision with radical radiotherapy is the preferred option. Features influencing relapse include size, architecture, the presence or absence of necrosis, and cytological nuclear grade.51 However, the factor of overriding importance is the completeness of surgical excision as indicated by free margins.52 Management options have recently been reviewed,53 and three randomised trials are in progress. The results of two trials (NSABP B-17 and B-24, and EORTC 10853) have been reported, the EORTC trial in abstract only.54,55 In B-17 local excision alone (403 patients) and local excision plus radiotherapy (411 patients) are compared. At a median follow-up time of eight years, local relapse was reported in 104 (25.8%) of the non-irradiated group (53 invasive) versus 47 (11.4%) of the irradiated patients (17 invasive). The EORTC trial, which included 1011 patients, had a similar design. At a median follow-up time of 51 months, the cumulative incidence of ipsilateral local recurrence was reduced in the radiotherapy arm (9% v 16%), this including both non-invasive and invasive cancers.56 Only limited information on the completeness of excision is available.57 In the B-24 trial, of 1804 women with DCIS treated by local excision and radiation, half were randomly allocated to receive tamoxifen 20 mg daily for 5 years and half to receive placebo. At a median follow-up of 74 months in women treated by tamoxifen, the cumulative incidence of recurrent breast cancer in either breast was 8.0%, compared with 12.7% in the placebo group; 3.9% and 6.5%, respectively, were invasive.55 It is essential that, as with small invasive tumours, eligible patients with DCIS are entered into randomised trials so that best management can be determined on scientific grounds. A recent survey of practice by 110 surgeons in the south of England showed that, although all four options of local excision, radiotherapy and tamoxifen were being used electively, only 27% of patients were included in the UK trial which compares them, a lamentable disregard of the need for evidence-based practice.58 The future -- specialised, multidisciplinary services Mammographic screening has increased the complexity of breast cancer management. Women with breast cancer must be aware of these complexities, understand the reliability of diagnostic methods, the safety of breast conservation, reasons for not advising systemic therapy and policies of after-care and support. Only then can they participate in decision making. Their questions can no longer be answered with authority by an individual surgeon, but require multidisciplinary input by radiologists, clinical and medical oncologists and pathologists supported by a breast-care nurse or counsellor. The experience of multidisciplinary assessment within the screening service led to the development of a specialised service in Edinburgh for women with symptomatic breast disease. Initially sited in a small hospital equipped with mammographic and operative facilities, this unit has now been transferred to the large Regional Cancer Centre as the Edinburgh Breast Unit, which, although still having independent diagnostic and inpatient facilities, has ready access to sophisticated diagnostic and treatment methods, including computed tomography and magetic resonance imaging, radiotherapy, chemotherapy and all aspects of supportive care. In the UK, women are coming to expect comprehensive care by breast specialists. In Australia, with its emphasis on provision of healthcare by individual practitioners, as well as problems of distance between the major population centres, such a similar pattern may be more difficult to achieve but is likely to be demanded. Acknowledgements We are grateful to Ms Gil Morton for providing facilities in Melbourne for the initial preparation of this paper; to Mrs Ruby Wood for assistance, and to Professor James Garden and the Hunter Research Fund for support. References Breast cancer screening. Report to Health Ministers of England, Wales, Scotland and Northern Ireland by Working Group chaired by Sir Patrick Forrest, 1987. London: HMSO, 1987. Australian Institute of Health and Welfare. Breast and cervical cancer screening. Canberra: AIHW, 3-27. Brinkley B, Haybittle JL. The curability of cancer. Lancet 1975; 2: 951. Kerr GR, Kunkler IH, Langlands AO, Rodger A. (In)curability of breast cancer: a 30 year report of a series of 3933 cases. Breast 1998; 7: 90-94. Early Breast Cancer Trialists' Collaborative Group. Ovarian ablation in early breast cancer: overview of the randomised trials. Lancet 1996; 348: 1189-1196. Early Breast Cancer Trialists' Collaborative Group. 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A prognostic index in primary breast cancer. Br J Cancer 1982; 45: 361-366. Balslev I, Axelsson CK, Zedeler K, et al. The Nottingham Prognostic Index applied to 9149 patients from the studies of the Danish Breast Cancer Cooperative Group. Breast Cancer Res Treat 1994; 32: 281-290. Blamey RW, Day N, Young R, et al. The UKCCCR trial of frequency of breast screening. Breast 1999; 8: 215. Page DL, Dupont WD, Rogers LW, et al. Continued local recurrence of carcinoma 15-25 years after a diagnosis of low grade carcinoma in situ treated by biopsy only. Cancer 1995; 76: 1197-1200. Delaney G, Ung O, Bilous M, et al. Ductal carcinoma in situ. Part I: Definition and diagnosis. Aust N Z J Surg 1997; 67: 81-93. Silverstein MJ, Poller DN, Waisman JR, et al. Prognostic classification of breast ductal carcinoma in situ. Lancet 1995; 345: 1154-1157. Delaney G, Ung O, Cahill S, et al. Ductal carcinoma in situ. Part II: Treatment. Aust N Z J Surg 1997; 67: 157-165. Fisher B, Dignam J, Wolmark N, et al. 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Authors' details Department of Clinical and Surgical Sciences, University of Edinburgh, and Edinburgh Breast Unit, Western General Hospital, University of Edinburgh, Edinburgh, Scotland. A Patrick M Forrest, Kt, MD, FRCS, FRACS(Hon), Professor Emeritus. Elaine D C Anderson, MD, FRSCEd, Consultant Surgeon and Honorary Senior Lecturer. Reprints will not be available from the authors. Correspondence: Sir Patrick Forrest, 19 St Thomas Road, Edinburgh, EH9 2LR, Scotland, UK. patrick.forrestATed.ac.uk Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/> We appreciate your comments. 1: NHS Breast Screening Programme11Program instituted1987Age of women screened50-64 years (younger age under trial) Method of invitationBy personal letterCompliance ratesStrictly monitored (1995-96, 75.8%)Frequency of scanningEvery three years (optimum frequency under trial)Reading of mammogramsBy experienced radiologists only (read minimum of 5000 mammograms per year). Double reading variableQuality assurance/evaluationFor each specialty, regional and national quality assurance groups (including one for monitoring and evaluation) were set up. National coordinators and advisory committees publish annual reports. Strict auditing of clinical and pathological characteristics (size, node status, grade) of screen-detected cancers (Box 2)Data collectionNational Screening Evaluation Unit maintains a database for the whole UK programResearch organisationNational Breast Screening Reseach Committee of the UK Committee for Co-ordination of Cancer Research Back to text 2: Consistency of screening activity in women over 50 years in the UK NHS Screening ProgrammeVariable1995-961994-95Women invited1 517 0331 507 605Acceptance rate75.876.7Total screened1 222 3891 207 316Recalled for assessment62 682 (5.1%)63 925 (5.3%)Breast biopsy6496 (5.3/1000)6334 (5.2/1000)Benign biopsy2472 (2.0/1000)2000 (1.6/1000)Cancers detected6664 (5.4/1000) 6500 (5.4/1000)In situ (% of cancers)19.9%20.0%Invasive < 15 mm (% of cancers)42.1% 40.9% Back to text 3: Woman with a family history of breast cancer16-20 Genetic mutations: True familial breast cancer may be associated with mutations of BRCA1, causing breast and ovarian cancers and (in men) an increased incidence of cancer of the prostate; BRCA2, predominantly associated with cancer of the breast but also with other epithelial tumours; or p53, causing the rare Li-Fraumeni syndrome. Determining risk: Pedigree analysis is the important first step. In women with more than four family members with a dominant history of breast and ovarian cancer, a mutation of BRCA1 is associated with an 87% risk of either disease. In those with fewer affected family members, penetrance of a mutated gene may be lower, and the risk of breast or ovarian cancer is in the region of 20%-30%. Although breast cancer is more likely to be familial in young women, only a minority have mutations of either gene. In a study of 73 women with breast cancer diagnosed before age 32 years, common mutations of BRCA1 and BRCA2 were detected in only 12% and 2%, respectively.21 Genetic clinics: In the United Kingdom, as in Australia, genetic clinics have been established. In the UK, criteria for referral are based on national guidelines.22 Australian guidelines for genetic clinics, published by the National Breast Cancer Centre, are exemplary and should be stringently followed.23 The genetic service of the screening clinic in Edinburgh offers screening to women whose risk is three times that of the age-specific population risk (a lifetime risk greater than 24%). Screening starts at age 35 years or five years younger than the first index case and includes an annual physical examination and biennial mammographic examination to the age of 40 years; then annual mammography to the age of 50. In families at very high risk, the screening interval is reduced to 18 months in women over 50 years. Genetic testing of blood is currently used only for research. In those with a dominant family history, germline mutations of BRCA1 and BRCA2 are sought from the index case. Prophylactic mastectomy: In a large Mayo Clinic series of 639 women with a family history of breast cancer (214 high risk and 425 moderate risk), prophylactic mastectomy was associated with a reduction in the incidence of breast cancer of at least 90%.24 Modelling of life-years gained suggests that benefit from prophylactic mastectomy depends on age and penetrance of the gene, and women must be made aware of the likely benefits, risks and costs, while recognising that regular mammographic screening is a viable alternative to mastectomy.25 The uncritical use of genetic testing has inherent hazards, such as loss of insurance or employment, psychological distress, risk of prophylactic surgery and disruption of family relationships. Chemoprevention: In the National Surgical Adjuvant Breast and Bowel Project (NSABP) trial, 13 388 women considered to be at increased risk of breast cancer were randomly allocated to receive tamoxifen or placebo. Over a mean follow-up period of four years, 89 women who received tamoxifen developed invasive cancer compared with 175 cases in the placebo group, a reduction of 49%.26 Tamoxifen increased the risk of endometrial cancer, pulmonary embolism and deep vein thrombosis. Unfortunately, the NSABP trial was stopped and women in the control group were given tamoxifen before mortality data were available, but two other trials in Milan and London (which to date have shown no reduction in risk) will provide this.27,28 A large international trial (IBIS) is under way. Raloxifene (a selective oestrogen-receptor modulator), recently reported to decrease the risk of newly diagnosed breast cancer in postmenopausal women with no prior history of breast cancer,29 may also be suitable for chemoprevention in patients at high risk of breast cancer. Back to text 4: Trials of conservative therapy for early breast cancerTrialNumber of patientsFollow-up (years)Tumour size (cm)MarginsNSABP B-06*3118435≤ 4.0ClearToronto328377.6< 4.0ClearMilan335673.25< 2.5WideOrebro Uppsala343815≤ 2.0ClearScottish355856≤ 4.01 cmRelapse in ipsilateral breastTrialNode positiveSystemic therapyRadiotherapyNo radiotherapyNSABP B-06*3135.4%Node positive7.7%27.9%Toronto32NoneNone11.3% 35.2%Milan3330.5%Node positive0.3%10.2%Orebro-Uppsala34NoneNone2.3%18.4%Scottish3522.9%All5.8%24.5% *National Surgical Adjuvant Breast Project (B-06). Back to text

Editorial Erectile dysfunction in the Australian community This problem is both increasingly recognised and increasing in prevalence with the ageing of our population MJA 1999; 171: 342-343 Erectile dysfunction (ED) is the persistent inability to achieve and/or maintain an erection sufficient for satisfactory sexual activity.1 Worldwide, 100 million men are estimated to have some degree of ED, with around 30 million men in the United States1 and around one million men in Australia affected. With our ageing, but relatively fit, population the incidence of ED is certain to escalate. The first major community-based study on ED was the Massachusetts Male Aging Study (MMAS),2 an observational study (conducted from 1987 to 1989) of a random sample of men aged between 40-70 years living in and around Boston, Massachusetts. This study yielded, for the first time, an understandable concept of ED; comparable studies in Australia have been singularly lacking. The first report on the prevalence of ED in our community was a study by Chew et al from the Keogh Institute for Medical Research in Perth3 (formerly the Reproductive Medicine Research Institute). The generalisability of this 1996 study was limited as it only included men who presented to general practices in Perth. The South Australian community study by Pinnock and colleagues in this issue of the Journal,4 which recruited men from the general community through a 1997 household survey, provides data that are, firstly, drawn from a more general community sample than the one in the Perth study, and secondly, more suited to our own demographic situation than data from overseas surveys. The South Australian study confirms that age is the strongest contributing demographic factor to ED, with 60 years of age being the turning point where desire exceeds potency and sexual frequency diminishes.4 The MMAS found that 52% of men aged between 40 and 70 years had some form of ED, with almost 60% of 60-year-old men having this complaint.2 Both studies found that sexual function was also affected by risk factors such as smoking, hypertension, obesity and a high total cholesterol level with a low concentration of high density lipoprotein. Vigorous exercise was found to be protective. The Perth study also found diabetes mellitus (types 1 and 2) to be significant contributors to ED. It should be noted that Pinnock et al used a questionnaire based on the UCLA Prostate Cancer Index that covered sexual function parameters including desire and orgasm, frequency of intercourse, prostate surgery and erectile function. As this index has not been validated in patients who do not have prostate cancer, its use in a randomly based population study represents a methodological flaw. A more appropriate questionnaire for this study would have been the better-known International Index of Erectile Function (IIEF),5 a 15-question survey that includes similar parameters, assesses intercourse and overall satisfaction, but excludes questions related to prostate cancer. The higher incidence of ED reported in the South Australian study4 compared with the MMAS2 probably reflects improvements in public awareness and keenness to discuss and report ED over the past 10 years. The study by Pinnock et al4 clearly shows that cardiovascular disease and ED have similar risk factors and present in a similar age group. Thus, it seems possible that, by improving their risk factor profile, men may benefit both their cardiovascular health and their sexual function. Pinnock et al also suggest non-cancer prostate surgery appears a more important contributor to ED than previously recognised. Erectile dysfunction is clearly an established and recognised male health problem -- one that is decreasingly being regarded as an inevitable consequence of ageing. The estimated 10% of men currently seeking help will increase, as more men will seek help in the future. Doctors will need to improve their skills in obtaining patients' sexual histories as more men request help. A full assessment of men, with emphasis on cardiovascular risk factors, will help direct the consultation to discussion of sexual matters -- it makes good sense to combine cardiac and sexual issues. Sildenafil is the first effective oral medication for ED, and its arrival on the market was well timed with the increasing interest in ED and the increasing numbers of men wanting a simpler treatment. Initial media interest over coital deaths associated with sildenafil has abated, and the drug is now accepted as a safe treatment when prescribed within the recommended guidelines. These guidelines advise caution when prescribing sildenafil to male cardiac patients who may not be fit enough to engage in sexual activity. Sildenafil is also absolutely contraindicated in men receiving nitrate therapy and those who use amyl nitrite "poppers". When sildenafil is contraindicated or fails to achieve the desired result, the use of injectable vasoactive agents is appropriate. Penile injection therapy is still considered the "gold standard", having been used for over 10 years. Alprostadil is the only approved injectable prostaglandin medication available on the Pharmaceutical Benefits Scheme. Alprostadil is also available as an intra-urethral pellet. Vacuum erection devices have been available for over 20 years and are still an acceptable choice for some men. Penile prostheses may be used in more difficult cases. The Australian community-based studies on male sexual function show a pattern similar to that in overseas studies, and highlights two important points in this era of increasing demand for treatment for ED: Doctors need to understand "normal" sexual function for men at different age groups, as knowing the effects of ageing on sexuality is important when counselling patients and advising on treatment; and Knowing that an apparently healthy patient presenting with ED may have underlying cardiovascular disease can advantage the patient's health outcome, and conversely, reducing a patient's cardiovascular risk factors may benefit both cardiovascular health and sexual function; the implications for sexual function may add weight to the arguments against obesity, smoking and excessive alcohol intake. Michael P Lowy Sexual Health Physician Australian Centre for Sexual Health St Luke's Hospital Complex, Sydney, NSW NIH Consensus Conference. Impotence. NIH Consensus Development Panel on Impotence. JAMA 1993; 270: 83-88. Feldman HA, Goldstein I, Hatzichristou DG, et al. Impotence and its medical and psychosocial correlates: results of the Massachusetts Male Aging Study. J Urol 1994; 151: 54-61. Chew KK, Earle CM, Stuckey BGA, et al. Erectile dysfunction in general medical practice. A study in Perth, Australia. Int J Impotence Res 1997; 9 (Suppl 1): A17. Pinnock CB, Stapleton AMF, Marshall VR. Erectile dysfunction in the community: a prevalence study. Med J Aust 1999; 171: 353-357. Rosen RC, Riley A, Wagner G, et al. The international index of erectile function (IIEF): a multidimensional scale for assessment of erectile dysfunction. J Urol 1997; 49: 822-830.

Michael P Lowy

Editorial Screening, case finding and evidence-based guidelines There are functional questions about the nature of screening and the exact clinical scenarios to which screening guidelines apply MJA 1999; 171: 344-345 Screening has been defined as "the examination of asymptomatic people in order to classify them as likely or unlikely to have a disease".1 When public health authorities recommend screening for otherwise healthy people they assume a substantial degree of responsibility. Clear evidence should exist that the disease in question can be identified at an earlier and more treatable stage in its natural history. Moreover, the resulting fall in morbidity or mortality should be achieved without too great a burden of adverse effects. In particular, the side effects of the procedures necessary to establish a diagnosis and those associated with the treatments employed should not be excessive. Screening for prostate cancer has spurred considerable controversy, particularly since the introduction of prostate-specific antigen (PSA) testing.2,3 Most authorities within Australia and other countries recommend against such testing.4 The reasons include a lack of confidence that present interventions improve the prognosis of lesions discovered at screening. Furthermore, the interventions available (surgery and radiotherapy) are associated with a fairly high frequency of impotence and incontinence.5 These may be a high price to pay in the absence of proven benefit. Negative sentiments about routine prostate cancer screening have been incorporated into guidelines by four Australian bodies.6-9 In this issue of the Journal, Girgis et al examine the impact of such guidelines on the behaviour of general practitioners faced with a 58-year-old man requesting screening at the behest of his wife.10 They found that 90% of respondents would accede to the patient's request. After being acquainted with the Australian guidelines, three-quarters of the respondents would still choose to test the patient. Only 15% of respondents were confident that the guidelines would assist their case if a patient whom they had refused to test subsequently developed prostate cancer and sued. Few believed that they were at risk of being sued if patients suffered complications of investigation or treatment of which they had not been warned before screening. The authors conclude that evidence-based guidelines have little influence on GPs' approach to prostate cancer screening and raise the issue of "more deliberate implementation". They also regard the lack of confidence in a legal defence derived from national evidence-based guidelines as troubling and recommend that steps be taken to clarify their legal standing. As readers of the discussion in the Journal's Internet peer review trial would be aware,11 these conclusions have been challenged and have raised fundamental questions about the nature of screening and the exact clinical scenarios to which screening guidelines apply. In practice, screening can be carried out in a variety of settings. These range from organised mass population screening to advice provided to a single patient presenting to a doctor on account of some other problems (the latter is referred to as case finding). The common feature is that the medical profession has taken the initiative to promote the testing, and most screening guidelines have been developed with this implicit assumption. If this view is accepted, then a request by a patient to have a PSA test would not qualify as screening. When the request has been made by an asymptomatic patient without any particular concerns, the risk-benefit ratio is likely to be similar to that of a typical screening scenario, and it would be appropriate to be guided by the same advice. In other words, in a setting strictly as described by Girgis et al, where the patient requested testing at the suggestion of his wife, it might well be appropriate to be guided by the same published guidelines for prostate cancer screening. If special concerns about the presence of prostate cancer have led to the request, a GP might reasonably conclude that the extra component of reassurance is sufficient to justify the test. However, men with uncomplicated lower urinary tract symptoms should be advised that there are no data to suggest that they are at increased risk of prostate cancer.9 In real life clinical practice other complexities may also arise and must be taken into account. When patients seek PSA testing, simple refusal is rarely an option for GPs wishing to successfully balance their varied roles of therapist, educator, friend, small businessman and guardian of the public purse. Most GPs would agree that their principal task is to provide a balanced account of the pros and cons of testing. This would include the fact that a positive test could initiate a potentially costly chain of events that might leave the person incontinent and/or impotent without improving his life expectancy. If these facts have been conveyed accurately and the patient still requests testing then continued refusal may be seen as unreasonable and paternalistic. For a simple screening investigation such as PSA, where controversy is known to exist, it is difficult to be critical of practitioners who would provide testing. The other key issue raised by Girgis et al is the extent to which defensive medicine influences the use of clinical investigations in Australia. The fact that 46% of GPs perceived a medicolegal risk if they failed to accede to the patient's request, despite being presented with evidence that the testing was inappropriate, illustrates the extent of this problem. It has been anticipated that the provision of clinical practice guidelines might assist practitioners dealing with controversial clinical problems by providing a legally defensible approach with which to manage patients. However, this study suggests that, at least in the case of prostate cancer screening, guidelines do not provide this reassurance. The authors point out that, unless the legal standing of guidelines can be clarified, they are unlikely to provide a useful response to the problem of defensive medicine. Like many vigorous controversies, the arguments about prostate cancer screening result from a lack of evidence of value rather than evidence of no value. The definitive information to guide practitioners will be derived from clinical trials large enough to establish the balance of benefits and costs in a population. Trials of this type are presently under way in both the United States and Europe.12,13 Findings are expected in 2002 or sometime thereafter. If these provide an unequivocal result, then the response of practitioners to various testing scenarios will be guided by much firmer evidence. John J McNeil Professor, and Head, Department of Epidemiology and Preventive Medicine Monash University, Melbourne,VIC Paul E O'Brien Professor, Department of Surgery Monash University, Melbourne, VIC Mornson AS. Screening. In: Rothman KJ, Greenland S, editors. Modern epidemiology. Philadelphia: Lippincott-Raven, 1998; 499. Mulley AG, Barry MJ. Controversy in managing patients with prostate cancer. Banish dogma, get more data [editorial]. BMJ 1998; 316: 1919-1920. Woolf SH. Screening for prostate cancer with prostate-specific antigen -- an examination of the evidence. N Engl J Med 1995; 333: 1401-1405. Feeney T. To screen or not to screen. In: Fundamentals of prostate cancer detection and treatment [web site]. <http://rattler.cameron.edu/ww/index.html>. Revised 27 January 1999. Accessed 1 September 1999. Coley CM, Barry MJ, Fleming C, et al. Early detection of prostate cancer. Part II: Estimating the risks, benefits, and costs. Ann Intern Med 1997; 126: 468-479. Australian Cancer Society. Prostate cancer screening: guidelines for health professionals. Cancer Forum 1995; 19: 47-50. Australian Health Technology Advisory Committee. Prostate cancer screening. Canberra: AGPS, 1996. Royal Australian College of General Practitioners. Guidelines for preventive activities in general practice. 4th ed. Sydney: RACGP, 1996; 26. National Health and Medical Research Council. Clinical practice guidelines. The management of uncomplicated lower urinary tract symptoms in men. Canberra: Commonwealth of Australia, 1997. Girgis S, Ward JE, Thomson CJH. General practitioners' perceptions of medicolegal risk. Using case scenarios to assess the potential impact of prostate cancer screening guidelines. Med J Aust 1999; 171: 362-366. Girgis S, Ward JE, Thomson CJH. Potential impact using case scenarios of guidelines discouraging prostate cancer screening on general practitioners' perceptions of medicolegal risk [second revised version with peer review discussion]. <http://www.mja.com.au/public/issues/iprs2/girgis/girgisframe.html>. Accessed 1 September 1999. Kramer BS, Brown ML, Prorok PC, et al. Prostate cancer screening: what we know and what we need to know. Ann Intern Med 1993; 119: 914-923. Auvinen A, Tammela T, Stenman U-H, et al. Screening for prostate cancer using serum prostate-specific antigen: a randomised population-based pilot study in Finland. Br J Cancer 1996; 74: 568-572. &copy1; 1999 Medical Journal of Australia.

Research A South Australian population survey of the ownership of asthma action plans Richard E Ruffin, David Wilson, Anne Marie Southcott, Brian Smith and Robert J Adams MJA 1999; 171: 348-351 Abstract - Introduction - Methods - Results - Discussion - References - Authors' details - - More articles on Respiratory medicine Abstract Objective: To examine the relationships between ownership of written asthma action plans, asthma morbidity, use of devices, and patients' perceptions of their asthma management. Design and setting: A random population survey (in 1996) of the South Australian population aged 15 years or over, using interviewers to administer a questionnaire. Participants: People who reported that they had current, doctor-diagnosed asthma. Main outcome measures: Prevalence of written asthma action plans; night-time awakenings from asthma; ownership of peak flow meters; and people's perceptions of their asthma management. Results: The ownership of asthma action plans by people with self-reported asthma was 33% and has declined since 1995 (42%; P < 0.001). Fifteen per cent were wakened weekly or more frequently by asthma symptoms. These people were more likely to have a peak flow meter and a written action plan, but less likely to consider they had been provided with enough information about their asthma, to feel comfortable managing their asthma, or to find it easy to see their doctor. Having a written asthma action plan was associated with regular corticosteroid use, understanding asthma, having enough information and owning a peak flow meter. Conclusions: Ownership of asthma action plans in South Australia is suboptimal. Before we develop new strategies to improve asthma outcomes, we must determine whether there is a need to target people with less severe asthma and/or improve the use of guidelines by health professionals. Introduction The Australian and New Zealand Asthma Guidelines, developed in 1989, provide a list of objectives that would be desirable to achieve for every person with asthma,1 and studies of the use of asthma management plans have shown improved health outcomes for people with asthma.2-4 In Australia there is evidence that the promotion of asthma plan guidelines by the Thoracic Society of Australia and New Zealand and the National Asthma Campaign has led to increased uptake of plans.1 In South Australia the prevalence of adults with asthma reporting that they had a written action plan almost doubled between 1992 and 1995.5 However, there is evidence that asthma management is not ideal.6-8In one study in Victoria, 45% of people who died of their asthma had been assessed as having only a history of mild or moderate asthma.6 In another study in Victoria that examined the asthma knowledge of asthma patients, the median score obtained was less than 50%.7The effective implementation of asthma management plans in Australia to date has been seriously questioned by some investigators,8 and Bauman et al have concluded that the treatment and management of asthma is suboptimal.9 Our study aimed to provide representative population information on the ownership of written asthma action plans and the relationship to asthma morbidity and management factors. Methods Survey The data for this study were collected in the 1996 South Australian Health Omnibus Survey,10 a representative survey of people aged 15 years or older (n = 3010; response, 71%) . The survey was a multistage, systematic, clustered area sample of people who live in metropolitan Adelaide and major country centres with a population of over 1000. The survey was selected from a random sample of Australian Bureau of Statistics collector districts. Within each collector's district a random starting point was selected and from this point 10 households were selected using a fixed skip interval. Hotels, motels, hospitals, nursing homes and other institutions were excluded. The person whose birthday was next in each selected household was interviewed in their home by trained health interviewers. There was no replacement for non-respondents. Up to five call-backs were made in an attempt to interview the selected person. The data were weighted by age, sex, and geographic region to the estimated resident population data so that the analysis would be representative of the South Australian population. The part of the survey form dealing with asthma is shown in the Box. A person was classified as having current asthma if they answered yes to the first three questions. Social class was determined by referring to the gradation of occupational prestige given in the Australian Standard Classification of Occupations.11 An asthma action plan was defined as "written instructions of what to do if your asthma is out of control." Data analysis Possession of an asthma management plan and frequency of wakening at night with asthma were used as the two dependent variables for univariate analyses,12 which examined the associations between these variables and reported asthma management, knowledge and attitudes to management. Before conducting multiple logistic regression analyses, the explanatory variables were examined for collinearity or interactions. Stratified analyses were used to check homogeneity of associations across different levels of predictor variables. Smoking status and the information that people with asthma perceive they have for dealing with worsening asthma were found to interact, with an effect of these variables on worsening asthma. An interaction term for the two independent variables was included in the logistic regression analysis for frequency of wakening at night. This interaction term proved significant (P = 0.03), indicating the need to split the model and conduct separate logistic regression analyses of smokers and non-smokers. Therefore, we conducted three logistic regression analyses, using "asthma plan", "waken weekly-non-smokers" and "waken weekly-smokers" as the three response variables. All variables found to be significant at the univariate stage (ie, P = 0.25)13 were entered into each logistic regression. Insignificant variables were progressively omitted until satisfactory models were found that explained possession of an asthma plan and frequency of wakening at night. Results The prevalence of asthma was 11.6% (95% CI, 10.3%-12.9%). Of the 349 survey respondents with asthma, 33% (95% CI, 30.8%-35.2%) had a written asthma action plan and 15.2% (95% CI, 13.7%-15.7%) were awakened by asthma weekly or more frequently. Age, sex, migrant status, education level and socioeconomic status made no significant difference to the rate of possession of an asthma action plan or the rate of wakening with asthma weekly or more frequently. Variables significantly associated with ownership of an asthma action plan at the univariate level are shown in Table 1; those significantly associated with wakening with asthma at night are shown in Table 2. In the multivariate analysis (Table 3), the variables that best described those who had an asthma action plan were: using corticosteroids, understanding the effects of worsening asthma, having a peak flow meter, and believing they have enough information to deal with worsening asthma. The variables that best described non-smokers who waken weekly or more often were: having a peak flow meter, having an asthma action plan, not believing they have enough information to deal with worsening asthma, and not feeling comfortable taking care of their asthma. Only one variable -- not finding it easy or convenient to access their doctor about asthma -- explained wakening weekly or more often for smokers. Discussion The data obtained in this representative population study paint a bleak picture of the effectiveness of asthma management in Australia. As even people with mild asthma can die of the disease,6 every person with asthma may need an action plan. Yet, seven years after the promulgation of Australian guidelines on the implementation of asthma action plans,1 only 33% of people with diagnosed asthma had a written plan. The current level of plan ownership is significantly lower than the 42.1% (P < 0.001) reported 12 months earlier using the same survey methods.5 This may mean that vigilance regarding asthma management is declining. Our study has some limitations. We have no objective data to identify levels of asthma severity and asthma control in the respondents. The validity of the perception questions as repeatable measures has not been verified. Because we focused on ownership of written action plans, our study does not tell us whether patients are making appropriate use of these plans or of verbal instructions. In the multivariate analyses, only use of preventer medication, ownership of a peak flow meter and self-reported understanding of asthma were associated with plan ownership. This association could suggest that the more severe cases have better asthma management. Proof for this requires prospective measures (eg, lung function, medication doses) to assess the two critical factors of asthma severity and asthma control. Such knowledge could inform us of the potential need to target people with less severe asthma. People with asthma with nocturnal symptoms were more likely than those without nocturnal symptoms to report possession of a peak flow meter, and to have asthma action plans, but were less likely to consider they had been provided with enough information about their asthma (non-smokers) or to find it easy to see their doctor (smokers) (Table 2). Thus, although asthmatics with a higher level of morbidity are more likely to receive physical materials to assist in self-care, they continue to have greater unmet needs for general practitioner access and information about asthma self-management. What is the way forward? Randomised studies of the implementation of asthma plans show that good educational and skill objectives can be achieved.2,14-16 However, the complexity of the asthma management problem makes it impossible to provide for every contingency the patient might face in dealing with asthma. Asthma management decisions can be difficult, because the patient, the daily situation, the science base and the disease are constantly changing.2 The objectives of patient asthma management are the development of skills and positive attitudes to problem-solving, accompanied by sufficient knowledge to make sense of changing morbidity and symptoms. A controlled trial evaluation of a brief asthma education program (2.5 to 3 hours group work) demonstrated substantial changes in illness behaviour.2 These programs show that giving the patient the necessary skills cannot be achieved within the normal constraints of general practice. Randomised controlled trials of asthma clinics, where there is an emphasis on self-management, have demonstrated improvements in a range of morbidity and other health-related outcomes in a community-based setting.17 We must identify other ways of training the patient and focus the clinician on that part of the education program that can be managed in general practice. There is evidence that regular review improves asthma outcomes.18 It is pertinent to consider the possibility that inadequate use of guidelines by health professionals may be contributing to the fall in action plan ownership. Ways to improve use of guidelines need to include developments in information technology. Trostle has suggested that the inability of some people to comply with a treatment regimen is an unavoidable byproduct of collisions between the clinical world and other competing worlds of work, family, friends and recreation.19 Often, the process required to inform and empower the patient is more than an educational task. Some of the traditional models of patient education based on health beliefs or compliance frameworks have been seriously questioned.20,21 Patients have to fit their medical problems and medical regimens into the context of their daily lives. In doing so they will vary their compliance with advice and instructions to accommodate the social, psychological, economic and physical influences which are part of their lives.21 We need research that clearly articulates the complexity and variability of how asthma management fits into the context of individual patients' lives. The National Asthma Campaign has provided a guide for health professionals to assist with effective patient communication, which is a starting point for corrective strategies.22 We therefore know what optimal management of asthma is, but its attainment is elusive. Future strategies must be guided by studies defining asthma severity and asthma control, studies identifying factors that influence the use of guidelines by professionals, and studies elucidating the context of asthma management for the individual. References Woolcock A, Rubinfeld AR, Seale P, et al. Asthma management plan, 1989. Med J Aust 1989; 151: 650-653. Yoon R, McKenzie DK, Bauman A, Miles DA. Controlled trial evaluation of an asthma program for adults. Thorax 1993; 48: 1110-1116. Comino EJ, Mitchell CA, Bauman A, et al. Asthma management in eastern Australia. Med J Aust 1996; 164: 403-406. Beasley R, Cushley M, Holgate ST. A self-management plan in the treatment of adult asthma. Thorax 1989; 44: 200-204. Adams R, Ruffin R, Wakefield M, et al. Asthma prevalence, morbidity and management practices in South Australia, 1992-1995. Aust N Z J Med 1997; 27: 672-679. Robertson C, Rubinfeld AR, Bowes G. Deaths from asthma in Victoria: a twelve-month survey. Med J Aust 1990; 152: 511-517. Rubinfeld AR, Dunt DR, McLure BG. Do patients understand asthma? A community survey of asthma knowledge. Med J Aust 1988; 149: 526-530. Bauman A, Young L, Peat JK, et al. Asthma under-recognition and under-treatment in an Australian community. Aust N Z J Med 1992; 22: 36-40. Bauman A, Mitchell CA, Henry RL, et al. Asthma morbidity in Australia: an epidemiological study. Med J Aust 1992; 156: 827-831. Wilson D, Wakefield M, Taylor A. The South Australian Health Omnibus Survey. Health Promotional J Aust 1992; 2: 47-49. Kelley JL, Evans MDR. Using ASCO for socio-economic analysis: assessment and conversion into status and prestige indices. Canberra: Research School of Social Sciences, Australian National University, 1988. SPSS for Windows. Release 8.0 [computer program]. Chicago, IL: SPSS Inc, 1998. Hosmer DW, Lemeshow S. Applied logistic regression. New York: John Wiley, 1989. Wilson-Pessano SR, McNabb WL. The role of patient education in the management of childhood asthma. Prev Med 1985; 14: 670-687. Clark NM, Feldman CH, Evans D, et al. Managing better: children, parents and asthma. Patient Educ Counsell 1986; 8: 27-38. D'Sousa WD, Crane J, Burgess C, et al. Community-based asthma care: trial of a "credit card" asthma self-management plan. Eur Respir J 1994; 7: 1260-1265. Lahdenso A, Haajtela T, Herrala J, et al. Randomised comparison of guided self-management and traditional treatment of asthma over one year. BMJ 1996; 312: 748-752. Asthma management handbook 1998. Melbourne: National Asthma Campaign, 1998. Trostle JA. Medical compliance as an ideology. Soc Sci Med 1988; 18: 1299-1308. Carter WB. Psychology and decision making: modelling health behaviour with multiattribute theory. J Dental Educ 1992, December: 800-807. Morris SL, Schulz RM. Medication compliance: the patients' perspective. Clin Ther 1993; 15: 593-606. Asthma adherence: a guide for health professionals. Melbourne: National Asthma Campaign, 1999. (Received 19 Apr, accepted 26 Aug, 1999) Authors' details The Queen Elizabeth Hospital, Adelaide, SA. Richard E Ruffin, FRACP, MD, Head, Division of Medicine, and Michell Professor of Medicine, University of Adelaide; Anne Marie Southcott, MB BS(Hons), FRACP, Acting Director, Respiratory Medicine; Brian Smith, PhD, FRACP, Director, Clinical Epidemiology and Health Outcomes Unit, and Senior Lecturer, University of Adelaide. Centre for Population Studies in Epidemiology, Department of Human Services, Adelaide, SA. David Wilson, PhD, MPH, Head. Channing Laboratory, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Robert J Adams, MB BS, FRACP, Research Fellow. Reprints: Professor R E Ruffin, Department of Medicine, University of Adelaide, The Queen Elizabeth Hospital Campus, 28 Woodville Road, Woodville, SA 5011. rruffinATmedicine.adelaide.edu.au Survey questions Have you ever had asthma? Was your asthma confirmed by a doctor? Do you still have asthma? If answer yes to these questions, then: Do you have an asthma action plan (written instructions of what to do if your asthma is out of control)? Do you have a home nebuliser for asthma treatment? Interviewer: if "yes" prompt "have you used it in the last 12 months?" What preventive (not reliever) medicine do you use regularly for your asthma? None - Intal - Becotide - Becloforte Pulmicort - Tilade - Other (specify) Which of the statements shown on this card do you feel are true of your preventer medication? Works by relieving narrowed breathing tubes quickly Needs to be used when you feel unwell Works by slowly reducing inflammation in the breathing tubes Must not have the dose changed Don't know How often do you awaken during the night with asthma? Nightly - Most nights - About twice a week - Weekly - Monthly - Less often than monthly Only at certain times of the year (ie seasonal) Never In the last 12 months have you had any hospital admissions for asthma where you stayed at least one night in hospital? In the last 12 months have you had any days lost from work, school or home duties from asthma? How many days would you estimate? What would you do if you had a bad attack of asthma and six puffs of your reliever (eg, ventolin, respolin) had not helped? Which of these statements shown on this card most closely matches what you would be likely to do? Wait another two hours and take more reliever medication Seek medical advice Take another six puffs of reliever medication and see what happens Call an ambulance Get someone to take you to hospital Do something else (specify) What feelings would you have if you had to get help for a bad attack of asthma? Which of the statements shown on this card most closely match how you would be feeling? You feel that you have failed You would feel embarrassed You do not want to bother others It is the right thing to do You know you will be OK because of past experience Something else (specify) I am now going to read out a number of statements and show you a card for each of them. Could you please tell me which number from 1 to 5 best reflects the way you feel. I am the sort of person who understands all about my asthma Always - Often - Sometimes - Rarely - Never - Don't know/other If I took care of my asthma myself, most of the time, I would . . . Manage well Manage sometimes Not manage at all Don't know/other If I were having a severe attack of asthma I would feel comfortable about going to a doctor or hospital Very comfortable Comfortable Don't mind Uncomfortable Not comfortable at all Don't know/other Going to see a doctor for help with my asthma is Easy and convenient Not easy nor convenient Don't know/other I have information to use (such as "Asthma Action Plan" or other instructions) to deal with worsening asthma. Yes, all I need Some No, none at all Don't know/other Other questions were asked about smoking status, educational level and migrant status. Back to text 1: Variables associated with ownership of an action plan*VariableSubjects (n = 349)%Odds ratioWrong about CS effect10332.01.0Correct about CS effect162†44.41.7 (0.98-2.94) P = 0.04Don't use CS regularly14721.81.0Use CS regularly20241.62.56 (1.54-4.26) P < 0.01No home nebuliser28229.11.0Have home nebuliser6750.72.51 (1.41-4.48) P < 0.01No peak flow meter29626.61.0Have peak flow meter5371.76.99 (3.50-14.14) P <0.01Don't always understand asthma8516.51.0Understand asthma26438.63.19 (1.65-6.27) P < 0.01Not enough information11715.51.0Enough information23255.56.77 (3.98-11.56) P <0.01Feel bad getting help4721.31.0Getting help OK30235.12.26 (1.04-4.90) P = 0.04No hospital admission within 12 months 33432.1 1.0Hospital admission1560.03.17 (1.00-10.32) P = 0.05No days lost from work/school30231.11.0Days lost from work/school4746.81.95 (1.00-3.79) P = 0.05CS = corticosteroids. * Variables tested but not found to be significant were: sex, age, migrant status, educational level, socioeconomic status, weight, access to doctor, uncomfortableness dealing with asthma, perception of dealing with asthma, comfortableness in going to hospital if required, exercise, smoking status, and smoking bans at home. †Only those who regularly used preventive medicine for their asthma (n = 265) were asked about its effects. Back to text 2: Variables associated with the likelihood of wakening with asthma on a weekly basis or more frequently*VariableSubjects (n = 349)%Odds ratioWrong about CS effect1038.71.0Correct about CS effect162†25.83.63(1.60-8.45) P < 0.01No home nebuliser28212.81.0Have home nebuliser6730.81.96 (0.96-3.95) P = 0.04No peak flow meter29612.81.0Have peak flow meter5330.83.02 (1.45-6.27) P < 0.01Not easy to see doctor6033.31.0Easy access to doctor28911.80.27 (0.13-0.53) P < 0.01Uncomfortable taking care of asthma 4836.2 1.0Comfortable taking care30112.30.25 (0.12-0.52) P < 0.01Perception of self-management good 3813.7 1.0Perception poor31129.42.62 (1.09-6.25) P = 0.0 3No days lost from work/school30213.61.0Days lost from work/school4727.72.42 (1.11-5.25) P = 0.02CS = Corticosteroids. * Variables tested but not found to be significant were: sex, age, migrant status, educational level, socioeconomic status, weight, regular use of corticosteroids, not always understanding asthma, not having enough information, feeling bad getting help, comfortableness in going to hospital if required, exercise, smoking status, smoking bans at home, and having an asthma action plan. †Only those who regularly used preventive medicine for their asthma (n = 265) were asked about its effects. Back to text 3: Logistic regression analyses of variables associated with ownership of an asthma management plan and frequency of wakening at night with asthma (n = 349)VariableOdds ratioAsthma planNo peak flow meter1.0Have peak flow meter4.32 (2.91-8.43)Don't always understand asthma 1.0Understand asthma2.01 (1.01-4.02)Not enough information1.0Enough information4.32 (2.11-8.85)Don't use corticosteroid regularly1.0Use corticosteroid regularly2.08 (1.21-3.58)Waken weekly (non-smokers)No peak flow meter1.0Have a peak flow meter7.32 (2.59-20.07)Not enough information1.0Enough information0.12 (0.04-0.39)Uncomfortable taking care of asthma1.0Comfortable taking care0.30 (0.14-0.77)No asthma action plan1.0Asthma action plan2.79 (1.09-7.15)Waken weekly (smokers)Not easy to see doctor1.0Easy to see doctor0.28 (0.10-0.79)All results significant, P < 0.05. Back to text

