Volume 169 Issue 2

Analysing potential harm in Australian general practice: an incident-monitoring study Alice L Bhasale, Graeme C Miller, Sharon E Reid and Helena C Britt MJA 1998; 169: 73-76 For editorial comment, see Kidd & Veale Abstract - Introduction - Method - Results - Discussion - Acknowledgements - References - Authors' details - - ©MJA1998 Abstract Objective: To collect data on incidents of potential or actual harm to general practice patients and to evaluate the possible causes of these incidents. Design: An observational study of incidents of potential harm based on a modified critical incidents technique. A non-random sample of general practitioners (GPs) anonymously submitted incident reports contemporaneously. Setting and participants: Australian general practices between October 1993 and June 1995. During the study period, 324 GPs participated at some time. Main outcome measures: GP-reported free-text descriptions of incidents and structured responses for preventability, potential for harm, immediate consequences, predicted long-term outcomes, type of incident, contributing factors, mitigating factors, and additional resource use. Results: 805 incidents were reported -- 76% were preventable; 27% had potential for severe harm. No long term harm was predicted for 66% of incidents. Incidents could relate to pharmacological management (51 per 100 incidents), non-pharmacological management (42 per 100 incidents), diagnosis (34 per 100 incidents) or equipment (5 per 100 incidents). The most common contributory factors were poor communication between patients and healthcare professionals and actions of others (23 per 100 incidents each) and errors in judgement (22 per 100 incidents). Conclusion: Human errors and preventable system problems were identified. The incident monitoring technique provided useful data which could be applied to incident prevention strategies. Introduction Increased interest in quality improvement in healthcare has led to greater recognition that errors occur. The Harvard Medical Practice Study1,2 and the Quality in Australian Health Care Study3 retrospectively reviewed hospital medical records to identify and quantify adverse events caused by the hospital care provided. These studies have provided important insight into rates of adverse outcomes. In Australia, around 16% of admissions studied were associated with an adverse event.3Following the success of incident monitoring in anaesthetics,4,5 in 1993 the Commonwealth Review of Professional Indemnity Arrangements for Health Care Professionals initiated pilot incident-monitoring studies in six medical specialties. The aim of this study was to test the incident-monitoring method in general practice. An important difference between studies such as the Harvard Medical Practice Study and incident-monitoring studies is that no claims of generalisability are made in the latter. Incident monitoring cannot estimate prevalence. It provides detailed contextual information about specific processes and situations that can lead to adverse patient outcomes. Such information is then used to make specific recommendations. The objectives of this study were to test a mechanism for obtaining incident reports from GPs; to gain an understanding of the type of incidents occurring in general practice and hence areas of potential harm; and to identify areas which might benefit from intervention. Method The method has been described in detail elsewhere.6 Participating general practitioners reported incidents contemporaneously, on purpose-designed reporting forms. An incident was broadly defined as "an unintended event, no matter how seemingly trivial or commonplace, that could have harmed or did harm a patient". This criterion included "near misses" -- where the harm may have been averted, but the potential for harm existed. All GP members of the Australian Sentinel Practice Research Network and the Central, Southern, Western and Wentworth Area Health Sentinel Networks in Sydney were asked by letter to participate. Others volunteered when reporting was offered as a Quality Assurance option through the Royal Australian College of General Practitioners (RACGP). Reports were anonymous and information was protected from subpoena by the Health Insurance Act 1973 (Cwlth).7 The reporting form included both free text and fixed-response questions. Information requested included GP characteristics and the patient's age, sex and health problems associated with the incident. Free text descriptions were elicited of the incident, its consequences, and contributing and mitigating factors; the outcome; and the GP's opinion of the incident's preventability. Fixed-choice responses included the type of incident, contributing factors, mitigating factors, potential for harm, immediate consequences, and predicted long term outcomes. All fixed-choice questions included an "other" category to allow continuing development of categories. Quantitative descriptive analysis was used to describe the main features of the data for all 805 incidents