Volume 171 Issue 2

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