Richard E Ruffin · David Wilson · Brian Smith · Robert J Adams

Abstract Objective: To ascertain general practitioners' perceptions of medicolegal risk when screening for prostate cancer, and explore the potential impact of three national guidelines on perceptions and clinical practice. Design: Postal survey in August 1997. Participants: 219 randomly selected GPs in New South Wales (65% response rate). Main outcome measures: Response to case scenarios; perceptions of medicolegal risk and protection afforded by national guidelines before and after reading extracts of three national guidelines; ratings of current and potential strategies to increase GPs' sense of medicolegal protection. Results: 90% (95% CI, 86.5%-94.3%) would screen an asymptomatic male patient and 61% (95% CI, 54.2%-67.2%) indicated GPs would be at risk if they did not screen. Although significant changes in responses were found after respondents had read guideline extracts, 46% (95% CI, 39.5%-52.7%) continued to perceive medicolegal risk if screening was not performed. About two-thirds (65%; 95% CI, 59.9%-72.5%) supported a clear statement about the legal status of guidelines in a court of law to increase their sense of medicolegal protection. Conclusions: Even when made aware of national evidence-based guidelines against prostate cancer screening, GPs in our survey perceived limited hypothetical medicolegal protection. Introduction In Australia, the risk of medical litigation has increased. For general practitioners, the risk of being sued doubled from 1:160 in 1990 to 1:84 in 1994.1 If doctors believe these risks are substantial, this belief alone may influence their clinical behaviour.2-5Medicolegal risk may be reduced if practice is within existing clinical practice guidelines.6 Prostate cancer screening represents a "test-case" for such guidelines.7 Although there is no evidence that premature mortality from prostate cancer will be reduced by screening (see Box 1), Australian men report high rates of testing.12,13 GPs use prostate-specific antigen (PSA) assays for screening, either alone or combined with digital rectal examination (DRE).11,14,15 Current tests cannot distinguish innocuous from aggressive malignancy.16 Treatment options for men with localised prostate cancer currently available are "unnecessary for some and insufficient for others".17 On current evidence, men's quality of life may be diminished by anxiety, unnecessary treatment and adverse complications if screening is recommended.16 Unsurprisingly, 39% of GPs surveyed in 1995 indicated that prostate cancer screening guidelines would be "extremely" or "very" useful.18 Three sets of guidelines ensued, each recommending against screening.9,19,20 Yet, Pinnock et al recently reported that there is "anecdotal evidence that general practitioners are concerned that if a PSA test is not offered, and prostate cancer is later diagnosed, they may be seen as negligent".13 In a US survey, physicians who perceived that a patient who develops prostate cancer would be successful in suing his physician if he had not been previously screened were more likely to report using PSA tests to screen than those who perceived that such litigation would be unsuccessful.21 No published Australian research has quantified the influence of medicolegal concerns on prostate cancer screening. We designed this study to ascertain GPs' perceptions of medicolegal risk when asked to screen for prostate cancer, and, by using case scenarios, to assess the potential impact of national guidelines on their views. Methods Questionnaire The first section of our self-administered questionnaire commenced with this case scenario: Mr Smith, a 58-year-old employed repairman, presents to his regular GP after prompting by his wife to have a test for prostate cancer. He has no urinary symptoms, no family history of prostate cancer and has not had a vasectomy. GPs were asked: when they had last had a similar request; what should be done; whether the GP would be at risk medicolegally if she or he either did or did not perform either or both tests for screening purposes; what they would do if they were the GP and which test(s) they would advise as being the best available. We also randomised respondents to receive one of two versions of the case scenario which were identical, except that in one the patient was an architect, and in the other he was a repairman. We next provided verbatim the policies of the Australian Cancer Society,9 the National Health and Medical Research Council (NHMRC)19 and the Royal Australian College of General Practitioners (RACGP)20 about screening for prostate cancer, and asked if the respondents were aware of each guideline and whether, having read excerpts from all three, they would change their answers to the initial scenario. We then repeated the first scenario and questions. Our second case scenario read as follows: Imagine the following scenario with the earlier patient, Mr Smith. Having presented for a PSA test, you discouraged him from having it. Imagine that six months later, he is diagnosed with prostate cancer after a blood test organised by a locum. He then proceeds with a formal complaint against you because you did not do the test when he first requested it. We asked respondents to indicate if the three guidelines would protect them in the event of such a complaint, the extent to which such a possibility influenced their practice, and their perceptions of the likelihood of such a scenario. We next asked respondents to indicate their opinion of each of seven statements about prostate cancer screening, using a five-point Likert scale. Respondents then ranked five current and 14 potential strategies to increase GPs' sense of medicolegal protection in this aspect of clinical practice. The questionnaire concluded with six sociodemographic questions. Survey administration and analysis We purchased a list of all NSW GPs from a commercial company and randomly selected 400 names. Questionnaires and reply-paid envelopes were mailed in mid-1997, after an advance telephone prompt. At Day 16, non-responders received a reminder letter. At Day 35, a second questionnaire was posted to remaining non-responders. Two weeks after the second mail-out, a research assistant telephoned any remaining non-responders. The initial sample size was calculated to yield at least 200 questionnaires for analysis, thereby permitting independent and paired univariate analyses. Descriptive statistics were calculated, using SPSS version 6.0.22 We used univariate analysis to examine differences in GPs' responses to either repairman or architect scenarios. Univariate analysis was also performed to determine significant associations between respondents' beliefs and five nominated outcome variables. For these analyses, categories were collapsed into dichotomous variables. McNemar's χ2 was used to determine differences in GPs' responses to the scenarios before and after reading the three guidelines. The Royal Prince Alfred Hospital Ethics Committee approved the study. Results Of the 400 randomly selected GPs, 64 were ineligible (2 dead, 9 retired, 25 not in general practice, 5 on extended leave, 8 outside Australia, 15 uncontactable). From the 336 eligible GPs, 219 (65%) usable questionnaires were received. Our sample comprised 161 male respondents (74%) and 55 female respondents (26%), compared with 68% and 32%, respectively, for the NSW reference sample.23 Median age of our respondents was 47 years (range, 28-70 years); half had been in general practice for more than 17 years (range, 1-47 years) and 127 (58%) worked in the Sydney metropolitan area, somewhat comparable with the NSW reference sample (51% aged 45 years or over and 70% practising in Sydney).23 As only proportions (not actual numbers) for the NSW sample have been published,23 statistical testing of response bias was precluded. Responses to Scenario 1 Of the 219 GPs, 116 (53%) had received the repairman version of the case scenario and 103 (47%), the architect. There was no significant difference in GPs' answers to management of a patient's request for screening before (odds ratio [OR], 0.6; 95% CI, 0.19-1.85; P = 0.4) or after (OR, 0.79; 95% CI, 0.38-1.63; P = 0.5) reading the guidelines. Responses to all scenarios were therefore combined irrespective of patient occupation. More than two-thirds (95% CI, 62.8%-75.0%) of the participating GPs had had a request for prostate cancer screening from an asymptomatic man within the previous week (21.9%; 95% CI, 16.4%-27.4%) or the previous month (47.0%; 95% CI, 39.9%-53.2%). Of the total sample, 52.5% (95% CI, 45.9%-59.1%) indicated that PSA and DRE in combination should be done if a man requested a screening test and 55.3% (95% CI, 48.7%-61.9%) would perform the two tests (Box 2). The proportion of GPs perceiving that the GP would be at medicolegal risk if she or he did not screen for prostate cancer (61.2%) was significantly higher than that perceiving a risk if she or he did screen (15.1%; OR, 0.13; 95% CI, 0.03-0.44; P < 0.001) (Box 3). Only a quarter of the sample was aware of all three guidelines used in our survey (24.2%; 95% CI, 18.5%-29.9%). After reading the guidelines, significantly more respondents perceived less medicolegal risk if not proceeding to screening (Box 3). In addition, more respondents perceived risk if proceeding to screening (Box 3). Twenty-eight per cent (95% CI, 21.96%-33.8%) indicated that, given the three sets of guidelines, the GP would be protected medicolegally if screening tests were not performed (Box 3). Responses to Scenario 2 In the second case scenario, 14.6% (95% CI, 9.92%-19.3%) of respondents thought that the three guidelines would "most likely" protect them in the event of such a complaint. Respondents who thought such a scenario would "most likely" or "likely" influence their practice (68.9%; 95% CI, 62.8%-75.0%) were significantly more likely than those indicating it "unlikely" (23.7%; 95% CI, 18.1%-29.3%) to consider such a scenario could happen (OR, 2.72; 95% CI, 1.48-5.0; P = 0.0001). Compared with respondents who had stated, after reading the three Australian guidelines, that they would not screen an asymptomatic man, those who had stated they would screen were significantly less likely to indicate that guidelines would protect them medicolegally (OR, 0.08; 95% CI, 0.03-0.19; P < 0.001). Respondents who did not indicate that the GP would be at risk medicolegally if she or he did not perform any screening test were significantly more likely to consider that the guidelines would protect them than those who did (OR, 8.76; 95% CI, 4.45-17.23; P < 0.001). GPs who had reported that they would change their response to the case scenario after reading the guidelines presented in the survey were significantly more likely to think that the guidelines would protect them compared with those who had reported that they would not (OR, 2.55; 95% CI, 1.34-4.88; P = 0.004). GPs' views about influences on prostate cancer screening Box 4 summarises responses to seven statements about prostate cancer screening in general practice. Of the sample, 87.2% (95% CI, 82.8%-91.6%) "strongly agreed" or "agreed" that patients' decisions to be screened should be based on full disclosure of what is known about diagnosis and treatment of early prostate cancer. Respondents were significantly more likely to agree that a GP could be sued by a patient who subsequently developed prostate cancer for not performing a PSA test than by a patient who subsequently experienced adverse consequences of treatment resulting from a PSA test which had been performed (OR, 2.98; 95% CI, 1.22-8.34; P = 0.01). GPs' views of strategies to increase their sense of medicolegal protection In rating five current strategies to increase their sense of medicolegal protection, 50% (95% CI, 43.6%-56.8%) of respondents considered guidelines based on systematic reviews of the evidence as "very important", followed by NHMRC endorsement (44%; 95% CI, 37.2%-50.3%), quality of patient information (44%; 95% CI, 37.2%-50.3%) and availability of patient information about prostate cancer screening (38%; 95% CI, 31.96%-44.8%). A minority (11%; 95% CI, 6.9%-15.1%) were unsure of the impact of the current adversarial court system, which is seen as adversarial rather than conciliatory. With regard to potential strategies, there was strong support for written advice about the legal status of guidelines and inviting GP peers as well as specialists as expert witnesses in court (Box 5). Discussion Evidence-based guidelines appear to have little influence on GPs confronted by an asymptomatic man requesting prostate cancer screening. At least 90% of respondents in our study would proceed with at least one screening test (DRE, PSA, or both in combination). Furthermore, a significant majority of respondents considered the GP in the first scenario would be "at risk" medicolegally if she or he did not screen, and more so than if she or he did screen. Awareness of national guidelines was low. Surveys repeatedly demonstrate poor penetration of guidelines into general practice,24 generating interest in more deliberate implementation.7,25,26Our proxy for assessing the impact of guidelines on clinical practice augurs poorly for their influence in reducing perceptions of risk of being sued. Although, after reading the guidelines, significantly fewer considered the GP was at risk if she or he did not screen, only 28% indicated the GP was protected medicolegally by three sets of evidence-based guidelines when complying with their recommendations against screening. Even fewer (15%) considered protection would be afforded them if a man, having been diagnosed elsewhere with prostate cancer, then proceeded to initiate legal action for previous failure to screen. Those who perceived such a situation was likely were also more influenced by it in their practice. In contrast, those who would not screen were more likely to feel protected by guidelines. Most of the respondents supported a clear statement about the legal status of guidelines in a court of law. This is in contrast to the recommendation of a forum held in 1997 to examine legal implications of guidelines.27 Our results also confirm the observation of Pinnock et al that prostate cancer screening can be motivated by medicolegal concerns.13 In the US, physicians' self-reported screening correlates with their views about a medical malpractice vignette.21 Our findings suggest this to be the case also in Australia, prompting us to agree that "if physicians perform PSA tests at least to some extent out of fear of malpractice, then the standard of care may eventually be set by these defensive practices".21 GPs nonetheless support "informed decision-making" by men themselves. Specifically, 88% of the respondents "agreed" or "strongly agreed" that men's decisions to be screened should be based on "full disclosure" of what is known about the diagnosis and treatment of early prostate cancer. Two methodological caveats are recognised. First, the validity of our use of scenarios before and after exposure to guidelines has not been formally tested against actual behaviour. However, we know of no other feasible method to examine perceptions of medicolegal risk on test-ordering. Second, our response rate (65%) was lower than we had hoped, but the professional and demographic characteristics of our sample were comparable with the NSW GP profile. In summary, GPs in our survey perceived limited medicolegal protection from evidence-based guidelines. Their lack of confidence in a legal defence based on national guidelines is troubling. Those strategies suggested by GPs as important in increasing their sense of medicolegal protection could be considered further by health departments, medical defence organisations and clinical colleges. Acknowledgements The study was conducted while S Girgis was completing the NSW Health Department Public Health Officer Training Program. We thank Geoff Hirst for advice; Drs Buhagier, Stan, Gordon, Foran, Reid, Young, McGuigan and Sladden for their comments as GPs on questionnaire drafts; Nancy Harding for research support; Margaret Lesjak for assisting with telephone prompts; and Neil Donnelly for statistical advice. References Keaney MA. Is there a medical litigation crisis? Individual viewpoints on the perceived medical litigation crisis. Is litigation increasing? Med J Aust 1996; 164: 178-179. Weisman C, Morlock L, Teitelbaum M, et al. Practice changes in response to maplractice litigation climate. Results of a Maryland physician survey. Med Care 1989; 27: 16-24. Kessler D, McClellan. Do doctors practice defensive medicine? National Bureau of Economic Research working paper series. Cambridge, 1996. Summerton N. Positive and negative factors in defensive medicine: a questionnaire study of general practitioners. BMJ 1995; 310: 27-29. Hancock L. Defensive medicine and informed consent: a research paper. Review of professional indemnity arrangements for health care professionals. Canberra: AGPS, 1993. Barratt A, Bates P. O tell me the truth about evidence. Aust N Z J Public Health 1997; 21: 441-444. Ward J. Prostate cancer screening: too much, too soon? Cancer Forum 1998; 22: 18-23. Report of the US Preventive Services Task Force. Guide to clinical preventive services. 2nd ed. Baltimore: Williams & Wilkins, 1996; xlii. Australian Cancer Society. Prostate cancer screening: guidelines for health professionals. Cancer Forum 1995; 19: 47-50. Wald N, Morris J. What is case-finding? J Med Screening 1996; 3: 1. Ward J, Young J, Sladden M. General practitioners' views and use of tests to detect early prostate cancer. Aust N Z J Public Health 1998; 22: 374-380. Ward J, Hughes AM, Hirst G, Winchester L. Men's estimates of prostate cancer risk and self-reported rates of screening. Med J Aust 1997; 167: 250-253. Pinnock C, Weller D, Marshall V. Self-reported prevalence of prostate-specific antigen testing in South Australia: a community study. Med J Aust 1998; 169: 25-28. Sladden M, Dickinson J. General practitioners' attitudes to screening for prostate and testicular cancer. Med J Aust 1995; 162: 410-413. Ward J, Gupta L, Taylor N. Do general practitioners use prostate-specific antigen as a screening test for early prostate cancer? Med J Aust 1998; 169: 29-31. Hirst G, Ward J, Del Mar C. Prostate cancer screening: the case against. Med J Aust 1996; 164: 285-287. Whitmore W. Management of clinically localised prostate cancer: an unresolved problem. JAMA 1993; 269: 2676-2677. Gupta L, Ward J, Hayward R. Future directions for clinical practice guidelines: needs, lead agencies and potential dissemination strategies identified by Australian general practitioners. Aust N Z J Public Health 1997; 21: 495-499. Australian Health Technology Advisory Committee. Prostate Cancer Screening. Canberra: AGPS, 1996. Royal Australian College of General Practitioners. Guidelines for preventive activities in general practice. 4th ed. Sydney: RACGP, 1996; 26. Collins M, Fowler F, Roberts R, et al. Medical malpractice implications of PSA testing for early detection of prostate cancer. J Law Med Ethics 1997; 25: 234-242. SPSS for Windows [computer program]. Version 6.0. Chicago Ill: SPSS Inc, 1992. Commonwealth Department of Health and Family Services. General practice in Australia: supplementary tables 1997. Canberra: GP Branch, 1997; 19. (Publication no. 1838.) Gupta L, Ward J, Hayward R. Clinical practice guidelines in general practice: a national survey of recall, attitudes and impact. Med J Aust 1997; 166: 69-72. Hirst G. Clinical practice guidelines -- to what end? [letter]. Med J Aust 1997; 167: 288. Puech M, Ward J, Hirst G, Hughes AM. Local implementation of national guidelines: what do general practitioners suggest will work? Int J Qual Health Care 1998; 10: 339-343. Pelly JE, Newby L, Tito F, et al. Clinical practice guidelines before the law: sword or shield? Med J Aust 1998; 169: 330-333. (Received 7 Oct 1998, accepted 5 Jul 1999) Authors' details Needs Assessment and Health Outcomes Unit, Sydney, NSW. Seham Girgis, MB ChB, MPH, Public Health Officer; Jeanette E Ward, PhD, FAFPHM, Director, and Clinical Associate Professor, Department of Public Health and Community Medicine, University of Sydney. Australian Institute of Health, Law and Ethics, Sydney, NSW. Colin J H Thomson, BA, LLM, Executive Officer. Reprints: Associate Professor J E Ward, Needs Assessment and Health Outcomes Unit, Central Sydney Area Health Service, Locked Bag 8, Newtown, NSW 2042. jwardATnah.rpa.cs.nsw.gov.au 1: Defining "screening" for prostate cancer "Screening" is defined as the testing of asymptomatic individuals to detect risk factors or preclinical disease which has not manifested itself clinically.8 A screening test must satisfy two major requirements to be considered worthwhile: The test must be able to detect the target condition earlier than without screening and not produce large numbers of false positive and false negative results; Screening for and treating persons with early disease should improve the likelihood of favourable health outcomes compared with treating patients when they present with signs or symptoms of disease.8 Community-based randomised controlled trials are in progress to assess whether prostate cancer screening reduces the risk of premature mortality from prostate cancer among men offered it.9 When the results of these trials are published in the peer-reviewed scientific literature, data with which to calculate men's mortality risk in the absence of screening and risk reduction in its presence will be publicly available. The absence of evidence of effectiveness of prostate cancer screening to reduce premature mortality explains why four Australian authorities have recommended against it. Until such evidence is available, "case finding" by GPs who order PSA tests and/or perform DREs on asymptomatic men inadvertently implies prostate cancer screening is worthwhile, even though its effectiveness is yet unproven.10 Inadequate efforts to disseminate evidence-based guidelines to Australian GPs compound this misguided clinical practice, now known to be incorporated at disturbingly high rates in preventive health check-ups.11 In the scenario used in our survey, a 58-year-old man presents to his regular GP after prompting by his wife to have a test for prostate cancer. Testing in this context equates with screening, irrespective that the man has requested it himself. Back to text 2: Tests recommended by general practitioners in response to a patient request before and after reading extracts from the national guidelines (n=219)Which test should be done?Which test would you do?BeforeAfterBeforeAfterDRE and PSA53%37%55%43%DRE alone31%19%28%18%PSA alone4%7%7%12%Neither10%32%6%19%†DRE = digital rectal examination. PSA = prostate specific antigen. *McNemar's χ2 = 47.02; P < 0.001. †McNemar's χ2 22.78; 1 df; P < 0.001. Bold indicates a response consistent with the national guidelines. Where columns do not add to 100%. Data are missing. Back to text3: General practitioners' perception of medicolegal risk before and after reading the guidelines (n=219BeforeAfterIs the GP at risk medicolegally if she or he does not perform either or both tests for screening?Yes61%46%No26%42%Unsure13%11%McNemar χ2=20.02; 1 df; P < 0.0001Is the GP at risk medicolegally is she or he does perform either or both tests for screening?Yes15%19%No69%62%Unsure16%18%McNemar χ2=4.05; 1 df; P = 0.041Given the three recommendations, is the GP protected medicolegally if she or he does not perform either or both tests for screening?Yes-28%No-33%Unsure-33%Bold indicates a response consistent with the national guidelines. Where columns do not add to 100%, data are missing. Back to text4: General practitioners' views about seven statements pertinent to prostate cancer screening (n=219)Strongly agreeAgreeUnsureDisagreeStrongly disagreePatients' decisions to be screened should be based on full disclosure of what is known about the diagnosis and treatment of early prostate cancer46%42%5%6%1%A positive PSA test result may cause unnecessary anxiety for the patients25%62%3%9%1%A GP could be sued for not ordering a PSA test for someone who subsequently develops cancer of the prostate.16%43%12%20%7%A positive PSA test result leads to investigations and treatments of unknown effectiveness10%44%14%27%3%A GP could be sued for ordering a PSA test for someone who subsequently experiences adverse consequences from treatment6%18%25%35%16%A positive PSA result will lead to investigations associated with unacceptable morbidity3%20%21%49%6%Patients should sign a 'consent form' explaining benefits and potential complications of PSA testing before the GP orders it7%14% 23%41%14%Where rows do not add to 100%, data are missing. Back to text 5: Percentage of respondents rating as "very important" 14 potential strategies to increase a sense of medicolegal protection (n=219) GuidelinesClear statement about the legal status of the guidelines in a court 65%That guidelines summarise any relevant medicolegal judgments44%Public educationPamphlets for patients about prostate cancer screening tests in languages other than English 49%Mass media campaign targeting men older than 50 years which reassures men that screening is ineffective44%A standard consent form explaining benefits and consequences of prostate-specific antigen screening which would need to be signed by the man before he has the test29%A standard consent form also available in languages other than English27%CourtsRequiring a peer expert GP as well as a specialist as expert witnesses66%Legislation that a false screening report does not of itself establish negligence59%Requiring all expert witnesses refer to evidence-based guidelines in court56%Requiring peer expert GPs instead of expert specialists as expert witnesses53%Expert panels to advise the judge instead of juries49%A system of "No fault compensation"46%Removing cases of malpractice from the adversarial legal system46%Juries to include members with medical backgrounds in medicolegal cases35% Back to text

Seham Girgis · Jeanette E Ward

Editorial Breaking bad news: explaining cancer diagnosis and prognosis Doctors and nurses need training in communicating information about cancer and responding to patients' concerns MJA 1999; 171: 288-289 For related articles see Prince, Lobb et al & Naganathan et al Most patients, if they have cancer, want to be told about it, and they want to know what the likely treatments are, the side effects of treatment and their prognosis.1 A clear understanding of prognosis can be particularly important in conditions such as breast cancer, because patients need prognostic information to make informed decisions about systemic treatment. So, how can this information best be communicated? Based on a literature review and recommendations of a consensus panel of doctors (with input from patients with cancer), Girgis and Sanson-Fisher2 published some useful guidelines on conveying information to patients about serious disease or death. Their guidelines included ensuring privacy and allowing adequate time, assessing patients' understanding, giving information about diagnosis and prognosis simply and honestly, avoiding euphemisms, encouraging patients to express feelings, being empathic, giving a broad but realistic time-frame concerning prognosis, and arranging a review. The crucial question is how well these recommendations are followed in clinical practice, as discussing prognosis should be part of the process of breaking bad news. Audiotape recordings of consultations have shown that doctors break the bad news of a cancer diagnosis to patients in a predictable and routine way regardless of patients' individual information needs.3 Although the doctors gave reassurance that something could be done, few attempted to elicit patients' thoughts and feelings about the symptoms and their cause. They gave the information in a consistent order -- diagnosis, the relevant evidence, the need for further investigations, the treatments being considered and the probable outcome -- with no heed to which issues patients wished to address first. Obvious verbal and non-verbal cues of distress were not acknowledged and patients' immediate concerns were not explored. This consultation structure led patients to believe they were not entitled to talk about their feelings or their major concerns. Consequently, their preoccupation with these feelings and concerns meant that they did not assimilate the information and advice given. On being interviewed at the end of the consultation, patients reported that they were left with important, but undisclosed, concerns and also felt that the information given had been inadequate for their needs. The important article by Lobb and colleagues4 published in this issue of the Journal looks at one aspect of breaking bad news to cancer patients -- explaining prognosis to women with breast cancer. It was clear from the women's answers to a questionnaire and a clinical vignette that many had problems understanding prognostic information in the form it is usually presented. The women also varied considerably in what prognostic information they would like to receive and how they preferred it to be presented. The study's findings showed that not all women will desire or understand standard methods of giving prognostic information. It has been suggested that giving patients the opportunity to talk with nurses after consultations in which they have been told they have cancer, or have been given complex information about cancer prognosis, would result in their disclosing concerns and misunderstandings and these could then be fed back to the treating clinicians.5 However, this solution ignores important evidence that nurses are just as reluctant as doctors to acknowledge patients' distress and elicit their underlying concerns.6 Like doctors, nurses in these situations have been found to adopt behaviours designed to prevent further disclosure.7 These "blocking behaviours" include telling patients that any distress is normal, switching the subject to neutral topics, giving information and advice before patients' concerns have been identified, focusing only on physical aspects of the condition, and using leading, closed and multiple questions.7 Doctors and nurses avoid exploring patients' feelings and concerns because they fear that it will provoke too much emotion, which could be harmful to patients.8 They feel that their training has not equipped them with the necessary skills to explore these issues and respond appropriately.9,10 Feeling that they are not being supported emotionally and practically by colleagues and supervisors has also been linked to a greater use of these "blocking behaviours".6,11 The lack of adequate training of doctors and nurses in communicating information to patients with cancer can have important negative psychological consequences for the patients. The development of clinical anxiety and depression is more likely when patients have unresolved concerns and perceive that they have been given inadequate information.12,13 So, how can these communication deficiencies be remedied? The data collected by Lobb et al4 could be used as a basis for ongoing research to identify how best to structure and describe prognostic information so that concepts such as "median survival" and "relative risk" are made understandable. It would then be possible to develop training programs in communication skills that teach doctors how to elicit patients' preferences for information about prognosis. The use of intradisciplinary10 and multidisciplinary workshops14 has been advocated. While objective evidence of the value of intradisciplinary workshops is awaited, multidisciplinary workshops have proved successful in helping doctors and nurses acquire key communication skills.14 Despite workshops being effective in changing key communication behaviours, it is not certain how much of what is learnt is applied to clinical practice. Two randomised trials are being conducted in the United Kingdom in an effort to determine this. The Cancer Research Campaign (CRC) Psychosocial Oncology Group is studying whether training doctors in small groups enables them to be more effective in communicating with patients and better able to cope with breaking bad news and dealing with patient concerns. The CRC Psychological Medicine Group is assessing whether senior doctors benefit from six sessions of individual feedback on their "bad news" consultations and whether this results in better patient recall and less patient distress in future consultations (as measured by a patient interview and the Hospital Anxiety and Depression Scale), as well as a reduction in the level of burnout in the doctors themselves. Without systematic training, the breaking of bad news and discussions of cancer prognosis are likely to fall short of existing guidelines and patients' needs and expectations. Consultations of this type can be difficult and painful. Yet, for too long, we have expected doctors and nurses to undertake these difficult tasks without the necessary training and support. G Peter Maguire Consultant Psychiatrist; and Director Cancer Research Campaign Psychological Medicine Group, Manchester, UK Meredith C, Symonds P, Webster L, et al. Informational needs of cancer patients in West Scotland: cross sectional survey of patients' views. BMJ 1996; 313: 724-726. Girgis A, Sanson-Fisher RW. Breaking bad news: consensus guidelines for medical practitioners. J Clin Oncol 1995; 13: 2449-2456. Maguire P. Breaking bad news. Cambridge: Cambridge Handbook of Psychology, Health and Medicine, 1998: 273-275. Lobb EA, Butow PN, Kenny DT, Tattersall MHN. Communicating prognosis in early breast cancer: do women understand the language used? Med J Aust 1999; 171: 290-294. Watson M, Denton S, Baum M, Greer S. Counselling breast cancer patients: a specialist nurse service. Counselling Psychol Q 1988; 1(i): 23-31. Wilkinson SM. Factors which influence how nurses communicate with cancer patients. J Adv Nurs 1991; 16: 677-688. Maguire P. Barriers to psychological care of the dying. BMJ 1985; 291: 1711-1713. Maguire P, Faulkner A, Booth K, et al. Helping cancer patients disclose their concerns. Eur J Cancer 1996; 32A: 78-81. Maguire P, Faulkner A. How to improve the counselling skills of doctors and nurses in cancer care. BMJ 1988; 297: 847-849. Fallowfield L, Lipkin M, Hall A. Teaching senior oncologists communication skills: Results from phase 1 of a comprehensive longitudinal programme in the United Kingdom. J Clin Oncol 1998; 16: 1961-1968. Booth K, Maguire P, Butterworth T, Hillier VT. Perceived professional support and the use of blocking behaviours by hospice nurses. J Adv Nurs 1996; 24: 622-527. Parle M, Jones B, Maguire P. Maladaptive coping and affective disorders in cancer patients. Psychol Med 1996; 26: 735-744. Fallowfield LJ, Hall A, Maguire GP, Baum M. Psychological outcomes of different treatment policies in women with early breast cancer outside a clinical trial. BMJ 1990; 301: 575-580. Maguire P, Booth K, Elliott C, Jones B. Helping health professionals involved in cancer care acquire key skills -- the impact of workshops. Eur J Cancer 1996; 32A: 1486-1489.

Research Communicating prognosis in early breast cancer: do women understand the language used? Elizabeth A Lobb, Phyllis N Butow, Dianna T Kenny and Martin H N Tattersall MJA 1999; 171: 290-294 For related articles see Maguire, Prince & Naganathan et al Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Oncology Abstract Objectives: To determine the degree to which women with early breast cancer understand the prognostic information communicated by clinicians after breast cancer diagnosis, and their preferences for how this information is presented. Design: Cross-sectional survey conducted within two months of breast cancer diagnosis, using a self-administered written questionnaire. Participants and setting: One hundred women attending five Sydney teaching hospitals and one country hospital, who were diagnosed with early stage breast cancer between January and December 1997. Results: The 100 respondents represented 70% of the 143 women originally approached to participate. Many respondents did not fully understand the language typically used by surgeons and cancer specialists to describe prognosis: 53% could not calculate risk reduction (with adjuvant therapy) relative to absolute risk; 73% did not understand the term "median" survival; and 33% believed a cancer specialist could predict an individual patient's outcome. Women in professional/ paraprofessional occupations understood more prognostic information than non-professional women. There was no agreement on the descriptive equivalent of a "30%" risk, nor the numerical interpretation of a "good" chance of survival. Forty-three per cent of women preferred positively framed messages (eg, "chance of cure"), and 33% negatively framed messages (eg, "chance of relapse"). The information women most wanted was that relating to probability of cure, staging of their cancer, chances of treatment being successful, and 10-year survival figures with and without adjuvant therapy. Conclusions: Our results suggest that misunderstanding is responsible for women's confusion about breast cancer prognosis. Clinicians should use a variety of techniques to communicate prognosis and risk, and need to verify that the information has been understood. Introduction To make informed decisions women with breast cancer must understand what their prognosis is without systemic treatment, and the likely advantages and disadvantages of treatment. While most Australian doctors now tell cancer patients their diagnosis,1 prognosis is less commonly discussed.2 Reticence to provide prognostic information is often based on concerns that the information will be overwhelming, not understood or will destroy hope.3,4 However, it is not clear whether the information itself, or the language used, is the critical feature. Many patients have a poor understanding of their disease and their prognosis,5,6 or have difficulty recalling the information they have been given about their disease.7,8 Similarly, women at risk of developing breast cancer commonly misreport individual and population risk.9 Denial and minimisation of risk are also common psychological reactions to cancer risk notification after screening procedures.10 If it were possible to determine whether patients cannot understand the terminology or mathematics of risk information, or, rather, prefer not to be told or do not absorb the information, clearer directions for best clinical practice in discussing prognosis could be established. Most previous studies on risk communication in cancer have not dealt specifically with issues pertinent to women with breast cancer. In two studies that did, the women surveyed were well down the treatment path and their experience of learning their prognosis was long past.5,11 To our knowledge, there are no reports of women's understanding of specific prognostic information in early breast cancer. We investigated women's understanding of prognostic information and their preferences for the way the information on the risk of their breast cancer recurring after surgery is presented to them. Methods Survey subjects Women were recruited through their treating physician. To ensure input from a range of women, five urban centres attracting referrals from populations with different socioeconomic profiles (Royal Prince Alfred, Royal North Shore, Prince of Wales, St George, and Westmead hospitals, all in Sydney, New South Wales) and one rural centre (Tamworth Hospital, Tamworth, NSW) were approached to participate in the study. Thirteen breast surgeons and 13 medical oncologists from these centres were invited to participate in the study and all agreed. One hundred and forty-three consecutive women newly diagnosed with stage I or II breast cancer at any of the six treatment centres between January and December 1997 were contacted by letter to request their participation. The women received the letter within 2-4 weeks of making their own decisions about adjuvant treatment and within 2 months of their initial diagnosis. (The timing of questionnaire administration was carefully considered to maximise the saliency of the issues while avoiding distressing women making their own treatment decisions.) The letter was followed up by a phone call from the research coordinator, who obtained verbal consent for participation and then sent out the questionnaire by mail. One centre opted to send women a letter signed by their oncologist inviting them to participate in the study. The survey sample included patients of surgeons and medical oncologists in both private and public practice. Women from a non-English-speaking background with insufficient knowledge of English to complete the questionnaire, and women presenting with a second cancer, were excluded. Questionnaire We gathered the data using a self-administered written 17-item questionnaire, designed on the basis of a review of the literature; an analysis of 20 audiotapes of initial oncology consultations with breast cancer patients (collected from two centres -- Royal Prince Alfred Hospital and Westmead Hospital -- during another study undertaken between 1995 and 199712); and expert consultation (a working party set up by the National Breast Cancer Centre). The 20 audiotapes were transcribed and the contents analysed to identify the range of ways in which prognosis was conveyed to patients (eg, absolute and relative risk, cumulative risk, numerical or non-numerical probability, and individual versus population risk). The questionnaire investigated women's understanding of and preferences for these different formats used by doctors for disclosing prognosis and risk information. In addition, a standard hypothetical scenario of adjuvant therapy in early stage breast cancer was included, and women responded to questions applying to that scenario (Box 1). Six of the questions explored women's understanding of different ways in which the risk of breast cancer recurring after surgery could be presented. Two sample questions are shown in Box 2. A "don't know" option was not offered in the items relating to "understanding" in order to force a choice and allow an analysis of common errors in interpretation. The remaining questions focused on the importance of different prognostic information to women's decision making, and on their preferences for presentation of risk - for example: percentages versus numbers (eg, "70%" v. "7 in 10"); numerical versus verbal descriptions of risk (eg, "30%" v. "small"); and positively framed versus negatively framed statements (eg, "70% chance of remaining free of cancer" v. "30% chance of the cancer coming back"). The questionnaire also elicited the women's demographic data and details of their breast cancer diagnosis and treatment (Box 3). Statistical analysis Appropriate sample sizes were calculated using the SAM sample size software package.13 Sample size calculations were based on effect sizes from related studies in patients' level of recall after a variety of interventions. In an Australian study measuring understanding of information presented in an oncology consultation, a sample size of 47 per group was sufficient to detect statistically significant differences of 7% (P < 0.005) in recall between groups. Thus, in a comparison of two patient subgroups (eg, young v. old), a total sample size of 100 would allow us to detect a similar difference in responses in the two groups. A sample size of 100 would also allow detection of a difference of 30% or more (felt to be clinically significant) between subgroups in the proportion of women preferring one presentation of risk versus another, with a power of 0.8 and a significance level of 0.05. A "total understanding" score was calculated by summing correct responses to the six items assessing "understanding". The summary score was normally distributed (K-S Lilliefors .0514). Descriptive statistics were used to identify the percentage of patients understanding and preferring different risk information. Analysis of variance (ANOVA), Student's t tests and χ2 tests of association were used to examine the relationship between demographic variables and outcomes, as appropriate; two-sided tests were used.15 Ethical approval Approval was granted for this study by the Ethics Committee of the University of Sydney, the Central Sydney Area Health Service, the Southern Sydney Area Health Service, and individual hospital ethics committees at Westmead, Royal North Shore and Tamworth hospitals. Results Of the 118 women who agreed to participate in the survey, 100 returned questionnaires (70% of the original 143 women contacted). Demographic data Demographic characteristics of the participants are presented in Box 3. Their mean age was 56 years and most were city dwellers. Just over half had completed the Higher School Certificate, university or some form of tertiary training. The percentage of women with tertiary qualifications was 42% (compared with 37% in the general Australian population16).. Nearly two-thirds worked (or had worked) in professional or paraprofessional occupations, and 22% were working in occupations related to medicine (eg, doctor, nurse, medical receptionist, technician). Questionnaire responses A summary of the women's responses to the questionnaire is given in Box 4. Discussion We have identified some of the problems women with breast cancer experience when trying to interpret prognostic information presented by their doctors. Our results support the hypothesis that it is misunderstanding, not denial, that causes confusion. A considerable number of women in our study did not clearly understand some of the language used to describe the risk of breast cancer recurrence after surgery or how additional treatment might benefit them. Moreover, the response from this group of relatively highly educated women probably represents a "best case" scenario, and, if anything, one might expect understanding to be poorer in the general population of women with breast cancer. These findings have implications for informed consent. Clinicians need to explain what type of prognostic information can be given, and enquire how much of this information women want to hear. They should check very carefully how women have interpreted the information presented to them, and must not assume that, because a woman has already consulted a number of specialists, her prognosis has been conveyed to her and clearly understood. This applies to all patients with breast cancer, but especially those who work in unskilled occupations. It might be argued that our sample was not truly representative, as (i) the women surveyed, having recently been told their diagnosis, may not have been in the best frame of mind to answer the questionnaire clearly and impartially; and (ii) we did not include a similar group of women who had never had breast cancer. Furthermore, patient responses may have been different had the questions concerned personal experience rather than a hypothetical case scenario.5,9,10,19 However, data from Degner et al20 suggest that views expressed by people diagnosed with cancer differ considerably from those of the well population, which underscores the importance of surveying those who have actually been diagnosed with cancer. In addition, we felt that a typical case vignette was the most appropriate tool to control for the influence of individual disease variables and treatment protocols; to reduce the positive bias associated with evaluating one's own treatment team; and to examine all aspects of risk communication in adjuvant therapy. Creative measures to assist women in understanding risk statistics are needed. Bunker et al have recently proposed that a life table constructed from published statistics on national morbidity and mortality may be used to display the likelihood of developing or dying of a disease at any given moment.21 A similar approach could be used to display the likelihood of disease recurrence and premature death after cancer diagnosis. We believe that these and other information aids may contribute to informed patients' involvement in treatment decisions, and a more realistic understanding of prognosis. Acknowledgements We thank Dr Afaf Girgis, Dr Lyn Mann, Ms Kate White, Ms Joan Wilson and Ms Kim Hobbs for their assistance and advice; also the 26 clinicians who participated in this project, and the women who so willingly filled out the questionnaire. The research was funded by the National Health and Medical Research Council National Breast Cancer Centre of Australia. References Charlton RC. Breaking bad news. Med J Aust 1992; 157: 615-621. Butow PN, Kazemi J, Beeney LJ, et al. When the diagnosis is cancer: patient communication experiences and preferences. Cancer 1996; 77: 2630-2637. Oken D. What to tell cancer patients: a study of medical attitudes. JAMA 1961; 175: 1120-1128. Beisecker AE, Helmig I, Graham D, et al. Attitudes of oncologists, oncology nurses and patients from a women's clinic regarding medical decision making with older and younger breast cancer patients. Gerontologist 1994; 34: 505-512. Siminoff LA, Fetting JH, Abeloff MD. Doctor-patient communication about breast cancer adjuvant therapy. J Clin Oncol 1989; 7: 1192-1200. Sheldon JM, Fetting JH, Siminoff LA. Offering the option of randomized clinical trials to cancer patients who overestimate their prognoses with standard therapies. Cancer Invest 1993, 11: 57-62. Dunn SM, Butow PN, Tattersall MHN, et al. General information tapes inhibit recall of the cancer consultation. J Clin Oncol 1993; 11: 2279-2285. Mackillop WJ, Stewart WE, Ginsburg AD, Stewart SS. Cancer patients' perceptions of their disease and its treatment. Br J Cancer 1988; 58: 355-358. Evans DR, Blair V, Greenhalgh R, et al. The impact of genetic counselling on risk perceptions in women with a family history of breast cancer. Br J Cancer 1994; 70: 934-938. Lerman C, Rimer BK, Engstrom PF. Cancer risk notification: psychosocial and ethical implications. J Clin Oncol 1991; 9: 1275-1282. Hughes KK. Decision making by patients with breast cancer: the role of information in treatment decision selection. Oncol Nurs Forum 1993; 20: 623-628. Brown R, Dunn S, Butow P. Meeting patient expectations in the cancer consultation. Ann Oncol 1997; 8: 877-882. Glasziou P. SAM 2.1: a sample size calculator [computer program]. Sydney: NHMRC Clinical Trials Centre, University of Sydney, 1992. Armitage P, Berry G. Statistical methods in medical research. Oxford: Blackwell Scientific, 1994: 397. SPSS Advanced Statistics, TM6.1. Chicago; SPSS Inc, 1994. Australian women's year book. Canberra: Australian Bureau of Statistics, 1997. Degner LF, Kristjanson LJ, Bowman D, et al. Information needs and decisional preferences in women with breast cancer. JAMA 1997; 277: 1485-1492. Bilodeau BA, Degner LF. Informational needs, sources of information, and decisional roles in women with breast cancer. Oncol Nurs Forum 1996; 23: 691-696. Marteau TM. Framing of information: its influence upon decisions of doctors and patients. Br J Soc Psychol 1989; 28: 89-94. Degner LF, Sloan JA. Decision making during serious illness: what role do patients really want to play? J Clin Epidemiol 1992; 45: 941-950. Bunker JP, Houghton J, Baum M. Putting the risk of breast cancer in perspective. BMJ 1998; 317: 1307-1309. (Received 4 Jan, accepted 11 May, 1999) Authors' details University of Sydney, Sydney, NSW. Elizabeth A Lobb, BAdEd, MAppSci, Associate Lecturer, Medical Psychology Unit. Phyllis N Butow, PhD, MPH, Executive Director, Medical Psychology Unit; and Research Co-ordinator, Department of Psychological Medicine, Royal North Shore Hospital. Dianna T Kenny, PhD, MA, Associate Professor of Psychology, Faculty of Health Sciences. Martin H N Tattersall, MD, FRACP, Professor of Cancer Medicine, Department of Medicine. Reprints: Ms E A Lobb, Associate Lecturer, Medical Psychology Unit, Department of Psychological Medicine, University of Sydney, NSW 2006. Email: lizlobbATblackburn.med.usyd.edu.au 1: Hypothetical breast cancer scenario used in the questionnaire Sheila is a 54-year-old woman with breast cancer. Sheila has gone through the menopause. Sheila chose to have her breast cancer (tumour) removed by a lumpectomy, but she also had some of the lymph glands in her armpit removed. Sheila was advised to have radiotherapy after her lumpectomy. Sheila's breast cancer was small, and the lymph nodes under her arm were not affected with cancer. Her tumour contained receptors to oestrogen, suggesting that it may be sensitive to the effects of hormones. Sheila's doctor uses this information to decide if she would benefit from additional treatment. Sheila understands that any additional treatment other than surgery is called "adjuvant" therapy. Adjuvant therapy means giving treatment now after her surgery to try to prevent the cancer returning in the future. Following her breast cancer surgery, Sheila was told of her risk of having her cancer return (her prognosis) if she has no further treatment. This risk can be expressed in different ways. Back to text 2: Examples of questions to assess women's understanding of relative risk reduction Example A: Sheila's doctor told her that 30% of women with a cancer similar to hers will have their cancer come back within 5 years. If Sheila has additional treatment, the risk of her cancer coming back will be reduced by 30%. Tick one only If Sheila has additional treatment this means the risk of her cancer coming back within 5 years is zero. If Sheila has additional treatment this means the risk of her cancer coming back within 5 years is 21%. If Sheila has additional treatment this means the risk of her cancer coming back within 5 years is 30%. Example B: If Sheila's doctor says the median time for her breast cancer to return without further treatment is about 5 years, he/she means: The average time for Sheila's cancer to return is 5 years That 50% of women with breast cancer like Sheila's will have their cancer return within 5 years That the women whose cancer will come back will have it come back within 5 years I don't understand the word "median" Back to text 3: Demographic characteristics of the respondents (n = 100) to a questionnaire about provision of information on breast cancer prognosis*CategoryNumber of participantsAge (mean, 56 years; range, 35-88 years)Postcode City82 Country18Educational level Non-tertiary58 Tertiary42Occupation Professional/paraprofessional63 Non-professional36Marital status Married58 Other41English as first language84Working in medicine-related occupation22Time since diagnosis 1-2 months71 ≥3 months26Treatment for breast cancer Lumpectomy only14 Mastectomy only17 Lumpectomy + R38 Lumpectomy +R + C15 Mastectomy + C15Family member/friend with breast cancer Yes61 No38* Not all categories sum to 100 because of missing data. R = radiotherapy; C = chemotherapy. Back to text 4: Summary of questionnaire responses Understanding of risk Risk concepts tested Absolute risk of relapse: -- 86% of respondents gave a correct response. 30% relative risk reduction, with therapy, of an absolute risk of 30% (sample question A, Box 2): -- 47% gave a correct response; -- 28% thought additional treatment would reduce the risk of relapse to zero; and -- 25% thought the risk would remain at 30%. Median 5-year survival (sample question B, Box 2): -- 27% answered correctly; -- 43% thought it meant "average" survival; -- 10% thought that half the women not having adjuvant therapy would have their breast cancer return within 5 years; and -- 20% did not understand the term "median". Interpretation of a graphical representation of risk: -- 80% of respondents answered correctly. Distinguishing individual risk from population risk: -- 66% gave correct response. -- The remaining women believed that their cancer specialist knew whether or not they would respond to treatment. Association with demographic variables Mean number of correct responses, 3.4 (95% CI, 3.08-3.6); only one woman answered all six questions correctly. Women in professional employment (mean number of correct responses, 3.6 [95% CI, 3.2-4.0]) or paraprofessional employment (mean number of correct responses, 3.4 [95% CI, 3.0-3.8]) understood more prognostic information than women in non-professional employment (mean number of correct responses, 2.5 [95% CI, 1.7-3.4] [F2,87 = 4.24, P = 0.02]). No other variables were found to be associated with understanding of risk (eg, working in a medically related field; having tertiary qualifications; having had surgery, radiotherapy and/or chemotherapy for breast cancer; or time elapsed since consultation in which prognosis was discussed). Interpretation of words versus statistics There was no consistency in respondents' interpretation of "a good chance of remaining free of cancer" in statistical terms, nor agreement on the non-numerical interpretation of "a 30% risk" (17% thought it was a very high or high risk, 34% that it was a medium risk, and 49% that it was a low risk). Preferences for language 44% of respondents preferred "a 70% chance of cure", 13% preferred "a 7 in 10 chance", and the remainder had no preference. 53% of women preferred "a 30% chance of cancer coming back", 38% preferred "a small chance of cancer coming back", and the remainder had no preference. 49% of non-tertiary-educated women versus 24% of tertiary-educated women preferred the descriptive option (a "small" chance) (χ22 = 8.17, P = 0.02). 43% of women preferred the wording "70% chance of cure", 33% preferred "30% chance of the cancer coming back", and 25% had no preference. Preferences for framing of information Reasons given for choosing positively framed prognostic information: "a more positive/optimistic statement" and "encourages determination to manage treatment positively". Reasons given for choosing negatively framed prognostic information: "it emphasises the importance of additional treatment" and "more specific/precise". Importance attributed to prognostic information (Table) Over 90% of respondents regarded information about their chances of being cured, the staging of their cancer, and the chances that the recommended treatment would work as very important to their decision making. Nearly two-thirds of women regarded the 10-year survival rate with adjuvant therapy as very important information, and 45% wanted to know this rate without adjuvant therapy. These percentages are considerably higher than documented in previous studies.17,18 Women's ratings of the importance of different types of prognostic informationPrognostic informationVery importantSomewhat importantNot importantMy chances of being cured94%2%4%What things about my cancer influence my chances of being cured (eg, size of my cancer, whether lymph nodes are involved, etc)92%6%2%The chances that the recommended treatment will work91%7%2%How many women in my situation choosing to have the recommended treatment would be alive in 10 years60%29%11%Statistics about long term outcome of breast cancer50%32%18%How many women not choosing to have the recommended treatment are alive in 10 years45%35%20%The longest anyone in my situation has lived34%19%47%The shortest anyone in my situation has lived30%14%56%The risk of my cancer shortening my life compared with other life events (eg, heart disease, old age)45%23%32%The average time people in my situation have lived44%28%28%Back to text