received, using SAS.8 No significance testing was carried out as it would have been invalid because of the nature of the study and sample. Qualitative analysis of textual data was carried out for 500 incidents. This analysis involved examination of groups of events for common causes, situations and contributing factors. Results GP response Of 510 GPs initially approached, 214 accepted. A further 110 GPs volunteered during the study. Between October 1993 and June 1995, 805 reports were received from 324 enrolled participants. As all reports were anonymous, reporting rates could not be calculated. However, a GP-generated personal identification number on most reports allowed estimation of the number of reports received from each identification number. There were 241 GPs who submitted at least one report, and 82 unidentified reports. The proportion of each sex and the proportion from rural practices among the respondents were equivalent to the overall GP population at that time.9 However, only 16% of respondents had less than 10 years' experience, whereas in a national sample in 1990-1991 about 30% of GPs had less than 10 years' experience.10 Patients Of the 805 incidents, 58% involved female patients. Almost one-third of incidents involved patients over 65 years old (median age, 50 years; range, 0-98 years). Younger patients (0-24 years) were least likely to be involved in incidents (Figure). Compared with the overall age-sex distribution of patients attending GP consultations, women older than 75 years and infants were over-represented in the incidents reported.9 Age and sex of patients involved in reported incidents. Incidents Incidents were categorised as pharmacological, non-pharmacological, diagnostic or equipment events (Box 1). Pharmacological events were most frequent. The most common incident type overall was omitted or delayed treatment. A high degree of overlap between non-pharmacological and diagnostic events was noted -- 79 incidents involved both types. GPs thought 76% of the incidents were preventable (Box 2) and 11% were unpreventable. They were undecided about the remaining 13%. More than one-third of the incidents resulted in additional use of resources. While pharmacological incidents were most often reported, they were also largely considered preventable (79%) and the least harmful potentially and in the long term. In contrast, diagnostic events were less preventable and more harmful (Box 2). Of the 38 deaths reported, 30 involved a diagnostic incident. Major immediate consequences were reported in 17% of incidents, and 4% resulted in the patient's death (Box 2). GPs predicted that most incidents would cause no long term harm, but that 7% would result in the future death of the patient. Mitigating and contributing factors Incident outcomes were more frequently mitigated by chance factors than through systematised fail-safe or preventive procedures. The most frequently reported mitigating factors were good fortune, early intervention by the GP, and the patient's good physical condition (Box 3). Ineffective communication and problems in coordination between healthcare services were frequent contributing factors (Box 4). Actions or involvement of others in caring for patients were also frequently cited. Assessment-related mistakes constituted another cluster of contributing factors (eg, errors in judgement, failure to recognise significant signs and symptoms, and inadequate patient assessment). Insufficient use of standard resources and protocols by the GP was also recognised. GPs reported being tired, rushed or late in 10% of incidents, but GP memory lapses and stressful situations were least frequently cited as contributing factors. There were no obvious associations between specific contributing factors and incident type. Qualitative analysis Qualitative analysis of free-text responses identified four broad problem groups: communication, procedural, clinical and external problems. More comprehensive descriptions are available elsewhere.11,12Communication problems: Most communication problems between GPs and patients occurred when patients did not understand some aspect of their condition, the management plan or the treatment. Patients with mental health problems or lacking English language skills were particularly at risk. Some serious pharmacological incidents occurred when patients misunderstood instructions and took newly prescribed drugs in addition to, rather than instead of, a previously prescribed medication. Poor communication also manifested as clinical error in inadequate history taking. There were also problems with communication between healthcare providers. Clinical information about the outcomes of hospital referrals or admissions, the expected role of the GP in post-discharge care, specialists' recommendations for management and results of tests or investigations was often not communicated between GPs and other healthcare providers, or was too late to be of use. Unclear or uninformative medical records caused a number of incidents, and