Elizabeth A Lobb · Phyllis N Butow · Dianna T Kenny

Editorial Diagnosing osteoporosis: the value of quantitative ultrasound Currently, screening by quantitative ultrasound does not appear to be a good deal MJA 1999; 171: 295-296 For related articles see Maguire, Lobb et al & Naganathan et al Towards the end of the 20th century, the problems of diagnosis have not really changed. These remain how to evaluate the risk of disease, and then how to explain risk reduction clearly to patients. What has changed is our ability to predict risk, and to reduce that risk by the powerful public health, pharmacological or surgical interventions now available. What has this to do with osteoporosis, a microarchitectural disorder leading to fragility fracture? Osteoporosis is a classic chronic disorder in which the actual individual risk of clinical disease (in this case future fracture) is often difficult to quantify. The situation is similar for hypertension and hypercholesterolaemia. A few statistics may aid risk evaluation. A risk of 5%-10% or greater over five years of any osteoporotic fracture (arms, legs, pelvis, spine or rib) is generally regarded as requiring intervention. Interventions can reduce fracture risk by about 15%-50%.1,2 To prevent one fracture in such a population, between 20 and 133 patients need to be treated for five years. The risk of osteoporotic fracture depends on age. In women over the age of 65 years, the five-year risk rises dramatically from 5%, and to 20% in women over the age of 90 years.3 The presence of a previous osteoporotic fracture at least doubles the risk of future fracture.4-6 What does bone densitometry have to do with risk evaluation? It is this: when bone density is measured by dual energy x-ray absorptiometry (DEXA), then, for each standard deviation that the result falls below the mean for the individual's age (the Z score), the future risk of fracture doubles. Thus, an individual with a Z score of 22 has a fourfold greater risk of fracture than the average person of the same age. In a 65-year-old, this would give an actual five-year risk of fracture of about 30%. Because the bone density of fracture populations is independent of age, the concept of a standard deviation unit with respect to a fixed, low-risk population -- healthy 20-30-year-olds -- has been introduced (the T score) (see Figure). Significant microarchitectural deterioration (osteoporosis) is defined in bone density terms as a T score of -2.5 or less. Patients with a T score in this range have at least 5.65 times the risk of fracture relative to normal young individuals. However, their absolute five-year risk of fracture is related to the actual population risk at their age; for women aged 65-70 years this is about 18%.2 Factors other than age and bone density contribute to calculation of absolute fracture risk. Particularly important is a previous history of osteoporotic fracture. Currently, bone density risk evaluation by DEXA or quantitative computed tomography is supported by rebates from the Health Insurance Commission (HIC) for patients at high risk based on clinical information. Rebates are for evaluation of individuals who have had an osteoporotic fracture; who have clinical risk factors, such as corticosteroid treatment or premature menopause; or who have had osteoporosis diagnosed on a previous bone density test. The HIC will not fund the first bone density test in unselected individuals, otherwise known as population screening. This is because it is currently considered that bone density testing and the interventions consequent on finding high-risk individuals do not fulfil Australian cost-effectiveness criteria. However, individuals who do not meet current HIC criteria for bone density testing often decide to pay for the test themselves. How should we advise the HIC or the individual patient about the most effective screening for osteoporosis? Based on the epidemiology of fracture in Australia, it could be argued that, as well as the categories of high risk patients already outlined, all women aged 65-75 years should have bone density testing. This is because the population risk of future fracture rises dramatically in this age group. If screening is performed at an earlier age, the benefits are diluted by the small number of patients with detectable osteoporosis and the lack of controlled trial evidence that treatment prevents fracture at these ages when event rates are low. Could ultrasound become a "front end" to DEXA testing? In this issue of the Journal, the article by Naganathan et al7 is a useful contribution to the debate, providing a framework for considering the value of ultrasound screening. Naganathan et al report a simple method for calculating the benefits of testing bone structure by ultrasound compared with the current "gold standard" of DEXA. They achieved this by comparing the pre- and post-test probabilities of DEXA-defined osteoporosis (T score ≤ -2.5 at spine or hip sites) after ultrasound testing. Interestingly, they showed that 37% of their selected population had a normal combined quantitative ultrasound score, and that this finding completely excluded DEXA-defined osteoporosis. However, based on these data, an ultrasound test does not seem to be a good deal either for the individual patient or for the HIC, should it fund screening. The cost of screening 100 patients with ultrasound ($40 each) plus DEXA for those with abnormal ultrasound results ($80 x 63) would be $9040; the cost of screening with DEXA alone would be only $8000. Thus, both patients and the HIC should be advised not to pay for commercial ultrasound testing as a "front end" to DEXA at present. What about the future -- could ultrasound replace DEXA as the "gold standard" for predicting fracture? The answer is yes, possibly. The evidence-based approach would demand large prospective studies showing that ultrasound is better and cheaper than DEXA in predicting fracture, and that patients treated on the basis of ultrasound testing have a reduced risk of fracture compared with those who are not treated. To date, a couple of studies have taken the first steps to show effective fracture prediction in elderly women.8,9 It has taken 20 years to validate DEXA as a clinically useful predictor of patients who should be treated to prevent fracture, so don't hold your breath over ultrasound! Richard L Prince Associate Professor, University Department of Medicine Sir Charles Gairdner Hospital, Perth, WA Reprints: Associate Professor R L Prince, University Department of Medicine, Sir Charles Gairdner Hospital, Nedlands, WA 6009. Eddy DM, Johnston CC, Cummings SR, et al. Osteoporosis: review of the evidence for prevention, diagnosis and treatment and cost-effectiveness analysis. Osteoporos Int 1998; 8 Suppl 4: S7-S80. Cummings SR. Effect of alendronate on risk of fracture in women with low bone density but without vertebral fracture: Results from the Fracture Intervention Trial. JAMA 1998; 280: 2077-2082. Sanders KM, Seeman E, Ugoni AM, et al. The age- and gender-specific rate of fractures in Australia: a population based study. Osteoporos Int 1999. In press. Ross PD, Genant HK, Davis JW, et al. Predicting vertebral fracture incidence from prevalent fractures and bone density among non-black, osteoporotic women. Osteoporos Int 1993; 3: 120-126. Wasnich RD, Davis JW, Ross PD. Spine fracture risk is predicted by non-spine fractures. Osteoporos Int 1994; 4: 1-5. Cummings SR, Nevitt MC, Browner WS, et al. Risk factors for hip fracture in white women. N Engl J Med 1995; 332: 767-773. Naganathan V, March L, Hunter D, et al. Quantitative heel ultrasound as a predictor of osteoporosis. Med J Aust 1999; 171: 297-300. Bauer DC, Gluer CC, Cauley JA, et al. Broadband ultrasound attenuation predicts fractures strongly and independently of densitometry in older women. Arch Intern Med 1997; 157: 629-634. Porter RW, Miller C, Grainger D, Palmer SB. Prediction of hip fracture in elderly women: a prospective study. BMJ 1990; 301: 638-641. Back to text

Richard L Prince

Editorial Nurses in Australia: their role today and tomorrow The old stereotypes are long gone and the new nurse is developing swiftly MJA 1996; 164: 520-521 May 12 is International Nurses' Day, in tribute to nurses and the role they play in delivering health care. In Australia, the nature of this role has changed significantly over the past three decades. The momentum for this change has come in response to forces from both within and without the profession: the women's movement of the 1970s dramatically altered expectations of work for this once almost totally female workforce;1 in the 1980s, tertiary education was introduced; and in the 1990s, nursing has not escaped the impact of deregulation of the labour market, multiskilling and the drive towards greater efficiency and productivity in the face of economic pressures. Impact of tertiary education Newly qualified nurses are now the product of a liberal education, quite different from the hospital-based education of the past. Indeed, all nurses have embraced the tertiary opportunities that the transfer of nurse education has provided. The demand for places to convert certificate or diploma qualifications to degrees remains strong in the 34 universities with faculties or schools of nursing in Australia.2 So, too, does the demand for places for graduate diplomas and higher degrees; about half the schools of nursing offer doctoral programs3 and the number of nurses who have gained doctorates is increasing. This has in turn led to the creation of more chairs of clinical nursing (18 as of March 1996, with more pending [Professor S McKinley, Secretary to the Australian Professors of Clinical Nursing Association, personal communication]). As well as providing education, universities have promoted and stimulated research that is contributing to the developing knowledge base for nursing practice. This work, together with hospital-based research and that of newly established nursing research centres, is crucial to the evolution of the nurse's role and to the provision of evidence-based care unique to nursing. In fact, increased scientific knowledge and resulting new technologies and treatment methods are increasing the complexity of nursing practice. And in the constant interplay between education and research, education to maintain and develop new practical skills has become a critical necessity. Other influences Influences apart from those of education and research have led to further developments in the role of nurses. At times, blurred boundaries with the roles of other health workers have resulted, with accompanying dilemmas. For example, economic forces have led to the increasing employment of less skilled workers who have taken on some of the work of nurses, mostly outside the regulatory framework that governs nurses -- grave questions about accountability and duty of care need to be answered. For example, to whom and for what are personal care attendants, with no knowledge of drugs, accountable in administering prescribed medications without supervision? Indeed, the general decline in resources and the restructuring of service delivery systems will continue to impact on the role of nurses. Advancing technology is also associated with yet-to-be-resolved legal and ethical dilemmas in the role of nurses (as for all health practitioners) -- dilemmas, such as euthanasia and assisted suicide, that are no longer remote but immediate and omnipresent. Expanding roles The expansion of the nurse's role is challenging the existing statutory limitations on nursing practice. For example, nurses in intensive care units are at the cutting edge of technological innovation and often undertake activities once thought to be the sole province of medical practitioners.4 Nurses in remote areas have long been expected to act outside the boundaries of the nurse's role and have articulated the case for an expanded role (e.g., the right to prescribe some medications or to order pathological tests).5,6 Further, nurses in women's health services in most States and Territories find the absence of such rights (including also the right to refer clients to specialist services) prevents delivery of optimal patient care.7 A review of existing nursing roles with new and expanded boundaries is almost complete in New South Wales.8 The Nurse Practitioner Review, sponsored by the New South Wales Health Department, started in November 1993 and has included 10 pilot projects to evaluate three models of nursing roles with expanded responsibilities: Nurse Practitioner Remote Area, Nurse Practitioner General Practice and Nurse Practitioner Area and District Health. Within the context of each practice, extra responsibilities include ordering diagnostic procedures, prescribing and receiving or making referrals. The scope that the nurse practitioner role offers for advanced practice in nursing is a major attraction for nurses. And, given the developments in their preparation and the growth of nursing knowledge, it is a role that nurses are ready to fulfil. Within the wider context of all health care professions, nurses wish to work collaboratively, as team members, and to be consulted about their views on people's health care needs. They wish to be acknowledged for the contribution they make to patient recovery and to maintaining people's health and for the care and support they give to the dying; nurses are arguably the health professionals most intimate with people's lives and they recognise their resulting position of privilege and trust. And, in the challenging climate of change continually impacting on so many aspects of the nursing role, at least one aspect will persist: nurses will continue to support the values of caring and comfort that have always underpinned their practice. Elizabeth C Percival Executive Director, Royal College of Nursing, Canberra, ACT Helen M Hamilton Project Officer, Royal College of Nursing, Canberra, ACT Beaumont M. The professional role of a national nursing organisation. In: Gray G, Pratt R, editors. Issues in Australian nursing 2. Melbourne: Churchill Livingstone, 1989; 247-261. Report of the national review of nurse education in the higher education sector: 1994 and beyond. Canberra: AGPS, 1994: 143. Royal College of Nursing, Australia. Directory of higher education nursing courses. Sydney: New Hobson Press, 1996. Bucknall T, Thomas S. Clinical decision making in critical care. Aust J Adv Nurs 1995; 13 (2): 10-17. Kreger A. Remote area nursing practice: a quest for education. Report to the Council of Remote Area Nurses Inc. CRANA, 1991: 57-60. Buckley P, Gray G. Across the spinifex: registered nurses working in rural and remote South Australia. Adelaide: School of Nursing, Flinders University, 1993: 143. New South Wales Health Department. Role and function of nurse practitioners in New South Wales. Discussion paper. Sydney: NSW Health, 1992: 7, 13-17. (NSW State Health Publication No. [NB] 93-120.) New South Wales Health Department. Nurse Practitioner Review Stage 2. Vol 2. Sydney: NSW Health, 1993. A1/1-A5/1-20. (NSW State Health Publication No. [NB] 93-120.) ©MJA 1999 © 1999 Medical Journal of Australia.

Elizabeth C Percival · Helen M Hamilton

Research Evaluation of the PAPNET system in a general pathology service Annabelle Farnsworth, Fay M Chambers and Colin S Goldschmidt MJA 1996; 165: 429-431 Abstract - Introduction - Methods - Results - Discussion - References - Disclaimer of conflict of interest - Authors' details - - More articles on Obstetrics & gynaecology and women's health Abstract Objective: To compare the results of an automated rescreening device (PAPNET) with manual screening of Papanicolaou (Pap) smears. Design: All normal or technically unsatisfactory smears and a random sample of abnormal smears on manual screening were submitted for PAPNET rescreening. Setting: Large general pathology laboratory in Sydney between January and September 1995. Results: Of 54 658 PAP smears classified on manual screening as normal, 266 were reclassified as abnormal after PAPNET screening (32 atypical squamous cells of uncertain significance, 217 low-grade squamous intraepithelial lesions and 17 high-grade intraepithelial lesions). Of the random sample of 1022 smears classified on manual screening as abnormal, all high-grade intraepithelial lesions (122 smears) and squamous cell carcinomas (2 smears) were also detected by PAPNET, and 112 were reclassified as normal by PAPNET (14 atypical squamous cells of uncertain significance and 98 low-grade squamous intraepithelial lesions). Histological follow-up confirmed 15 of the 17 smears classified as high-grade intraepithelial lesions on PAPNET screening and detected a further seven that had been classified by PAPNET as either atypical squamous cells of uncertain significance or low-grade squamous intraepithelial lesions. Conclusions: When used as a quality-control measure in a general pathology laboratory, the PAPNET automated screening system detects higher numbers of abnormal PAP smears than manual screening. Introduction Papanicolaou (Pap)-smear examination has been shown to lower mortality and morbidity from cervical cancer,1 but the screening test itself is imperfect. False negative results (when a smear is reported as normal but has been taken from a woman with a high-grade lesion in her cervix) have been reported to be between 10%-20%.2The failure of Pap smears to detect some high-grade abnormalities is the result of either sampling or laboratory error.2 Sampling error occurs when the person taking the smear fails to collect the abnormal cervical cells because of either poor technique or the small size or localised nature of the lesion.3 Laboratory error is usually caused by the screening cytologist failing to detect the abnormal cells on the slide. Screening of Pap smears is a labour-intensive task requiring a high degree of skill and concentration. Even in laboratories using well-recognised quality control measures and staffed by highly trained cytologists, many high-grade abnormalities remain undetected by routine manual screening. These may also be missed on a manual rescreen.3 PAPNET is an automated interactive system for analysis of Pap smears which has been shown to detect abnormalities that were repeatedly missed on manual screening.4,5 We introduced the PAPNET system into our laboratory in January 1995 as a quality-control measure for rescreening of all negative (normal) smears. Here, we compare the detection of abnormalities by PAPNET with those detected by manual screening in our laboratory, and report on the histological follow-up of the PAPNET cytopredictions and the work practices of cytologists using this system. Methods Our laboratory is a large general practice in Sydney with a referral base covering metropolitan and country areas of New South Wales. During the period of our survey (23 January to 30 September 1995), all Pap smears were screened manually using routine methods. Quality assurance measures used in the study (e.g., rescreening and follow-up of abnormal smears) were routine procedures used in our laboratory. All smears considered "normal" (negative) and "technically unsatisfactory" on routine manual screening, together with a random sample of smears considered "abnormal" on routine screening during the same period, were submitted for PAPNET analysis. Smears were considered technically unsatisfactory when a confident report could not be given because of scanty material, or obscuring of cellular detail by blood, inflammation, cellular degeneration or air drying. The abnormal smears were randomly selected from the recent file of atypical smears. The PAPNET rescreening was undertaken blind to the results of manual screening. (See Box 1 for a description of the PAPNET technology.) Interim reports were generated for smears considered normal and technically unsatisfactory, and, after the slide review was completed in the laboratory, a final report was issued incorporating the PAPNET findings. Reporting terminology was based on the Bethesda system of reporting cervical/vaginal cytological diagnoses.6 A record was kept of the number of cases each cytologist was able to review per day with PAPNET. The number of slides that required manual rechecking and complete rescreening was also recorded. This involved the cytologists using the light microscope to recheck individual abnormal cells that were tagged on the PAPNET monitor. If these cells were considered to be significantly atypical, the whole slide was rescreened. If any degree of abnormality was found after rescreening, the slide was submitted to the cytopathologist for checking. To test the specificity of PAPNET, histological follow-up was performed for all patients who had an additional lesion predicted by PAPNET and were recommended to have colposcopy for this lesion. As follow-up of cytological predictions can take many months, the process was expedited and, where possible, histology results are given. In some cases, follow-up was still pending or the referring doctor had decided to follow-up by repeated observation and Pap smears. These are designated as "follow-up to come". In some cases, follow-up was unavailable; the referring doctor had been unable to contact the patient, the patient had moved or had decided to proceed no further with management. These cases are designated as "lost to follow-up". Results During the 10-month period of this survey, 60 317 Pap smears were submitted to the laboratory for examination. These smears are categorised in Box 2 (cytopredictions). The results fall within suggested National Cervical Screening Programme standards for reporting categories of technically satisfactory smears. PAPNET screening was performed on 54 658 smears classified on manual screening as negative (or within normal limits) and 1819 smears classified as technically unsatisfactory. Of the 3840 smears classified on manual screening as abnormal, 1022 smears (27%) were randomly selected and submitted for PAPNET screening: 807 low-grade squamous intraepithelial lesions, 122 high-grade squamous intraepithelial lesions, 91 atypical squamous cells of uncertain significance, and two cases of squamous cell carcinoma. Manual screening compared to PAPNET screening Of the smears classified as negative on manual screening, 266 were reclassified as abnormal after PAPNET rescreening, including 17 reported as high-grade squamous intraepithelial lesions (Box 3). This represents a 7% increase in abnormal smears after PAPNET rescreening. All of the 122 smears reported as high-grade squamous intraepithelial lesions and both squamous cell carcinomas detected on manual screening were also detected by PAPNET (Box 3). Fourteen (15%) of the 91 smears reported as atypical squamous cells of uncertain significance and 98 (12%) of the 807 reported as low-grade squamous intraepithelial lesions were reclassified as negative on PAPNET rescreening (Box 3). Histological follow-up of PAPNET cytopredictions Histology confirmed an abnormality in 28% of smears reported as atypical squamous cells of uncertain significance and 61% reported as low-grade squamous intraepithelial lesions (Box 4). Of the 17 smears reported as high-grade squamous intraepithelial lesions on PAPNET rescreening, 15 (88%) were confirmed on histology (Box 4). Three of the 32 cases reported as atypical squamous cells of uncertain significance and four of the 31 reported as low-grade squamous intraepithelial lesions (where colposcopy was recommended) were also shown to have a high-grade lesion on histological biopsy. In total, there were an extra 22 histologically confirmed high-grade lesions not detected on manual screening, of which 15 were detected by PAPNET. Cytologists' work practices In our laboratory, cytologists manually screened between 25 and 50 slides (mean, 42; standard deviation [SD], 6) per day. The large SD reflected the range of experience among the laboratory's cytologists, who alternate between gynaecological and non-gynaecological cytology. PAPNET rescreening was included in this rotation. After training, cytologists performing PAPNET rescreening were able to screen between 100 and 160 slides (mean, 126; SD, 15) per day. This included loading and unloading the tapes, viewing and assessing the images on the PAPNET screen, documentation and generating patient reports. The number of cases submitted for limited rechecking varied between 10%-90%, depending on the cytologist. The number requiring complete rescreening by a senior cytologist varied between 0 to 10 per cytologist per day and averaged five per day. The number of cases submitted to a cytopathologist by each cytologist averaged one per day. Discussion Pap smears remain the highest-volume pathology test that is not automated. Attempts have been made to automate this complex process for nearly 40 years, but it is only recently that advances in the development of automated systems have occurred which offer practical advantages in a laboratory. Although the detection rate of abnormalities on manual screening was well within normal standards in our study, PAPNET rescreening was able to detect an increased number of abnormal Pap smears. This increase was not associated with a loss of specificity, as often occurs with increased detection by manual screening.3 Many studies have shown the ability of PAPNET rescreening to detect a significant number of abnormal Pap smears when compared with manual screening, but these have been predominantly smaller studies using archived material.8,9 Our study was undertaken as part of the routine workflow in a laboratory processing a large number of smears and is the first Australian study to compare the two screening systems. The reported increase in detection of abnormalities in other studies has been as high as 16%,10 and the company which developed PAPNET (Neuromedical Systems Inc., New York, USA) claims increases of up to 30%. The increase in our study was much smaller (7%), with most detected abnormalities being low-grade lesions. However, we believe this increase was worthwhile given the reasonably high rate of detection on manual screening and the large volume of routine smears processed. Boon et al. reported the results of a large series of smears that were not double-screened, but had been either manually screened or PAPNET screened. Higher detection rates of abnormalities were found in the PAPNET group. Our study is the first report of a large series in which all negative smears were screened both manually and by PAPNET. Our study showed that the PAPNET system could be feasibly integrated into a routine working laboratory situation. It was a valuable educational and quality assurance tool. Cytologists found it easy to use and were able to review slides at three to four times their manual-screening rate. From our experience, cytologists did not become complacent in their manual screening, but rather became more cautious knowing that all the negative smears would be examined by a computerised device. The additional work for cytopathologists and senior cytologists was not great. PAPNET is only one of a number of automated cytology systems currently available as an additional test for routine Pap-smear screening. We did not undertake a comparison of other automated systems or their cost-effectiveness. Further studies on the cost-effectiveness of PAPNET testing and its efficacy for use in public health screening programs are needed. It may be that automated testing technology will replace current screening methods in the future. Disclaimer of conflict of interest This work was conducted independently. Neither Douglass Hanly Moir Pathology nor any of the individual authors has any financial or other association with the suppliers of the PAPNET service, Neuromedical Systems Inc. References Mitchell HS, Giles GG. Cancer diagnosis after a report of negative cervical cytology. Med J Aust 1996; 164: 270-273. Koss LG. The Papanicolaou test for cervical cancer detection. A triumph and a tragedy. JAMA 1989; 261: 737-743. Boscha MC, Rietveld-Scheffers PEM, Boon ME. Characteristics of false negative smears tested in the normal screening situation. Acta Cytol 1992; 36: 711-716. Koss LG, Hin E, Schreiber K, et al. Evaluation of the PAPNET cytologic screening system for quality control of cervical smears. Am J Clin Pathol 1994; 101: 220-229. Boon M, Kok CP. Neural network processing can provide means to catch errors that slip through human screening of Pap smears. Diagn Cytopathol 1993; 9: 411-416. The Bethesda system of reporting cervical/vaginal cytologic diagnoses: revised after the second National Cancer Institute Workshop, April 29-30, 1991. Acta Cytol 1993; 37: 115-124. Royal College of Pathologists of Australasia. Performance Standards for Australian Laboratories Reporting Cervical Cytology. Sydney: RCPA Quality Assurance Programs, 1995. Rosenthal DL, Acosta D, Peters RK. Computer-assisted re-screening of clinically important false negative cervical smears using the PAPNET testing system. Acta Cytol 1996; 40: 120-126. Sherman ME, Mango LJ, Kelly D, et al. PAPNET analysis of reportedly negative smears preceding the diagnosis of a high grade squamous intraepithelial lesion or carcinoma. Mod Pathol 1994; 7: 578-581. Elgert PA, Suhrland MJ, Re E, et al. Prospective quality control of cervical smears using the PAPNET system [abstract No. 5]. In: Abstracts of the Scientific Session of the 42nd Annual Scientific Meeting of the American Society of Cytology; 1994 Nov 1-6; Chicago. Acta Cytol 1994; 38: 793-805. Boon ME, Kok LP, Beck S. Histologic validation of neural network assisted cervical screening: comparison with the conventional procedure. Cell Vision 1995; 2: 23-27. (Received 10 Jan, accepted 14 Aug 1996) Authors' details Douglass Hanly Moir Pathology, 95 Epping Road, North Ryde, NSW. Annabelle Farnsworth, MB BS, FRCPA, Cytopathologist. Fay M Chambers, MB BS, FRCPA, Cytopathologist. Colin S Goldschmidt, MB BCh, FRCPA, Cytopathologist. Reprints: Dr A Farnsworth, Douglass Hanly Moir Pathology, 95 Epping Road, North Ryde 2113. Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/> We appreciate your comments. 1: The PAPNET system. PAPNET consists of a scanning apparatus and a review station.4 In Australia, the cervical slides are sent to Hong Kong for the initial scanning. The scanning apparatus includes an automated microscope with an attached video camera which transmits images to a primary classifier. Selected images are then passed into a neural net computing unit which chooses the 128 highest-ranking images for storage on an optical disk or digital tape, which is sent back to Australia for display at the review station. The review station is located in the cytology laboratory where manual screening takes place. The 128 recorded images are displayed in panels on a high-resolution colour monitor and are reviewed by a cytologist. If an abnormality is suspected, the original slide is manually checked and, if necessary, manually rescreened. Back to text 2: Categories of Pap smears on manual screening (23 January to 30 September 1995). CytopredictionNumber of smearsNegative*54 658 (90.6%)Low-grade squamous intraepithelial lesions 2974 (4.9%)High-grade squamous intraepithelial lesions 432 (0.7%)Atypical squamous cells of uncertain significance434 (0.7%)Technically unsatisfactory1819 (3%)Total60 317 (100%)* Cellular appearance was within normal limits. Back to text 3: PAPNET rescreening of PAP smears classified as normal and abnormal on manual screening. CytopredictionNormal smears: manual screeningPAPNET rescreeningAbnormal smears: manual screeningPAPNET rescreeningNegative*54 65854 359--112Atypical squamous cells of uncertain significance--329177Low-grade squamous intraepithelial lesions--217807709High-grade squamous intraepithelial lesions--17122122Squamous cell carcinoma--022Technically unsatisfactory18191852---- * Cellular appearance was within normal limits. The 112 negative smears on PAPNET screening had been classified on manual screening as atypical squamous cells of uncertain significance (14 smears) and low-grade squamous intraepithelial lesions (98 smears). Back to text 4: Histological follow-up of PAPNET cytopredictions. Histological follow-up PAPNET-detected abnormalitiesNegative/inflammation*Low-grade squamous intraepithelial lesionsHigh-grade squamous intraepithelial lesionsFollow-up to comeLost to follow-upTotalAtypical squamous cells of unknown significance66371032Low-grade squamous intraepithelial lesions21544631High-grade squamous intraepithelial lesions 01150117 *Cellular appearance was within normal limits. Back to text

Annabelle Farnsworth · Fay M Chambers · Colin S Goldschmidt

Research Investigation of a cluster of leukaemia in the Illawarra region of New South Wales, 1989-1996 Victoria J Westley-Wise, Bernard W Stewart, Irene Kreis, Paolo F Ricci, Anthony Hogan, Chris Darling, Steve Corbett, John Kaldor, Neill H Stacey, and Pauline Warburton MJA 1999; 171: 178-183 For editorial comment, see Cartwright Abstract - Introduction - Methods - Results - Discussion - Conclusions - Follow-up - Acknowledgements - References - Authors' details - - More articles on Haematology Abstract Objectives: To investigate a cluster of leukaemia among young people and assess the plausibility of a disease-exposure relationship. Design: Descriptive analysis of population-based leukaemia incidence data, review of evidence related to the causation of leukaemia, assessment of environmental exposures to known leukaemogens, and resulting risks of leukaemia. Setting: Illawarra region of New South Wales, Australia, focusing on suburbs between the Port Kembla industrial complex and Lake Illawarra (the Warrawong area). Main outcome measures: Standardised incidence ratios (SIRs) for leukaemia; current measured and past estimated ambient air benzene concentrations; and expected leukaemia cases attributable to estimates of ambient air benzene concentrations. Results: In 1989-1996, 12 leukaemia cases among Warrawong residents aged less than 50 years were observed, more than the 3.49 cases expected from the rate in the rest of the Illawarra region (SIR, 343.8; 99% CI, 141.6-691.7). These people lived in suburbs immediately to the south-southwest of a coke byproducts plant (a major industrial source of benzene, one of the few known leukaemogens). The greatest excess was among 15-24-year-olds (SIR, 1085.6; 99% CI, 234.1-3072.4). In 1996, ambient air concentrations of benzene averaged less than 1 part per billion (ppb). Since 1970, ambient air concentrations of benzene were estimated to have averaged up to 3 ppb, about one-thousandth of the level at which leukaemia risk has been identified in occupational epidemiological studies. Using the risk assessment model developed by the US Environmental Protection Agency, we estimate that past benzene levels in the Warrawong area could have resulted in 0.4 additional cases of leukaemia in 1989-1996. Conclusions: The excess occurrence of leukaemia in the Warrawong area in 1989-1996 is highly unusual. Current environmental benzene exposure and the reconstructed past environmental benzene exposure level are too low to explain the large excess of leukaemia. The cause of the cluster is uncertain. Introduction In July 1996 the Illawarra Public Health Unit (located in the Wollongong/Port Kembla region, New South Wales) was notified that four former students of a local high school had been diagnosed with leukaemia since 1989. Preliminary investigations established that a cluster of at least 11 people aged less than 40 years who had lived in suburbs near the school had been diagnosed with leukaemia since 1989. On the basis of New South Wales cancer registration data, only about 2 to 3 cases would have been expected. Established causes of leukaemia include occupational benzene exposure, ionising radiation, chemotherapeutic agents, and some inherited and congenital conditions.1-5 Coke byproduct plants are a recognised source of occupational, and potentially of environmental, benzene exposures.1,6,7 The people in the cluster lived in suburbs adjacent to the Port Kembla industrial complex, which includes coke ovens and an associated byproducts plant. We report the investigation of the Illawarra region leukaemia cluster and discuss the plausibility of a disease-exposure relationship. Methods Our investigation followed published guidelines for cancer cluster investigations.8-10 The main components were evaluations of: the pattern of leukaemia incidence in the Illawarra region, with specific attention to residential areas near the Port Kembla industrial complex; environmental exposure to known and putative leukaemogens; and the plausibility of a disease-exposure relationship (whether past environmental exposures to known leukaemogens could explain the excess leukaemia occurrence). The NSW Cancer Council Ethics Committee approved the study. Case finding and investigation Active and passive case-finding methods were used to identify all people resident in the Illawarra region (Wollongong, Shellharbour and Kiama Local Government Areas) aged less than 50 years who had been diagnosed with leukaemia in 1989-1996. The cut-off at age 50 years was chosen as the index cases were young and the age interval 40-50 years represents a natural change in leukaemia occurrence, when the leukaemia risk begins to rise steeply. We actively identified cases from bone marrow aspirate reports, hospital discharge and day-only admission data, and discussions with clinicians in Sydney and Wollongong, community members and organisations. The population-based New South Wales Central Cancer Registry provided the passive case-finding data. For each leukaemia case, we sought to review the medical record and interview the patient and/or a relative to obtain or confirm information about dates of birth and diagnosis, leukaemia cell-type, genetic and medical risk factors, residential and school histories, and personal and/or parental occupational histories. Occurrence evaluation Leukaemia incidence was analysed in eight areas within the Illawarra region with a similar population size (about 20 000-30 000 in 1986), including the area close to the Port Kembla industrial complex (Area 1) (Figure 1). Leukaemia incidence rates in the whole Illawarra region, and each of the eight areas within it, were compared with rates in a reference population by calculating standardised incidence ratios (SIRs) as a means of indirect age standardisation.11 The reference population used was "Urban NSW" (Sydney, Wentworth, Central Coast, Hunter and Illawarra administrative health areas). The calculation of rates was based on place of residence at diagnosis. Using Central Cancer Registry data, we calculated leukaemia SIRs for males and females and for people aged less than 50 years for four five-year periods which had Census years as their mid-points: 1974-1978, 1979-1983, 1984-1988 and 1989-1993. The SIR is the ratio of the number of cancer cases in a study population to the number of cases expected according to the age-specific rate in the reference population (multiplied by 100). For the Illawarra region, leukaemia rates could be calculated to 1996. Thus, for 1989-1996, leukaemia SIRs were calculated for each of the Illawarra areas. In Area 1, they were also classified by age group and cell-type (according to ICD-9),12 using the rest of the Illawarra region as the reference population. Australian Bureau of Statistics (ABS) census data for 30 June 1976, 1981, 1986 and 1991 were used for urban NSW reference populations.13 For the Illawarra region, the ABS provided population data by postcode. Exact Poisson confidence intervals (CI) around the SIRs were estimated.14 CIs were set at 99%, rather than 95%, to reduce the possibility of identifying a chance excess of cancer as statistically significant. SIRs and CIs were calculated with SAS for Windows version 6.11. NSW Central Cancer Registry data and urban NSW population data were accessed from NSW Health's Health Outcomes Information and Statistical Toolbox, a repository of health-related databases for New South Wales. Environmental monitoring and historical exposure reconstruction We undertook an extensive review of the literature on risk factors for and causes of leukaemia, and on carcinogenic effects of occupational and environmental exposures. The environmental assessment focused on exposure to known leukaemogens from the 1970s to 1996. It involved interviewing representatives from industry, government agencies, local residents and workers; inspecting relevant sites; reviewing government, industry and press reports; and collecting and reviewing information on environmental and occupational exposure for residents and workers. The NSW Environment Protection Authority (EPA) and BHP Steel began daily ambient air benzene monitoring in September 1996 in the residential areas nearest the plant (Figure 2). Monitoring was also conducted at three control sites. The EPA used the standard protocol developed by the US Environmental Protection Agency (US EPA) for assessing toxic organic compounds in ambient air.15 BHP used personal samplers, adapted to a stationary role, which collected organic vapours onto an active adsorbent medium by drawing air through the sampler. Both the EPA and BHP analysed the samples with gas chromatography at laboratories registered with the National Association of Testing Authorities. We estimated environmental benzene exposure from the main local sources before September 1996. Using methods developed by the US EPA,16 we estimated levels of emissions from the coke production facilities for each year since 1970 (based on levels in 1996, adjusted for changes in plant equipment and processes and changes in coke and benzene production). Information related to benzene emissions from motor vehicles and other petroleum sources, including Roads and Traffic Authority data on local traffic volumes, was used to provide an upper estimate of the extent to which emissions from these other major local sources may have differed in previous years relative to 1996. Risk estimation The US EPA's benzene risk assessment model of dose-response17 was used to estimate the number of excess leukaemia cases expected in Area 1 between 1989-1996. It was assumed that the Area 1 population had breathed ambient air (70 kg person breathing 20 m3 of air daily) with benzene concentrations equivalent to the estimated maximum annual average concentration since 1970 for the maximally exposed site, continuously over a lifetime (24 hours per day for 70 years). Results Case finding and investigation The same cases were identified by both active and passive case-finding methods. We identified 44 Illawarra residents aged less than 50 years who were diagnosed with leukaemia in 1989-1996. These included 12 people resident in Area 1 at diagnosis, and a 13th person who had moved out of Area 1 a few months before diagnosis (Table 1). None of these 13 people from Area 1 were found to have genetic or medical risk factors for leukaemia. Nor had they ever worked in the production of coke or its byproducts. Six were diagnosed with acute lymphoblastic leukaemia (ALL), four with chronic myeloid leukaemia (CML), and three with acute myeloid leukaemia (AML). Immunophenotypic features and leukaemic classifications revealed no unusual patterns. Six people have died. Of the nine people from Area 1 aged 20 years or less, seven had lived there all their lives, and two for about 11 years. Four attended the same high school in the late 1980s, with three being in the same school year; these three people had leukaemia of different cell-types. Occurrence evaluation For the four five-year periods between 1974-1993, leukaemia incidence in the Illawarra region, and each of its areas, was not significantly different to that throughout urban New South Wales.18 The incidence of total cancers and other specific cancers (including lymphoma and multiple myeloma) was also not significantly higher in Area 1.18However, leukaemia incidence among Area 1 residents aged less than 50 years in 1989-1996 was more than three times higher than in the rest of the Illawarra region (12 cases observed, versus 3.49 expected; SIR, 344; P = 0.0003) (Table 2). The SIR was more than 200 for all leukaemia cell-types, and was significantly increased for ALL (Table 3). The greatest excess of leukaemia was among teenagers and young adults. Among 15-24-year-olds, five cases were observed, versus 0.46 expected (SIR, 1086; 99% CI, 234.1-3072; P = 0.0001). Environmental monitoring and reconstruction of historical exposure The Port Kembla industrial complex contains heavy industries such as copper smelting, sulphuric acid and superphosphate manufacture, petroleum depots, and Australia's largest steelworks, which includes coke ovens and their byproducts plant. In spring and summer, the predominant wind direction is from the northeast; hence, the residential area where the people with leukaemia lived received the greatest exposure from industrial emissions in the region. Benzene was the only known leukaemogen for which local environmental exposures may have been relevant. While ionising radiation is also an established leukaemogen, and there is evidence that exposure to occupational ethylene oxide or 1,3-butadiene can cause leukaemia,3-5 no specific local environmental sources of these agents were identified. At the byproducts plant, coke oven gases are distilled into a benzene- toluene-xylene commercial product (which is 80% benzene), while past practices (until 1977) separated them. The closest residences are more than 1 km from the plant, with all but two Area 1 cases residing 1-3 km from the plant. The other major benzene sources in Area 1 are motor vehicles and petroleum storage tanks. Both EPA and BHP monitoring found that ambient air benzene concentrations in Area 1 averaged less than one part per billion (ppb) in 1996 (Table 4), typical of urban sites in Sydney.19 Analysis of benzene, toluene and xylene ratios in the EPA's samples indicated that about 50% of the benzene was from petroleum. Annual average ambient air benzene concentrations at the most exposed site within Area 1, since 1970, are estimated to have been up to about 3 ppb. Roads and Traffic Authority data showed that traffic volumes in Area 1 have not changed appreciably since the 1970s.20 Local petroleum storage tanks had a greater storage capacity in previous years, which may have been associated with higher emissions.20 Risk estimation The estimated maximum annual average ambient air benzene concentration in Area 1 of 3 ppb is only about one-thousandth of concentrations at which leukaemia risk has been detected in occupational studies.1 The World Health Organization (WHO) has concluded that occupational exposure to an average of 1 part per million (1 ppm, ie 1000 ppb) over a working lifetime has been associated with no statistical increase in leukaemia deaths.1Using the US EPA benzene risk assessment model,17 if a population of 17 500 people (the number of people in Area 1 aged less than 50 years in 1991) had all breathed air with an average benzene concentration of 3 ppb over a lifetime, at the most 0.2 excess leukaemia deaths (or 0.4 cases) would have been expected in 1989-1996. Discussion This investigation into the reported cluster found a highly significant excess leukaemia occurrence in the Warrawong area, particularly among teenagers, in 1989-1996. Estimated past environmental benzene levels are too low to explain this excess. Cluster studies Cancer cluster studies have rarely provided insights into aetiology.3,8-10,21,22 Studies of very rare diseases with well-defined, high exposures are the most likely to yield conclusive results.22 However, these circumstances, in the context of geographic (spatial or spatiotemporal) clusters, are uncommon.10,22 Disease clusters occur continually in any population, and as such represent "expectedly unexpected" events.9,22Drawing boundaries tightly around people observed in clusters inadvertently identifies and overestimates disease excesses.21,22 However, in this study, the geographic, age and time criteria setting the boundaries were not defined or varied to influence the magnitude of the observed excess. Area 1 was a natural geographic grouping of postcodes bounded by industrial zones, Lake Illawarra and the Pacific Ocean. It included suburbs and a postcode area in which no cases were resident. The age range 0-49 years was broad given that the reported cluster was among teenagers. On the other hand, the most recent period analysed (1989-1996) was preceded by a period in which few leukaemia cases were diagnosed.18 Possible leukaemogens Several known leukaemia causes and risk factors were excluded as explanations for the cluster: ionising radiation, ethylene oxide, 1,3-butadiene, and genetic and medical risk factors. For other agents considered, such as dioxins, pesticides, and heavy metals, evidence is lacking of a causal relationship between these agents and leukaemia, despite numerous studies conducted worldwide.5 Although benzene is structurally related to carcinogenic polycyclic hydrocarbons, these agents are generally associated with lung and some other cancers, but not leukaemia.23 Similarly, the influence of genetic polymorphisms, specifically within the cytochrome P450 family, has been associated with lung cancer rather than leukaemia.24Viruses have been causally associated with the rare hairy cell leukaemia and adult T-cell leukaemia.4,5 They have also been suspected to cause leukaemia in childhood and adolescence, but there is still little convincing evidence that they play an important role.4,5,25 Several studies have associated parental smoking with childhood leukaemia.3,26 While many other parental occupational and/or personal exposures (including pesticides, benzene, solvents, petroleum products, and spray paints) have also been implicated in childhood leukaemia, most relevant studies have used poor exposure measures, with inconsistent results.2,3 To our knowledge no leukaemia "clusters" have been reported and investigated in close proximity to industrial facilities similar to those in the Warrawong area. Occupational exposure during steel and coke production has been causally associated with an increased risk of lung and certain other cancers, but not leukaemia.23,27-29 Benzene Benzene was the only known human leukaemogen to which people in Area 1 had potentially significant environmental exposures. Despite the inevitable focus on the steelworks and coke byproducts plant as a benzene source, petrol exhaust and tobacco smoke (the primary source of benzene for smokers, and relevant to non-smokers through passive smoking) are the most significant sources in urbanised populations.1 Food and water are not major sources of benzene exposure,30 and the possibility of contamination of the water supply in Area 1 with benzene from local sources was examined and excluded.20While other haematological malignancies have been associated with occupational benzene exposure,31-36 the evidence has been considered strongest for AML,1 which affected only three people in this cluster. However, a recent review concluded that the few available studies of leukaemia cell-types do not indicate larger or more consistent elevations in risk for AML than for other cell-types.36 Study strengths and limitations Studies of geographic cancer clusters must typically deal with poor information about environmental exposures.22 In this study we had to rely on estimates of past environmental benzene exposure, but several factors suggest that the emission estimates for the coke production facilities are accurate. An independent audit of the emissions estimates concluded that the underlying assumptions were robust and that the emissions inventory was calculated as accurately as possible without an onsite testing program.37 The estimated past annual average ambient air benzene concentration in the maximally exposed part of the Warrawong area, 3 ppb, was similar to concentrations measured38-40 and modelled41 at similar distances from byproducts plants overseas. Measured occupational benzene exposures for Port Kembla byproducts plant workers between 1979 and 199642 were similar to occupational monitoring results for byproducts plant workers from the United States43 and Britain in the 1980s.29,44Using the US EPA benzene risk assessment model,17 even if we assume that average ambient air benzene concentration in Area 1 was 30 ppb (rather than the estimated 3 ppb), this level of exposure would still only explain up to four excess leukaemia cases. Given that the observed leukaemia excess was primarily among young people, the default assumption of 70 kg adults used in our risk estimate is also likely to have slightly overestimated the risk, and hence the number of expected cases. Consistent with public health principles, the US EPA benzene risk assessment model, which uses data from studies of US rubber and chemical workers,36,45,46 is itself based on assumptions that would exaggerate rather than minimise risk, including a linear relationship between exposure to genotoxic carcinogens and leukaemia risk. However, results from some animal studies suggest that a non-linear response may be more biologically plausible.47,48 If this applies to benzene-induced human leukaemia, application of the US EPA model may considerably overestimate risks in the low exposure range. More plausible are biologically based multistage stochastic models for chemical carcinogenesis, which account for cellular birth, death, initiation, promotion and other biological processes, each stage being linked by a stochastic transition probability that accounts for exposure (or dose).47,48 Such models are likely to produce lower estimates of leukaemia risk for low levels of environmental exposure. However, large uncertainties are inherent in any conversion of risk estimates from animal studies or occupational studies to risk estimates for benzene exposure in the general community. Many people -- children, people of reproductive age, those with other risk factors -- may have susceptibilities to leukaemia quite different from those of the male workers studied in occupational studies. Animal and human studies have begun to clarify the potential risk associated with relatively high transient and/or intermittent benzene exposure49 versus cumulative exposure, but the relationship is still poorly understood for low dose extrapolations. In addition, people in the community are exposed to a variety of agents, which may have as yet unidentified additive and possibly synergistic effects. Conclusions On current knowledge, the recent ambient air benzene concentrations in the Warrawong area represent a negligible leukaemia risk, and the estimated past benzene concentrations are too low to explain the large excess of leukaemia cases that occurred in 1989-1996. However, factors such as variation in susceptibilities of individuals and population groups such as children, the possible effects of intermittent and high transient benzene exposures, and interactions between different agents, mean that we cannot exclude a causal association between leukaemia occurrence among young people in the Warrawong area and chemical exposures. Follow-up A feasibility study is being undertaken to examine the potential for relating disease to chemical exposures through a case-control study. Broadly, chemical exposures of interest are personal exposures (environmental and individual, to benzene and industrial emissions in general) and parental exposures (focusing on those with prior evidence of an association with leukaemia). In addition, routine surveillance of leukaemia and lymphoma is continuing, as is ambient air monitoring for benzene and other hazardous pollutants in the Warrawong area. Acknowledgements We gratefully acknowledge the assistance given by the individuals with leukaemia and their relatives, and other community members who participated in the investigation's Community Reference Group. We give special thanks to members of the Illawarra Leukaemia Investigation Steering Committee for their commitment and contributions: Giovanna Crocco and David Gilmour (Community Reference Group), Richard Willison and Trevor Dunn (Illawarra Public Health Unit), Joe Woodward and Craig Lamberton (NSW Environmental Protection Authority), Ron Hales (Wollongong City Council), and Christine Ewan (University of Wollongong). Many individuals and organisations assisted in and supported the study, but we would particularly like to thank the following organisations: NSW Health; Illawarra Area Health Service; New South Wales Cancer Council; BHP Port Kembla; NSW Environmental Protection Authority; and the University of Wollongong. We also thank John Marthick (University of Wollongong) and Paddy Ranasinghe (Illawarra Public Health Unit) for preparing the maps. References World Health Organization. Benzene (Environmental Health Criteria No. 150). Geneva: International Programme on Chemical Safety, 1993. Ross JA, Davies SM, Potter JD, Robison LL. Epidemiology of childhood leukaemia, with a focus on infants. Epidemiol Rev 1994; 16: 243-272. Cartwright RA, Staines A. Acute leukaemias. Clin Haematol 1992; 5: 1-26. Finch SC, Linet MS. Chronic leukaemias. Clin Haematol 1992; 5: 27-56. Tomatis L, editor. Cancer: causes, occurrence and control (IARC Scientific Publications No. 100). Lyon: International Agency for Research on Cancer, 1990. Fishbein L, O'Neill IK, editors. Benzene and alkylated benzenes. Environmental carcinogens: methods of analysis and exposure measurement, vol. 10 (IARC Scientific Publications No. 85). Lyon: International Agency for Research on Cancer, 1988. United States Environmental Protection Agency. National emission standards for hazardous air pollutants; regulation of benzene; response to public comments. US Federal Register 1984, 40 CFR Part 61, AD-FRL-2523-7. Centers for Disease Control. Guidelines for investigating clusters of health events. MMWR Morb Mortal Wkly Rep 1990, 39 (R-11): 1-23. Bender AP, Williams AN, Johnson RA, Jagger HG. Appropriate public health responses to clusters: the art of being responsibly responsive. Am J Epidemiol 1990; 132 Suppl 1: S48-S52. Fiore BJ, Hanrahan LP, Anderson HA. State health department response to disease cluster reports: a protocol for investigation. Am J Epidemiol 1990; 132 Suppl 1: S14-S22. Breslow NE, Day NE. Statistical methods in cancer research. Vol II. Lyon: International Agency for Research on Cancer, 1987. World Health Organization. Manual of the International Statistical Classification of Diseases, Injuries and Causes of Death. 9th Revision. Geneva: WHO, 1977. Australian Bureau of Statistics. Estimated resident populations by age and sex in statistical local areas, New South Wales (Catalogue. No. 3209.1, 30 June 1976, 1981, 1986, 1991). Canberra: ABS, 1978, 1983, 1988, 1993. Daly L. Simple SAS macros for the calculation of exact binomial and Poisson confidence limits. Comput Biol Med 1992; 22: 351-361. United States Environmental Protection Agency. Compendium of methods for the determination of toxic organic compounds in ambient air. 2nd edition. Compendium method TO-14A. Determination of volatile organic compounds (VOCs) in ambient air using specially prepared canisters with subsequent analysis by gas chromatography (EPA/625/R-96/010b). Cincinnati, OH: Center for Environmental Research Information, 1999. <http://www.epa.gov/ttn/amtic/files/ambient/airtox/to-14ar.pdf> Accessed 5 July 1999. United States Environmental Protection Agency. AP-42, 5th ed., vol. I. Chapter 12: metallurgical industry. 12.2 Coke production [draft]. Research Triangle Park, NC: Emission Factor And Inventory Group, US EPA, 1995. <http://www.epa.gov/ttn/chief/ap42pdf/c12s02.pdf>. Accessed 5 July 1999. [No longer available, but see final version at <http://www.epa.gov/ttn/chief/ap42/ch12/final/c12s02.pdf> Accessed 10 May 2001. United States Environmental Protection Agency. Integrated risk information system (IRIS). Benzene (CASRN 71-43-2). 16 October 1998. Cincinnati, OH: Environmental Criteria and Assessment Office, Office of Health and Environmental Assessment, Office of Research and Development, Cincinnati, 1996. <http://www.epa.gov/ngispgm3/iris/subst/0276.htm> Accessed 5 July 1999. Westley-Wise V, Hogan A. Report on the occurrence of leukaemia (1974-96) and other cancers (1974-93) in the Illawarra. Illawarra Area Health Service. Wollongong 1997. Wadge A, Salisbury J. Benzene. National Environmental Health Forum Monographs, Air Series 2. National Environmental Health Forum, South Australian Health Commission, Adelaide,1997. Kreis I, Willison R. Environmental assessment related to a leukaemia cluster. University of Wollongong. Wollongong 1997. Olsen SF, Martuzzi M, Elliott P. Cluster analysis and disease mapping -- why, when and how? A step by step guide. BMJ 1996; 313: 863-866. Rothman KJ. A sobering start for the cluster busters' conference. Am J Epidemiol 1990; 132 Suppl 1: S6-S13. International Agency for Research on Cancer. Polynuclear aromatic compounds. Part 3, Industrial exposures in aluminium production, coal gasification, coke production, and iron and steel founding. IARC Monographs on the evaluation of the carcinogenic risk of chemicals to humans, vol. 34. Lyon: IARC, 1984. Wormhoudt LW, Commandeur JNM, Vermeulen NPE. Genetic polymorphisms of human N-acetyltransferase, cytochrome P450, glutathione-S-transferase, and epoxide hydrolase enzymes: relevance to xenobiotic metabolism and toxicity. Crit Rev Toxicol 1999; 29: 59-124. Alexander FE. Viruses, clusters and clustering in childhood leukaemia: a new perspective? Eur J Cancer 1993; 29A: 1424-1443. Sorahan T, Lancashire RJ, Hulten MA, Stewart AM. Childhood cancer and parental use of tobacco: Deaths from 1953 to 1955. Br J Cancer 1997; 75: 134-138. Redmond CKA, Strobino BR, Cypress RH. Cancer experience among coke byproduct workers. Ann N Y Acad Sci 1976; 217: 102-115. Swaen GM, Slanged JAM, Volovics A, et al. Mortality of coke plant workers in the Netherlands. Br J Indust Med 1991; 48: 130-135. Hurley JF, Cherrie JW, Maclaren W. Exposure to benzene and mortality from leukaemia: results from coke oven and other coal product workers. Br J Indust Med 1991; 48: 502-504. Wallace L. Environmental exposure to benzene: an update. Environ Health Perspect 1997; 104: 1129-1136. Yin SN, Hayes RB, Linet MS, Li GL, et al. A cohort study of cancer among benzene-exposed workers in China: overall results. Am J Indust Med 1996; 29: 227-235. Hayes RB, Yin S-N, Dosemeci M, Li G-L, et al. Benzene and the dose-related incidence of hematologic neoplasms in China. J Natl Cancer Inst 1997; 89: 1065-1071. Rinsky RA, Alexander B, Smith MD, Hornung R, et al. Benzene and leukaemia: an epidemiological risk assessment. N Engl J Med 1987; 136: 1044-1050. Christie D, Robinson K, Gordon I, Bisby J. A prospective study in the Australian petroleum industry. I. Mortality. Br J Indust Med 1991; 48: 507-510. Wong O. An industry wide mortality study of chemical workers occupationally exposed to benzene. II. Dose response analyses. Br J Indust Med 1987; 44: 382-395. Savitz DA, Andrews KW. Review of epidemiologic evidence on benzene and lymphatic and hematopoietic cancers. Am J Indust Med 1997; 31: 287-295. Holmes Air Sciences 1997. Air quality report: review of BHP report to the Illawarra Area Health Service Leukaemia Task Force. Report prepared for the NSW Environment Protection Authority. Sydney: Holmes Air Sciences, 1997. Harkov R, Olsakovsky AC, Fillo JP. Determining the ambient impacts of coke and coke by-products manufacturing on selected pollutant levels in neighboring communities: I -- results from a six-month ambient air benzene monitoring study. Air toxics and volatile organic compounds: papers from the 84th Annual Meeting and Exhibition of the Air and Waste Management Association, Vancouver, 1991. Vol 6. Pittsburgh: Air and Waste Management Association, 1991. GDCh (Society of German Chemists) Advisory Committee on Existing Chemicals of Environmental Relevance. Benzene. Weinhmam, VCH Verlagsgesellschaft, 1988. In: World Health Organization. Benzene (Environmental Health Criteria No. 150). Geneva: WHO, 1993: 36. Fentiman AF, Neher MB, Kinzer GW, et al. Environmental monitoring benzene (PB-295 641). Prepared for US EPA. Springfield, VA: Battelle Columbus Laboratories, National Technical Information Service, 1979. In: IARC. Some industrial chemicals and dyestuffs (IARC monographs on the evaluation of the carcinogenic risk of chemicals to humans, vol. 29). Lyon: IARC, 1982. United States Environment Protection Agency. Benzene emissions from coke byproduct recovery plants -- background information for proposed standards (EPA-450/3-83-016a). Research Triangle Park, NC: Office of Air Quality Planning and Standards, 1984. BHP Flat Products Division. Report to the Illawarra Area Health Service. Port Kembla: BHP Flat Products Division, 1997. Runion HE, Scott LM. Benzene exposure in the United States, 1978-1983: an overview. Am J Indust Med 1985; 7: 385-393. Drummond L, Luck R, Afacan AS, Wilson HK. Biological monitoring of workers exposed to benzene in the coke oven industry. Br J Indust Med 1988; 45: 256-261. Rinsky RA, Young RJ, Smith AB. Leukemia in benzene workers. Am J Indust Med 1981; 2: 217-245. Ott MG, Townsend DT, Fishbeck WA, Langner RA. Mortality among workers occupationally exposed to benzene. Arch Environ Health 1978; 33: 3-10. Cox LA Jr, Ricci PF. Reassessing benzene cancer risks using internal doses. Risk Analysis 1992; 12: 401-409. Cox LA Jr, Ricci PF. Dose-response non-linearities for benzene revisited: A reply to C Crump. Risk Analysis 1993; 14: 485-486. (Received 2 July 1998, accepted 18 May 1999) Authors' details Illawarra Public Health Unit, Illawarra Area Health Service, Wollongong, NSW. Victoria J Westley-Wise, MPH, FAFPHM, Director; Anthony Hogan, MSc(Hons), PhD, Public Health Officer. Children's Cancer Research Institute, Sydney Children's Hospital, Sydney, NSW. Bernard W Stewart, PhD, FRACI, Research Director; now Head of Cancer Control Program, South Eastern Sydney Area Health Service. University of Wollongong, Wollongong, NSW. Irene Kreis, PhD, FAFPHM, Senior Lecturer; Paolo F Ricci, MSc, PhD, Professorial Fellow. BHP Steel Flat Products Division, Wollongong, NSW. Chris Darling, MSc(Occup Med), FAFOM, Occupational Health Advisor. NSW Health Department, Sydney, NSW. Steve Corbett, MPH, FAFPHM, Manager. National Centre for HIV Epidemiology and Clinical Research, University of New South Wales, Sydney, NSW. John Kaldor, PhD, Deputy Director, and Professor of Epidemiology. University of Sydney, Sydney, NSW. Neill H Stacey, BSc(Hons), PhD, Associate Professor. Illawarra Regional Hospital, Illawarra Area Health Service, Wollongong, NSW. Pauline Warburton, MB BS, FRACP, Director. Reprints: Dr V J Westley-Wise, Illawarra Public Health Unit, PO Box 66, Keiraville, NSW 2500. Email: vwestATdoh.health.nsw.gov.au Figure 1 (above): Map of the Illawarra region, showing areas used for comparing leukamia incidence. Back to textFigure 2 (below): Map of the Warrawong area (central portion of area 1), showing the location of the four ambient air monitoring stations. Back to textBack to textBack to textBack to textBack to text

Victoria J Westley-Wise · Bernard W Stewart · Irene Kreis · Paolo F Ricci · Anthony Hogan · Chris Darling · Steve Corbett · John Kaldor · Neill H Stacey · Pauline Warburton

Healthcare Hepatitis C: an economic evaluation of extended treatment with interferon Alan Shiell, Sue Brown and Geoff C Farrell MJA 1999; 171: 189-193 Abstract - Introduction - Methods - Results - Discussion - References - Authors' details Abstract Objectives: To re-evaluate the cost effectiveness of treating hepatitis C virus (HCV) infection with interferon alfa (IFα) in Australia, taking into account changes in clinical practice. Design: A decision-analytic method (Markov model) was used to simulate the costs and effects of 6 months and 12 months of treatment with IFα versus no treatment (conventional management). Both costs and effects were modelled over 30 years. Data sources: Published meta-analysis of the effectiveness of treatment, professional judgement about treatment protocols, scheduled medical fees, diagnosis-related costs for hospital admission, and a literature search for quality-of-life weights. Patients: A hypothetical cohort of 1000 patients with chronic HCV infection aged 40 years at the start of treatment. Main outcome measures: Incremental costs per life-year gained and per quality-adjusted life-year (QALY) gained. Results: Compared with no treatment, IFα treatment for 6 months results in an extra 94.2 life-years or 320.1 QALYs at an extra cost of $1.8 million (after discounting at 3%) in a cohort of 1000 patients. Discounted cost per life-year gained is $19 110, which is about a quarter of the cost reported in 1994. The discounted cost per QALY gained is $5625. Extended treatment for another 6 months results in an additional 89.0 life-years saved or 170.8 QALYs gained at an incremental discounted cost of $15 835 per life-year gained and $8250 per QALY gained. Conclusions: The cost effectiveness of IFα treatment for HCV infection has improved as a result of better patient selection, cost reductions and enhanced effectiveness of extended treatment. The results are sensitive to assumptions made about quality of life and the discount rate. Introduction Infection with the hepatitis C virus (HCV) is an important public health problem in Australia. It is estimated that there are at least 100 000 people carrying the virus and that up to 10 000 new cases are diagnosed each year.1 As many as 85% of those with acute HCV infection will develop chronic infection, and, of these, a significant proportion will develop cirrhosis and hepatocellular carcinoma (HCC). The only approved treatment for chronic HCV infection, interferon alfa (IFα), is expensive, has significant adverse effects and is effective in only 10%-35% of patients. The cost effectiveness of treatment is uncertain. Decision-analytic techniques have been used to simulate the expected costs and effects of treatment, and several economic evaluations of IFα have been published.2-7 The only Australian study (published in 1994)3 estimated the cost per life-year gained by treatment with IFα to be $33 000 in patients with cirrhosis at the start of treatment and $71 000 for patients without cirrhosis. These figures are substantially higher than those reported elsewhere, reflecting a more cautious view of the long term effectiveness of IFα and the exclusion of the broader benefits of therapy, such as its assumed effects on employment and production capacity. The impact that IFα has on the natural history of HCV infection is now better known. Treatment is discontinued in patients who fail to show a response after 12 weeks, with no reduction in effectiveness but with substantial cost savings. Further, several studies have shown benefits of extended treatment over 12 months rather than 6 months, and this has become the recommended treatment period in most countries including Australia. The effect that this has on cost effectiveness is not clear, as both costs and benefits are likely to increase. Our aim is to update our previous estimate of the cost effectiveness of IFα in the treatment of chronic HCV infection.3 Under section 100 of the Health Act 1953 (Cwlth) (Highly Specialised Drugs Program), subsidised treatment is restricted to patients with no signs of cirrhosis at start of treatment and we have restricted our analysis to such patients. Methods The costs and effects of IFα treatment were simulated by a decision-analytic method (the Markov model) in a hypothetical cohort of 1000 patients with chronic HCV infection aged 40 years at start of treatment (the mean age at diagnosis is 42 years). Both costs and effects were modelled over 30 years. The cost effectiveness of treatment with IFα over 6 months versus no treatment (ie, conventional management only) was re-evaluated, incorporating changes in clinical practice, treatment costs and the price of IFα. The incremental costs and effects of moving from 6 months to 12 months' treatment were then estimated. The software used was Microsoft Excel 97. The assumptions and methods for the decision analytic technique are shown in the Box. Results The net cost of 6 months' treatment with IFα for chronic HCV infection (ie, the cost of treatment minus the cost of conventional management of the disease) was estimated to be $1800 per patient after discounting at 3%. Treatment with IFα results in an extra 94.2 discounted life-years saved or 320.1 additional (discounted) QALYs (Table 2). The incremental cost per life-year saved was $19 110, which is about a quarter of the cost reported in our previous study.3 The incremental cost per QALY gained was $5625. Extending treatment from 6 to 12 months results in an additional 89.0 discounted life-years gained or 170.8 discounted QALYs at incremental costs of $15 835 per life-year gained and $8250 per QALY gained. Average cost per unit of outcome increases as the duration of the model is reduced. As duration of the model acts as a proxy for age at the start of treatment, this finding suggests that treatment is less cost effective in older age groups. The sensitivity analysis (Table 3) suggests that the results for 6 months' treatment are robust with respect to assumptions made about rates of disease progression, the long term effectiveness of IFα, the price of IFα and the exclusion of patients not responding after 12 weeks. The most important variables are the choice of discount rate and the adjustment for quality of life (Table 3). Relatively minor adjustments to the quality-of-life weight for treatment have a large effect on cost per QALY gained. In the extreme, the adverse effects of treatment offset any gains in quality of life brought about by disease resolution. The effect of 12 months' treatment over 6 months' treatment is also sensitive to changes in the discount rate and the duration of the model and, in addition, is more sensitive to assumptions made about disease progression and treatment effectiveness. Discussion Our results suggest that the cost per life-year gained from 6 months' treatment with IFα is lower than when it was first evaluated in an Australian context in 1994.3 This change is attributable to three main factors: a reduction in the cost of treating people with IFα; a reduction in the price of IFα itself; and cessation of treatment at 12 weeks in those who fail to show a reduction in serum alanine aminotransferase levels. The latter has been clinical policy in Australia since IFα was first listed for public subsidy in 1994, but our initial evaluation preceded this.3Quality adjustment of the outcomes also has a substantial effect on the cost-effectiveness ratios, suggesting that the major impact of IFα treatment is on improving quality of life rather than increasing life expectancy through the prevention of cirrhosis. There is also the relief offered to those in whom the infection is resolved. However, the sensitivity of the results to changing assumptions about the effect of the disease and its treatment on quality of life reinforces the need for further research into the subjective impact of HCV infection. Only one other study has considered the cost effectiveness of 12 months' versus 6 months' therapy.7 Consistent with our results, it concluded that treatment over 12 months may be cost effective, except in patients older than 60 years of age. The cost-effectiveness ratios reported here compare favourably with many other public health interventions, such as screening for breast and cervical cancer.20,21 However, there are problems in comparing the results of economic evaluations, particularly when different methods have been used.22 Furthermore, if the benefits of extended treatment with IFα are to be realised within a limited healthcare budget, then some other program or activity must be dropped or reduced in scale to accommodate the increase in expenditure. Thus, before drawing conclusions about cost effectiveness, one should compare the benefits of IFα treatment with the benefits of the other program or activity affected.23 See Box for summary points. Caution is especially warranted when, as in this case, a decision-analytic model has been employed, as it is often difficult to assess the validity of the assumptions made. The protracted nature of HCV infection, however, makes it difficult to assess the cost effectiveness of treatment by another means.24,25 Decisions on when and how to use IFα have to be made with available data. However, our comprehensive sensitivity analysis showed that, for most of the assumptions made, the results appear to be robust. The exceptions are the two subjective variables -- the utility attached to different disease endpoints and the rate at which future costs and benefits are discounted. HCV infection is not the benign disease it was once believed to be, but little is known about the impact it has on people's lives or the lengths to which they might go for relief. Our results are particularly sensitive to assumptions made about the relative effect of living with chronic infection, and its associated risks of long term sequelae versus the known risks and the uncertain effectiveness of treatment. Individual attitudes to risk and time preference will affect the perceived cost effectiveness of treatment. Further research is needed to examine the personal and social impact of HCV infection and the utility of its treatment.26 References Australian Health Ministers' Advisory Council. National Hepatitis C Action Plan, October 1994. Canberra; AGPS, 1994. 2. Garcia de Ancos JL, Roberts JA, Dusheiko GM. An economic evaluation of the costs of a-interferon treatment for chronic active hepatitis due to hepatitis B or C virus. J Hepatol 1990; 11: S11-S18. Shiell A, Briggs A, Farrell G. The cost-effectiveness of alpha interferon in the treatment of chronic active hepatitis C. Med J Aust 1994; 160: 268-272. Dusheiko GM, Roberts JA. Treatment of chronic type B and C hepatitis with interferon alfa: an economic appraisal. Hepatology 1995; 22: 1863-1873. Joliet E, Vanlemmens C, Kerleau M, et al. Cost-effectiveness analysis of the treatment of chronic hepatitis C. Gastroenterol Clin Biol 1997; 21: 336-338. Bennet WG, Inoue Y, Beck R, et al. Estimates of the cost-effectiveness of a single course of interferon-a 2b in patients with histologically mild hepatitis C. Ann Intern Med 1997; 127: 855-865. Kim WR, Poterucha JJ, Hermans JE, et al. Cost-effectiveness of 6 and 12 months of interferon-a therapy for chronic hepatitis C. Ann Intern Med 1997; 127: 866-874. National Institutes of Health Consensus Development Panel statement: management of hepatitis C. Hepatology 1997; 26(3 Suppl 1): 2S-10S. Fattovitch G, Giustina G, Degos F, et al. Morbidity and mortality in compensated cirrhosis type C: a retrospective follow-up study of 384 patients. Gastroenterology 1997; 112: 463-472. Australian Bureau of Statistics. Deaths: Australia 1994. Canberra: ABS, 1994. (Catalogue No. 3302.0.) Poynard T, Leroy V, Cohard M, et al. Meta-analysis of interferon randomized trials in the treatment of viral hepatitis C: effects of dose and duration. Hepatology 1996; 24: 778-789. Carithers RL Jr, Sugano D, Bayliss M. Health assessment for chronic HCV infection: results of quality of life. Dig Dis Sci 1996; 41: 75S-80S. Davis GL, Balart LA, Schiff ER, et al. Assessing health-related quality of life in chronic hepatitis C using the Sickness Impact Profile. Clin Ther 1994; 16: 334-343. Foster GR, Goldin RD, Thomas HC. Chronic hepatitis C virus infection causes a significant reduction in quality of life in the absence of cirrhosis. Hepatology 1998; 27: 209-212. National Health and Medical Research Council. A strategy for the detection and management of hepatitis C in Australia. Canberra: NHMRC/AGPS, 1997. Commonwealth Department of Health and Family Services. Medical Benefits Schedule. Nov 1996. Canberra; AGPS, 1996. Commonwealth Department of Health, Housing, Local Government and Community Services. Manual of Resource Items and their Associated Costs. Canberra: AGPS, November 1993. Drummond MF, Brandt A, Luce B, Rovira J. Standardising methodologies for economic evaluation in health care. Int J Technol Assess Health Care 1993; 9: 26-36. Gold MR, Siegel JE, Russell LB, Weinstein MC, editors. Cost-effectiveness in health and medicine. New York: Oxford University Press, 1996: 230. AHMAC Breast Cancer Screening Evaluation Committee. Breast screening in Australia: future directions. Canberra: Australian Institute of Health and Welfare, 1990. AHMAC Cervical Cancer Screening Evaluation Committee. Cervical Screening in Australia: options for change. Canberra: Australian Institute of Health and Welfare, 1991. Salkeld G, Davey PD, Arnolda G. A critical review of health-related economic evaluations in Australia: implications for health policy. Health Policy 1995; 31: 111-125. Birch S, Donaldson C. Cost-benefit analysis: dealing with the problems of indivisible projects and fixed budgets. Health Policy 1987; 7: 61-72. Bennet WG, Pauker SG, Davis GL, Wong JB. Modeling therapeutic benefit in the midst of uncertainty: therapy for hepatitis C. Dig Dis Sci 1996; 41: 56S-62S. Koff RS, Seeff LB. Economic modeling of treatment of chronic hepatitis B and chronic hepatitis C: promises and limitations. Hepatology 1995; 22: 1880-1885. Owens DK. In the eye of the beholder: assessment of health-related quality of life. Hepatology 1998; 27: 292-293. (Received 20 Nov 1998, accepted 3 May 1999) Authors' details Social and Public Health Economics Research Group (SPHERe), Department of Public Health and Community Medicine, University of Sydney, Sydney, NSW. Alan Shiell, MSc(Econ), Honorary Research Associate. Medical Benefits Fund of Australia, Sydney, NSW. Sue Brown, MPH, BPharm, Pharmacy Manager, Provider Relations. Department of Medicine, Westmead Hospital, University of Sydney, NSW. Geoff C Farrell, MD, FRACP, Storr Professor of Medicine. Reprints will not be available from the authors. Correspondence: Mr A Shiell, Social and Public Health Economics Research Group (SPHERe), Department of Public Health and Community Medicine, University of Sydney (A27), NSW 2006. Email: alansATpub.health.usyd.edu.au Assumptions and methods for the decision analytic technique Natural history of hepatitis C (HCV) Chronic HCV infection to cirrhosis: The rate of progression was assumed to be 20% at 20 years,8 consistent with experience in patients attending liver clinics, but is higher than in a community sample. Cirrhosis to hepatocellular carcinoma (HCC): Rates of progression range from 1% to 4% per year and are higher in older age groups.8 We have assumed an annual rate of 1.4% (14% over 10 years), which is the lowest rate from more than 10 published studies from Europe and Japan.9 The small chance of HCC developing in patients without cirrhosis (< 0.25% per year)8 was ignored. Cirrhosis to advanced liver failure: We assumed that 20% of the cohort would progress to advanced liver failure over 10 years from the onset of cirrhosis.8 Death: All patients developing HCC or advanced liver failure were assumed to die within 2 years of diagnosis. Deaths from other causes were estimated from Australian life tables.10 Effectiveness of IFα treatment Previous evaluation: In our previous evaluation,3 we assumed that 6 months' treatment with IFα would be effective in 20% of cases overall and 26% of cases without cirrhosis at the start of treatment. A recent meta-analysis by Poynard et al11 suggests that a sustained response is achieved in 14%-22% of cases treated with 3 million international units (miu) of IFα over 6 months, and in 28%-38% of patients treated with the same dose for 12 months or longer. Our estimates of the effectiveness of treatment were based on the assumption of an 18% sustained response rate after IFα treatment for 6 months and a 35% sustained response rate after 12 months' treatment, with both rates subject to sensitivity analysis. Quality of life Chronic HCV infection has been described as largely asymptomatic, with less than 20% of patients developing non-specific symptoms such as fatigue.8 However, recent studies suggest that it has an impact on quality of life.12-14 People with chronic HCV infection scored significantly lower than a comparable but healthy population on various generic health measures, such as the 36-item short-form health survey (SF-36).12 Side effects of treatment: Mild side effects of IFα are common and most patients will experience flu-like symptoms which diminish over time. Less transient effects -- fatigue, irritability, depression, thyroid disease and skin disorders -- are more troublesome and cause some patients to discontinue treatment. Less than 2% of patients will experience severe side effects.8 Quality-adjusted life-years (QALYs): The impact of the disease (including its sequelae and treatment with IFα) on quality of life can be incorporated into the analysis by weighting the life-years gained according to their quality, thus generating an estimate of quality-adjusted life-years, or QALYs. These weights are usually calibrated on a scale of 0 to 1, where 0 is equivalent to death and 1 to a year of life in full health. Subjective impact of the disease: A major shortcoming is a lack of understanding of the subjective impact of the disease. In the absence of patient-generated weights, other authors have used quality-of-life weights based on clinical judgement or small scale surveys.4,6,7 The weights are 0.8-0.95 for chronic hepatitis, 0.7-0.8 for compensated cirrhosis, 0.28-0.5 for decompensated cirrhosis, and 0.1-0.25 for hepatocellular carcinoma. The weights we used were adapted from those derived by Kim et al,7 as these were the only ones based on patient judgement (Table 1). In the baseline case, it was assumed that treatment had no additional adverse effect on quality of life -- an assumption relaxed in the sensitivity analysis. Costs of treatment Estimates of the treatment costs for each of the main clinical endpoints were based on clinical protocols as specified by the National Health and Medical Research Council (NHMRC)15 and the clinical opinion of one of the authors (G C F). The protocols were costed using the Medicare Benefits Schedule for medical services,16 and Australian national diagnosis-related groups (AN-DRG-3.1) for hospital admissions (Table 1).17 See Appendix for details. All costs are in Australian dollars at 1996 prices. Cirrhosis: A weighted cost was computed on the basis of specified treatment protocols for each of the main clinical manifestations of cirrhosis. The weights reflect the estimated proportion of patients likely to experience each state.6 It was further assumed that 2% of patients experiencing cirrhosis would undergo a liver transplant each year and that 25% of cirrhotic patients would experience at least one episode of septicaemia requiring hospital admission. IFα: The unit cost of IFα reflected its price to the healthcare system. It was assumed that treatment would be given at a rate of 3 miu three times a week for either 24 or 48 weeks and would be discontinued in people who did not show a reduction in serum alanine aminotransferase (ALT) levels after 12 weeks. Experience in Australia suggests that 26% of people will fail to respond in this period and will discontinue treatment (R G Batey, Deputy Dean, and Professor of Gastroenterology, Faculty of Medicine and Health Sciences, University of Newcastle, Newcastle, NSW, personal communication). Other costs: Lost production capacity caused by morbidity and premature mortality associated with HCV infection was not considered.18 Other patient costs, such as the use of community services and alternative medicine, were also omitted. This biases the findings against treatment with IFα. Cost effectiveness of IFα treatment The cost effectiveness of treatment for 6 months is expressed as the additional cost per QALY gained over and above no treatment (conventional management). The incremental cost effectiveness of 12 months' treatment over 6 months' treatment is also reported. Future costs and outcomes were discounted at both 3% and 5% (as recommended by Gold et al19). Undiscounted results are also presented and the effect of using a higher discount rate is assessed in the sensitivity analysis. (Discounting is the process whereby costs and benefits occurring at different points in time are made commensurate with each other.) Sensitivity analysis The robustness of the results was examined by sensitivity analysis (given the uncertainties inherent in the modelling approach). Key variables included in the sensitivity analysis were response rates, rates of disease progression, time to develop sequelae, costs of treatment, percentage of patients excluded at 12 weeks, age groups, the discount rate, and the adjustment for quality of life. Back to text 1: Baseline assumptions: values and costs used in the Markov modelValueRangeDisease transition probabilities From chronic infection to cirrhosis20%10%-30% From cirrhosis to advanced liver failure20%10%-30% From cirrhosis to hepatocellular carcinoma14%7%-21%Effectiveness of treatment Long term response after 6 months18%14%-24% Long term response after 12 months35%26%-38% Discontinue treatment after 12 weeks because of lack of response26%13%-39%Health state (quality of life) weights Chronic infection0.950.80-1.00 Cirrhosis0.750.50-0.90 Advanced liver failure0.250.10-0.40 Hepatocellular carcinoma0.250.10-0.40 Treatment with interferon alfa (IFα)0.950.80-0.95 Resolved infection1.001.00-1.00Treatment episode costs*$$Medical management of chronic infection405200-600Treatment with IFα 6 months' treatment including discontinuing treatment2 8001 975-3 630 12 months' treatment including discontinuing treatment5 1503 620-6 670Cirrhosis (weighted average)2 8251 400-4 200 Management of compensated cirrhosis660330-990 Diuretic-sensitive ascites1 880940-2 820 Refractory ascites13 6406 820-20 460 Variceal haemorrhage (Year 1)5 8502 925-8 775 Hepatic encephalopathy (Year 1) 6 3753 190-9 565 Hepatocellular carcinoma (Year 1)8 8654 435-13 290 Liver transplant (Year 1)92 52546 265-138 790 Septicaemia5 3002 650-7 950Terminal care28 40014 200-42 600Back to text 2: Summary of costs and outcomes of interferon treatment for chronic hepatitis C infection in a hypothetical cohort of 1000 patients Treatment durationNet costs ($)Lives saved Life-years savedQALYs gainedUndiscounted(a) 6 months1 185 55512.0176.3 531.4(b) 12 months2 013 84523.4 342.7830.7(c) Increment828 290 11.3166.5299.3Discounted (3%)(a) 6 months1 800 3807.694.2320.1(b) 12 months3 209 34514.7183.2490.9(c) Increment1 408 9657.189.0170.8Discounted (5%)(a) 6 months2 049 6455.763.9237.7(b) 12 months3 694 02011.1124.2359.5(c) Increment1 644 3755.460.3121.8Treatment DurationCost/life saved ($)Cost/ life-year saved ($)Cost/ QALY gained ($)Undiscounted(a) 6 months98 7106 7202 230(b) 12 months86 2355 875 2 425(c) Increment73 0204 9752 765Discounted (3%)(a) 6 months238 52519 1105 625(b) 12 months218 67017 520 6 540(c) Increment197 64515 835 8 250Discounted (5%)(a) 6 months360 37032 095 8 620(b) 12 months334 02029 750 10 275(c) Increment306 120 27 265 13 505 Incremental cost and outcomes (a) 6 months' treatment with interferon v. no treatment; (b) 12 months' treatment with interferon v. no treatment; (c) 12 months' treatment with interferon v. 6 months' treatment. Net costs = costs of treatment minus costs of conventional management of the disease. QALY = quality-adjusted life-year. Back to text 3: Discounted costs of interferon treatment for chronic hepatitis C infection per life-year and per quality-adjusted life-year (QALY) gained under best and worst case scenarios (sensitivity analysis)Treatment for 6 months v. no treatmentCosts ($) per QALY (Baseline = $5 625)Costs ($) per life-year (Baseline = $19 110)VariableRangeBest caseWorst caseBest caseWorst caseRate of cirrhosis10%-30% 3 2409 6459 20548 820Time to cirrhosis (years)10-304 09010 29011 64537 470Rate of sequelaeComposite*5 1156 26512 95037 590 Liver failure10%-30% Hepatocellular carcinoma7%-21%Time to sequelae (years)5-155 4955 77516 21522 970Long term response rateComposite3 3908 26511 68027 600 6 months14%-24% 12 months26%-38%Cost of interferon per dose$13-$393 0358 12010 31027 595Cost of health service useComposite4 0657 18513 81024 410 Chronic infection50%-150% Cirrhosis50%-150% Terminal care50%-150%Discontinue treatment at 12 weeks13%-33%5 2406 01017 81020 415Duration of model (years)20-404 30512 95012 89049 090Discount rate0-10%2 23018 6206 72589 900Quality-of-life weightsComposite (See Table 1)2 08028 03019 110† 19 110†Treatment for 12 months v. 6 months Costs ($) per QALY (Baseline = $8 250)Costs ($) per life-year (Baseline = $15 835)VariableBest caseWorst caseBest caseWorst caseRate of cirrhosis3 80019 8257 02542 270Time to cirrhosis (years)5 21012 6859 32026 455Rate of sequelae6 98010 16510 76531 040 Liver failure Hepatocellular carcinomaTime to sequelae (years)7 8358 72513 49518 970Long term response rate 4 36063 1758 125214 105 6 months 12 monthsCost of interferon per dose 4 15512 3407 91023 475Cost of health service use 5 48511 01010 53521 135 Chronic infection Cirrhosis Terminal care at 12 weeks 6 8109 58513 07518 595Duration of model (years) 7 20017 3009 75541 910Discount rate2 76533 4754 97578 310Quality-of-life weights 7 5309 81015 835†15 835† * Composite refers to the aggregate effect on cost per unit of outcome of changing all subsidiary variables simultaneously. †Quality adjustment has no effect on the number of life-years saved. Back to text Summary points Costs and benefits of healthcare interventions have to be considered in the context of a limited healthcare budget. The cost effectiveness of interferon alfa (IFα) treatment of chronic hepatitis C infection in Australia has improved since it was first evaluated in 1994. The major effect of IFα therapy is on improving quality of life, not life expectancy. More research is required on the impact of chronic hepatitis C infection and IFα treatment on quality of life. Back to text APPENDIX 1 Treatment episode costs Back to article 1: Medical management of chronic infection Resource categoryNumberUnit costTotal Cost Specialist visits2112.65225.30 Pathology Liver function test219.8039.60 Alfa fetoprotein219.9039.80 Ultrasound1101.70101.70 Total 406.40 2: Treatment with interferon (6 months) including workup Resource categoryNumberUnit costTotal Cost Specialist review initial consultation194.1594.15 subsequent consultation647.15282.90 Interferon (allowing for drop out)0.871889.281643.67 Pathology Full blood count717.20120.40 Liver biopsy1130.35130.35 Liver function test719.80138.60 International normalisation ratio112.4012.40 Thyroid function test341.00123.00 PCR380.00240.00 Anti-HCV113.7013.70 Total2799.17 3: Treatment with interferon (12 months) including workup Resource categoryNumberUnit costTotal Cost Specialist review initial consultation194.1594.15 subsequent consultation1447.15660.10 Interferon (allowing for drop out)0.813 755.253 041.74 Pathology FBC1517.20258.00 Liver biopsy1130.35130.35 LFT1519.80297.00 International normalisation ratio112.4012.40 Thyroid function test441.00164.00 PCR680.00480.00 Anti-HCV113.7013.70 Total5151.44 4: Management of compensated cirrhosis Resource categoryNumberUnit costTotal Cost GP visits424.5098.00 Specialist visits initial1110.75110.75 subsequent355.45166.35 Pathology LFT219.8029.60 AFP419.9079.60 Ultrasound283.95167.90 Total662.20 5: Management of diuretic-sensitive ascites Resource categoryNumberUnit costTotal Cost Inpatient admissions0.331980.00653.40 Day-only admissions1455.00455.00 Specialist review initial visit1110.75110.75 subsequent visit555.45277.25 Pathology LFT419.8079.20 Creatinine417.7571.00 AFP219.9039.80 FBC217.2034.40 Prothrombin time212.4024.80 Medication Aldactone 200 mg/day199.0699.06 Procedures Paracentesis138.2038.20 Total1882.86 6: Management of refractory ascites Resource categoryNumberUnit costTotal Cost Day-only admissions26455.0011 830.00 Specialist review initial visit1110.75110.75 subsequent visit555.45277.25 Pathology LFT419.8079.20 Creatinine417.7571.00 AFP219.9039.80 FBC217.2034.40 Prothrombin time212.4024.80 Medication Norfloxacillin 200 mg/tds0.33545.15179.90 Procedures Paracentesis2638.20993.20 13,640.30 7: Management of variceal haemorrhage - Year 1 Resource categoryNumberUnit costTotal Cost Hospital admission11980.001980.00 Day-only admissions5455.002275.00 Specialist review initial visit1110.75110.75 subsequent visit555.45277.25 Pathology LFT419.8079.20 Creatinine417.7571.00 AFP219.9039.80 FBC217.2034.40 Prothrombin time212.4024.80 Medication Propanolol182.4982.49 Procedures Oesophagoscopy (+ anaesthetic)3291.95875.85 Total5850.40 8: Management of hepatic encephalopathy - Year 1 Resource categoryNumberUnit costTotal Cost Hospital admission2.41980.004752.00 Specialist review initial visit1110.75110.75 subsequent visit555.45277.25 Pathology LFT419.8079.20 Creatinine417.7571.00 AFP219.9039.80 FBC217.2034.40 Prothrombin time212.4024.80 Medication Lactulose 60 mls1734.96734.96 Procedures Diagnostic endoscopy (+ anaesthetic)1213.75213.75 Paracentesis138.2038.20 Total6376.11 9: Management of hepatocellular carcinoma - Year 1 Resource categoryNumberUnit costTotal Cost Hospital admission (diagnosis)16947.006947.00 Inpatient admission17846.907846.90 Specialist visits initial visit1110.75110.75 subsequent visits955.4555.45 Pathology LFT419.8079.20 Creatinine417.7571.00 AFP219.9039.80 FBC217.2034.40 Prothrombin time212.4024.80 Procedures Paracentesis138.2038.20 Total8866.60 10: Other hospital admissions Reason for admission/treatmentRateUnit cost ($) Liver transplant (+ associated admissions)0.0292,527 Major infection (septicaemia)0.255,300 Terminal care - Advanced liver failure28,400 - hepatocellular carcinoma28,400 Back to text