inadequate records resulted in poor communication within practices. Incorrect or unclear labelling of drugs resulted in administration of the wrong drug, and inappropriate drugs were dispensed because of poor handwriting on prescription forms. Such errors were often compounded by similar medication names (eg, Teldane/Feldene, Microlax/ Murelax). Procedural problems: The main procedural error was failure to check medical records. Diagnostically, procedural error manifested in poor application of the differential diagnosis, when the correct diagnosis was inappropriately rejected because of insufficient or incorrect examination, or was not included in the differential diagnoses and was therefore not evaluated. In non-pharmacological incidents, treatment procedures may have been neglected (eg, not checking for anaesthesia before an excision). In equipment incidents, machines were not properly checked before use (eg, leads or tubes were disconnected) or were not well maintained (eg, unfilled emergency oxyviva equipment). Lack of protocols for ensuring action on results of tests and investigations meant that important results were filed unseen or left until the GP who ordered the test was next in the surgery. Recall systems were often inadequate, preventing recall of patients for follow-up tests and investigations and resulting in missed or delayed diagnosis or management. Clinical problems: These consisted of incidents that could only be attributed to human error. In pharmacological incidents, clinical errors occurred where an inappropriate drug was chosen; in non-pharmacological incidents, where the wrong treatment was chosen; in diagnostic incidents, where symptoms and signs were not recognised (eg, chest pain considered to be musculoskeletal); and in equipment incidents, where equipment was used inappropriately. External problems: External problems involved factors outside the GP's control, such as actions of other healthcare providers, equipment faults or unavailability, disease-related factors, and unpredictable drug effects. Patient-related factors included non-compliance, age, level of comprehension, and psychological condition. Discussion The diversity of incidents reflects the heterogeneous nature of general practice and its context within the healthcare system. Nevertheless, it was possible to isolate recurrent themes and errors and to identify incidents that occurred because of system problems or other preventable factors. Pharmacological incidents were most frequent and could be prevented through clearer prescription writing, double-checking of doses and potential interactions, and improved patient understanding. Unexpected drug reactions (eg, to previously well-tolerated drugs) and idiosyncratic complications were largely beyond GPs' control. However, compilation of this information may be useful to reinforce or add to data collected elsewhere. Diagnostic incidents had the most serious outcomes. While management of test results and lack of recall systems contributed to these incidents, many occurred while the patient was under another medical practitioner's care, or were caused by the diagnostic decision-making processes of GPs. Patient misunderstanding was a factor in many incidents. This might be addressed by improved GP awareness to ensure full patient understanding. However, information management problems require "hard-wired" solutions -- structures and systems that ensure better outcomes. In particular, opportunities for errors may be reduced by better recall systems for follow-up and for regular tests and screening,13 better transfer of medical information between healthcare providers, clearer writing of prescriptions, and better maintenance and use of medical records. Information technology could help by streamlining some of the administrative functions, particularly prescription writing, which appears to be adversely affected when GPs are tired, rushed, or running late. Limitations to the validity of our data include the non-random nature of the sample, limited recognition of incidents, selectivity in reporting incidents, and the lack of an alternative perspective. (We did not seek the patients' perspective because of the controversial nature of the data.) However, issues we identified as important have been described by other researchers. Many of the issues pertaining to pharmacological incidents have been described in a study of adverse drug events in United States hospitals.14 Similarly, the problems of multiple prescribing in the elderly have been well summarised, and opportunities for improvement in the management of polypharmacy have been identified.15 Prescription clarity has also been recognised as an area of potential misunderstanding.16 In critical incident studies, incidents are sampled until "saturation" (until no new incident types are reported).17 While these 805 incidents may not reach saturation, they demonstrate at least some of the types of incidents occurring in Australian general practice. Logically, where inadequate systems are widely