Alan Shiell · Sue Brown · Geoff C Farrell

Editorial Acne and acne scarring: why should we treat? Reasons for early medical intervention, and options for treatment of scarring MJA 1999; 171: 62-63 Acne is so common that one could argue that it is a normal occurrence in human development. Its prevalence has been estimated at 95%-100% in 16-17-year-old boys and 83%-85% in 16-17-year-old girls.1 The initial presentation is usually comedonal acne, progressing to inflammatory lesions within 2-3 years,2 then rising in incidence and severity to reach its most serious stage between the ages of 14 and 17 years in girls and 16 and 19 years in boys.1 Development of comedonal acne at an early age, in girls at least, appears predictive of more severe disease in later years.3 Acne will mostly resolve by the age of 23-25 years; nevertheless, 1% of men and 5% of women still bear acne lesions at 40 years of age.4So, is acne a disease worthy of treatment, or a normal occurrence that should be ignored, as it will eventually cease to be a problem for most affected individuals? Concern about acne is one of the commonest reasons for young patients to consult a medical practitioner, so the direct cost of consultations and of the diversion of medical services needs to be taken into account in any assessment of the value of treating this apparently "normal" life event. Added to this, we are seeing the development of increasing antibiotic resistance in Propionibacterium acnes,5 a problem exacerbated by long term and widespread use of often suboptimal doses of antibacterial agents. So how can one justify treatment? Firstly, acne as a condition is aesthetically and sometimes physically unpleasant. Severe cystic acne causes pain, recurrent bleeding and purulent discharge. In rare instances, patients with acne develop severe systemic toxicity and require treatment in hospital. Before isotretinoin was introduced, such patients were extremely difficult to treat. Secondly, it can cause great distress in adolescents at a time when they are probably least able to deal psychologically and socially with the unsightliness of active acne. Being so readily visible (affecting the face in 99% of cases6), acne can reduce employment prospects7 and create interpersonal difficulties.8 Affected adolescents report more social isolation and self-consciousness than their unaffected peers8 and experience more embarrassment, social inhibition, unhappiness, anxiety, and dissatisfaction with their facial appearance.9 Finally, acne scarring can cause devastating long term psychic trauma for the sufferer and it has been suggested that such scarring may be a risk factor for suicide, particularly in men.10As current treatments for acne are very effective, scarring could be avoided in many cases by adequate medical intervention early in the course of the disease. Successful treatment of cystic acne with isotretinoin appears to reduce anxiety and depression in patients.11 Anti-androgen hormonal treatments such as cyproterone acetate and spironolactone, topical preparations such as adapalene, azelaic acid, topical antibiotics and retinoic acid may help to replace or augment long term antibiotic therapy, ensuring a sufficient armamentarium to keep the incidence of acne scarring to a minimum. Unfortunately, scarring may affect up to 95% of patients with acne. The degree of scarring is related to the severity and duration of acne before adequate therapy is instituted. One study found that a time delay of up to three years between acne onset and adequate treatment was sufficient to cause facial scarring in either sex, although keloidal or hypertrophic truncal scarring was more common in men.12 The same study established that superficial inflamed papular acne and cystic acne could both produce scarring, a finding with important implications for our healthcare system, which subsidises isotretinoin for failed therapy in nodulocystic disease only. If hypertrophic scarring occurs it should be dealt with by such measures as intralesional steroids, silicone sheeting or vascular laser treatment, as required. However, most scarring in acne is atrophic rather than hypertrophic in nature, with destruction and dissolution of supporting tissues. In the young, most scars will initially improve, the erythema will subside and the scars mature over the first two to three years. After this initial improvement the scarring is quiescent, but, over time, as facial tone declines and facial fat stores are resorbed, the scars will become more noticeable. With ageing, the facial skin starts to sag and seems to literally hang on the scars. The inelastic strands of scars bind the skin, giving it an uneven, cascading appearance. This is amplified by other age-related changes such as the resorption of skeletal and soft tissues. Remedial approaches to acne scarring have improved over the years. The older, less successful treatments such as dermabrasion and chemical peeling have been replaced by the use of resurfacing infrared lasers such as CO2 lasers13 and, more recently, erbium lasers14 to better remove and tighten the skin. An understanding that replacement of the atrophied structures in the dermis and subcutaneous tissues is necessary in severe cases of acne scarring has led to the development of superior dermal and subcutaneous augmentation techniques. Dermal and subcutaneous augmentation is possible by a number of autologous techniques, including dermal grafting,15 lipocytic dermal augmentation,16 fat transfer17 and, more recently, the implantation of autologous collagen and cultured and expanded autologous fibroblasts. Non-autologous augmentation is also possible by way of injections of bovine collagen, fibrin foam, hyaluronic acid or polymethylmethacrylate microspheres. For "punched out" ("ice pick") scars, none of these methods is useful. For these a range of punch techniques is used, involving coring out of scars with an appropriately sized cylindrical instrument, followed by suturing or graft application. Punch techniques can be used to treat many scars at a single operation, and may be combined with resurfacing techniques such as infrared laser treatment.18 Subcision (dermal scarification) is another helpful technique, in which dermal undermining of scars is used to improve the scar tissue by two mechanisms: (i) direct breaking of scar attachments, and (ii) intentional injury of the dermis to induce laying down of new collagen.19 All of these techniques are valuable tools for practitioners seeking to improve the outcome of treating acne scarring, but it would be better still if the problem never arose. A preventable condition such as postacne scarring should be one deserving of the earliest, best and most effective treatment. Gregory J Goodman President, Skin and Cancer Foundation Melbourne, VIC Burton JL, Cunliffe WJ, Stafford I, Shuster S. The prevalence of acne vulgaris in adolescence. Br J Dermatol 1971; 85: 119-126. Lucky AW, Biro FM, Huster GA, et al. Acne vulgaris in early adolescent boys: correlations with pubertal maturation and age. Arch Dermatol 1991; 172: 210-216. Lucky AW, Biro FM, Simbartl LA, et al. Predictors of severity of acne vulgaris in young adolescent girls: results of a five-year longitudinal study. J Pediatr 1997; 130: 30-39. Cunliffe WJ, Gould DJ. Prevalence of facial acne vulgaris in late adolescence and in adults. BMJ 1979; 1: 1109-1110. Cooper AJ. Systematic review of Propionibacterium acnes resistance to systemic antibiotics. Med J Aust 1998; 169: 259-261. Cunliffe WJ. The acnes. London: Dunitz, 1989. Cunliffe WJ. Unemployment and acne. Br J Dermatol 1986; 115: 386. Schachter RJ, Pantel ES, Glassman GM, Zweibelson I. Acne vulgaris and psychologic impact on high school students. N Y State J Med 1971; 24: 2886-2890. Wu SF, Kinder BN, Trunnell TN, Fulton JE. Role of anxiety and anger in acne patients: a relationship with the severity of the disorder. J Am Acad Dermatol 1988; 18: 325-333. Cotterill JA, Cunliffe WJ. Suicide in dermatological patients. Br J Dermatol 1997; 137: 246-250. Rubinow DR, Peck GL, Squillace KM, Gantt GG. Reduced anxiety and depression in cystic acne patients after successful treatment with isotretinoin. J Am Acad Dermatol 1987; 17: 25-32. Layton AM, Henderson CA, Cunliffe WJ. A clinical evaluation of acne scarring and its incidence. Clin Exp Dermatol 1994; 19: 303-308. Goodman GJ. Facial resurfacing using a high-energy, short-pulse carbon dioxide laser. Australas J Dermatol 1996; 37: 125-131. Stuzin JM, Baker TJ, Baker TM. CO2 and erbium:YAG laser resurfacing: current status and personal perspective. Plast Reconstr Surg 1999; 103: 588-591. Goodman GJ. Laser assisted dermal grafting for the correction of cutaneous contour defects. Dermatol Surg 1997; 23: 95-99. Coleman WP 3d. Lipocytic dermal augmentation. In: Klein AW, editor. Tissue augmentation in clinical practice. Procedures and techniques. New York: Marcel Dekker, 1998: 49-62. Coleman SR. Long-term survival of fat transplants: controlled demonstrations. Aesthetic Plast Surg 1995; 19: 421-425. Johnson WC. Treatment of pitted scars: punch transplant technique. J Dermatol Surg Oncol 1986; 12: 260-265. Orentreich DS. Subcutaneous incisionless (subcision) surgery for the correction of depressed scars and wrinkles. Dermatol Surg 1995; 21: 543-549.

Gregory J Goodman

Editorial Asthma in general practice: action plans or planned actions There's more than one way to implement effective asthma management in general practice Peter G Gibson MJA 1999; 171: 67 Good general practice is integral to effective asthma management. Asthma prevalence and hospitalisations are high, and, although we don't yet know how to reverse the rise in asthma prevalence, we know that severe exacerbations can be reduced by inhaled corticosteroid therapy and by effective education that involves an individualised, written action plan and regular medical review.1The burden of illness from asthma is concentrated in general practice, but studies of asthma education have mainly been conducted in hospitals. We need to transfer the improvements seen in these randomised trials to Australian general practice. Several approaches have been tried, including public health initiatives conducted by the National Asthma Campaign (NAC), practice audit,2,3 and nurse-run asthma clinics.4 In this issue of the Journal, Abdulwadud et al provide data showing just how different asthma can be in general practice to asthma in a specialist setting.5 Predictably, asthma is less severe in general practice.5 Medication use and understanding about asthma are similar, but fewer general practice patients have a written action plan and understand how to respond to an asthma emergency. Thus, for Australia, where inhaled corticosteroid use is already high, educational interventions in general practice should focus on the early management of exacerbations using written action plans and on smoking cessation. Also in this issue, Heard et al report their trial of a combined nurse educator/general practitioner asthma clinic.6 As part of the intervention, patients attending the asthma clinic received action plans and education about asthma. Patients in the control group also received action plans from their doctors, so that by the end of the study about 70% of patients had a written action plan and 80% were taking inhaled preventer medication. Asthma morbidity was reduced in both groups, and the asthma clinic did not prove to be any better than regular review of asthma by a general practitioner. Presumably outcomes in the control group improved because the participating general practitioners, who were caring for patients in both intervention and control groups, modified their behaviour by appropriately following proven guidelines. This problem is common in studies of asthma education, where blinding is seldom used and participation in the study is enough to improve management. Thus, this article compares asthma clinics to enhanced medical care, and a direct comparison with usual medical practice is lacking. What can we learn from this? Firstly, that the improvements in asthma mordibity that follow education and medical review can be achieved in general practice in Australia, and can be achieved in several ways. Regular review of asthma control and issuing an action plan by a general practitioner can be as effective as a special asthma clinic. General practitioners can now be confident that modifying their practice will improve asthma control. We know that this is needed, as surveys indicate that, although more people use action plans since the NAC, their use is still unacceptably low.7 General practitioners can choose between setting up an asthma clinic or implementing a structured program of regular review in their practices. The NAC and asthma liaison officers within the divisions of general practice are implementing suggested schemes at present. Regular review could turn into complacency, where a general practitioner feels that his or her current practice is satisfactory and that people with asthma are well managed. The best way to avoid this is to conduct regular quality control of asthma management. There are some simple interventions with asthma audit that do reap rewards for patients and doctors alike.2,3 Special asthma clinics also need to conduct regular quality control of their services, as when they provide asthma education without general practitioner consultations and action plans there is no benefit to patients.8 Structured asthma management programs, whether by systematic regular review or a special asthma clinic, will need to be adapted to the organisational structure of the practice. This can be done fairly simply in practices with several doctors. It is more difficult to do so in solo practices, but here it is even more important, as patients from small practices have a higher admission rate for asthma than those from larger practices.9 General practitioners need to adapt the National Asthma Campaign's six-point asthma management plan to their practices and ensure that all patients with asthma understand their disease, have a set of written instructions about when and how to treat exacerbations (all people with asthma are at risk of exacerbations), and are prescribed optimal therapy to control symptoms and exacerbations. Special asthma clinics or a system of regular education and review will suffice, provided that the processes and outcomes are monitored to ensure success. Organising the process of care for asthma in general practice and defining how to do it may be just as important as educating the doctor about what to do. Most general practitioners understand asthma management. Effective implementation is the issue. Peter G Gibson Staff Specialist, Respiratory Medicine John Hunter Hospital, Newcastle, NSW Gibson PG, Wilson AJ, Coughlan J, et al. The effects of self-management asthma education and regular practitioner review in adults with asthma. In: Cates C, DuCharme F, Gibson PG, et al. Airways module. Cochrane database of systematic reviews, issue 4. Oxford, UK: Update Software, 1998. Bryce FP, Neville RG, Crombie IK, et al. Controlled trial of an audit facilitator in diagnosis and treatment of childhood asthma in general practice. BMJ 1995; 310: 838-842. Feder G, Griffiths C, Highton C, et al. Do clinical guidelines introduced with practice based education improve care of asthmatic and diabetic patients? A randomised controlled trial in general practices in east London. BMJ 1995; 311: 1473-1478. Charlton I, Charlton G, Bloomfield J, et al. Audit of the effect of a nurse-run asthma clinic on workload and patient morbidity in general practice. Br J Gen Pract 1991; 41: 227-231. Abdulwadud OA, Abramson MJ, Light L, et al. Comparison of patients with asthma managed in general practice and in a hospital clinic. Med J Aust 1999; 171: 72-75. Heard AR, Richards IJ, Alpers JH, et al. Randomised controlled trial of general practice based asthma clinics. Med J Aust 1999; 171: 68-71. Comino EJ, Mitchell CA, Bauman A, et al. Asthma management in eastern Australia, 1990 and 1993. Med J Aust 1996; 164: 403-406. Premaratne UN, Sterne JAC, Marks GB, et al. Clustered randomised trial of an intervention to improve the management of asthma: Greenwich asthma study. BMJ 1999; 318: 1251-1255. Griffiths C, Sturdy P, Naish J, et al. Hospital admissions for asthma in East London: associations with characteristics of local general practices, prescribing, and population. BMJ 1997; 314: 482-486.

Peter G Gibson

Research Randomised controlled trial of general practice based asthma clinics Adrian R Heard, Ian J Richards, John H Alpers, Louis S Pilotto, Brian J Smith and Julie A Black MJA 1999; 171: 68-71 See also Gibson & Abdulwadud et al Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on General practice and primary care Abstract Objective: To compare the effects on asthma morbidity of asthma clinics based in general practice with standard general practice care. Design and setting: A randomised controlled trial in eight general practices. Patients, general practitioners and outcomes assessors were not blinded to treatment allocation. Participants: 195 patients with asthma aged 5-64 years; 191 completed the trial. Intervention: Three asthma clinic sessions over six months involving nurse counselling, education about asthma management, spirometry and consultation with the general practitioner. Main outcome measures: Patients reporting days lost from work or school, number of days lost, the presence of morning or nocturnal asthma symptoms, use of an action plan, medication use, current smoking, hospitalisation, and emergency visits. Results: Asthma clinics were associated with a greater reduction in nocturnal symptoms, an increase in the ownership of peak flow meters and an increase in the number of patients commencing or resuming smoking. Both control and intervention groups showed similar improvement in days lost from work or school, the presence of symptoms, use of an action plan and taking reliever medication. Conclusion: Our study does not show that asthma clinics are more effective than standard general practice care in reducing asthma morbidity. It is uncertain how much of the improvement in outcomes was due to the asthma clinic, the influence of the study itself upon patients and practitioners, or other factors, such as the tendency for a patient's asthma management to improve over time. Introduction Asthma is the most common chronic disease in children and a leading cause of morbidity in adults in Australia.1,2 Asthma clinics may be a way of improving comanagement practices between health professionals and people with asthma. They involve trained nurses conducting asthma education, peak flow readings and spirometry with asthma patients, combined with a brief general practitioner review. Asthma clinics are an integral part of general practice in the United Kingdom, but have yet to gain acceptance in Australia.3 One reason for this might be that studies have not provided conclusive evidence that these clinics reduce morbidity.4-9 This may be because regular general practitioner review10 and/or asthma education11 is the key element in reducing asthma morbidity, and therefore only studies comparing asthma clinics with patients receiving irregular reviews are likely to show significant differences in outcomes. In this study, we used a randomised controlled trial design to test whether asthma clinics (intervention) were more effective in reducing morbidity from asthma than standard medical treatment (control). The clinics used the Patient Management System, a recognised model for operating asthma clinics.12 Methods Ethical approval Ethics approval for the study was obtained through the Royal Australian College of General Practitioners' ethics committee at the RACGP national office. Recruitment A previous major study of asthma self-management found a 50% reduction in the number of people reporting at least one day lost from work.6 We calculated that to detect a similar reduction in a study with 80% power and a 95% confidence interval a sample size of 170 was required. Patients were recruited from eight general practices staffed by 42 general practitioners. Consent was sought from all people with asthma aged 5-64 years attending these practices during three months of 1997. Subjects were individually randomised within practices into intervention and control groups. This meant that each participating general practitioner potentially saw both intervention and control patients. A randomisation chart was set up for each participating practice at Asthma South Australia, and general practitioners and the asthma educators were informed of a subject's treatment allocation before the baseline interview. Thus, patients, doctors and outcome assessors were not blinded as to who had received the intervention and who were controls. Intervention Each general practice operated one three-hour asthma clinic session per week. The asthma educators in the trial were practising registered nurses with extensive experience in respiratory care. Their component of the clinic session involved education in asthma management strategies, including a written asthma management plan, spirometry and instruction on using peak flow meters, inhalers and an asthma diary card. The session ended with a consultation by the general practitioner. Each asthma clinic patient was asked to attend three asthma clinic sessions within the six months of the study. Gathering outcomes data We conducted a telephone interview using adapted questions from the Southampton Morbidity Index13 and questions relating to clinical practice14 at the beginning and end of the study. Our outcome measures included number of patients reporting days lost from work or school, number of days lost, use of an action plan, medication use, current smoking, the level of morning or nocturnal asthma symptoms, hospitalisation, emergency visits, and number of home visits by the general practitioner. Data analysis All data were analysed on an intention-to-treat basis. For analysis, we categorised morning and nocturnal symptoms as "at least weekly" or "less frequently/never" to distinguish regular from irregular symptoms and to maintain adequate numbers of participants in each of the two categories. We analysed the number of days lost from work with both linear and logistic regression. Linear regression was conducted on the difference in the number of days lost from work between baseline and six months, and was adjusted for clustering by doctor. For logistic regression, also adjusted for clustering by doctor, the variable was divided into two categories (two or fewer days lost and three or more days lost), representing better-controlled and less well controlled asthma, respectively. The statistical analyses for all other study factors used logistic regression, adjusted for baseline measurements and clustering by treating doctor. We also conducted a longitudinal analysis using χ2 tests to examine changes in the intervention and control groups over the six months of the trial. Odds ratios and 95% confidence intervals (95% CIs) were calculated for all outcome measures. All tests were conducted using the Stata statistical software package.15 Results Patients Over the three-month recruitment period, 195 people entered the study, and 191 (97 in the clinic group and 94 controls) completed both interviews (Box 1). The demographic profile of the control group (mean age, 26.3 years, 95% CI, 22.3-30.2; proportion of males, 45%, 95% CI, 34%-55%) was similar to the intervention group (mean age, 27.5 years, 95% CI, 23.6-31.4; proportion of males, 42%, 95% CI 32%-52%). Although there were no records of the number of eligible subjects across all participating practices, an audit of all patients seeing general practitioners at two of the eight practices showed a participation rate of 45.1% of all asthmatics. The main reasons for non-participation were either the general practitioner's failing to ask the patient for consent or the patient's refusing consent. The average age of non-participants (mean age, 20.8 years, 95% CI 17.1-24.5) was not significantly different from that of participants (mean age, 21.4 years, 95% CI 17.1-25.7) in the two audited practices. Of the 97 people in the clinic group, 67 completed the three planned clinic sessions, 17 attended only one or two sessions, and 13 failed to attend any sessions. Outcomes There was no difference between the clinic and control groups at baseline for dichotomous study variables (Box 2), which provided evidence for effective randomisation. There was a low incidence of hospitalisation and emergency department attendance in both groups. At six months, however, waking at night at least weekly due to asthma and current smoking were significantly different between the two groups, as was ownership of a peak flow meter (Box 3). There were no differences reported at six months in patients' having discussed trigger factors with their general practitioner or receiving an action plan from their general practitioner. Unlike the dichotomous outcome variables, the mean number of days lost from work was significantly different between the treatment groups at baseline, with a high level of variability in the control data (intervention group mean, 2.62, 95% CI 1.84-3.40; control group mean, 5.37; 95% CI 3.46-7.29). There was no difference in the number of days lost from work at six months in the intervention group compared with the control group (intervention group mean, 2.09, 95% CI 0.91-3.27; control group mean, 2.66; 95% CI 1.66-3.66). Linear regression to compare the number of days lost at six months minus those at baseline between intervention and control participants showed a significant reduction in number of days lost in the control group compared with the intervention group (P = 0.04). Logistic regression comparing two or fewer days lost with three or more days lost showed a non-significant trend towards fewer days lost from work at six months in the intervention group (odds ratio, 0.50; 95% CI 0.24-1.03). Longitudinal analyses within the clinic and control groups showed a trend towards decreasing morbidity over the six-month period, with a 13% decrease in the number of people reporting days lost from work, school or usual activities in both groups (intervention group odds ratio, 0.57, 95% CI 0.31-1.06; control group odds ratio, 0.57, 95% CI 0.31-1.06). Longitudinal analyses also showed that the reported issuing of action plans increased significantly in both groups (intervention group odds ratio, 11.25, 95% CI 3.07-41.21; control group odds ratio, 3.94, 95% CI 1.53-10.10). An increase in the discussion of trigger factors was only significant for the control group (intervention group odds ratio, 2.6, 95% CI 0.84-8.02; control group odds ratio, 3.72, 95% CI 1.36-10.21). Discussion Our study does not show that asthma clinics are more effective than standard general practice care in reducing asthma morbidity. We observed an improvement in most of the outcome measures in both the intervention and control groups. Outcomes for patients who attended an asthma clinic had few differences from those in the control group. The intervention group was less likely to be woken "at least weekly" at night due to asthma. This may signal better home management of asthma in the intervention group, an outcome that is anticipated by guidelines16 but challenged in recent studies.17 Ownership of peak flow meters increased among the intervention group during the course of the study, probably because the asthma educators promoted the use of peak flow readings for asthma self-management. More people in the intervention group either adopted or recommenced smoking during the study. Smoking cessation advice was not included as part of the study intervention. In intensive interventions such as asthma clinics, smokers should be identified to ensure that smoking cessation is achieved or maintained if possible. In this study there were few reports of hospitalisations and emergency department visits at baseline, reflecting our broad inclusion criteria, which did not focus on severe asthmatics. Outcomes which were infrequent in this study may be significant in much larger studies. In relation to days lost from work or school, the significant difference between the intervention and control groups at baseline, the high variability at baseline in the control group and the different findings between the logistic and linear regressions at six months do not allow an adequate understanding of the effect of the intervention. The lack of difference between groups in the proportion of participants who had discussed trigger factors with their doctor and who had received an asthma action plan raises one of the possible explanations for the limited differences observed in this study. Baseline levels of both these clinical practice indicators are usually around 40%-60%,14 and were within that range at baseline in our study. Yet the frequency of both indicators increased substantially over the six months for both groups, which might suggest that clinical practice for the control subjects was contaminated as a result of general practitioners' seeing both intervention and control subjects. Other explanations may be: The asthma clinic in itself makes no difference to the outcomes being measured, and that a simpler intervention, such as regular general practitioner review, is the critical factor. The results of a review of asthma education support this.10 Whether the presence of an asthma clinic in a general practice increases the rate of general practitioner review is unknown. A possible Hawthorne effect.18 With general practitioners and patients being unblinded to the study, it is possible that both increased behaviours which led to better asthma self-management outcomes. People with asthma tend to show improved outcomes over time. This effect is likely to be enhanced after a visit to a general practitioner where management decisions are made. The data showing that the number of people reporting days lost from work or school decreased in both intervention and control groups support this explanation. Baseline data may have been biased because subjects were randomised into treatment groups before the baseline interview, and some subjects may have been aware of their treatment status at the baseline interview. Whatever reasons led to the apparent improvement in outcomes, a factor that may have contributed to the lack of difference between intervention and control groups may be the poor compliance with the intervention regimen. Nearly one-third of patients from the intervention group did not comply with the required three clinic visits, and 13% did not attend any visits. The outcome of this study holds some lessons for future randomised controlled trials in general practice. The major limitation of the study was the randomisation by patient rather than practice, which may lead to modification of general practitioner behaviour towards the control group as well as the intervention group, thus increasing the chance of contamination of controls and the Hawthorne effect. The inability to blind general practitioners and patients to the patient's treatment allocation also limited the study. The participation rate of less than 50% is lower than the rate considered desirable for randomised controlled trials, but compares favourably with other community-based studies.6,19 This study also demonstrates that, in general practice, larger, longer-term or more targeted studies (such as to more severe asthmatics) are required to show differences, especially for variables such as hospitalisation for asthma, which have a relatively low incidence among most general practice patients. Conducting this study for a longer period would also have allowed it to run over the full range of seasons, which is preferable for studies of seasonal diseases such as asthma. Acknowledgements We would like to thank the two nurses who conducted the asthma clinics, and Kieran McCaul from the Department of Human Services, South Australia, for statistical advice on the final drafts of the article. Thanks also go to the doctors and staff at the following participating practices: Angaston Medical Centre, Brooker Clinic, Greenwith Medical Centre, Golden Grove Medical Centre, Flinders Clinic, Nuriootpa Medical Centre, North Plympton Medical Centre and Tanunda Medical Centre. This study was made possible through a grant from the Department of Human Services, Adelaide, South Australia. References Abramson M, Kutin J, Czarny D, et al. The prevalence of asthma and respiratory symptoms among young adults: Is it increasing in Australia? J Asthma 1996; 33: 189-196. Peat JK, Toelle BG, Gray EJ, et al. Prevalence and severity of childhood asthma and allergic sensitisation in seven climatic regions of New South Wales. Med J Aust 1995; 163: 22-26. Barnes G, Partridge MR. Community asthma clinics: 1993 survey of primary care by the National Asthma Task Force. Qual Health Care 1994; 3: 133-136. Jones KP, Mullee MA. Proactive, nurse-run asthma care in general practice reduces asthma morbidity: scientific fact or medical assumption? Br J Gen Pract 1995; 45: 497-499. Lahdensuo A, Haahtela T, Herrala J, et al. Randomised comparison of guided self-management and traditional treatment of asthma over one year. BMJ 1996; 312: 748-752. Mayo PH, Richman J, Harris HW. Results of a program to reduce admissions for adult asthma. Ann Intern Med 1990; 112: 864-871. Martys C. Asthma care in Darley Dale: general practitioner audit. BMJ 1992; 304: 758-760. Evans D, Mellins R, Lobach K, et al. Improving care for minority children with asthma: Professional education in public health clinics. Paediatrics 1997; 99: 157-164. Charlton I, Charlton G, Broomfield J, et al. Audit of the effect of a nurse run asthma clinic on workload and patient morbidity in a general practice. Br J Gen Pract 1991; 41: 227-231. Gibson P, Coughlan J, Abramson M, et al. The effects of self-management education and regular practitioner review in adults with asthma. (Cochrane Review). In: The Cochrane Library, Issue 2. Oxford: Update Software; 1998. Bauman A. Effects of asthma patient education upon psychological and behavioural outcomes. Int Rev Health Psych 1993; 2: 199-212. Charlton I, Antoniou AG, Atkinson J, et al. Asthma at the interface: bridging the gap between general practice and a district general hospital. Arch Dis Child 1994; 70: 313-318. Jones K, Charlton I, Middleton M, et al. Targeting asthma care in general practice using a morbidity index. BMJ 1992; 304: 1353-1356. Beilby J, Wakefield M, Ruffin R. Reported use of asthma management plans in South Australia. Med J Aust 1997; 166: 298-301. StataCorp. Stata Statistical Software: Release 5.0. [computer program]. College Station, Texas: Stata Corporation, 1997. The Thoracic Society of Australia and New Zealand. Peak flow meter use in asthma management. Med J Aust 1996; 164: 727-730. Garrett J, Fenwick J, Taylor G, et al. Peak expiratory flow meters (PEFMs): who uses them and how does education affect the pattern of utilisation? Aust N Z J Med 1994; 24: 521-528. Rice B. The Hawthorne effect: persistence of a flawed theory. Psychol Today 1982; 16: 71-74. Garrett J, Fenwick J, Taylor G, et al. Prospective controlled evaluation of the effect of a community based asthma education centre in a multiracial working class neighbourhood. Thorax 1994; 49: 976-983. (Received 4 May 1998, accepted 31 May 1999) Authors' details SA HealthPlus, Department of Human Services, Adelaide, SA. Adrian R Heard, BSocAdmin, MPH, Senior Project Officer. Centre for Health Care Evaluation, Bedford Park, SA. Ian J Richards, BApplSc, MPH, Project Officer. Flinders Medical Centre, Bedford Park, SA. John H Alpers, MD, FRACP, Director, Respiratory Unit. North Western Adelaide Health Service, Woodville South, SA. Louis S Pilotto, FAFPHM, PhD, Senior Consultant. Brian J Smith, FRACP, PhD, Senior Lecturer, Department of Medicine. Asthma SA, Royston Park, SA. Julie A Black, BNG, Chief Executive Officer. Reprints will not be available from the authors. Correspondence: Mr A R Heard, SA HealthPlus, PO Box 65, Rundle Mall, SA 5000. Email: Adrian. HeardaATdhs.sa.gov.au Back to textBack to textBack to text

Adrian R Heard · Ian J Richards · John H Alpers · Louis S Pilotto · Brian J Smith · Julie A Black

Research Comparison of patients with asthma managed in general practice and in a hospital clinic Omar A Abdulwadud, Michael J Abramson, Larry Light, Francis C K Thien and E Haydn Walters MJA 1999; 171: 72-75 See also Heard et al & Gibson Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Respiratory medicine Abstract Objectives: To compare knowledge and attitudes about asthma, self-management skills and impact of asthma on quality of life between patients managed in general practice (GP) and in a hospital clinic. Design: Cross-sectional survey with six months' follow-up. Patients and setting: 105 adults with asthma: 61 from the Alfred Hospital Asthma and Allergy Clinic, Melbourne, and 44 from nearby general practices, in 1994-1995. Main outcome measures: Patient sociodemographic and clinical characteristics; patient knowledge, attitudes and beliefs about asthma; self-management skills; and impact of asthma on quality of life. Results: GP patients were more educated (P = 0.04) and more likely to smoke (P = 0.04) and to have mild asthma (P = 0.04) than hospital patients; they were less likely to use theophylline (P = 0.006) and to have exercise limitation (P = 0.03), and had fewer previous hospital admissions (P = 0.01). Impact of asthma on quality of life was greater in the hospital group than in the GP group. At baseline, the GP group were less likely to have written asthma action plans (P = 0.018), and were less able to manage rapid onset attacks than the hospital group (P = 0.02). More subjects in the hospital group than the GP group felt their asthma was severe (P = 0.02) and were optimistic about their asthma improving (P = 0.03). GP patients increased their knowledge about asthma significantly (P = 0.002) over six months. Conclusions: Patients with asthma managed in general practice and in hospital differ in clinical parameters, quality of life and attitudes to asthma. Future educational initiatives should take such differences into account. Introduction Asthma is the third most common reason for consultations with general practitioners (GPs) in Australia,1 but is both under-recognised and undertreated.2 The finding that GPs were the usual source of routine asthma treatment for 89% of the people who died of asthma3 demonstrates that GPs have the primary management role even in severe asthma.4To guide both doctors and patients, in 1989 the Thoracic Society of Australia and New Zealand developed the "six-point" Australian Asthma Management Plan (AMP).5 This was adopted by the National Asthma Campaign (NAC) at its inception in 1990. While the Royal Australian College of General Practitioners is a partner in the NAC, the plan was originally drawn up by hospital-based specialists. There is concern among GPs that they do not have sufficient time and knowledge to devise action plans and counsel patients about asthma management,4 as suggested in the AMP. The effectiveness of patient education about asthma as proposed in the AMP has not been widely evaluated in general practice. Only one such study has been reported,6 and only one nationwide survey of selected GPs was conducted before the launch of the NAC intervention.7 We aimed to examine patient knowledge about asthma and its management, self-management skills, impact of asthma on quality of life, and attitudes to asthma. We compared these between patients managed in general practice and in a hospital clinic over a six-month period that coincided with widespread advertising and dissemination of the AMP. Methods Design and setting The study was a cross-sectional survey with six months' longitudinal follow-up during 1994-1995. There was no intervention, and patients received their usual care from their GPs or hospital specialists. The study was conducted at the Alfred Hospital Asthma and Allergy Clinic, Melbourne, Victoria, and at 13 general practices near the hospital. Fourteen GPs were recruited by a practising GP (L L). The study was approved by the Ethics Review Committee at the Alfred Hospital. Subjects Consecutive patients being seen for asthma at the participating general practices were nominated by their GPs. Of 54 patients invited to participate, 44 were recruited (nine refused or did not respond and one died). Sixty-one patients were recruited from the Alfred Clinic. Inclusion and exclusion criteria were reported previously.8 All patients gave written informed consent. Diagnosis of asthma was based on American Thoracic Society criteria.9 Assessments Clinical and demographic characteristics of patients were determined by questionnaire. The term "priority asthmatic" was given to asthmatics who had severe and precipitately acute attacks of asthma; they had usually (but not necessarily) been admitted to an intensive care unit. Forced expiratory volume in 1 second (FEV1) was obtained from the records of the lung function laboratory, and predicted FEV1 at baseline was calculated for males and females separately, as suggested by Gibson et al.10 The mean daily peak expiratory flow (PEF) variability was estimated from patient diaries.5 Severity of asthma was classified as mild, moderate or severe based on medication use, as reported previously.8 Medication was grouped into generic categories. Outcome measures Patients completed the Asthma General Knowledge,11 Quality of Life,12 Self-Management Skills,13 and Attitudes and Beliefs14 questionnaires on entry and six months later. Selection of these outcomes was based on the asthma education targets and outcome measures proposed by the National Asthma Campaign.15 Statistical analysis Data were analysed with the SAS for Windows statistical package.16 Categorical variables were summarised as percentages, and associations were tested in contingency tables by χ2 tests. For continuous variables that were normally distributed, differences in mean scores were assessed by Student's t test. For continuous variables that were not normally distributed, the Wilcoxon signed rank and rank sum tests were used. Results Participation Follow-up questionnaires were returned by 39 of the 44 (87%) GP patients (with five of those with the most severe asthma lost to follow-up) and by 47 of the 61 (77%) hospital patients (with the remaining 14 either lost to follow-up or not responding). Subject characteristics Characteristics of the two patient groups are shown in Box 1. They were similar in age and sociodemographic characteristics, including occupation (data not shown), except that the GP group had a significantly higher proportion of tertiary-educated people and of current smokers than the hospital group. GP patients had less exercise limitation and milder asthma than the hospital patients, and were less likely to have been admitted to hospital and to have priority asthma. There was no significant difference in lung function or other clinical parameters (data not shown). GP patients were significantly less likely to use theophylline and to have a written asthma action plan than hospital patients. Proportions using β-agonists, anticholinergics, and inhaled or oral steroids and owning peak flow meters were not significantly different in the two groups. Asthma outcome measures Asthma knowledge: Asthma General Knowledge scores did not differ significantly between the GP and hospital groups either at baseline (means, 20.2 and 20.5 out of 31, respectively) or six months later. Scores increased in both groups over the six months, but the increase was significant only in the GP group (P = 0.002), which had a mean score increase of 1.66 (95% confidence interval [CI], 0.58 to 2.76) compared with 0.83 (95% CI, 20.39 to 2.03) in the hospital group. Quality of life: Scores for impact of asthma on quality of life are shown in Box 2. Impact at baseline was significantly greater in the hospital group than in the GP group for total quality of life and the subcategories of breathlessness, social disruption, and concern for health, but not mood disturbance. After six months, impact had significantly decreased in the hospital group for all these parameters except mood disturbance, but there was no significant change in the GP group. Despite the significant decrease in the hospital group, impact was still significantly greater than in the GP group for total quality of life (P = 0.03), social disruption (P = 0.008) and concern for health (P = 0.04). None of the improvements in quality of life differed significantly between the two groups over six months. Self-management skills: At baseline, the hospital group had a significantly higher median score for knowledge about self-management of a rapid onset asthma attack than the GP group (P = 0.02), but the two groups had similar scores for a slow onset attack (Box 3). After six months, the hospital group had significantly improved its slow onset scenario score (P = 0.02), but the GP group had not. Overall, there was no difference in the median change over six months in scores for either scenario between the two groups. Attitudes and beliefs about asthma: Patients' attitudes and beliefs about their asthma are shown in Box 4. At baseline, hospital patients were significantly more likely than GP patients to believe that their asthma was severe, but also that it would improve in the future. After six months, hospital patients were significantly less optimistic (P = 0.03), and the difference in this parameter between the two groups was no longer significant. The proportion of patients who said they could do everything they wanted regardless of the effect it might have on their asthma did not differ significantly between the two groups at baseline, but at follow-up hospital patients were significantly less likely to say this than GP patients. More hospital than GP patients wished their doctor would talk more to them about their asthma at both baseline and six-month follow-up, but the difference was significant only at follow-up. Concomitantly, fewer hospital patients than GP patients felt that their doctor had told them everything they wanted to know about their asthma; the difference was significant at both baseline and follow-up. Discussion We found that our samples of GP and hospital patients with asthma differed in sociodemographic and clinical parameters, quality of life, self-management skills and attitudes and knowledge about asthma. Some of our findings about the GP sample were more positive than reported previously. Use of inhaled steroids was significantly higher than found in random community samples,17,18 possibly because our sample of GP patients had more severe asthma, or because of industry promotion of these drugs.18 It is also possible that this form of treatment has become more acceptable in our group of GPs, many of whom had a particular interest in asthma. Use of peak flow meters and prevalence of written action plans in the GP patients were also higher than previously reported,17,18 but, once again, this finding may be confounded by the group of GPs studied. Actual prevalence of peak flow meter use and written action plans may be substantially lower in more typical general practices. There was some evidence from our study that implementation of the AMP may have improved, especially in general practice, over the period of our study. However, despite NAC recommendations, half of the hospital patients and three-quarters of the GP patients had no written asthma action plans; and about a third of the hospital patients and half of the GP patients did not have access to a peak flow meter. While our study sheds no light on the reasons for these findings, it demonstrates that there was room for improvement in asthma management in both settings, but particularly in general practice. Asthma knowledge among the GP patients was similar to that among the hospital patients at baseline, but improved more over the six months to follow-up. This was possibly due to the GP patients' higher educational level, our interaction with them during the study or better than average care from their doctors. As doctors had recruited the patients to the study, they may have put more effort into educating them before follow-up, although we have no evidence for this. The absence of any significant improvement in quality of life among the GP patients after six months suggests that insufficient attention may be given to this aspect of asthma. Furthermore, the potential selection bias towards milder disease and the loss to follow-up of five of those with more severe asthma from the GP group may have biased the results away from detecting improvement. Overall, the general practice group had better quality of life than the hospital group. This would be expected, as the GP group had milder disease with fewer hospital admissions. It is surprising that mood disturbance was the only category which did not differ between the two groups at baseline. Possibly moods such as sadness, depression and frustration are similar in all patients regardless of the severity of asthma. At baseline, the GP group was less able to manage the rapid onset attack, perhaps because they were likely to have experienced fewer such attacks. The hospital group improved their ability to manage slow onset attacks significantly over six months. Maybe their doctors educated them informally, although they did not have access to the results of the questionnaires. Alternatively, participants may have improved their answers with practice, but as this did not happen in the GP group it is unlikely. There was little difference in attitudes and beliefs about asthma between groups. However, at six months, the hospital group was significantly less optimistic about their asthma improving in the future than the GP group. This could result from the difference in asthma severity between the two groups, which resulted in hospital patients having a more realistic appreciation of their poor prognosis after education. At six months, more of the hospital patients than GP patients also wished that their doctors would tell them more about their asthma. Perhaps this reflects a low level of communication between doctors and patients in the hospital asthma clinic compared with general practice and requires further study. This study has some limitations. The GP patients may not be representative of the total general practice population, and recruiting interested GPs may have biased results. In the absence of any viable alternative strategy, evaluation focused on patients rather than GPs. Despite potential sampling and selection biases, the results highlight the impact of patient education among patients attending general practices and the differences between GP and hospital patients. Future educational initiatives should take such differences into account. The type and scope of patient education in general practice and hospitals should be thoroughly evaluated to identify areas in which GPs and specialists could be trained and supported more effectively. Continued dissemination and implementation of the Australian AMP is required to improve the self-management skills of patients in general practice. Acknowledgements We acknowledge a public health postgraduate research scholarship from the National Health and Medical Research Council. Dr Andrew Forbes, Jan Driver and Michael Bailey provided statistical support. We are grateful to the general practitioners who participated in the study. Drs Guy Marks, Rae Allen and Bonnie Sibbald gave permission to use their questionnaires. Dr John Kolbe gave permission to use his scoring system for the asthma attack scenarios. References Bridges-Webb C, Britt H, Miles DA, et al. Morbidity and treatment in general practices in Australia 1990-1991. Med J Aust 1992; 157 Suppl: 1-56. Tse M, Cooper C, Bridges-Webb C, Bauman A. Asthma in general practice. Opportunities for recognition and management. Aust Fam Phys 1993; 22: 736-741. Robertson CF, Rubinfeld AR, Bowes G. Deaths from asthma in Victoria: a 12 month survey. Med J Aust 1990; 152: 511-517. Antic R. Asthma in Australia: the current understanding. Overview of a national series of interactive meetings for general practitioners. Sydney: Excerpta Medica, 1993. Woolcock A, Rubinfeld AR, Seale JP, et al. Asthma management plan, 1989. Med J Aust 1989; 151: 650-653. Byrne DM, Drury J, Mackay RC, et al. Evaluation of the efficacy of an instructional program in the self-management of patients with asthma. J Adv Nursing 1993; 18: 637-646. Tse M, Bauman A, Bridges-Webb C. Asthma management in general practice. Aust Fam Phys 1991; 20: 1085-1092. Abdulwadud O, Abramson M, Forbes A, et al. Evaluation of a randomized controlled trial of adult asthma education in a hospital setting. Thorax 1999; 54: 493-500. American Thoracic Society. Standards for the diagnosis and care of patients with chronic obstructive pulmonary disease (COPD) and asthma. Am Rev Respir Dis 1987; 136: 225-244. Gibson J, Gallagher H, Johansen A, Webster I. Lung function in an Australian population: spirometric standards for non-smoking adults. Med J Aust 1979; 1: 292-295. Allen RM, Jones MP. The validity and reliability of an asthma knowledge questionnaire used in the evaluation of a group asthma education self-management program for adults with asthma. J Asthma 1998; 35: 537-545. Marks GB, Dunn SM, Woolcock AJ. A scale for the measurement of quality of life in adults with asthma. J Clin Epidemiol 1992; 45: 461-472. Sibbald B. Patient self care in acute asthma. Thorax 1989; 44: 97-101. Sibbald B, Collier J, D'Souza M. Questionnaire assessment of patients' attitudes and beliefs about asthma. Fam Pract 1986; 3: 37-40. National Asthma Campaign (NAC) National Asthma Strategy. Goals and targets. Melbourne: National Asthma Campaign, 1994. SAS Institute Inc. SAS language guide for personal computers, the SAS system for Microsoft Windows. Release 6.10. Cary, NC: SAS Institute Inc, 1994. Abramson MJ, Kutin JJ, Rosier MJ, Bowes G. Morbidity, medication and trigger factors in a community sample of adults with asthma. Med J Aust 1995; 162: 78-81. Comino EJ, Mitchell CA, Bauman A, et al. Asthma management in eastern Australia, 1990 and 1993. Med J Aust 1996; 164: 403-406. (Received 28 Sep 1998, accepted 7 Jun 1999) Authors' details Department of Epidemiology and Preventive Medicine, Monash Medical School, The Alfred Hospital, Melbourne, VIC. Omar A Abdulwadud, PhD, Postdoctoral Fellow; Michael J Abramson, PhD, FRACP, Associate Professor. Department of Allergy and Clinical Immunology, Monash Medical School, The Alfred Hospital, Melbourne, VIC. Larry Light, MB BS, Clinical Assistant; Francis C K Thien, MD, FRACP, Staff Physician. Department of Respiratory Medicine, Monash Medical School, The Alfred Hospital, Melbourne, VIC. E Haydn Walters, DM, FRACP, Professor, and Director of Respiratory Medicine. Reprints: Associate Professor M J Abramson, Department of Epidemiology and Preventive Medicine, Monash Medical School, The Alfred Hospital, Prahran, VIC 3181. Email: Michael. AbramsonATmed.monash.edu.au Back to textBack to textBack to text Back to text

Omar A Abdulwadud · Michael J Abramson · Larry Light

Editorial Necrotising arachnidism Does the white-tailed spider deserve its bad name? MJA 1999; 171: 98 In this issue of the Journal, Pincus et al1 report a series of cases of local tissue injury, varying from small to extensive ulceration and necrosis, following confirmed or suspected spider bites, a condition often labelled "necrotising arachnidism". Spider bite is hardly a rare injury, but has generally been considered mild, with the exception of bites by widow spiders, such as our redback spider (Latrodectus hasselti), funnelweb spiders (Atrax and Hadronyche species) and recluse or fiddleback spiders (Loxosceles species).2 While the former two groups of spiders are native to Australia, the recluse spiders are not. Their necrotic bite has been a problem in the Americas and elsewhere, but not in Australia. In 1976, Southcott brought Loxosceles to the attention of Journal readers, reporting its occurrence in Adelaide and Sydney.3 From the late 1970s an increasing number of patients have been presenting to doctors throughout Australia with bites resulting in local tissue injury, ranging from a tiny ulcer through to very extensive areas of full-thickness skin necrosis.2,4 Following a report of one such case in the Journal,5 Sutherland, in an editorial entitled "Watch out, Miss Muffet!", speculated on causative organisms, mentioning, in particular, the white-tailed spider (currently designated Lampona cylindrata).6 Since then Australian poisons information centres have seen a steady increase in calls about definite or suspected spider bite, and such calls are now the single most common reason for calling a poisons information centre,7 with a 30% increase in calls related to spider bite in the last two years alone. Casual conversation with many urban general practitioners will often reveal that they see a small but growing number of cases of suspected spider bite resulting in local tissue injury, varying from mild to quite severe. Currently, there is no system for national collection of these case data to ascertain the true extent of the problem, nor to confirm that numbers of cases are rising. In many cases the bite is ascribed to the white-tailed spider, despite a singular lack of evidence. The white-tailed spider is a common native urban spider, frequently found in homes, where it roams in search of prey.2 Published venom research and case reports of bites have been reviewed and do not reveal evidence that this spider commonly causes tissue injury.8,9 There are only four published case reports of tissue injury and in none of these cases was the spider formally identified.10-12Pincus et al add a further 12 cases, but in only three cases was the spider formally identified by an expert. In two this was a white-tailed spider, while the third case involved a black house spider (Badumna species). This adds to the still scarce case reports of necrotic bites by identified spiders and, most importantly, provides three cases with expert identification. Of the two confirmed white-tailed spider bite cases reported, one developed shallow ulcers only, the other a small ulcer that healed within one month. Both cases are therefore at the mild end of the necrotising arachnidism spectrum. What is the mechanism of injury in necrotising arachnidism and how might we treat it? Recluse spiders have been studied in detail, but the mechanism of venom injury is still contentious.2 Worse, in North America, where these spiders are native and frequently cause bites, there is neither concordance on treatment nor a clearly effective treatment.2 Experience there does suggest that early surgical debridement may extend the lesion, that early skin grafting usually fails, that antibiotics are unhelpful unless there is a clearly identified and targeted secondary infection and that no specific therapy is helpful, with the possible exception of hyperbaric oxygen therapy.2 This treatment for necrotising arachnidism is being tried in a number of hyperbaric units around Australia, with mixed but encouraging success.11 It is probably time to formalise this by running a multicentre trial to establish the validity and indications for this form of treatment. In the only two cases I have seen in South Australia where a spider was clearly caught biting and subsequently identified, it was a recluse spider (Loxosceles), not a white-tailed spider.2 In my experience with many cases of necrotising arachnidism over nearly 20 years, the white-tailed spider is often suspected but never confirmed to be the culprit. In most cases, a spider is found in the house after the bite and an unsubstantiated link is made. The increasing tendency of the media and the medical profession to blame the white-tailed spider for necrotising arachnidism is unfortunate, as it establishes a common belief that the cause is known when in truth it is not. In Brazil, wolf spiders were long blamed for necrotising arachnidism until a detailed study showed that recluse spiders were the culprits.13 A concerted effort to determine which species of spiders (or perhaps some other organism) can cause necrotising arachnidism should become a prime focus for research in this field. Once a cause is known, specific treatments can be more reliably investigated and preventive measures devised. Julian White Clinical Toxinologist Women's and Children's Hospital, Adelaide, SA Pincus GL, Winkel KD, Hawdon GM, Sutherland SK. Acute and recurrent skin ulceration after spider bite. Med J Aust 1999; 171: 99-102. White J, Cardoso JL, Fan HW. Clinical toxicology of spider bites. In: Meier J, White J, editors. Handbook of clinical toxicology of animal venoms and poisons. Boca Raton: CRC Press, 1995: 259-329. Southcott RV. Spiders of the genus Loxosceles in Australia. Med J Aust 1976; 1: 406-408. Sutherland SK. Spider bites in Australia; there are still some mysteries [editorial]. Med J Aust 1983; 2: 597. Spring W. A probable case of necrotizing arachnidism. Med J Aust 1987; 147: 605-607. Sutherland SK. Watch out, Miss Muffet! [editorial]. Med J Aust 1987; 147: 531. New South Wales Poisons Information Centre. 1998 Annual Report. Sydney: New Children's Hospital, 1999. White J, Hirst D, Hender E. 36 cases of bites by spiders, including the white-tailed spider, Lampona cylindrata. Med J Aust 1989; 150: 401-403. Atkinson RK, Wright LG. Studies of the necrotic actions of the venoms of several Australian spiders. Comp Biochem Physiol 1991; 98: 441-444. Grey M. A significant illness that was produced by the white-tailed spider, Lampona cylindrata [letter]. Med J Aust 1989; 151: 114-116. Skinner MW, Butler CS. Necrotising arachnidism treated with hyperbaric oxygen. Med J Aust 1995; 162: 372-373. Chan SW. Recurrent necrotising arachnidism. Med J Aust 1998; 169: 642-643. Ribeiro LA, Jorge MT, Piesco RV, Nishioka S deA. Wolf spider bites in Sao Paulo, Brazil; a clinical and epidemiological study of 515 cases. Toxicon 1990; 28: 715-717.

Julian White

Notable Case Acute and recurrent skin ulceration after spider bite We reviewed the records of the Australian Venom Research Unit and The Alfred Hospital Department of Hyperbaric Medicine from January 1992 to July 1998 and found 15 cases of skin ulceration after spider bite that could be followed up with the patient and the treating physician. Fourteen patients had skin ulceration attributed to white-tailed spider bites but in only three was this confirmed. One patient had skin necrosis after a confirmed black house spider bite. Recurrent skin ulceration occurred in nine of the 15 patients. Steven J Pincus, Kenneth D Winkel, Gabrielle M Hawdon and Struan K Sutherland MJA 1999; 171: 99-102 See also White Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Insects, bites and stings Introduction Spider bite is the single commonest reason for inquiries to the Victorian Poisons Information Centre, with over 1300 calls recorded in 1997.1 Most people with spider bite require no specific treatment and suffer only minor symptoms, but a small number develop necrotic skin lesions associated with significant morbidity.2-4 One series reported no significant illnesses in 36 bites,5 and only seven definite cases of skin necrosis after spider bite have been published in Australia.3,4,6,7 This paucity of reports has led to debate as to the ability of Australian spiders to cause skin necrosis (necrotising arachnidism). We performed a retrospective analysis of case records of suspected necrotising arachnidism in Australia to better define its clinical features and to compare it with loxoscelism, a well-recognised cause of skin ulceration in the Americas. Methods Patients were identified from records of inquiries from clinicians between January 1992 and July 1998 held by the Australian Venom Research Unit and cases referred to the Hyperbaric Unit of the Alfred Hospital, Melbourne. Initial case-finding criteria were a history of spider bite with subsequent ulceration or necrosis at the bite site. Only cases in which both the patient and primary treating doctor were contactable by telephone were included (with the informed consent of both patient and doctor). In the patient interview we asked for demographic details, the method of identification of the spider, details of ulcerative or necrotic lesions and any other related problems, treatment, outcome details and relevant past medical history. This information was confirmed with the patient's doctor, who was also asked about details of investigations, treatments and outcomes. Results Fifteen cases were identified from more than 600 patients with skin lesions but without confirmed spider bite. In 14 cases (Box 1) the spider was said to be a white-tailed spider (Lampona species) but in only three cases was this identification confirmed. One case involved two black house or black window spiders (Badumna species; see Box 2). All of the spider bites were to the limbs, and involved blistering, ulceration or necrosis of the skin. Thirteen were described as painful. Five patients experienced ongoing disability, and one required amputation of the hand and distal forearm. Four of the 15 patients experienced systemic symptoms (fever), and three had ulcers that were culture-positive for Staphylococcus species (one positive for Streptococcus species also). Nine patients had recurrent lesions, involving recurrent breakdown or blistering of the skin after healing, or breakdown of skin grafts used to treat non-healing ulcers. Oral or intravenous antibiotics (including doxycycline, penicillin or flucloxacillin) were given to 14 patients. Other treatments included dressings, antihistamines, topical and oral corticosteroids, hyperbaric oxygen therapy and skin grafting. Discussion A major difficulty in the clinical study of spider bite is accurately identifying the spiders involved. Our series included 11 cases in which a spider was witnessed to bite the patient but was not captured for identification, one case where the spider was captured and identified by a clinician, and three cases where the spider was captured and identified by an expert arachnologist. White-tailed spiders are distinctive, but in most of these cases absolute attribution to Lampona is not possible. Window spiders are relatively nondescript, and therefore less likely to be correctly identified unless captured and formally identified by an arachnologist. Four cases of skin loss attributed to bites from Lampona have been previously reported.3,4,7 Two of these (Cases 54 and 137) are included in this study, as both patients were reported to the AustralianVenom Research Unit independently. Several cases of bites from Badumna species have been published. These patients mostly experienced significant sickness, without skin loss.2,8 Some skin loss was reported in the case of a male black house spider bite.6 The case presented here (Box 2) is the first to link the female spider to skin necrosis. It has been suggested that many cases of suspected necrotising arachnidism in Australia may be the result of bites from spiders of the genus Loxosceles, a group associated with necrotising arachnidism on several continents.9 While it is probable that some Australian cases of necrotising arachnidism might be attributed to this spider, it would be difficult to implicate Loxosceles in the cases reported here. The lesions reported in this series show similarities but also significant differences from those caused by Loxosceles. As with Loxosceles, the initial bite appears to be relatively painless, with pain developing over the next 12-24 hours, accompanied by local erythema and oedema, then blister formation and ulceration.10 However, Loxosceles produces a deep ulcer, with a rolled edge and necrotic base, extending into and sometimes through subcutaneous fat to expose underlying muscle.10,11 By contrast, most ulcers reported here were superficial, being confined to the epidermis and dermis. Another important difference appears to be the site of bites that progress to significant ulceration. Significant Loxosceles lesions occur in areas of abundant subcutaneous fat, with involvement extending beyond the margins of the skin necrosis.11 The lesions reported here occurred in areas of little or no subcutaneous fat. An infectious aetiology has been proposed for necrotising arachnidism in Australia,12 but the concept that Mycobacterium ulcerans might be such an agent13 was subsequently challenged.14Bacillus, Staphylococcus and Penicillium species have been cultured from several spider venoms, including that of a Lampona species.14 Only three of the 15 patients in our series had ulcers which grew any microorganisms, but, as 14 patients had been treated with antibiotics, infective organisms may have been cleared before cultures were prepared. However, the absence of cultured organisms and poor clinical response to antibiotic therapy seen in many patients suggests that this condition is more complex than simple skin infection. Nine of the 15 patients in our case series had recurrent ulceration. This problem had not been reported in Australia until very recently.7 There are several American reports of lesions attributed to Loxosceles that have resulted in chronic non-healing ulcers and recurrent ulceration. These were felt to be secondary to induction of a pyoderma gangrenosum-like disease process.15 Pyoderma may follow a minor injury and may be aggravated by surgery.16 It is typically associated with systemic immune abnormalities, but up to 50% of cases are described as "idiopathic". Spider bite may act as a trigger to precipitate this condition in susceptible individuals. Several patients in our case series had histological findings consistent with pyoderma, and surgical intervention may have been associated with a poorer outcome. Although no patient in this series received corticosteroids at the doses recommended for pyoderma, long term topical corticosteroids may have slowed progression of the lesion in case 14. Prospective study of the value of this treatment in cases of necrotising arachnidism should be considered. Management of necrotising arachnidism remains an area of debate, and there is limited information upon which to make recommendations for the Australian situation. At least for Loxosceles envenomations, conservative management appears to be the best primary treatment. This should include tetanus prophylaxis and routine wound care. Early ice water application to bites is recommended to counter inflammation. Initial studies proposed early excision and grafting of ulcers,11 but more recent experience suggests that this may worsen the lesion and delay healing.17 Hyperbaric oxygen therapy is gaining popularity in general wound management. Animal models have produced conflicting results on the value of this type of treatment for Loxosceles lesions.18,19 Treating ulcers attributed to Lampona bites with hyperbaric oxygen therapy appears to have a marked clinical benefit.4 Acknowledgements We thank Mr Albert Ong, of the Pathology Department, Gladstone Base Hospital, for permission to reproduce his photograph of a patient, Dr Robert Raven and Mr Phil Lawless of the Arachnology Department of the Queensland Museum, and Ms Catriona McPhee and Dr Ken Walker of the Museum of Victoria for spider identification and photographs, and Dr Ian Miller, Director of the Hyperbaric Unit at the Alfred Hospital in Melbourne, for assistance in collecting patient information. This study would not have been possible without the assistance of the many other clinicians and patients involved. We thank the Victorian Department of Human Services, CSL Limited, BHP Community Trust and Snowy Nominees for financial support, and Dr Anna Young and Dr Tony Pennington for helpful discussion. Call NASTY! To address the paucity of clinical data on necrotising arachnidism the Australian Venom Research Unit, together with the Monash Medical Centre's Department of Emergency Medicine, is conducting a long term prospective study of the outcome of spider bite. Clinicians and the public are encouraged to report definite spider bites (with spider captured) immediately after the bite. The on-call investigator can be contacted via the Monash Medical Centre switch (telephone: 03 9550 1111) as the NASTY Study (Necrotising Arachnidism Study). Definitive identification of the spider involved by an arachnologist is essential to advance our understanding of this condition. References Victorian Poisons Information Centre Annual Report 1997. Melbourne: Royal Children's Hospital, 1998. Sutherland SK. Australian animal toxins. The creatures, their toxins and care of the poisoned patient. Melbourne: Oxford University Press, 1983. Gray M. A significant illness that was produced by the white-tailed spider, Lampona cylindrata. Med J Aust 1989; 151: 114-116. Skinner MW, Butler CS. Necrotising arachnidism treated with hyperbaric oxygen. Med J Aust 1995; 162: 372-373. White J, Hirst D, Hender E. 36 cases of bites by spiders, including the white-tailed spider, Lampona cylindrata. Med J Aust 1989; 150: 401-403. Macmillan DL. Envenomation by a window spider [letter]. Med J Aust 1989; 150: 16. Chan S. Recurrent necrotising arachnidism [letter]. Med J Aust 1998; 169: 642-643. Tingate TR. Envenomation by the common black window spider [letter]. Med J Aust 1991; 154: 291. White J, Cardoso J, Fan H. Clinical toxicology of spider bites. In: Meier J, White J, editors. Clinical toxicology of animal venoms and poisons. Boca Raton: CRC Press, 1995. Atkins JA, Wingo CW, Sodeman WA, Flynn JE. Necrotic arachnidism. Am J Trop Med Hyg 1957; 7: 165-184. Auer AI, Hershey FB. Proceedings: Surgery for necrotic bites of the brown spider. Arch Surg 1974; 108: 612-618. Harvey MS, Raven RJ. Necrotising arachnidism in Australia: a simple case of misidentification [letter]. Med J Aust 1991; 154: 856. Oppenheim B, Taggart I. More in spider venom than venom? Lancet 1990; 335: 228. Atkinson RK, Farrell DJ, Leis AP. Evidence against the involvement of Mycobacterium ulcerans in most cases of necrotic arachnidism. Pathology 1995; 27: 53-57. Rees RS, Fields JP, King LE. Do brown recluse spider bites induce pyoderma gangrenosum? South Med J 1985; 78: 283-287. Callen JP. Pyoderma gangrenosum. Lancet 1998; 351: 581-585. Rees RS, Altenbern DP, Lynch JB, King LE, Jr. Brown recluse spider bites. A comparison of early surgical excision versus dapsone and delayed surgical excision. Ann Surg 1985; 202: 659-663. Strain GM, Snider TG, Tedford BL, Cohn GH. Hyperbaric oxygen effects on brown recluse spider (Loxosceles reclusa) envenomation in rabbits. Toxicon 1991; 29: 989-996. Maynor ML, Moon RE, Klitzman B, et al. Brown recluse spider envenomation: a prospective trial of hyperbaric oxygen therapy. Acad Emerg Med 1997; 4: 184-192. (Received 19 Oct 1998, accepted 1 Jun 1999) Authors' details Australian Venom Research Unit, Department of Pharmacology, The University of Melbourne, VIC. Steven J Pincus, MB BS, BSc(Hons), Research Registrar. Kenneth D Winkel, MB BS, FACTM, Director. Gabrielle M Hawdon, MB BS, MPH, Deputy Director. Struan K Sutherland, MD DSc, Honorary Principal Fellow. Reprints: Dr K D Winkel, Australian Venom Research Unit, Department of Pharmacology, The University of Melbourne, Parkville, VIC 3052. Email: k.winkelATpharmacology.unimelb.edu.au 1: Fourteen cases of acute and recurrent skin ulceration after suspected or confirmed white-tailed spider bite* Spider identity confirmed 1. A 27-year-old woman in Queensland was bitten on the leg by a female white-tailed spider (positively identified by one of the authors, SKS). She developed a pimple-like lesion that blistered and broke down to form a 2x2cm ulcer. She was treated with doxycycline, and healed over 1 month. 2. A 38-year-old man in Victoria was bitten on the calf by a female white-tailed spider (positively identified by the Victorian Museum). The bite was painful, itchy, erythematous and blistered, and progressed to shallow ulcers, while he became feverish. He was treated with doxycycline and antihistamines, and the original lesion healed over 10 days. He has since had multiple episodes of similar lesions, with a gradual decrease in frequency. 3. A 33-year-old man in New South Wales was bitten on the leg by a white-tailed spider (also sighted by the local medical officer). Initially the bite produced a small, red, painful lesion. Culture produced a scant growth of S. aureus. The patient was treated with doxycycline, and the lesion healed, then broke down at one month into a 6x6cm ulcer that healed over four months. Spider identity not confirmed (patient reported white-tailed spider bite, but no formal identification) 4. A 39-year-old man in Queensland was bitten on the shin. The bite was painful and progressed rapidly to a 20x10cm ulcer. He presented at one week, febrile with secondary infection. Staphylococcus and Streptococcus were cultured from the wound. He was treated with intravenous and oral antibiotics, but presented again three weeks later requiring further antibiotic treatment. The ulcer healed over the next month. 5.·A 38-year-old man in Tasmania was bitten at the base of the little finger. The lesion developed initially as a reddened disc with central darkening, progressing to a painful ulcer (1x2cm). S. aureus was cultured from the lesion. He was treated with intravenous and oral antibiotics without response. Hyperbaric oxygen therapy was applied five times, until the lesion developed a granulating base. 6. A 46-year-old man in New South Wales was bitten on the back of the hand by a white-tailed spider. The bite resulted in a painful, erythematous 5x5cm area of blisters that progressed to a chronic ulcer. He was unsuccessfully treated with routine wound dressings, oral and intravenous antibiotics, developed a claw hand and underwent amputation at the wrist. 7. A 46-year-old man in New South Wales was bitten on the shin. The bite resulted in an itchy, painful swelling with a 1cm necrotic area, and the patient became febrile. He was treated with flucloxacillin and penicillin, but the ulcer slowly increased in size with central necrosis, before eventually healing over one month. 8. A 51-year-old man in Queensland was bitten on the back of the hand. Blisters at the bite site progressed to a painful ulcer that had not healed two months after the bite, when the wound was debrided and repaired with a split skin graft. Two weeks later there was blistering and loss of the graft. Regrafting was also unsuccessful, leaving a persistent 15x8cm ulcer that took six months to heal. The lesion recurred once three years later. 9. A 35-year-old man in Victoria was bitten on the palm of the hand. The bite resulted in a painful lesion with central blistering. He was treated with antibiotics. The blister broke down to a shallow ulcer that resolved slowly over a month. The patient experienced several episodes of superficial blisters over the next year. A white-tailed spider (Lampona cylindrata, actual length 1-2 cm) -- the likely suspect in most of these cases of serious injury after spider bite. "Lampona group spiders are found throughout Australia; L. cylindrata is particularly common in disturbed and urban areas. These spiders live in crevices, under bark, rocks and leaf litter and often in houses. They attack and eat other spiders including black house spiders." -- Australian Museum online <http://www.austmus.gov.au/is/sand/whitspi.htm> Accessed 11 June 1999. 10. A 33-year-old woman in Victoria was bitten on the medial malleolus. Initially a red spot, the bite site blistered on Day 1, progressing to increasing inflammation and spreading ulceration resulting in multiple ulcers on the lower leg. A biopsy showed perivascular infiltration with polymorphic neutrophils and lymphocytes. The patient was unsuccessfully treated with antibiotics and routine dressings for four months before being referred for hyperbaric oxygen therapy. Twelve sessions of hyperbaric oxygen therapy led to resolution of the ulcer, but the patient experienced several recurrences of ulcers (1-2cm self-healing) per year thereafter. 11. A 69-year-old woman in Victoria was bitten on the medial malleolus. The bite resulted in pain, erythema, oedema, multiple blisters, progressing to dry shallow ulcers, with fever. The patient was treated with intravenous antibiotics and routine wound dressings without response. Blisters and swelling increased for 10 days, then healed over three weeks. Three months after the bite the patient experienced multiple episodes of small blisters that healed in 5-7 days. 12. A 25-year-old woman in Victoria was bitten on the foot. The bite resulted in an ulcer and erythema in the first web space and swelling to the ankle. The patient was treated with oral antibiotics. The lesion healed over one month, but recurred four times in the next six months, after which the patient had 10 sessions of hyperbaric oxygen therapy. There was a minor recurrence one year after the bite. 13. A 35-year-old man in Victoria was bitten on the shin. The bite resulted in painful, erythematous, swollen, multiple superficial ulcers. A biopsy showed dermal necrosis and vasculitis infiltrated by polymorphic neutrophils. The patient was treated with intravenous flucloxacillin and penicillin, oral augmentin, immobilisation and (after two months) with a split skin graft. The graft healed over one month, but the patient presented again a year after the bite with rapid breakdown of the graft. A regraft gave a poor result and recovery was slow.7 14. A 40-year-old woman in New South Wales was bitten on the arm. The bite resulted in a red spot that grew to 2cm and developed a necrotic centre at seven days, progressing to shallow ulcers in the mid-forearm (6x3cm). Biopsy showed dermal necrosis and mixed perivascular infiltrate. Treatment with tetracycline was ineffective, but topical and oral prednisolone appeared to slow the progression of the ulcer. The patient underwent hyperbaric oxygen therapy, with resolution of the ulcer, but she has experienced subsequent recurrences. *Identified from the Australian Venom Research Unit medical advisory service records and from the Alfred Hospital Department of Hyperbaric Medicine records. Back to text 2: Skin necrosis following bites from two Badumna spiders This is the first report of skin necrosis after the bite of a female black house spider. A previously well 55-year-old woman was bitten four times by two spiders that fell onto her forearm after she had sprayed them with insecticide. She felt an immediate stinging pain after the bite. The spiders were captured and later identified as female Badumna spiders (species indeterminate) (Dr Robert Raven, Museum Scientist, Arachnology, Queensland Museum, personal communication). She presented to hospital four days later with a painful, swollen forearm, was admitted and, although systemically well, was treated with intravenous flucloxacillin. Over the next three days, several ragged ulcers with necrotic bases developed within the swollen area. Microscopy of a swab of the ulcer showed numerous leukocytes, but no organisms were seen on gram stain nor subsequently cultured. After debridement, the ulcers were allowed to heal by secondary intention. The wounds healed slowly over the next few months and have not recurred. A black house or black window spider (Badumna insignis, actual length 1-1.5 cm). "Black house spiders are widely distributed in southern and eastern Australia. They are common in urban areas. Other Badumna group spiders are found throughout Australia. Black house spider webs form untidy, lacy silk sheets with funnel-like entrances. They are found on tree trunks, logs, rock walls and buildings (in window frames, wall crevices, etc.). Badumna longinquus often builds webs on foliage." -- Australian Museum online <http://www.austmus.gov.au/is/sand/widspi.htm> Accessed 11 June 1999. Back to text

Steven J Pincus · Kenneth D Winkel · Gabrielle M Hawdon · Struan K Sutherland

Health Care Establishing a collaborative service model for primary mental health care A collaborative project between general practitioners and mental health services, which links a consultation-liaison model with shared care, was piloted with success. This article provides a broad overview of the service model and the stages in its development. Graham N Meadows MJA 1998; 168: 162-165 Introduction - History of the CLIPP service - Activity of the service - Benefits and costs - Summary and prospects - Acknowledgements - References - Authors' details - - More articles on Psychiatry Introduction Improving collaboration between mental health services and general practitioners in caring for people with serious mental illness is an aim of Commonwealth Government policy.1,2 Recent documents examining the psychiatry workforce have also recommended stronger links between specialist and generalist services in this area.3-5 Mental health care needs may often be more appropriately met by general practitioners than by long term specialist care. This will be true for many patients with anxiety disorders and depression, but also for selected patients with psychotic disorders. General practitioner involvement with people with continuing mental illness may also provide an opportunity to address unmet physical health needs,6 and may ultimately have an impact on the high rates of physical morbidity and mortality associated with major mental disorder.7Various models of consultation-liaison links between psychiatric services and GPs have been described in reports from the United Kingdom.8-11 Although this area of activity in Britain was described as "the silent growth of a new service" in 1984,12 a more recent review noted that many such schemes had not proceeded beyond pilot phase. This review stressed the need for further evaluations, including cost-benefit evaluation, in response to this situation.13 In Australia, a pilot scheme in Newcastle, New South Wales, providing consultation-liaison attachments to GPs was initially reported positively,14 but a later viewpoint paper alluded to less encouraging aspects, and the project did not move beyond pilot phase.15 A recent survey of psychiatrists in South Australia suggests considerable enthusiasm for collaboration in consultation-liaison models,16 but revealed little actual activity in this area. The Consultation Liaison in Primary Care Psychiatry (CLIPP) service model developed in the Northwest Melbourne Area Mental Health Service promotes collaboration between GPs and public mental health services in managing psychiatric problems. CLIPP is now established, with recurrent funding from State public mental health services, and is being extended into another area mental health service. This article describes the CLIPP model and the activity involved in ensuring its continuation beyond the pilot phase. History of the CLIPP service In 1993, Health and Community Services Victoria received Federal Government National Mental Health Initiative funding expressly for promoting shared care initiatives in mental health. Early in 1994, staff of the Northwest Melbourne Area Mental Health Service and local GPs (represented by the Division of General Practice) proposed a pilot project, for which they were granted $97 000 over two years. These funds supported a half-time psychiatric nurse case manager for 18 months and most of the cost of a half-time psychologist project officer for two years. The area mental health service contributed about four half-day sessions per week of psychiatrist time. Consultation-liaison attachments, although they are well liked and help to improve GP confidence, have been criticised as doing little to enhance GPs' involvement with the care of the seriously mentally ill.15 Shared care arrangements for specific patients with serious mental disorder may result in GPs feeling that public mental health services are not helping them with the types of problems they see most frequently. We aimed to counter these problems by combining the two approaches. Consultation-liaison attachments were set up first. General practitioners were recruited by mail through the Division. Interested GPs were followed up with personal visits by project staff, then with fortnightly visits by a psychiatrist to each practice (similar to the British "liaison-attachment" model9). Details of the consultation-liaison attachment system are shown in Box 1. Three months after setting up these attachments, shared care was initiated by asking participating GPs to accept patients referred from the area mental health service. At this point, the number of psychiatrist consultation appointments for patients referred by GPs was generally reduced to two each session to allow time for discussion of the shared care patients referred from the area health service. Operation of the shared care system is described in Box 2. During 1995, consultation-liaison attachments were set up with seven group practices of between two and 12 GPs. By late 1995, all of these practices were accepting patients transferred from the area mental heath service. The CLIPP service was recognised by a National Mental Health Achievement Award in 1996, in the category of prevention and health promotion. The project was reported to Health and Community Services Victoria, with an account of the development, and a cost-benefit analysis supported by work carried out in the area mental health service.17 Activity of the service During its first two years, CLIPP provided care to over 220 patients through the clinical consultation-liaison service, patients having been referred by 31 of the 40 GPs from the seven participating group practices. It has facilitated the transfer of over 90 clients from the area mental health service into shared care with 28 GPs, including GPs from each participating practice. Box 3 lists the clinical diagnoses of the patients in these two groups. The most common single impediment to the transfer of care to GPs -- affecting about 15 patients -- is drug costs. Some regimens are free to patients under area mental health service care, but prohibitively expensive (under the Pharmaceutical Benefits Scheme) for others. A change to a rebated alternative drug may sometimes remove this impediment, but is not always clinically appropriate. One partial solution would be for a GP to see patients every two to four weeks for clinical monitoring, while the psychiatrist sees them around six-monthly, prescribing through the area mental health service pharmacy. Among patients transferred to GPs, telephone follow-up by area mental health service staff has found that 90% report being satisfied with their management. One year after transfer to GP care, 60% felt their physical health care had improved with the increased GP input. In some 20% of cases, review of GP case notes showed that newly identified physical health problems had been treated. Two patients whose care was transferred to GPs died of natural causes. No other cases have so far been lost to follow-up. An unexpected referral route developed during the pilot phase of the service, with public community mental health services making one or two referrals a month to GPs working with CLIPP. This is appropriate for patients who present directly to these specialist services, but whose needs could be as well, or better, met in this augmented primary care model. Benefits and costs The pilot project was reported to Human Services Victoria in June 1996. While the clinical service had been running for little over a year, and was hardly ready for summative evaluation, the following benefits could be claimed on the basis of a combination of qualitative and quantitative data. The model: provides a large number of courses of GP care, with (through consultation-liaison attachments) specialist assessment and supervision; provides a valued educational opportunity for interested GPs; complements general practice care with systematic monitoring and community outreach (provided by the area mental health service) when necessary. This augments the capacity of GPs to provide care to individuals with continuing mental disorder; allows area mental health care to be provided locally and with more flexibility; shows high levels of consumer acceptability; and promotes the physical health of clients transferred to GPs. A detailed cost-effectiveness report of the project is in press.18 Costing analyses included projecting estimates of the activity of the service forward up to two years, and examining the projected cost effectiveness that could be reasonably expected from the service over that time. A simplified version of this analysis can be rendered as follows. The total cost of the CLIPP service was compared with the cost of providing care through area mental health services for the 110 patients in CLIPP who would otherwise have been cared for in the area mental health service. This group comprised 90 patients transferred from the area mental health service to GPs, 10 patients seen in the consultation-liaison attachments who would otherwise have had their care transferred to the area mental health service, and 10 patients diverted from triage at the area mental health service to GPs. Two patterns of area mental health service care that would otherwise have been required for the patients transferred into shared care through CLIPP were identified. These were 1-25 community service contacts per year, and 25-50 such contacts per year. The median cost per case for area mental health service care was estimated to be $623 and $2261 per annum, respectively.17 The 110 patients transferred to the CLIPP service were estimated to have originated from these two groups in a ratio of 4:1 (88 patients at $623 and 22 patients at $2261 per annum). From these estimates, the annual costs of mental health service care for the 110 patients transferred to GPs within CLIPP is $104 566. By comparison, the total cost of the CLIPP program (including the cost of staff initally funded through the Commonwealth Government grant, and psychiatrists whose time was committed from area mental health service budgets) was estimated at within $1000 of this sum. Hence, the model can be argued to be cost neutral for the area mental health service, but with the advantages to patients described earlier. The evaluation report was positively received by Human Services Victoria. In late 1996, commitment was made to continue funding for the project through the Western Region of Human Services Victoria, and extended to developing another project along similar lines in a nearby area of metropolitan Melbourne. Further development of the service is now an active process of participation between Western Region as purchasers and the Western Health Care Network as providers, with the support of academic staff from the University of Melbourne. Summary and prospects It has been previously shown that GP consultation-liaison services can be implemented in Australia.14 In the CLIPP model, the strengths of the relationships established through consultation-liaison links have been harnessed in support of effective shared care. Combining these two activities means that a cost-effectiveness case can be presented which is more convincing than that for a consultation-liaison service alone. Experience of this development suggests that, if such schemes are to continue, they need to meet the needs and expectations of all stakeholders with purchaser and provider roles -- GPs, patients, case managers, psychiatrists, and mental health service managers. Current plans for further development of the CLIPP model include use of computer-based reminder systems to support GPs in managing transferred patients, and providing periodic group education sessions for participating GPs. Over the next three years, CLIPP will provide the setting for a Commonwealth Department of Health and Family Services examination of process and outcome in shared care (General Practice Evaluation Program Grant 518). The new study uses a quasi-experimental design to compare processes and outcomes of care in the shared care setting with those in a community mental health service. Further systematic analysis of the consultation-liaison service is under way. This will include description of GP referral patterns, management suggestions from psychiatrists, determinants of outcomes, and a further cost-benefit analysis. I believe CLIPP to be a very useful model for improving collaboration between GPs and psychiatric services. It has allowed a diverse group of practitioners to work together in ways that transcend funding and organisational barriers in the interests of sensible arrangements for the delivery of health care. Acknowledgements Human Services Victoria for funding through Western Metropolitan Region budgets, particularly Mr John Hedditch for support in expansion of the service. The Commonwealth Government for funding through Mental Health Initiative funding and General Practice Divisional resources; also, Dr Philip Hegerty of the Northwest Division, Dr Bob Long, and the many other GPs involved. The project team from the Northwest Area mental health services: Dr Lynette Joubert, Mr Guy Dobson, Dr Carol Harvey, Dr Rajeev Kumar, Dr Philip Price, and Dr Michael Wong. Western Health Care Network management staff, particularly Mr George Shaw, for support. Mr Paul Mcrone, health economist at the Institute of Psychiatry, London, for assistance with cost-benefit analyses. References Australian Health Ministers' Advisory Council. National mental health plan. Canberra: AGPS, April 1992. Commonwealth Department of Human Services and Health. Better health outcomes for Australians: national goals, targets and strategies for better health outcomes into the next century. Canberra: AGPS, 1994. Solomon S and Associates, Buckingham B and Associates, Epstein M. Report of consultancy for the mental health workforce committee on medical workforce financing arrangements. Melbourne: The Associates, 1993. McKay B and Associates. Proposals for change final report: optimum supply and effective use of psychiatrists. Canberra: Bernie McKay and Associates, 1996. McKay B and Associates. Issues and options supplementary paper: optimum supply and effective use of psychiatrists: Canberra: Bernie McKay and Associates, 1996. Brugha TS, Wing JK, Smith BL. Physical health of the long term mentally ill in the community. Is there unmet need? Br J Psychiatry 1988; 155: 777-781. Allebeck P. Schizophrenia: a life shortening disease. Schizophrenia Bull 1989; 15: 81-89. Strathdee G, King M. The interface between primary and secondary psychiatric care. In: Williams P, Wilkinson G, Rawmsley K, editors. The scope of epidemiological psychiatry: Essays in honour of Michael Shepherd. London: Routledge, 1989: 420-433. Creed F, Marks B. Liaison psychiatry in general practice: a comparison of the liaison-attachment scheme and shifted outpatient models. J R Coll Gen Pract 1989; 39: 514-517. Strathdee G, McDonald E. Innovations: establishing psychiatric attachments to general practice: a six stage plan. Psychiatr Bull 1992; 154: 72-76. Strathdee G. Psychiatrists in primary care: the general practitioner viewpoint. Fam Pract 1988; 5: 111-115. Strathdee G, Williams P. A survey of psychiatrists in primary care: the silent growth of a new service. J R Coll Gen Pract 1984; 34: 615-618. Gask L, Sibbald B, Creed F. Evaluating models of working at the interface between mental health services and primary care. Br J Psychiatry 1997; 170: 6-11. Carr VJ, Donovan P. Psychiatry in general practice: a pilot scheme using the liaison-attachment model. Med J Aust 1992; 156: 379-382. Carr VJ, Reid ALA. Seeking solutions for mental health problems in general practice. Med J Aust 1996; 165: 435-436. Barber R, Williams AS. Psychiatrists working in primary care: a survey of general practitioners' attitude. Aust N Z J Psychiatry 1996; 30: 278-286. Meadows G, Gielewski H, Falconer B, et al. The pattern of care model: a tool for planning community mental health services. Psychiatr Serv 1997; 48: 218-223. Meadows G, Joubert L, Mcrone P, Dobson G. Consultation, collaboration and cost effectiveness: reflections on four years of shared care in Melbourne. In: Ellis P, editor. Community care -- working together. Proceedings of the Geigy Psychiatric Symposium; 1997 Dec 3-5; Wellington, New Zealand. Sydney: Novartis. In press. Received 1 Sep, accepted 22 Dec, 1997 Authors' details Department of Psychiatry, University of Melbourne, Royal Park Hospital, Melbourne, VIC. Graham N Meadows, MRCP(UK), FRANZCP, Senior Lecturer. Reprints: Dr G N Meadows, Department of Psychiatry, University of Melbourne, Royal Park Hospital, Private Bag 3, PO Parkville, VIC 3052. E-mail: g.meadowsATmedicine.unimelb.edu.au 1: Format for consultation-liaison attachments in the CLIPP project Psychiatrists provide consultation services for any patient referred by GPs. This service is provided at the general practice clinic. For group practices, visits are usually fortnightly, and 2-3 patients are seen per consultation Specific forms, which include a global impression rating by the GPs, are used to document the consultancy request from the GPs and responses by psychiatrists; follow-up forms are completed by GPs after three months, and include a repeat of the previous global impression rating and a change score. These forms are complemented by face-to-face discussion between GPs and psychiatrists during the fortnightly consultation at the GP's clinic, during which any patient can be discussed, including those not seen personally by the psychiatrist. Psychiatrist consultations are generally specifically intended to leave continuing care of each patient with the GP. General practitioners have been remunerated at the hourly rate for "Divisional activities by GPs" through a Divisional seeding grant for time spent in discussion with psychiatrists. The Royal Australian College of General Practitioners recognises this activity as continuing medical education, and awards two CME points per hour, or one point per patient referred. Back to text 2: Format for shared care in the CLIPP project Case managers within the area mental health service identify candidate patients -- typically clinically stable, without recent relapse, with fair to good insight, and with some social support. Patients are referred to the CLIPP nurse, who prepares the transfer. A concise summary of diagnosis, history, and treatment adherence is prepared from the case notes. Impediments to transfer are identified and acted upon where possible; the outcome of this action is recorded. The CLIPP nurse drafts a management plan and arranges a first CLIPP appointment, at which the GP, psychiatrist and patient discuss the draft and establish the plan for continuing management. The GP takes over the primary responsibility for the care of the patient. A patient registration and tracking system maintained by area mental health service staff supports the GP in maintaining continuity of care and provides information about satisfaction and other quality assurance. As part of this tracking system, an administrator maintains an electronic diary of due dates for review of each patient. Clinical staff then review patients three-monthly by telephone contact with the patient and by checking the GP's case notes for continued contact. Management plans usually also recommend that psychiatrists review patients every 6-12 months. Back to text 3: Diagnoses of CLIPP service patients, by origin of referralBroad diagnostic category*Consultation- liaison referralsReferrals from mental health service to GPsDepression and dysthymia105 12Adjustment disorder40--Anxiety disorders281Problems related to substance abuse11--Schizophrenia856No diagnosis8Bipolar disorder711Eating disorder4--Pain disorder3 --Axis ii (personality disorder) diagnosis only2--Delusional disorder12Somatoform disorder1--Dementia of Alzheimer type1--Dissociative fugue1--Medication-induced movement disorder1--Schizoaffective disorder--10Brief psychosis--1Totals22193* From Diagnostic and statistical manual of mental disorders, fourth edition. Washington, DC: American Psychiatric Association, 1994. Back to text