used, similar events are likely to occur regularly rather than being related to individual characteristics or techniques. Continued collection and classification of events will elucidate more causal factors, particularly for the less common types of incidents. This study also resulted in a number of suggested interventions.18 Incident monitoring studies are intended to be continually used in improving systems. It is important to use the data for formulating interventions. This study has shown that such data can be collected in general practice, but the translation of findings into active change remains to be addressed. Acknowledgements We gratefully acknowledge the funding provided by the Commonwealth Review of Professional Indemnity Arrangements for Health Care Professionals. The project was conducted under the auspices of the RACGP. Recruitment of GPs and administration of the GP participants was carried out jointly by the Family Medicine Research Unit and the RACGP Research and Health Promotion Unit, South Australia. Other members of the research team made considerable contributions to running the project. Thanks must go to the GP participants for so generously sharing their experiences with us. References Brennan TA, Leape LL, Laird NM, et al. Incidence of adverse events and negligence in hospitalized patients: results of the Harvard Medical Practice Study I. N Engl J Med 1991; 324: 370-376. Leape LL, Brennan TA, Laird NM, et al. The nature of adverse events in hospitalized patients: results of the Harvard Medical Practice Study II. N Engl J Med 1991; 324: 377-384. Wilson RM, Runciman WB, Gibberd RW, et al. The Quality in Australian Health Care Study. Med J Aust 1995; 163: 458-471. Williamson JA, Mackay P. Incident reporting. Med J Aust 1991; 155: 340-343. Webb R, Currie M, Morgan CA, et al. The Australian incident monitoring study: an analysis of 2000 incident reports. Anaesth Intensive Care 1993; 21: 520-528. Britt H, Miller G, Steven I, et al. Collecting data on potentially harmful events: a method for monitoring incidents in general practice. Fam Pract 1997; 14: 101-106. Commonwealth of Australia. Health Insurance Act 1973. Declaration under section 106L. Commonwealth of Australia Gazette 1993; GN 31: 2269-2272. SAS [computer program]. Version 6.11. Cary, North Carolina: SAS Institute, 1995. General Practice Branch. Commonwealth Department of Health and Family Services. General Practice in Australia: 1996. Canberra: Commonwealth of Australia, 1996. Bridges-Webb C, Britt H, Miles DA, et al. Morbidity and treatment in general practice in Australia 1990-1991. Med J Aust 1992; 157 Suppl: S1-S56. Miller G, Britt H, Steven I, et al. Incident monitoring in general practice: a pilot study. Report to the Professional Indemnity Review, Commonwealth Department of Human Services and Health. Sydney: Royal Australian College of General Practitioners, 1995. Bhasale AL. Collecting data on potentially harmful events: evaluation of an incident monitoring technique in Australian general practice [master's thesis]. Sydney: University of Sydney, 1997. Bhasale AL, Norton KJ, Britt H. Tests and investigations. Indicators for better utilisation. Aust Fam Physician 1996; 25: 680-694. Leape LL, Bates DW, Cullen DJ, et al. Systems analysis of adverse drug events. JAMA 1995; 274: 35-43. Teng Liaw S. Drug interactions among the elderly. Aust Fam Physician 1997; 26: 355-357. Liddell MJ, Goldman SP. Attitudes to and use of a modified prescription form by general practitioners and pharmacists. Med J Aust 1998; 168: 322-325. Flanagan JC. The critical incident technique. Psych Bull 1954; 51: 327-359. Bhasale AL, Britt H, Miller G. Developing interventions which could reduce the occurrence of adverse patient incidents in general practice. Report to the Taskforce on Quality in Australian Health Care, Department of Human Services and Health, Canberra. Sydney: Family Medicine Research Unit, University of Sydney, 1995. (Received 4 Aug 1997, accepted 26 Mar 1998) Authors' details Department of General Practice, University of Sydney, Sydney, NSW. Alice L Bhasale, BSc(Psychol), MSc(Med), Senior Research Assistant, Family Medicine Research Unit; Graeme C Miller, MB BS, FRACGP, Medical Director, Family Medicine Research Unit; Sharon E Reid, MB BS, MPH, Lecturer; Helena C Britt, PhD, Director, Family Medicine Research Unit. Reprints will not be available from the authors. Correspondence: Ms A L Bhasale, Acacia House, Westmead Hospital, Westmead, NSW 2145. E-mail: alicebATgenprac.wsahs.nsw.gov.au - 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/>

Alice L Bhasale · Graeme C Miller · Sharon E Reid · Helena C Britt

Suicide among young Australians, 1964-1993: an interstate comparison of metropolitan and rural trends Michael J Dudley, Norman J Kelk, Tony M Florio, John P Howard and Brent G H Waters MJA 1998; 169: 77-80 See also Rosenman Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - ©MJA1998 Abstract Objectives: (i) To compare suicide rates in 15-24 year old men and women; and (ii) for 15-24 year old men, to investigate differences in suicide rates between metropolitan and rural areas, and changes in method-specific suicide rates and, in particular, firearm and hanging suicide rates in rural and metropolitan areas. Design: Retrospective analysis of Australian Bureau of Statistics (ABS) suicide data (1964-1993). Setting: All Australian States. Subjects: Young women and men aged 15-24 years who died by suicide. Results: Male youth suicide rates rose substantially over the 30 years in all Australian States, whereas female rates did not increase. Increases in suicide rates in young men in small rural towns consistently exceeded those in metropolitan areas in all Australian States. Metropolitan rates in 1964 were higher than those in small rural towns, but by 1993 the position was reversed. Medium-sized cities were the only areas where there was no consistent interstate trend. Differences were noted in suicide base rates in different States. High car exhaust suicide rates were noted in Western Australia, and high firearm suicide rates in Tasmania and Queensland. The ratio of firearm suicide rates in small rural areas to those in metropolitan areas rose in all mainland States, but the same ratio for hanging suicide rates changed little. Conclusions: All Australian States reflect national suicide trends in relation to sex and residential area. In some States, particular suicide methods predominate. A decreasing trend in overall firearm suicide rates in young men in all States from 1984 to 1993 conceals substantial increases in firearm suicide rates in small rural areas in all mainland States over the 30-year period. This, together with the marked rate ratio difference in firearm suicides between metropolitan and small rural areas, suggests that particular risk factors for suicide are operating in small rural areas. The fact that hanging rate ratios changed little suggests that more general factors in male youth suicide are also operating in all areas. A better understanding of similarities and differences in health risks faced by metropolitan and rural youth is required. Introduction Suicide rates for 15-24 year old Australian men have trebled since the early 1960s. However, these rate increases have not been uniform. In metropolitan areas they have doubled, but they have increased as much as 12-fold in towns with fewer than 4000 people. The rates for suicide with a firearm in 15-24 year old men have declined overall, and in metropolitan areas since the late 1980s, but they have continued to rise in rural areas. Rates of suicide by hanging have risen in all locations.1We aimed to answer questions about whether these national suicide trends are replicated at the State level. We wanted to know whether the trends for the larger States dominate the national picture, or whether the same fundamental trends are occurring in all States. Interstate analysis is also important, because health, education and welfare services are often organised and funded at a State level. Differences among the States have long been part of the Australian culture, and firearms legislation, in particular, is at present a State prerogative. In this article, we report suicide rates in young men and women (aged 15-24 years) in all Australian States and Territories, as well as suicide rates in young men by method of suicide, and by residential area, in all States, for 1964 to 1993. Methods Our methods are described in more detail elsewhere.1 Data on suicides and corresponding population data for subjects aged 15-24 years were sought from the Australian Bureau of Statistics (ABS) for the years 1964-1993. These data were de-identified, and an undertaking was given not to attempt to identify the subjects or to contact their families. Data concerning usual area of residence were available for all but 219 of 8537 people who had died by suicide. Subjects' usual place of residence was classified as: metropolitan areas of capital cities of each State; cities with populations >100 000; cities with populations >25 000; towns with populations >4000; or towns with populations <400. These cut-offs, chosen after consulting social geographical sources,2,3 approximate Australian urban groupings in order of size. Definitions of "metropolitan" and "rural" also follow guidelines given in these sources. Rates throughout are expressed as numbers of suicides per 100 000 of the at-risk population. Data were aggregated in 5-year epochs to enable longer-term trends to be discerned. Results Sex-specific suicide rates Suicide rates in 15-24 year old men rose substantially over the past 30 years in all Australian States and Territories, but rates in women of the same age did not (Figure 1). We will consider suicide rates in 15-24 year old men only in the remainder of the article. Method-specific suicide rates Considering the whole 30-year period, for 15-24 year old men, a clear trend exists, both nationally and for individual States, of a reduction in firearm suicide rates in the past 10-15 years, and of an increase in hanging suicide rates