Graham N Meadows

Clinical Practice The role of the general practitioner in the treatment of schizophrenia: specific issues This article provides practical guidelines for general practitioners in treating schizophrenia. Specific areas include pharmacological treatment, supportive therapy, depression and suicide, alcohol and drug abuse, sexuality, and physical health. Vaughan J Carr MJA 1997; 166: 143-146 Introduction - Drug therapy - Supportive therapy - Depression and suicide - Alcohol and drug abuse - Sexuality - Physical health - Conclusion - Acknowledgements - References - Authors' details - - More articles on Psychiatry This is the second in a two-part series. The first article was published in the MJA 20 January 1997 issue. Introduction This second paper in this series deals with more specific issues in the primary care treatment of patients with schizophrenia, and attempts to clarify the roles of general practitioners (GPs) and specialist services, highlighting the areas which may be especially well provided by GPs. Practical guidelines are provided in the Box. Drug therapy Systematic accounts of the drug treatment of schizophrenia are available,1,2 and only matters particularly relevant to GPs will be covered here. Antipsychotic drugs are still chosen mostly on the basis of side effects. Low potency drugs (e.g., chlorpromazine, thioridazine) are more likely to produce sedation, postural hypotension and anticholinergic side effects, while higher potency drugs (e.g., haloperidol, fluphenazine) tend to cause more extrapyramidal side effects, such as parkinsonism, acute dystonia and akathisia. Some newer drugs (e.g., risperidone) are said to be more benign in their side effect profile; further use and investigation may bear this out. Clozapine seems unique in having marked benefits for about one-third of otherwise "treatment resistant" patients; this drug is subject to stringent controls because of the associated risk of agranulocytosis. Antipsychotic drugs are only partially effective in controlling psychotic symptoms. Up to 30% of patients on maintenance drug treatment relapse within two years3 -- this is not entirely explained by poor compliance. A third or more of schizophrenic patients taking antipsychotic drugs continue to experience delusions and/or hallucinations, usually in attenuated form.4,5 Therefore, when psychotic symptoms persist after two or more antipsychotic drugs have been taken (separately), in adequate doses, for a cumulative total of 12 months, measures other than drug treatment are necessary. Firstly, factors that may be contributing to persistent symptoms (e.g., drug or alcohol abuse, relationship problems) should be identified and dealt with if possible, usually by a specialist. Secondly, where appropriate, effective non-pharmacological treatment strategies should be added to a suitable drug regimen. Several individual psychological (e.g., cognitive behaviour therapies) and family-oriented (e.g., training in problem-solving skills) interventions are available. These require specialist expertise, and GPs can be instrumental in locating appropriate providers of these treatments. With very few exceptions, only one antipsychotic drug should be used at a time. The dose should be the minimum required to maintain remission, and side effects should be absent or minimal. Excessive doses of antipsychotic drugs augment negative symptoms, impair cognitive function, mimic depression, undermine compliance by causing dysphoria and discomfort, produce higher rates of side effects that contribute to stigmatisation by rendering the patient more conspicuous, and can cause irreversible complications (e.g., tardive dyskinesia). Overmedication also interferes with rehabilitation. GPs can monitor antipsychotic drug use to ensure that doses are not unnecessarily high. Doses of haloperidol greater than 10 mg per day (or the equivalent) are not currently justified and approximately half this amount is now recommended, even less for first psychotic episodes. Adjunctive medication (e.g., lithium, carbamazepine) should only be used on specialist advice. There is no role for long term use of benzodiazepines, although they can be useful adjuncts in acute episodes, particularly when sedating a patient in an emergency. Long term use of anticholinergic drugs for the treatment of drug-induced parkinsonism should be avoided as they may mask the signs of tardive dyskinesia and impair cognitive function. The relapse signature: Patients and their families should be encouraged to monitor the patient's symptoms in association with GPs and specialist services. Each patient is said to have a unique relapse "signature"6 -- a sequential emergence of symptoms and signs which herald an impending relapse. There is often a "window" of 2-4 weeks in which such early warning signs appear,6 signalling the need to increase doses of antipsychotic drugs to prevent relapse. GPs should review with patients their typical sequence of warning signs so that they can correctly interpret them and make timely adjustments to the drug regimen. Non-compliance with medication is inevitable at some stage in most patients' treatment. It is said that 80% of patients are non-compliant with medication 40%-80% of the time.7 Reasons for this include medication side effects, complex dosing schedules, stigma, lack of knowledge or false beliefs about medication, and poor insight or denial of illness.7,8 Some patients reason that stopping medication will signify they are not ill.8 Some patients may prefer the psychotic state, either because of certain rewards from being ill (secondary gain) or difficulties in coping with normal expectations and responsibilities.8 Non-compliance may occasionally be an attempt to assert control or a manifestation of rebellion. Dealing with non-compliance requires a good working relationship, incorporating sound education about the illness and its management. Keeping dosing schedules simple and eliminating side effects are important strategies. Asking about medication and reasons for non-compliance in a non-judgemental way will encourage disclosure. One useful strategy is to assume episodic non-compliance and openly regard each occasion as a learning opportunity for the patient. Involving the patient in drug management, including allowing limited self-regulation of doses,8 together with self-monitoring of symptoms, will benefit the patient. Simply resorting to depot medications undermines the patient's collaborative role in health care. Arranging for medication to be taken under supervision, which is fraught with potential conflict, or seeking legal means of enforcing drug administration (e.g., community treatment orders), should only be a last resort. Supportive therapy GPs, preferably in conjunction with specialist services, can provide supportive therapeutic relationships which predict good outcomes in schizophrenia.9 In general, realistic goals should be set, which include protecting vulnerabilities, minimising stress and strengthening adaptive capabilities.8 Initial supportive techniques of reassurance, explanation and the opportunity for airing emotion can progressively incorporate education about the illness and its management, clarification of patients' "relapse signatures", the role of medication, and attention to daily living skills, social and occupational functioning. Counselling by GPs can help patients learn simple stress management techniques, anxiety control strategies and problem-solving skills for coping with non-psychotic (e.g., social) anxiety and depression linked to relationship problems or stressful life events. GPs should supplement self-monitoring of symptoms by examining patients' mental state at each appointment. This includes assessment of the status of psychotic symptoms and, although it is important not to dwell excessively on these, GPs should not avoid asking such questions as: Do your beliefs about . . . continue to trouble you?; or Have you been hearing voices in the past few weeks? Are you able to ignore them? What have you found helpful when they occur? Patients with schizophrenia learn three kinds of palliative coping techniques to deal with psychotic and other symptoms:10 cognitive control (e.g., reappraisal, self-instruction, acceptance, manipulation of attention); behavioural control or the generation and implementation of action alternatives (e.g., increased or decreased activity, diversion, withdrawal from stimulation, altered arousal); and social support recruitment. They can be helped to identify their usual coping techniques, modify and extend them. GPs can encourage patients to practise these by imagining they have a particular symptom and then implementing an identified coping strategy. Such rehearsal of coping skills may facilitate their successful transfer to everyday settings. Families of schizophrenic patients need support and GPs can provide education, aided by various leaflets and other publications on schizophrenia which are now readily available. GPs can also provide explanation, reassurance, advice and the opportunity to air emotional distress (especially anger, shame, sadness and guilt). Specialist services can provide various forms of more specific family counselling and education on schizophrenia. Schizophrenia is usually a prolonged illness of relapses and remissions, but the eventual outcome is better than was previously thought -- most patients make a good long-term social recovery (i.e., improved social relationships and self-care abilities).11 The early years are crucial in determining the patient's ultimate level of function and substantial gains may take years to become apparent. Depression and suicide Depressive symptoms are common in schizophrenia, especially during recovery after an acute psychotic episode (postpsychotic depressive disorder). However, it can be difficult to distinguish between the almost ubiquitous low level depressive symptoms in schizophrenia and a major depressive syndrome that will require specific treatment. The negative symptoms of schizophrenia and the effects of antipsychotic drugs can both mimic depression. Nevertheless, discerning clinicians can diagnose a major depressive episode. A specialist referral to help confirm the diagnosis may be required. Depressive disorders in schizophrenic patients can be treated as for similar conditions in other patients, including the use of antidepressant medication. The risk of such drugs triggering relapse of schizophrenic symptoms is small. Major risks include the risk of suicide by overdose, and appropriate precautions should be taken to guard against this. A course of antidepressant drugs at recommended daily doses can be added to the antipsychotic drug regimen for 6-12 months, together with whatever psychotherapeutic assistance is indicated. Between 10% and 13% of schizophrenic patients commit suicide,12 mostly during the first 10 years of the illness. There are no reliable guidelines for predicting and preventing suicide in these patients. The schizophrenic patient more likely to commit suicide is a young, single, unemployed, socially isolated man whose illness is marked by numerous exacerbations and hospital admissions for psychosis.12 He often has a past history of depression and/or attempted suicide, and perhaps a non-delusional, demoralising awareness of his deterioration, which is particularly acute if he has previously had some higher education and realises that his family's expectations and his own ambitions are unlikely to be fulfilled. Sensitive enquiry may reveal considerable underlying emotional distress with depressive symptoms, accompanied by feelings of hopelessness and inadequacy. If a GP recognises something like this pattern in a patient, then a thorough assessment should be undertaken and an urgent specialist referral should be made if the GP is concerned about the patient's risk of suicide. Alcohol and drug abuse In an Australian sample of 194 patients, we estimated that the six-month prevalence of alcohol or drug abuse or dependence in schizophrenic patients treated by community mental health services was 26.8% and the lifetime rate was 59.8% (unpublished data). Apart from tobacco and caffeine, the commonest substance abused was alcohol, followed by cannabis and amphetamines. Up to 74% smoked cigarettes and 40% smoked more than 40 cigarettes daily; 17% consumed more than 600 g of caffeine daily. Substance abuse in schizophrenia is increasing,13 is more common in young men with antisocial characteristics, and has been linked to poor compliance with treatment, increased hospital admissions, depression, suicide, assaultive behaviour, instability of accommodation and homelessness. In addition, alcohol and cannabis have both been associated with increased positive symptoms of schizophrenia.14,15Detecting substance abuse in schizophrenia is the first priority. GPs should use non-judgemental enquiry to become thoroughly familiar with the patient's current and past pattern of drug use, including tobacco, caffeine and alcohol, gauging the quantity, frequency and context of use. An undetected alcohol or drug problem should be suspected in patients who respond poorly to treatment. If necessary, a referral can be made to mental health services with special therapeutic programs for psychiatric and substance abuse comorbidity. If alcohol or drug abuse is detected in patients during remission, even when no immediate adverse consequences are apparent, the GP should first attempt to determine the patient's reasons for using those substances. The patient can then be informed in a matter-of-fact way about their detrimental effects on schizophrenia and general health, highlighting the extent to which alcohol, cannabis and amphetamines worsen psychotic symptoms and lead to relapse. The difficulty is that this information may not match the selective recollection of patients, who may even report certain benefits from using drugs. It is preferable not to argue, but to point out that all substances, including therapeutic agents, have a certain "margin of safety" between desired effects and adverse consequences, but that the "margin of safety" for some drugs is much narrower than others. Having indicated that complete abstinence is the safest course of action, a harm minimisation approach can be negotiated as a satisfactory compromise. A series of short-term achievable goals can be identified in sequence, including aiming to control levels of consumption (including issues of safe needle use, where relevant), then moving on to goals for reducing consumption, incorporating strategies for preventing relapse and parting from the alcohol and drug culture. Simultaneously, the GP can attend to factors that may be contributing to the patient's substance use, including resolution of interpersonal and practical problems (e.g., money, accommodation), with the help of other agencies if necessary, and encourage the development of additional coping skills and the pursuit of other interests. Sexuality There are very few systematically collected data about sexual functioning of schizophrenic patients. Their fertility rates are increasing,16 and schizophrenic women can be at increased risk of sexual exploitation and abuse.17 For patients with schizophrenia, sexual fulfilment contributes to self-esteem and well-being, and psychosexual function and capacity for intimacy are important prognostic factors. However, antipsychotic drugs can interfere with sexual activity and inappropriate sexual behaviours caused by the illness can lead to ostracism and loneliness. GPs should enquire about patients' relationships, sexual behaviours, sexual orientation, knowledge of sexuality and reproduction, need for contraception, and understanding of safe-sex practices. It can also be helpful to ascertain whether the patient experiences any sexual dysfunction, which is common,18 but not always due to medication, and ensure that the patient is informed about sexually transmitted diseases where necessary. Specific interventions may be appropriate. Physical health Patients with schizophrenia often have high rates of concurrent physical illness,19,20 especially cardiovascular and respiratory diseases.21 Among the risk factors for physical ill-health are smoking, alcohol and drug use, antipsychotic drugs, poor nutrition and hygiene, obesity, sedentary lifestyle, poverty and social isolation. Schizophrenic patients should be examined six-monthly for side effects and complications of antipsychotic drug use. Akathisia can be detected by observing the patient at rest, both seated and standing, and asking whether there are any subjective feelings of restlessness (especially in the legs)22 which may be present in the absence of objective signs. Observations of gait and posture will enable the characteristic tremor and bradykinesia of parkinsonism to be detected, while passive flexion and extension of the upper limbs will reveal cog-wheel rigidity.23 Examination for tardive dyskinesia can be conducted using the readily available Abnormal Involuntary Movement Scale (AIMS), which facilitates detection and quantification of the variety of orobuccal and choreoathetoid limb movements possible in this condition.24 Parkinsonism and akathisia should be dealt with by a reduction in the dose of antipsychotic drugs or by changing to a lower-potency drug. Anticholinergic agents should only be used in the short term for parkinsonism and are ineffective for akathisia; the latter can sometimes be controlled with propranolol. There is no effective treatment for tardive dyskinesia and decisions about its management should be made in consultation with a psychiatrist or other specialist. Patients over the age of 40 require an annual physical (and dental) examination, including measurement of blood pressure, examination of the cardiovascular and respiratory systems and skin, assessment of drug side effects, and urinalysis.25 This can also provide an opportunity for a systems review to help detect symptoms which patients may not report spontaneously. Thyroid function, full blood count and erythrocyte sedimentation rate should be determined. Vision and hearing can be checked, and a chest x-ray and electrocardiogram ordered25 if there is any indication of cardiovascular or respiratory disease. Breast examination and Pap smear in women should be performed as indicated for the general female population. Conclusion Although the long-term treatment of schizophrenia is multimodal and multidisciplinary, GPs are in a position to take an active, even central, role in the care of patients with this illness. Models of "shared care" for schizophrenia involving GPs as integral members of the treatment team are just beginning to be established. If they live up to their promise they will provide significant improvements in the comprehensive care of schizophrenic patients. To function effectively in this context most GPs will require some initial training and continuing education. Acknowledgements I am grateful to Associate Professor Patrick McGorry and Drs Peter Hopkins, Brian Masters, Steve Robinson and Tony Ryan for their comments on earlier drafts of this paper. References Keks NA, Kulkarni J, Copolov DL. Treatment of schizophrenia. Med J Aust 1989; 151: 462-467. Kane JM. Schizophrenia. N Engl J Med 1996; 334: 34-41. Davis J. Overview: maintenance therapy in psychiatry: I. Schizophrenia. Am J Psychiatry 1975; 132: 1237-1245. Silverstein ML, Harrow M. First-rank symptoms in the postacute schizophrenic: a follow-up study. Am J Psychiatry 1978; 135: 1481-1486. Johnstone EC, Owens DGC, Gold A, et al. Schizophrenic patients discharged from hospital: a follow-up study. Br J Psychiatry 1984; 145: 586-590. Birchwood M, Macmillan F, Smith J. Early intervention. In: Birchwood M, Tarrier N, editors. Innovations in the psychological management of schizophrenia. Assessment, treatment and services. Chichester: John Wiley & Sons, 1992: 115-145. Van Kammen DP, Marder SR. Dopamine receptor antagonists. In: Kaplan HI, Sadock BJ, editors. Comprehensive textbook of psychiatry. 6th ed. Baltimore: Williams & Wilkins, 1995: 1987-2022. Fenton WS, McGlashan TH. Schizophrenia: individual psychotherapy. In: Kaplan HI, Sadock BJ, editors. Comprehensive textbook of psychiatry. 6th ed. Baltimore: Williams & Wilkins, 1995: 1007-1018. Frank AF, Gunderson JG. The role of the therapeutic alliance in the treatment of schizophrenia: relationship to course and outcome. Arch Gen Psychiatry 1990; 47: 228-236. Carr V. Patients' techniques for coping with schizophrenia: an exploratory study. Br J Med Psychol 1988; 61: 339-352. Harding CM, Zubin J, Strauss JS. Chronicity in schizophrenia: fact, partial fact, or artifact? Hosp Community Psychiatry 1987; 38: 477-485. Caldwell CB, Gottesman II. Schizophrenics kill themselves too: a review of risk factors for suicide. Schizophr Bull 1990; 16: 571-589. Cuffel BJ. Prevalence estimates of substance abuse in schizophrenia and their correlates. J Nerv Ment Dis 1992; 180: 589-592. Duke PJ, Pantelis C, Barnes TRE. South Westminster Schizophrenia Survey: alcohol use and its relation to symptoms, tardive dyskinesia and illness onset. Br J Psychiatry 1994; 164: 630-636. Linszen DH, Dingemans PM, Lentor ME. Cannabis abuse and the course of recent-onset schizophrenic disorders. Arch Gen Psychiatry 1994; 51: 273-279. Lane A, Byrne M, Mulvany F, et al. Reproductive behaviour in schizophrenia relative to other mental disorders: evidence for increased fertility in men despite decreased marital rate. Acta Psychiatr Scand 1995; 91: 222-228. Darves-Bornoz JM, Lemperiere T, Degiovanni A, Gaillard P. Sexual victimization in women with schizophrenia and bipolar disorder. Soc Psychiatry Psychiatr Epidemiol 1995; 30: 78-84. Bhui K, Puffet A, Herriot P. A survey of sexual problems amongst psychiatric inpatients. Soc Psychiatry Psychiatr Epidemiol 1995; 30: 73-77. Brugha TS, Wing JK, Smith BL. Physical health of the long-term mentally ill in the community. Is there unmet need? Br J Psychiatry 1989; 155: 777-781. Honig A, Pop P, Tan ES, et al. Physical illness in chronic psychiatric patients from a community psychiatric unit. The implications for daily practice. Br J Psychiatry 1989; 155: 58-64. Vieweg V, Pandurangi A, Levenson J, Silverman J. Medical disorders in the schizophrenic patient. Int J Psychiatry Med 1995; 25: 137-172. Barnes TRE. A rating scale for drug-induced akathisia. Br J Psychiatry 1989; 154: 672-676. Simpson GM, Angus JWS. A rating scale for extrapyramidal side effects. Acta Psychiatr Scand 1970; 212 Suppl: 11-19. Kaplan HI, Sadock BJ, Grebb JA, editors. Kaplan and Sadock's synopsis of psychiatry: behavioural science, clinical psychiatry. 7th ed. Baltimore: Williams & Wilkins, 1994: 952. Burns T, Kendrick T. Schizophrenia. In: Pullen I, Wilkinson G, Gray DP, editors. Psychiatry in general practice today. London: The Royal College of Psychiatrists and the Royal College of General Practitioners, 1994: 194-208. Authors' details Discipline of Psychiatry, Faculty of Medicine and Health Sciences, The University of Newcastle, Newcastle, NSW. Vaughan J Carr, MD, FRANZCP, Professor of Psychiatry. Reprints: Professor V J Carr, Discipline of Psychiatry, Faculty of Medicine and Health Sciences, The University of Newcastle, Callaghan, NSW 2308. 1: Practical guidelines for specific aspects of primary care for patients with schizophrenia Pharmacological treatment Antipsychotic drugs should be chosen after considering their relative side effects. Use only one antipsychotic drug at a time When symptoms persist despite compliance, consider non-pharmacological strategies Use minimum dose required for maintaining remission and avoiding side effects Monitor symptoms: identify relapse signature Explore reasons for non-compliance and regard as a learning opportunity Encourage patient's role as a collaborator Supportive therapy Develop a supportive therapeutic relationship within which you: Set realistic goals Educate both patient and family Encourage symptom self-monitoring and coping skills Depression and suicide Depressive symptoms are common in schizophrenia. Treat as in other patients, with antidepressant drugs if necessary Consider risk of suicide Refer to specialist if necessary Alcohol and drug abuse Substance abuse is highly prevalent in schizophrenia, and has adverse effects on the course of the illness. Routinely enquire about substance use Strongly suspect if treatment response is poor Inform patient of adverse effects, and negotiate harm minimisation through short-term goals Refer to specialist if necessary Sexuality Normal sexual functioning can be affected by the illness and by antipsychotic medication. Discuss contraception Discuss safe sexual practices Try to ascertain any sexual dysfunction Physical health Schizophrenic patients have many risk factors for and high rates of concurrent physical disease. Examine six-monthly for side effects and complications of antipsychotic drugs Do a physical check annually for patients over 40 Back to text

Vaughan J Carr

In light of the emphasis on community care for schizophrenia and the increasing role likely to be played by general practitioners, this paper describes some of the general principles involved in the treatment of this disorder and provides a set of practical guidelines to assist general practitioners. Vaughan J Carr Introduction - Understanding the disorder - Symptoms - Early detection of psychosis - Diagnosis - Establishing a working relationship - Practice issues - Liaison with mental health agencies - Involuntary admissions - Conclusion - Acknowledgements - References - Authors' details - - More articles on Psychiatry This is part one of a two-part series. The second article appears in the MJA 3 February 1997 issue. Introduction Awareness of the importance of the general practitioner (GP) in the treatment of schizophrenia1-3 is growing. Factors contributing to this include continuing deinstitutionalisation (begun in the 1950s); the discovery in the 1960s and 1970s that GPs were the major providers of community psychiatric care;4,5 and the development of innovative community mental health service models in the 1980s,6,7 with recent efforts to integrate GPs into them.1,8Psychiatry texts suitable for assisting GPs in treating schizophrenic patients9,10 do not provide comprehensive practical guidelines for primary care. The two papers* in this series are intended to help fill this gap until specific primary care research provides more knowledge. Understanding the disorder Schizophrenia can be viewed in terms of a "vulnerability-stress" model,11 within which it manifests as a result of interactions between a biopsychological predisposition and environmental stress (see Figure). Vulnerability to schizophrenia is determined by premorbid risk factors, while environmental stressors are destabilising factors.12,13 For a given vulnerability-stress interaction, moderating influences may alter the illness threshold, thereby determining the occurrence of episodes of illness. Protective factors raise this threshold and perpetuating factors lower it. Treatment for schizophrenia is multimodal: antipsychotic medication and learned palliative coping techniques act on the underlying vulnerability; social support and instrumental coping (coping behaviours in relation to external rather than internal or disease-related events) help in adaptation to potentially stressful life events; and family interventions and rehabilitation strategies can augment protective factors or counter perpetuating influences. Symptoms Symptoms of schizophrenia are currently considered in three groups.14 These are: psychotic, or positive, symptoms (delusions and hallucinations); negative symptoms, representing loss of normal functions (flat affect, alogia, apathy, anhedonia-asociality and inattentiveness); and disorganisation symptoms (bizarre or disorganised behaviour, disjointed speech or formal thought disorder, incongruous affect). Schizophrenic patients often have other, traditionally non-schizophrenic, symptoms such as depression, anxiety, somatisation, phobias, obsessions, compulsions, and post-traumatic stress symptoms. Early detection of psychosis The longer psychotic symptoms go untreated, the worse the outcome.15-17 Therefore, early detection and treatment with antipsychotic drugs is crucial.17 Many patients who experience incipient psychotic symptoms consult their GP for some reason, placing the GP in a prime position to identify the problem early and make a prompt referral. There are two main facets to early detection: identifying individuals with prodromal symptoms before the emergence of frank psychosis; and recognising early or incipient psychotic symptoms.18,19Prodromal assessment: Schizophrenia cannot be diagnosed on the basis of prodromal symptoms alone because these are non-specific.20,21 They include impaired concentration, anxiety, depression, irritability, rebelliousness, social withdrawal, loss of interest or motivation, impaired function at school or work, deteriorating self-care, somatic complaints, restlessness, self-injury or suicide attempts, alcohol and drug abuse, emotional lability, and uncharacteristic aggression or poor impulse control. Also, it is important to note that the odd ideas or perceptions and peculiarities of speech or behaviour occurring in the prodromal stages of schizophrenia may also occur in normal adolescents.21 In schizophrenia, such phenomena may be present for two years or more, although usually not longer than 6-12 months, before the onset of psychotic symptoms.15,22 If such non-specific problems occur in an adolescent or young adult, they should be taken seriously, the possibility of schizophrenia kept in reasonable perspective, and the patient referred for psychiatric assessment with a letter detailing the main findings. While such an assessment in the prodromal phase may be inconclusive, it can be useful because, firstly, a positive encounter with a psychiatrist or mental health team establishes an important contact that can be resumed in the future. Secondly, the GP can provide ongoing support to the patient and family while diagnostic uncertainty prevails by acknowledging the problems identified and helping to implement any recommendations made by specialist services. Dismissing the problem ignores and invalidates the family's experience and may foster denial and thereby delay reassessment and hence eventual diagnosis and treatment. Thus, a useful short term measure may be a supportive counselling approach incorporating simple problem-solving strategies. Thirdly, it is important to monitor progress carefully in repeated clinical assessments, enlisting the cooperation of both patient and family, so that significant clinical change can be detected swiftly. Early psychotic symptoms: GPs are generally better able to detect psychiatric problems if they have good rapport with their patients, an interest in psychosocial problems, the ability to convey interest and concern, and good interviewing skills.23-25 The latter include appropriate eye contact, empathic responsiveness to cues of emotional distress, attentive posture, listening with few interruptions, an unhurried style, and the capacity to ask directive questions of a psychosocial nature. If indicated, GPs should ask, matter-of-factly and without embarrassment, a set of questions designed to elicit psychotic phenomena. For example: Do you hear noises or voices when there is no-one speaking or nothing to explain what you are hearing? What do they say? How many are there? Do they seem to be having a conversation among themselves about you?; or Do you have experiences that no-one else thinks are true, such as feeling you are under the control of some person or force that you can't explain, believing that the radio or TV are referring to you, thinking that others can read your mind, suspecting that someone is trying to hurt you?; or Is there some interference with your thinking such as thoughts being put into your head which are not your own, feeling that your thoughts are broadcast aloud so that other people can hear what you are thinking, feeling that thoughts are being taken out of your head against your will?. Patients experiencing their first early psychotic symptoms may deny or conceal such experiences. However, if asked these questions in the context of a confiding relationship, they may be able to acknowledge them for the first time. More harm is probably done if such symptoms persist undetected and untreated than would occur by asking about them in their absence. Having detected a possible new case of schizophrenia, referral to a psychiatrist or mental health service is imperative. While prolonged delays in the referral process are unacceptable, time should be taken to discuss the reasons for and purpose of the referral with the patient and efforts made to identify a psychiatrist or clinical service team suitable for the individual concerned. Diagnosis The diagnosis of schizophrenia is a specialist task. The current emphasis on detecting the earliest phase of onset of persistent psychotic symptoms -- for which antipsychotic drugs are indicated -- means that treatment may be initiated before a firm diagnosis can be made. Waiting for a confident diagnosis risks a poorer outcome. In general, psychiatric diagnoses are provisional hypotheses that may need revision as new information comes to light. Schizophrenia is particularly difficult to diagnose as there are several conditions that may mimic it and the pattern of psychotic symptoms tends to be relatively unstable early in the course of the illness.26-28For all these reasons, GPs should remain wary of a diagnosis of schizophrenia, even when long "established". If response to treatment is poor or the patient seems particularly sensitive to the adverse effects of treatment, a reappraisal of the diagnosis, including specialist reassessment, should be considered. Establishing a working relationship The cornerstone of successful treatment of schizophrenia is a good working relationship with the patient that embodies the principle of personal continuity of care over time.29,30 This is rarely possible in public mental health services and is not adequately provided by multidisciplinary teams. The GP, by providing long-term personal continuity of care,31 can fill this important gap in the patient's treatment even while the patient remains under the care of a community mental health team. If there is no well developed relationship between patient and GP before the onset of psychosis, one can be developed during the several 10-15-minute consultations per year which these patients tend to have with their GPs for renewal of prescriptions and other medical matters;6,32 the interview skills referred to previously are required. A trusting atmosphere can thus develop and be used as a basis for supportive therapy. Patients should be treated as autonomous adults, capable of mature decision-making and able to adopt a rational approach to the illness and its treatment. Fostering a collaborative partnership between patient and doctor for the joint management of the illness helps to counter the low self-esteem and lack of confidence that usually follows the experience of psychosis. Practice issues General practices should have a register or system for identifying the records of patients with schizophrenia31 to ensure regular reviews of patient progress, just as with diabetes or other chronic physical diseases. This also assists in auditing quality of care and patient outcomes. Management protocols for common problems in treating schizophrenia can be developed based on the case register. For example, missed appointments by schizophrenic patients are likely to portend relapse, deterioration in functioning, depression, suicidal preoccupations or an episode of drug or alcohol abuse. The management protocol could include having receptionist staff first notify the GP of a missed appointment, followed by telephone contact, home visit, or notifying the patient's community mental health team. It would also serve the patient's interests if the management protocol had the flexibility to handle unscheduled appointments -- frontal lobe impairments can make it difficult for schizophrenic patients to plan ahead or to appreciate the need to make appointments, and they may simply turn up unexpectedly. Also, in group practices, one GP should be identified as the primary care provider for a particular patient to facilitate the personal continuity of care. A standard record-keeping format with a checklist of items individually tailored for each patient may help to ensure that important clinical matters are not overlooked. Liaison with mental health agencies Close liaison between GPs and mental health services is crucial for the successful community treatment of schizophrenia by GPs. Well established lines of communication with the patient's psychiatrist or case manager are essential. Versions of the "shared care" model can provide practical support for GPs and facilitate their integration with mental health services in caring for schizophrenic patients. Divisions of general practice could be further encouraged to develop patterns of providing mental health care using innovative models of this kind. Involuntary admissions For acutely psychotic schizophrenic patients for whom involuntary hospitalisation may be indicated under the relevant mental health act, a coordinated approach involving the GP and the local mental health outreach team is the preferred option. If such a service is not available, the GP will first need to determine whether the patient's behaviour represents an immediate and substantial danger to others (e.g., presence of a weapon, demonstrably violent actions). In dangerous situations, GPs should first protect themselves and other people. The police should be involved if physical containment of the patient (including whatever restraint can be humanely applied using a minimum of force) is necessary. Only when the situation has been rendered reasonably safe should the GP venture to speak to the patient. If there is no immediate danger, the GP should approach the patient in a calm, non-threatening manner, avoiding confrontation, and conduct an interview in a safe place with whatever privacy is feasible, but with adequate assistance at hand.33 This can be provided by ambulance officers, medical or paramedical personnel and other responsible individuals. In either case, having interviewed the patient long enough to confirm, using whatever additional information is available from others, that the patient's condition meets the criteria for involuntary admission, then the GP should arrange that promptly according to the relevant mental health act. The patient should be informed of this and the legal status of the order explained simply and directly. Patients should be taken to hospital by ambulance (rather than police car) under appropriate supervision; this is both safer for patients, especially if sedated, and also underlines the medical nature of the problem. Police officers should accompany the patient in the ambulance if continued restraint is necessary. Transport by police vehicle should be avoided as it is invariably traumatising for the patient and conveys an entirely wrong message to the patient as to the nature of the situation. Sedating an involuntary patient in the community before transport to the hospital should be avoided if possible, as it may interfere with subsequent diagnostic assessment. However, sedation is clinically indicated (although the legality varies from State to State) for patients thought to be at high immediate risk of injuring themselves or others, who require restraint to enable transportation, or if transportation is likely to be of long duration.34 The patient may need to be restrained first or, alternatively, may accept medication on being confronted by the persuasive presence of enough people. Sedation can often be achieved by giving chlorpromazine (100 mg) or diazepam (10-20 mg) orally; severely agitated psychotic patients may require diazepam (10-20 mg, orally) together with haloperidol (5-10 mg, orally). Suitable parenteral medications include intramuscular injection of droperidol or haloperidol (5-10 mg) and/or midazolam (2.5-5 mg).34 If a high potency antipsychotic drug is administered parenterally, it should be accompanied by benztropine (2 mg, intramuscularly) to avoid serious acute dystonic reactions like laryngeal dystonia. Intramuscular injection of chlorpromazine is always contraindicated as it can cause an injection abscess, while that of diazepam is unsuitable because rates of absorption vary. Conclusion Today's GPs are well positioned to play a major role in the early detection of schizophrenia. Given the importance of early detection in successful treatment, the alert GP can have a considerable impact on the course of this illness. This contribution continues beyond the initial stages of the illness as GPs can help to optimise treatment and improve clinical outcome by providing personal continuity of care, maintaining close liaison with other mental health agencies, and making specific provision for schizophrenic patients using clinical practice registers and management protocols, as well as confidently handling emergencies. Practical recommendations are summarised in the Box. More specific issues will be covered in a subsequent article in the Journal. Acknowledgements I am grateful to Associate Professor Patrick McGorry and Drs Peter Hopkins, Brian Masters, Steve Robinson and Tony Ryan for their comments on earlier drafts of this paper. References Falloon IRH, Shanahan W, Laporta M, Krekorian HAR. Integrated family, general practice and mental health care in the management of schizophrenia. J R Soc Med 1990; 83: 225-228. Wilkinson G. The role of primary care physicians in the treatment of patients with long-term mental disorders. Int Rev Psychiatry 1991; 3: 35-42. Kendrick T, Burns T, Freeling P, Sibbald B. Provision of care to general practice patients with disabling long-term mental illness: a survey in 16 practices. Br J Gen Pract 1994; 40: 301-305. Shepherd M, Cooper B, Brown AC, Kalton G. Psychiatric illness in general practice. London: Oxford University Press, 1966. Goldberg DP, Kay C, Thompson L. Psychiatric morbidity in general practice and the community. Psychol Med 1976; 6: 565-569. Stein LI, Test MA. Alternative to mental hospital treatment. I. Conceptual model, treatment program, and clinical evaluation. Arch Gen Psychiatry 1980; 37: 392-397. Hoult J. Community treatment of the acutely mentally ill. Br J Psychiatry 1986; 149: 137-144. Jackson G, Gater R, Goldberg D, et al. A new community mental health team based in primary care: a description of the service and its effect on service use in the first year. Br J Psychiatry 1993; 162: 375-384. Goldberg D, Benjamin S, Creed F. Psychiatry in medical practice. 2nd ed. London: Routledge, 1994. Pullen I, Wilkinson G, Wright A, Gray DP, editors. Psychiatry in general practice today. London: The Royal College of Psychiatrists and the Royal College of General Practitioners, 1994. Zubin J, Spring B. Vulnerability: a new view of schizophrenia. J Abnorm Psychol 1977; 86: 103-126. McGlashan TH, Hoffman RE. Schizophrenia: psychodynamic to neurodynamic theories. In: Kaplan HI, Sadock BJ, editors. Comprehensive textbook of psychiatry. 6th ed. Baltimore: Williams & Wilkins, 1995: 957-968. Fenton WS, McGlashan TH. Schizophrenia: individual psychotherapy. In: Kaplan HI, Sadock BJ, editors. Comprehensive textbook of psychiatry. 6th ed. Baltimore: Williams & Wilkins, 1995: 1007-1018. American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 4th ed. Washington, DC: American Psychiatric Association, 1994. Loebel AD, Lieberman JA, Alvir JMJ, et al. Duration of psychosis and outcome in first-episode schizophrenia. Am J Psychiatry 1992; 149: 1183-1188. Johnstone EC, Crow TJ, Johnson AL, MacMillan JF. The Northwick Park study of first episode schizophrenia: I. Presentation of the illness and problems relating to admission. Br J Psychiatry 1986; 148: 115-120. Wyatt RJ. Neuroleptics and the natural course of schizophrenia. Schizophr Bull 1991; 17: 325-351. McGorry P, Kulkarni J. Prevention and preventively oriented clinical care in psychotic disorders. Aust J Psychopharm 1994; 7: 62-69. McGorry P, Rosen A, Carr V, Pantelis C. Innovations in the treatment of psychosis. In: Andrews G, editor. Specialization in psychiatry. Proceedings of the 1993 Geigy Symposium. Sydney: CIBA-Geigy, 1994: 157-232. Jackson HJ, McGorry PD, Dudgeon P. Prodromal symptoms of schizophrenia in first-episode psychosis: prevalence and specificity. Compr Psychiatry 1995; 36: 241-250. McGorry PD, McFarlane C, Patton GC, et al. The prevalence of prodromal features of schizophrenia in adolescence: a preliminary survey. Acta Psychiatr Scand 1995; 92: 241-249. Beiser M, Erickson D, Fleming JAE, Iacono WG. Establishing the onset of psychotic illness. Am J Psychiatry 1993; 150: 1349-1354. Marks J, Goldberg D, Hillier V. Determinants of the ability of general practitioners to manage common mental disorders. Psychol Med 1979; 9: 337-353. Goldberg D, Steele JJ, Johnson A, Smith C. Ability of primary care physicians to make accurate ratings of psychiatric symptoms. Arch Gen Psychiatry 1982; 39: 829-833. Goldberg DP, Jenkins L, Millar T, Faragher EB. The ability of trainee general practitioners to identify psychological distress among their patients. Psychol Med 1993; 23: 185-193. McGorry PD. Paradigm failure in functional psychosis: review and implications. Aust N Z J Psychiatry 1991; 25: 43-55. McGorry PD, Copolov DL, Singh BS. Functional psychosis: the case for a loosening of associations. Schizophr Res 1990; 3: 221-234. Stanton MW, Joyce PR. Stability of psychiatric diagnosis in New Zealand psychiatric hospitals. Aust N Z J Psychiatry 1993; 27: 2-8. McGlashan T. Intensive individual psychotherapy of schizophrenia: a review of techniques. Arch Gen Psychiatry 1983; 40: 909-920. McGlashan T, Keats CJ. Schizophrenia: treatment process and outcome. Washington: American Psychiatric Press, 1989. Burns T, Kendrick T. Schizophrenia. In: Pullen I, Wilkinson G, Wright A, Gray DP, editors. Psychiatry in general practice today. London: The Royal College of Psychiatrists and the Royal College of General Practitioners, 1994: 194-208. Melzer D, Hale AS, Burns T, et al. Community care for patients with schizophrenia one year after hospital discharge. BMJ 1991; 303: 1023-1026. Hyman SE. Manual of psychiatric emergencies. 2nd ed. Boston: Little Brown, 1988. Victorian Drug Usage Advisory Committee. Psychotropic drug guidelines. 3rd ed. Melbourne: Victorian Medical Postgraduate Foundation Therapeutics Committee, 1995. Discipline of Psychiatry, Faculty of Medicine and Health Sciences, The University of Newcastle, Newcastle, NSW. Vaughan J Carr, MD, FRANZCP, Professor of Psychiatry. Reprints: Professor V J Carr, Discipline of Psychiatry, Faculty of Medicine and Health Sciences, The University of Newcastle, Callaghan, NSW 2308. Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company. Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/> Vulnerability Premorbid risk factors Family history of schizophrenia Perinatal complications Attention deflicts Impaired arousal modulation impaired social competence coping deficits Moderating influences Protective factors Social support Family problem-solving skills Medication compliance Perpetuating factors Social impoverishment Critical or emotionally overinvolved family Unemployment Alcohol or drug abuse Stress Acute Life events Recent physical illness Psychoactive drugs Chronic Ongoing family conflict Poverty Academic or work pressures Vulnerability-stress model of schizophrenia. Back to text Practical recommendations for primary care management of schizophrenic patients Early detection of psychosis Be alert for: 1. Prodromal symptoms Refer patient for psychiatric assessment Monitor patient's progress Support and counsel patient and family 2. Incipient psychotic symptoms Ask psychological probe questions Refer promptly to a psychiatrist or mental health service Diagnosis Is a specialist task, but remains provisional. Therefore: Remain prepared to revise the diagnosis Consider specialist reassessment if there are problems with treatment Working relationship Is based on personal continuity of care. Therefore: Develop a trusting relationship with the patient Treat the patient as an autonomous adult Foster collaboration with the patient in managing the illness Practice issues As patients with schizophrenia have special needs: Maintain a patient register Develop management protocols for problems such as missed appointments, and include flexibility to allow for unexpected behaviour Liaison with mental health agencies Is essential for successful community treatment of schizophrenic patients. Therefore: Maintain communication with the patient's psychiatrist or case manager Involuntary admissions The medical nature of these circumstances needs to be emphasised. Therefore: Work with a mental health team if possible First ensure safety of self and others (involve police if necessary) Use a non-threatening, non-confrontational approach to the patient Determine whether criteria for involuntary admission are present Follow procedures of local mental health act Clearly explain and inform the patient of his or her legal status Ensure supervised transport to hospital (preferably by ambulance) Sedation may be clinically indicated Back to text

Vaughan J Carr

Editorial The human element of adverse events Is a certain level of error inevitable in healthcare? MJA 1999; 170: 404-405 The Quality in Australian Health Care Study (QAHCS),1 together with the Harvard study on which it was based,2 were groundbreaking studies that for the first time systematically revealed the nature and scale of iatrogenic injury in healthcare. Morbidity due to healthcare appears to be a major public health problem, and it is very unlikely that this problem is confined to Australia and the United States. The QAHCS revealed particularly high levels of adverse events (AEs), in part because it took a broader, quality-of-care approach rather than one focused on negligence and compensation. In this issue of the Journal, review and content analysis of textual summaries of the AEs by Wilson et al, the QAHCS team, have now yielded a deeper understanding of these events.3 The major categories of human error, accounting for over 70% of AEs, were: Failures in technical performance; Failure to decide and/or act on available information; Failure to investigate or consult; and A lack of care or failure to attend. Do the failures identified by the QAHCS team imply carelessness and/or incompetence on the part of healthcare staff? On occasions this may be so, but research on human error paints a more complex picture.4 Tempting though it may be to simply blame the doctors and nurses, identifying a failure in the process of care is usually just the first step in understanding the causes of AEs. This is especially so when the failure occurs not in some routine procedure, but in complex diagnostic or technical tasks, in which the term "error" may be a misleading oversimplification.5 Should we therefore accept that a certain level of error is inevitable in healthcare? We certainly should not accept such high levels of iatrogenic injury, much of which is preventable. In one sense, though, it is necessary to accept error. Before there can be any serious hope of reducing AEs there must first be a recognition of the frequency of error and of imperfect decision-making in healthcare, as is the case in other human activities.6 The next step, as the QAHCS team argues, is to look beyond the immediate failures to their deeper causes.3 Analyses of accidents in medicine and elsewhere have led to a much broader understanding of the causes of AEs, with less focus on individuals and more on pre-existing organisational factors. The conditions which give rise to failures in the process of care can be considered in a broad framework of individual, task, team, work environment and organisational factors.7 A failure to consult, for instance, may be due to overconfidence in a junior member of staff, inexperience, inadequate knowledge, delay in obtaining test results, or the unavailability of senior members of staff. Each of these problems may be specific to that occasion or may reflect more general problems: the attitudes of individual members of staff, the training policies of the hospital, poor supervisory practices, inadequate and haphazard systems of communication or interpersonal problems within a team. The National Taskforce on Quality in Australian Health Care produced a comprehensive, multifaceted plan of action to reduce healthcare injuries and deaths.8 The Taskforce was surely correct to see both the problem and the solution as multidimensional, as the systems approach implies. Safety programs in industries, involving sociotechnical systems with many similarities to medicine, target the tasks, teams and conditions of work, as well as ensuring that staff are highly skilled.4 Safety needs to be addressed both at the level of the particular clinical process and at the interpersonal and organisational levels. Where tasks can be clearly specified, then greater standardisation, clear guidelines and less reliance on the vagaries of human memory and vigilance are essential. Team and communication failures have been strongly implicated in many accident analyses and remedial measures can be straightforward. Systems have also been developed in industry to monitor the conditions of work, as well as the associated organisational factors and decisions that give rise to these conditions. The Taskforce recommendations have been widely supported9 and a number of working groups have been established by Australian health departments. In 1997, a National Expert Advisory Group on Safety and Quality in Australian Health Care was established, and their recommendations will be considered by the Health Ministers later this year. In the 1998 Australian Health Care Agreements, $658 million was allocated for quality improvements within the public health system over five years, and a further $253 million for, among other objectives, improving the integration of public hospital and community services. Welcome though these initiatives are, the pace of change nevertheless seems slow given the stark message of the original QAHCS study four years ago. The findings from QAHCS suggested that each year 50 000 Australians suffer permanent disability and 18 000 die at least in part as a result of their healthcare. Further evidence emerged in 1997 with the publication of AE rates in Victorian hospitals.10 Since then, thousands more Australians have presumably been injured or died through deficiencies in the healthcare system. Furthermore, the QAHCS found that AEs lost Australia over three million bed-days per annum. In its interim report, the National Expert Advisory Group pointed out that the extrapolated potential saving from preventable AEs in 1995-96 would be $4.17 billion.11 AEs also lead to increased disability benefits and time lost off work, which all impact on the Australian economy. Achieving change on the required scale will require a specific commitment from all healthcare providers, administrators and consumers, as well as unequivocal, sustained government support. It is hoped that 1999 will see the necessary consensus for urgent action from all the parties involved and the implementation of specific, carefully evaluated safety initiatives. It would be tragic if the "lack of care and failure to attend" and "failure to decide and act", revealed as causes of AEs, ultimately also applied to those professional and government bodies responsible for programs of prevention. Charles A Vincent Reader in Psychology, Clinical Risk Unit, Department of Psychology University College London, UK Wilson RM, Runciman WB, Gibberd RW, et al. The Quality in Australian Health Care Study. Med J Aust 1995; 163: 458-471. Brennan TA, Leape LL, Laird NM, et al. Incidence of adverse events and negligence in hospitalized patients. N Engl J Med 1991; 324: 370-376. Wilson RMcL, Harrison BT, Gibberd RW, Hamilton JD. An analysis of the causes of adverse events from the Quality in Australian Health Care Study. Med J Aust 1999; 170: 411-415. Reason JT. Understanding adverse events: human factors. In: Vincent CA, editor. Clinical risk management. London: BMJ Publications, 1995. Cook RI, Woods DD, Miller C. A tale of two stories: contrasting views of patient safety. Report of the National Patient Safety Foundation. Chicago: American Medical Association, 1998. Leape LL. Error in medicine. JAMA 1994; 272: 851-857. Vincent CA, Taylor-Adams S, Stanhope N. A framework for the analysis of risk and safety in medicine. BMJ 1998; 316: 1154-1157. The Final Report of the Taskforce on Quality in Australian Health Care. Canberra: AGPS, June 1996. Wilson RM, Harrison BT. Are we committed to improving the safety of health care. Med J Aust 1997; 166: 452-453. O'Hara D, Carson NJ. Reporting of adverse events in hospitals in Victoria 1994-1995. Med J Aust 1997; 166: 460-463. National Expert Advisory Group on Safety and Quality in Australian Health Care. Interim report - Commitment to quality enhancement. July 1998. <http://www.health.gov.au/about/cmo/neag.htm> Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/> We appreciate your comments.

Charles A Vincent

Research An analysis of the causes of adverse events from the Quality in Australian Health Care Study Ross McL Wilson, Bernadette T Harrison, Robert W Gibberd and John D Hamilton MJA 1999; 170: 411-415 For editorial comment, see Vincent Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Administration and health services The Quality in Australian Health Care Study (QAHCS), published in the Journal in 1995,1 reported that 16.6% of hospital admissions were associated with an iatrogenic patient injury, termed an adverse event (AE) (see Box 1). This compares with the rate of 3.7% for AEs in the Harvard Medical Practice Study (HMPS),2 and a rate of 17% in a more recent study with an alternative observational method of determining AEs.3 Fifty per cent of the AEs in the QAHCS were judged to have a high preventability score (4 or more on a scale of 1-6 of increasing likelihood of preventability).1 The disability caused by these adverse events ranged from temporary disability (fully resolved in one month) in 46.6% of AEs, to death in 4.9% of AEs. Although recording AEs emphasises only the "complications" of rather than the benefits derived from healthcare, AEs are of great significance to individual patients as well as to the whole healthcare system. Abstract Objective: To examine the causes of adverse events (AEs) resulting from healthcare to assist in developing strategies to minimise preventable patient injury. Design: Descriptions of the 2353 AEs previously reported by the Quality in Australian Health Care Study (QAHCS) were reviewed. A qualitative approach was used to develop categories for human error and for prevention strategies to minimise these errors. These categories were then used to classify the AEs identified in the QAHCS, and the results were analysed with previously reported preventability and outcome data. Results: 34.6% of the causes of AEs were categorised as "a complication of, or the failure in, the technical performance of an indicated procedure or operation", 15.8% as "the failure to synthesise, decide and/or act on available information", 11.8% as "the failure to request or arrange an investigation, procedure or consultation", and 10.9% as "a lack of care and attention or failure to attend the patient". AEs in which the cause was cognitive failure were associated with higher preventability scores than those involving technical performance. The main prevention strategies identified were "new, better, or better implemented policies or protocols" (23.7% of strategies), "more or better formal quality monitoring or assurance processes" (21.2%), "better education and training" (19.2%), and "more consultation with other specialists or peers" (10.2%). Conclusion: The causes of AEs or errors leading to AEs can be characterised, and human error is a prominent cause. Our study emphasises the need for designing safer systems for care which protect the patient from the inevitability of human error. These systems should provide new policies and protocols and technological support to aid the cognitive activities of clinicians. Introduction An additional analysis of data from the Quality in Australian Health Care Study (QAHCS)1 was undertaken in order to understand more fully the causes of the adverse events (AEs) identified and to assist in developing prevention strategies. Here, we describe the error or errors in the delivery of healthcare which led to the AEs. This contrasts with our previous report,1 which focused on the patient characteristics associated with AEs and the nature and consequences of the AEs. Methods The method of determining AEs in the QAHCS has been described previously.1 The AEs were re-examined with the specific goals of determining the causes for, or the underlying errors leading to, each AE. In addition, strategies that were judged to have the potential to prevent AEs were recorded. To obtain this information the first and subsequent review forms (RF1 and RF2 forms1) collected during the QAHCS were re-examined. The source material for these forms had been the hospital medical records, but neither the hospitals nor the medical records were revisited in this analysis. Categories for the causes of the AEs were devised by an iterative process during a three-day workshop. For this, we sought additional expertise in clinical epidemiology and qualitative research methods. Using these categories, the AEs recorded on the review forms were assessed by three of the senior medical specialists who had originally reviewed the medical records in the QAHCS. All the material from each AE was reviewed by only one reviewer, as the agreement between the medical reviewers in determining the presence or absence of an AE during the QAHCS was 80% (kappa, 0.55). A proforma was completed which asked the reviewer to identify the error and then classify it by human cause and preventive strategy. All AEs were also categorised into some of the processes of clinical care. Results for the "delay", "treatment" and "investigation" categories are presented. The categories were not mutually exclusive. These data were then entered into a database, merged with the original data from the QAHCS for each case and analysed. Two of the original total of 2353 AEs were missed in this review; thus, results are given for 2351 AEs. Our analysis provides the frequency of occurrence of each of the categories of causes of AEs, together with the proportion in each category resulting in permanent disability (including death) and the proportion with high preventability. Results Human error categories Box 2 shows the frequency of occurrence of each of the human error categories, and the proportion of the AEs in each category judged to have permanent disability and high preventability. Of the 2351 AEs, 1922 (81.8%) were associated with one or more human error categories. As the error categories were not mutually exclusive, the 1922 AEs were associated with 2940 causes. "Complication of, or failure in, the technical performance of an indicated procedure/operation" was the most frequent cause of AEs; examples of this category are shown in Box 3A. Human errors associated with categories of failure of cognitive function were the next most frequent cause of AEs (Box 2). These included "Failure to synthesise, decide and/or act on available information", "Failure to request or arrange investigation, procedure or consultation", and "Misapplication of, or failure to apply, a rule; or use of a bad or inadequate rule". The most frequent error category, "complication of, or failure in, the technical performance of an indicated procedure/operation", had a lower proportion of AEs with permanent disability (14.2%). The next five most frequent human error categories all had a high proportion of AEs with permanent disability (25% or more) (Box 2). This pattern was also seen in the proportions of AEs with death as the outcome: 2.2% in the first category, and 8% or more in each of the next five categories. Of the 1201 AEs having high preventability, 9 (0.7%) were not associated with a human error category; for the remaining 1192 AEs, 2051 causes were identified (Box 2). Delay categories The importance of timeliness to the quality of healthcare led to further analysis of all AEs to ascertain the nature and role of delay in their causation (Box 4A). Delays contributed to 20.0% of AEs: of these, delays in diagnosis accounted for 56.8% and treatment delays for 40.6%. Diagnostic delay was usually the failure to make, or attempt to make, a diagnosis of a patient's condition rather than just providing symptomatic or even no treatment. Treatment delay was when the diagnosis had been made but there was a delay in initiating specific therapy. Examples of AEs in the delay category are included in Box 3B. The AEs with delay categories were judged to have very high preventability (86%-90%) compared with the average (51.2%) for all AEs (Box 4A). Treatment categories AEs categorised as caused by a treatment error were also analysed (Box 4B). In 19.6% of all AEs, treatment error contributed to the cause. The majority of AEs in this group fell into the categories of "no or inadequate treatment" (51.5%), or "wrong or inappropriate treatment" (27.4%). As with AEs caused by delay, these AEs were judged to have much higher preventability than the average for all AEs. Examples of AEs involving treatment errors are shown in Box 3C. Investigation categories Analysis of the AEs caused by patient investigation issues is shown in Box 4C, and examples are given in Box 3D. There was a problem with clinical investigation in 10.7% of AEs. Paralleling the results in the treatment category, most (78.6%) of these AEs were in this category because an investigation was not done, rather than the investigation being inappropriate (3.6%), or not acted upon (15.5%). Consistent with other AEs that are attributed to cognitive failure, there was a very high percentage of these AEs rated as high preventability. Strategies for preventing AEs When describing AEs, preventability refers to the identification of an avoidable error that led to the adverse event. This is not to say that the error could be avoided on every occasion, and that the adverse event would not occur. Rather, it implies that, with the current state of knowledge and technology, it is possible to identify and avoid that particular error, and hence reduce the probability of an AE. The reviewers were making a judgement, having identified the error, on the particular strategy for a change in the healthcare system that could have prevented the AE. The outcomes of these judgements are given in Box 5. Nineteen (1.6%) of the 1201 high preventability AEs did not have a prevention strategy category. Of the 2613 prevention strategies identified in the 1182 AEs with high preventability, 24.7% (646) were for "better education and training", 20.9% (545) were for "new or better implemented policies or protocols" and 18.6% (486) were for "more or better formal quality monitoring or assurance processes". Discussion AEs are important to patients, healthcare providers and to the custodians and funders of health services. One estimate of the national cost to the Australian healthcare system of just the additional hospital bed-days (as a result of the AEs identified in 19921) is in excess of $800 million dollars per year.4 This estimate ignores any subsequent hospital admissions and out-of-hospital healthcare expenses, loss of productivity of the patients involved, and long term community costs of permanent disability from AEs. It also ignores the benefits received from healthcare. Providing insights into how AEs occur can help in developing prevention strategies to reduce the frequency and severity of patient injuries during healthcare. Our review and analysis of the AE data from the QAHCS have shown that the causes of AEs or errors leading to AEs can be characterised, and that human error is a prominent cause. It is important to recognise that human error is inevitable for even the best-trained and best-qualified healthcare providers. Weed has recently pointed out that the unaided human mind is incapable of performing consistently at the necessary level to provide optimal healthcare.5 However, other studies6 have noted that the label "human error" is prejudicial and non-specific; it may retard rather than advance our understanding of how complex systems fail. It is postulated that within complex systems error is a symptom of organisational problems, and this is likely to apply to healthcare. Therefore, we need a healthcare-system response to error that moves the system towards being as "failsafe" as possible rather than one that blames the clinician who may have erred. Examples from the more frequently studied area of adverse drug events7 would be decision-support technology for antibiotic prescribing,8 with its demonstrated benefits, and electronic prescribing to reduce prescribing and transcription errors in hospital.9 Our analysis identified broad functional categories that are linked to the processes that make up the system of healthcare delivery and hence cut across specialties, diagnosis-related groups (DRGs) and particular patient groups. The sample size is large enough to provide useful information even when several AEs could not be classified into the categories chosen, or insufficient information was available to indicate cause. On the other hand, several factors bias the information available for assessing AEs because of an emphasis on procedures and short term outcomes and possible under-reporting of the contribution of the supporting systems to the cause of the AEs. Firstly, because the original data source was the hospital medical record, the information available about AEs is biased towards the patient involved and away from other potentially important contextual events at the time. Further, the medical record often focuses more on the actions of clinicians involved in direct or procedural patient intervention, and less on the actions of other staff or systems with a more supportive role. These and other factors will lead to an emphasis on procedures and short term outcomes, and a possible under-reporting of the contribution of supporting systems in causing AEs. Finally, information about subsequent or prior hospitalisations is usually only available if the patient attended the same hospital on all occasions. Having acknowledged these potential limitations, cognitive failure (Box 2) appears to have a role in 57% of all the causes of AEs, and most of the AEs involved were judged to be of high preventability and to have caused significant disability. These AEs were largely associated with errors of omission rather than commission. Does this represent a minimum "obligatory" error rate resulting from a combination of human error and our healthcare system, and hence which cannot be improved? Our data are not able to answer this question unequivocally, but we believe they show sufficient opportunities for moving the system towards a failsafe mode to suggest that the answer is no. Until recently there has been an under-recognition of the role and responsibilities of the healthcare system and its custodians in providing a "safe environment" using systems-improvement tools.10 One response to these data should be to look at the factors in healthcare delivery that may interfere with the cognitive or technical performance of healthcare providers. Insufficient use of information technology to assemble the necessary information at the time of decision-making may increase error. Another important factor is fatigue, which has already been shown to increase error in doctors.11 Sleep deprivation may have a much more significant role in human error in healthcare than the current work-load patterns pay heed to, but more research is needed. Other factors that may be important include the level of supervision provided to junior staff, and the pervasive effect of the culture of medical practice, which can unhelpfully portray error as individual failure or deviation from perfection.12 Our study method does not provide direct information about the role of these factors. The high proportion of causes of AEs involving cognitive failure must represent a manifestation of human error occurring in a system that is not patient protective, if one accepts that these practitioners are appropriately trained and competent by international standards. Our study provides clear guidance on methods for improvement, with "new, better, or better implemented policies or protocols" accounting for 24% of prevention strategies identified for the AEs, "quality monitoring and assurance processes" accounting for 21%, and "better education and training" for a further 19%. In summary, improvement is needed in the agreed processes of care, supported by information systems that allow general dissemination of current knowledge of diseases or treatments, and information on outcomes of care for each patient, through appropriate quality processes. Simple examples are the availability of practice guidelines and protocols at the point-of-care, and the use of automated reminders for patients and practitioners when a particular test or follow-up is required. In addition, having adequate patient "outcome" information in a form that can be benchmarked is a powerful tool in identifying unacceptable variation. Acknowledgements We acknowledge the contributions of Professor B Armstrong, Professor W R Runciman, Professor R Holland, Dr T Robertson and Dr A Hobbes. References Wilson RMcL, Runciman WB, Gibberd RW, et al. The Quality in Australian Health Care Study. Med J Aust 1995; 163: 458-471. <eMJA pdf> Brennan TA, Leape LL, Laird N, et al. Incidence of adverse events and negligence in hospitalised patients: results of the Harvard Medical Practice Study I. N Engl J Med 1991; 324: 377-384. Andrews LB, Stocking C, Krizek T, et al. An alternative strategy for studying adverse events in medical care. Lancet 1997; 349: 309-313. The Final Report of the Taskforce on Quality in Australian Health Care. Appendix 7. Canberra: AGPS, June 1996. <http://www.health.gov.au/pubs/hlthcare/toc.htm> Weed LL. New connections between medical knowledge and patient care. BMJ 1997; 315: 231-235. Cook RI, Woods DD. Operating at the sharp end: the complexity of human error. Human performance in anaesthesia: a corpus of cases. Report to the Anaesthesia Patient Safety Foundation, 1991. Columbus, Ohio: The Ohio State University: 255-307. Classen DC, Pestonick SL, Evans RS, et al. Adverse drug events in hospitalised patients: excess length of stay, extra costs and attributable mortality. JAMA 1997; 227: 301-306. Evans RS, Pestonick SL, Classen DC, et al. A computer-assisted management program for antibiotics and other anti-infective agents. N Engl J Med 1997; 338: 231-238. Bates DW, Boyle DL, Vander Vliet MB, et al. Relationship between medication errors and adverse drug events. J Gen Intern Med 1995; 10: 199-205. Leape LL. A systems analysis approach to medical error. J Eval Clin Pract 1997; 3: 213-222. Nocera A, Khursandi DS. Doctors' working hours: can the profession afford to let the courts decide what is reasonable. Med J Aust 1998; 168: 616-618. Leape LL. Error in medicine. JAMA 1994; 272: 1851-1857. (Received 4 May 1998, accepted 20 Jan 1999) Authors' details Royal North Shore Hospital, Sydney, NSW 2065. Ross McL Wilson, MB BS, FRACP, Senior Specialist in Intensive Care; Director of QARNS (Quality Assurance Royal North Shore); Bernadette T Harrison, RN RM, Manager QARNS. University of Newcastle, Newcastle, NSW 2308. Robert W Gibberd, PhD, Associate Professor, Department of Statistics; and Director of Health Services Research Group. John D Hamilton, MB BS, FRCP, Professor of Medicine, Faculty of Medicine and Health Sciences. Reprints: Dr R McL Wilson, Director of QARNS, Royal North Shore Hospital, Pacific Highway, St Leonards, NSW 2065. Email: rwilsonATdoh.health.nsw.gov.au Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/> 1: Terms and definitions Adverse event (AE): An AE was defined as an injury or complication which resulted in disability or prolongation of hospital stay and was caused by the healthcare received rather than by the disease from which the patient suffered. The AE either occurred during the hospital admission, or during an earlier contact with healthcare services, and was responsible for all or part of the hospital admission. Error: An act of commission or omission that caused, or contributed to the cause of, the unintended injury. for errors of commission this will usually be the immediate morbid consequences of the error for errors of omission this will usually be the continuation of, and consequences of, an existing morbid state that could have been cut short, or had a better outcome, if the error had not occurred. Prevention strategy: Changes in the system in which an error occurred that mayreduce the probability of the error occurring increase the probability that the error would be remedied before an unintentional injury occurredPreventability: Preventability of an AE was assessed by the detection of "an error in management due to the failure to follow accepted practice at an individual or system level"; accepted practice was taken to be "the current level of expected performance for the average practitioner or system that manages the condition in question". Back to textBack to text 3. Examples of categories of causes of adverse events and preventability scoresA. Human error categories Example 1: A 50-year-old man sustained a bowel perforation from colonoscopy for investigation of abdominal pain. Laparotomy required. Category: "Technical performance". Preventability score: 3. Example 2: A 71-year-old man required six operations for femoral hernia repair. Category: "Technical performance". Preventability score: 2. Example 3: A 32-year-old woman had persisting severe back pain after two laminectomies, three myelograms, one decompression/fusion, and three thecal/epidural injections over 18 months. In pelvic traction at the time of review. Category: "Technical performance". Preventability score: 4. Example 4: A failed attempt at percutaneous endoscopic gastrostomy on a 32-year-old woman was followed by an open procedure. The patient died 9 days later. Autopsy revealed acute peritonitis, subphrenic abscess and bilateral pneumonia. There did not appear to have been an antemortem diagnosis of intra-abdominal sepsis, or any specific treatment for it. Category: "Technical performance". Preventability score: 6. B. Delay in diagnosis and/or treatment categories Example 1: Diagnosis of cancer of the colon was delayed until the patient, a 62-year-old woman, presented with a ruptured caecum and peritonitis from an obstructing tumour. In hospital 3 months earlier with a history suggestive of cancer of the colon and iron-deficiency anaemia, but no investigation performed. Categories: Diagnosis delay, violation of protocol or rule; failure to synthesise, decide or act on available information; lack of care/attention. Preventability score: 5.5. Example 2: A 28-year-old man with abdominal pain was treated with cholecystectomy. Gallbladder was macroscopically and histologically normal. Small bowel lymphoma was eventually diagnosed and treated, with resolution of the presenting symptoms. Categories: Diagnosis delay; failure to synthesise, decide or act on available information; failure to request or arrange an investigation, procedure or consultation. Preventability score: 5. C. Treatment categories Example 1: A 52-year-old man with known asthma was prescribed a beta-blocker for hypertension. This resulted in acute respiratory failure leading to artifical ventilation and tracheostomy. Categories: Wrong or inappropriate treatment; misapplication of or failure to apply a rule; failure to synthesise, decide or act on information. Preventability score: 6. Example 2: A 54-year-old man developed gastrointestinal bleeding (haemoglobin level, 45 g/L) while receiving non-steroidal anti-inflammatory drugs and steroids for rheumatoid arthritis. This required hospital admission and blood transfusion, at which time the correct diagnosis of osteoarthritis was made. Categories: Wrong or inappropriate treatment; acting on insufficient information; failure to request or arrange an investigation, procedure or consultation. Preventability score: 5.5. Example 3: Hospitalisation and surgical intervention for septic arthritis that followed steroid injection into a joint. Categories: Unclassified treatment; technical; lack of care/attention. Preventability score: 4.5. D. Investigation categories Example 1: A 75-year-old woman died from acute renal failure after developing gentamicin toxicity. Gentamicin was used to treat an infected pleural effusion, and drug levels were not measured. Categories: Investigation not performed; failure to request or arrange an investigation, procedure or consultation; lack of care/attention. Preventability score: 5. Example 2: A 58-year-old woman had recurrent hospital admissions for chest pain and impaired cardiac function without specific investigation, and hence a reduction in treatment options. Categories: Investigation; violation of protocol or rule; failure to synthesise, decide and/or act on available information. Preventability score: 5. Back to text 4: Contribution of delay, treatment and investigation categories to adverse events (AEs). Values are number (%) of AEsPermanentHighA. Delay categoryFrequencydisabilitypreventabilityDiagnostic delay267 (56.8%)93 (34.8%)231 (86.5%)Treatment delay191 (40.6%)53 (27.7%)172 (90.1%)Administrativedelay12 (2.6%)3 (25.0%)11 (91.7%)Total470 (100%)149 (31.7%)414 (87.9%) B. Treatment categoryNo or inadequatetreatment237 (51.5%)72 (30.4%)176 (74.3%)Wrong/inappropriatetreatment126 (27.4%)35 (27.8%)96 (76.2%)No or inadequateprophylaxis41 (8.9%)9 (22.0%)34 (82.9%)Treatmentunclassified36 (7.8%)7 (19.4%)28 (77.8%)Missed treatment20 (4.4%)4 (20.0%) 16 (80.0%)Total460 (100%) 127 (27.6%)350 (76.1%) C. Investigation categoryInvestigationnot performed198 (78.6%)81 (40.9%)171 (86.4%)Investigationnot acted on39 (15.5%)13 (33.3%)36 (92.3%)Investigationinappropriate9 (3.6%)2 (22.2%)9 (100.0%)Investigationunclassified6 (2.4%)2 (33.3%)5 (83.3%)Total252 (100%)98 (38.9%)221 (87.7%)Back to text 5: Frequency of occurrence of categories of prevention strategies and the proportion of adverse events (AEs) judged as causing permanent disability or having high preventability. Values are number (%) of AEsPermanentHighCategoryFrequencydisabilitypreventabilityNew, better, or better implementedpolicies or protocols884 (23.7%)206 (23.3%)545 (61.7%)More or better formal quality monitoringor assurance processes790 (21.2%)186 (23.5%)486 (61.5%)Better education and training715 (19.2%)160 (22.4%)646 (90.3%)Consultation with other specialistsor peers391 (10.5%)133 (34.0%)294 (75.2%)Don't know341 (9.2%)51 (15.0%)186 (54.5%)Better access to, or transfer of, information135 (3.6%)40 (29.6%)100 (74.1%)Discharge procedures and protocols122 (3.3%)27 (22.1%)100 (82.0%)Other89 (2.4%)22 (24.7%)46 (51.7%)Changes in organisation management88 (2.4%)22 (25.0%)75 (85.2%)Changes in organisation culture77 (2.1%)26 (33.8%)66 (85.7%)More or better personnel72 (1.9%)29 (40.3%)53 (73.6%)More or better equipment or otherphysical resources22 (0.6%)8 (36.4%) 16 (72.7%)Total3726 (100%)*910 (24.4%)2613 (70.1%) * Total is greater than the number of AEs (2351) as the categories were not mutually exclusive. Back to text

Bernadette T Harrison · Robert W Gibberd · John D Hamilton

Healthcare Acupuncture in Australian general practice: patient characteristics Gary Easthope, Gerard F Gill, Justin J Beilby and Bruce K Tranter MJA 1999; 170: 259-262 For editorial comment, see Bensoussan See also Acupuncture in Australian general practice: practitioner characteristics Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Complementary medicine Abstract Objective: To ascertain the incidence of acupuncture claims and the characteristics of patients claiming for acupuncture. Design: Secondary analysis of Health Insurance Commission data on claims for acupuncture performed by a medical practitioner. Participants: A summary of all Medicare acupuncture claims for financial years 1984-85 to 1996-97 and a random sample of patients claiming a Medicare rebate in calendar year 1996. Main outcome measures: Claims for acupuncture by patients' State, sex, age, and the socioeconomic disadvantage index of patients' residences. Results: Between 1984-85 and 1996-97 the number of acupuncture claims increased, but declined as a proportion of total Medicare claims. In 1996, 1.16% of patients claimed for acupuncture, which constituted 0.5% of all Medicare claims. Adjusting for age and socioeconomic disadvantage, women were more likely than men to claim for acupuncture (odds ratio, 1.40; 95% confidence interval, 1.36-1.45). This sex difference is proportionately greater than that for all medical services. Propensity to claim for acupuncture increased with age, peaking at 65-69 years, then declining. Acupuncture claims were more likely in areas just above those assessed as having the greatest social disadvantage. Conclusion: The number of acupuncture claims has increased since 1984. As a proportion of all Medicare claims, acupuncture has remained stable since declining in 1991-92. This suggests that acupuncture is now an established complementary medical practice. Introduction People in the United States,1,2 Canada,3,4 the Netherlands,5,6 the United Kingdom7,8 and Australia9 are increasingly using medicines that are not part of the conventional pharmacopoeia and seeking therapies that are not taught in the conventional medical undergraduate curriculum. A South Australian community study reported that 48.5% of respondents had used such alternative medicines and 20.3% had visited a non-medical practitioner of alternative therapies.10Some general practitioners, as well as non-medical practitioners, provide alternative therapies. Such provision ranges from 16% of general practitioners in Australia,11 Britain12,13 and Canada14 to 30% in New Zealand.15,16 In addition, the proportion of doctors who refer patients to non-medical therapists ranges from 59%-72% in Britain12,13 to 60% in the United States,17 68% in Canada,14,18 80% in New Zealand15,16 and 90% in Holland.6 In Australia one such therapy, acupuncture, is of particular interest in that, although it is used by doctors as part of their normal general practice in many countries, including the UK,13 Canada14 and Holland,6 it is used most extensively by doctors in New Zealand15,16 and Australia.11 Acupuncture is not part of the standard medical curriculum in Australia, but it is recognised as a standard medical therapeutic technique in that it attracts a Medicare rebate (as item 173) when it is performed by a medical practitioner. Other alternative therapies do not attract a rebate or are not so clearly specified. Given this level of government recognition and its use by one in seven Australian general practitioners,11 acupuncture can be considered an addition to general practice in Australia -- a complementary, rather than an alternative, therapy. In this article we examine the characteristics of patients claiming for acupuncture provided by general practitioners, as an extension of our previous report on the characteristics of general practitioners using acupuncture.11 Methods The Health Insurance Commission provided two datasets on the claims submitted by patients involving acupuncture, where those services were provided by medical practitioners. The first dataset was time-series data for the financial years 1984-85 to 1996-97. It includes the number of services and benefits claimed for acupuncture (1984-1990, item 980; 1991-1997, item 173) by State/Territory, age and sex. The second dataset consisted of all Medicare services claimed by patients in the calendar year 1996 -- each case representing an individual patient. We analysed a 1:10 systematic random sample of these data, which included 1 575 173 patients. The data included five variables that measured the frequency of acupuncture claims, frequency of non-acupuncture items, sex, age groupings and postcode. Postcodes were reclassified into 62 categories (consolidated to 12 for presentation) derived from an Australian Bureau of Statistics socioeconomic disadvantage index (SDI).19 SDI groupings were used as proxy measures of socioeconomic status. The 1996 data were analysed using the SAS procedure proc logistic.20 A logistic regression model was fitted to the data to analyse a dichotomous dependent variable (1 = acupuncture service claims, 0 = other service claims). Models were also fitted to four dependent variables representing acupuncture use as quartiles of total service use (ie, 0-25%, 26%-50%, 51%-75%, 76%-100%). Logistic regression odds ratios adjusted for sex, age and SDI were calculated. The University of Tasmania Ethics Committee (Human Experimentation) approved the study. Results Time-series data Between 1984 and 1996, claims for acupuncture rose in all States and Territories except South Australia, where claims began to decrease in 1989, and the Northern Territory, where they began to decrease in 1990. However, in proportion to total Medicare claims, there has been decreased relative demand for acupuncture (Figure). This general Australian decline is echoed in all States and Territories except New South Wales, where demand has fluctuated at a low level. Of particular interest is the order of States and Territories in use of acupuncture throughout the whole time period, with consistently high proportions of claims in Tasmania and South Australia and low levels of claims in the Northern Territory and New South Wales. Separate analyses (not shown) indicate that women make about two-thirds of all claims, except in the Northern Territory, where women make only 55% of claims. When age is examined by sex the picture is more complex. In 1996-97, boys aged 14 years or younger (51.6%; 95% CI, 50.5%-52.7%) were slightly more likely than girls (48.5%; 95% CI, 47.3%-49.5%) to make claims for acupuncture, whereas among older people the pattern was 35% men (95% CI, 34.9%-35.1%) and 65% women (95% CI, 64.9%-65.1%). From 1984 to 1987 claims for both men and women increased with age, peaking at age 55-64 years. However, from 1988 the peak age for women shifted to 45-54 years. There has also been an increase in claims among people 70 years or older, from 7.25% in 1984 to 18% in 1996. 1996 sample data In 1996, acupuncture claims accounted for about 0.5% of all HIC claims for medical services. Of the 1 575 173 patients in our sample, 18 219 (1.16%) claimed for acupuncture. Most patients (16 039; 88.0%) claimed for 10 acupuncture services or fewer, but a small proportion (519; 2.8%) claimed for more than 20 services. High use of acupuncture is only weakly associated with high use of other Medicare services (Pearson's r = 0.07; P < 0.0001). Analyses of the 1996 data (not shown) suggest that, while women (52.7%; 95% CI, 52.6%-52.8%) are more likely than men (47.3%; 95% CI, 47.2%-47.4%) to claim for all types of medical services, their claims for acupuncture are proportionately higher, with 61.7% of those claiming for acupuncture being women (odds ratio [OR], 1.45). These sex differences remain after adjusting for age and SDI (Box). However, acupuncture claims expressed as quartiles (ie, 0-25%, 26%-50%, 51%-75%, 76%-100%) by sex show a different pattern. Sex-based differences tend to decrease as the proportion of acupuncture claims rises. From a logistic regression model (not shown) controlling for age and SDI, no sex-based differences were found for acupuncture claims in the group claiming acupuncture as 76%-100% of all claims (OR, 1.03; 95% CI, 0.91-1.16). As a proportion of all claims, acupuncture claims increased linearly with age (Box), peaking for the 65-69 years age group, then declining. Acupuncture claims tend to be highest in the areas just above the most socioeconomically disadvantaged. Patients in SDI area 2 are 1.7 times (95% CI, 1.58-1.85) more likely to have claimed for acupuncture than those in the area 6 reference group, although the odds ratios for other SDI categories do not exceed 1.3 (Box). Discussion Acupuncture was claimed for by about one in every 100 patients in 1996 and in 1996-97 constituted about 0.5% of all Medicare claims. Although the number of acupuncture claims has increased in the past 13 years, such claims have decreased as a proportion of total Medicare claims. The consistent State/Territory differentials in acupuncture claims are difficult to explain. One possible factor may be ease of access to providers because of the small size of Tasmania and the concentration of the South Australian population in Adelaide. Another may be that these two States have high unemployment, and Medicare-funded acupuncture, unlike medication or physiotherapy, does not require patients to pay for treatment. Acupuncture claims are made more by women than men, and are age-related. The differential between claims made by women and men is greater than the usual disproportion for medical-service claims. This finding appears to lend support to previous research that suggests women are more receptive to alternative techniques.9,10,21 However, this apparent receptiveness varies by age, with boys more likely than girls to receive acupuncture. Further, the peak age for acupuncture claims by women has varied, shifting in 1988 from 55-64 years to 45-54 years. These age variations suggest that the decision to use acupuncture is not solely a function of women's receptiveness to alternative therapies, but is a function of either sex/age-based differences in presenting complaints or doctors' changing willingness to use acupuncture. The increase in claims for acupuncture by middle-aged and elderly patients is also likely to relate to the presenting complaints of patients, or perhaps the lack of success of conventional treatment in alleviating their problems. However, the very weak relationship between high Medicare claims and high acupuncture claims suggests that acupuncture is being used as an alternative to, rather than in conjunction with, other treatments. Whether acupuncture is used after other treatments have failed, as suggested by American2 and Canadian21 research, cannot be ascertained from these HIC data. However, focus groups conducted by one of us (G E) with general practitioner users of acupuncture suggest that it is seen by family doctors as most useful for chronic pain, a symptom more likely to present in middle-aged and elderly patients.22 The higher rate of claims for acupuncture in areas in the lower levels of the SDI scale is contrary to most previous research on alternative therapies,9,10,21 which suggests they are used predominantly by wealthier segments of the community. The fact that these data relate to a Medicare-funded complementary procedure is important in considering this divergence from previous findings. Differences in the rate of acupuncture claims by SDI are not related to the proportion of doctors providing acupuncture in different SDI areas.11 This suggests either that the use of acupuncture is demand-driven rather than supply-driven or that doctors providing acupuncture in low-SDI areas do so to a greater extent through Medicare funding than their colleagues in other SDI areas. However, we recognise that a degree of caution is necessary when interpreting the SDI results, as postcode-based SDI measures may be subject to misclassification error.23 The funding system for Australian healthcare (Medicare and the Health Insurance Commission) provided data which are not available anywhere else in the world. This, coupled with the fact that acupuncture attracts a Medicare rebate if performed by a doctor, enabled us to produce this study, the only national-level study of the characteristics of patients treated with acupuncture. However, the advantages of this dataset are also its disadvantages. The data do not include acupuncture services provided by doctors conducted privately or for insurance companies. Nor do they include the provision of acupuncture by non-medical practitioners. Therefore, these results are not representative of overall acupuncture use or alternative therapies in general. Nevertheless, our results are important at the national level. Acupuncture, a therapy not taught in the standard undergraduate medical curriculum, has been adopted by doctors and used as a complementary therapy throughout Australia. The current Medicare rebate for acupuncture is $18.45, $2.55 less than a standard consultation. Doctors choosing acupuncture are not doing so for monetary reasons. For some doctors it is now an established complementary therapy, apparently chosen for clinical reasons, and a therapy used more frequently with women and elderly patients than with men or young adults and children. Acknowledgements The authors wish to thank the Government Employees Medical Research Fund, which provided funds to conduct the research. References Eisenberg DM, Kessler RC, Foster C, et al. Unconventional medicine in the United States. Prevalence, costs and patterns of use. N Engl J Med 1993; 328: 246-252. Astin JA. Why patients use alternative medicine: results of a national study. JAMA 1998; 279: 1548-1553. Northcott HC, Bachynsky JA. Concurrent utilization of chiropractic, prescription medicines, nonprescription medicines and alternative health care. Soc Sci Med 1993; 37: 431-435. Blais R, Maiga A, Aboucar A. How different are users and non-users of alternative medicine? Can J Public Health 1997; 88: 159-162. Menges LJ. Regular and alternative medicine: the state of affairs in the Netherlands. Soc Sci Med 1994; 39: 871-873. Visser GJ, Peters L. Alternative medicine and general practitioners in The Netherlands: towards acceptance and integration. Fam Pract 1990; 7: 227-232. Thomas KJ, Carr J, Westlake L, Williams BT. Use of non-orthodox and conventional health care in Great Britain. BMJ 1991; 302: 207-210. Vincent C, Furnham A, Willsmore M. The perceived efficacy of complementary and orthodox medicine in complementary and general practice patients. Health Education Research 1995; 10: 395-405. Lloyd P, Lupton D, Weisner D, Hasleton S. Choosing alternative therapy: an exploratory study of sociodemographic characteristics and motives of patients resident in Sydney. Aust J Public Health 1993; 17: 135-144. MacLennan AH, Wilson DH, Taylor AW. Prevalence and cost of alternative medicine in Australia. Lancet 1996; 347: 569-573. Easthope G, Gill GF, Beilby JJ, Tranter BK. Acupuncture in Australian general practice: practitioner characteristics. Med J Aust 1998; 169: 197-200. Anderson E, Anderson P. General practitioners and alternative medicine. J R Coll Gen Pract 1987; 37: 52-55. Wharton R, Lewith G. Complementary medicine and the general practitioner. BMJ 1986; 292: 1498-1500. Verhoef MJ, Sutherland LR. Alternative medicine and general practitioners. Opinions and behaviour. Can Fam Physician 1995; 41: 1005-1011. Hadley CM. Complementary medicine and the general practitioner: a survey of general practitioners in the Wellington area. N Z Med J 1988; 101: 766-768. Marshall RJ, Gee R, Israel M, et al. The use of alternative therapies by Auckland general practitioners. N Z Med J 1990; 103: 213-215. Borkan J, Neher JO, Anson O, Smoker B. Referrals for alternative therapies. J Fam Pract 1994; 39: 545-550. Goldszmidt M, Levitt C, Duarte-Franco E, Kaczorowiski J. Complementary health services: a survey of general practitioners' views. CMAJ 1995; 153: 29-35. Castles I. Information paper: 1991 census. Socio- economic indexes for areas. Canberra: AGPS, 1994. (Catalogue no. 2912.0.) SAS for Windows [computer program]. Version 6.12. Cary, North Carolina: SAS Institute, 1996. Kelner M, Wellman B. Health care and consumer choice: medical and alternative therapies. Soc Sci Med 1997; 45: 203-212. Astin M, Lawton D, Hirst M. The prevalence of pain in a disabled population. Soc Sci Med 1996; 42: 1457-1464. Hyndman JCG, Holman CDJ, Hockey RL, et al. Misclassification of social disadvantage based on geographical areas: comparisons of postcodes and collectors district analyses. Int J Epidemiol 1995; 24: 165-176. (Received 28 Aug, accepted 11 Dec, 1998) Authors' details School of Sociology and Social Work, University of Tasmania, Hobart, TAS. Gary Easthope, MA, PhD, Associate Professor; Bruce K Tranter, BA, PhD, Lecturer. Division of Community and Rural Health, University of Tasmania, Launceston, TAS. Gerard F Gill, MAE, FRACGP, Clinical Senior Lecturer. Department of General Practice, University of Adelaide, SA. Justin J Beilby, MPH, FRACGP, Senior Lecturer. Reprints will not be available from the authors. Correspondence: Dr G Easthope, School of Sociology and Social Work, University of Tasmania, GPO Box 252-17, Hobart, TAS 7001 Email: Gary. EasthopeATutas.edu.au Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/> Acupuncture claims (Medicare Benefits Schedule item 980 from 1984 to 1990; item 173 after 1990) by State and Territory (A), and as a proportion of all claims (B), from financial year 1984-85 to 1996-97. Back to text Characteristics of patients who claimed for acupuncture provided by general practitioners in 1996 (Medicare Benefits Schedule item 173)Number (%) Odds ratio* (95% CI) Sex (n = 18219)Women11233 (61.7%) 1.40 (1.36-1.45) Men6986 (38.3%) 1 Age (n=18219)0-4 years85 (0.5%) 0.08 (0.06-0.10) 5-9 years133 (0.7%) 0.13 (0.11-0.15) 10-14 years263 (1.4%) 0.28 (0.24-0.32) 15-19 years474 (2.6%) 0.49 (0.44-0.54) 20-24 years758 (4.2%) 0.69 (0.63-0.75) 25-34 years2314 (12.7%) 1 35-44 years3438 (18.9%) 1.55 (1.47-1.63) 45-54 years3672 (20.2%) 1.98 (1.88-2.09) 55-64 years3016 (16.6%) 2.36 (2.23-2.49) 65-69 years1447 (7.9%) 2.51 (2.35-2.68) 70-74 years1168 (6.4%) 2.39 (2.23-2.57) 75-79 years818 (4.5%) 2.33 (2.15-2.53) > 80 years633 (3.5%) 1.34 (1.23-1.47) Socioeconomic disadvantage index of claimants (n = 17961) High socioeconomic disadvantage1 300 (1.7%) 1.33 (1.18-1.50) 2 844 (4.7%) 1.71 (1.58-1.85) 3 1047 (5.8%) 1.33 (1.24-1.43) 4 1640 (9.1%) 1.23 (1.16-1.31) 5 2650 (14.8%) 1.27 (1.20-1.34) 6 2283 (12.7%) 1 7 2512 (14.0%) 1.20 (1.13-1.26) 8 2136 (11.9%) 1.20 (1.13-1.27) 9 1734 (9.7%) 1.29 (1.21-1.37) 10 1350 (7.5%) 1.25 (1.17-1.34) 11 864 (4.8%) 1.22 (1.13-1.32) 12 601 (3.3%) 1.34 (1.22-1.46) Low socioeconomic disadvantage * Multiple logistic regression odds ratios adjusted for sex, age and socioeconomic disadvantage index score dummy variables (model chi-squared, 12797.77; df, 25; P < 0.001). Dichotomous dependent variable (1 = acupuncture service claims, 0 = other service claims). CI = confidence interval. Source: Health Insurance Commission 1996. Back to text

Gary Easthope · Gerard F Gill · Justin J Beilby · Bruce K Tranter