over the whole period at a substantially greater rate than the increase by all other methods. Car exhaust suicide rates also increased at a greater rate than the overall increase, especially in Western Australia, but to a lesser extent than suicide by hanging. Suicides by poisoning did not increase proportionally in any States or nationally. Hanging is now the most common method of youth suicide in most States, exceeding firearms as a means of suicide in all States except Queensland and Tasmania. In the most recent epoch, firearm suicide rates were highest in Tasmania and Queensland (Figure 2). Residence-specific suicide rates In all States, suicide rates in 15-24 year old men have increased substantially in metropolitan areas, but the greatest increases have been recorded for towns with a population under 4000. In 1964 in four States (New South Wales, Victoria, Queensland, Western Australia), metropolitan suicide rates exceeded those of small rural areas, but by 1993 the position was reversed (Figure 3). New South Wales Suicide rates in 15-24 year old men rose consistently in all residential categories except cities with over 25 000 people. Sydney's rates rose least (1.6-fold), smaller towns (population, <4000) rose the most (9.9-fold), and Newcastle- Wollongong (2.7-fold) and towns with populations over 4000 (3.8-fold) were intermediate. Victoria Suicide rates in 15-24 year old men rose in all residential areas. Melbourne's rates began from a low baseline, and in 1964 rate differences between Melbourne and smaller towns (population, <4000) were less marked than in NSW. Melbourne's rates rose least (4.2-fold), smaller towns with fewer than 4000 people the most (34.5-fold), and Geelong (5.7-fold) and larger towns (population, >4000) (5.5-fold) were intermediate. Queensland Suicide rates in 15-24 year old men in Brisbane trebled, and rates for the Gold Coast and Sunshine Coast, areas with a high population growth, which both now exceed 100 000 people, peaked in the mid 1970s, but then fell. Rates in cities (population, >25 000 and larger towns (population >4000) increased 1.7- and 1.9-fold, respectively, but in smaller towns (population, <4000) the increase was 31.6-fold. South Australia Differences in suicide rates in 15-24 year old men between metropolitan and small rural areas were less marked in States with lower populations. Adelaide's suicide rate for young men rose 2.7-fold, and in towns with populations under 4000 it rose 5.5-fold. Rates in larger towns (population, >4000) increased 1.8-fold. High rates in cities with populations >25 000 were based on small numbers. Western Australia Suicide rates in 15-24 year old men in Perth rose 2.5-fold and rates in smaller towns (population, <4000) rose 7.0-fold. Rates in larger towns (population, >4000) fluctuated, rising 3.2-fold overall. Tasmania Tasmania's suicide rates in 15-24 year old men have been consistently high. While Hobart's rates have more than doubled, rates in smaller towns (population, <4000) have risen 3.6-fold. Trends elsewhere were inconsistent, although high rates have been recorded. Firearm and hanging suicide rates for metropolitan and small rural areas Suicide with firearms or by hanging, the most common methods, account for between a half and two-thirds of suicides in 15-24 year old men in each State, so these have been analysed by place of residence. In all States the ratio of the firearms suicide rate in small rural areas to the firearms suicide rate in metropolitan areas rose substantially over the 30-year period. In contrast, this ratio for suicide rates by hanging remained much the same or rose minimally over the same period. Thus, the national trend for a reduction in firearm suicide rates conceals a continuing rise in firearm suicide rates in rural areas in all States. These increases were especially pronounced in Victoria and Queensland (41.5- and 36.7-fold respectively), while Tasmania's rates remained high throughout the period (Figure 4). Discussion National youth suicide trends according to sex of the subject are reflected in the rates of all the individual States: suicides in 15-24 year old men rose substantially, whereas those in 15-24 year old women did not change in the past 30 years. The disproportionate increase in suicide rates in young men in small rural areas nationally is also occurring consistently in all Australian States. Certain data limitations should be noted. Coroners often must exercise subjective judgements in determining verdicts, which may lead to possible systematic differences in rates between different States and over time; Errors may also arise from unstandardised methods of recording suicides, especially earlier in the study period;1 Population data may fluctuate in minor ways with changing residential area boundaries, notably with some towns being absorbed into larger cities; and The data do not allow inferences about particular local geographical areas (see for comparison National Injury Surveillance Unit data4). However, it is unlikely that changing coronial verdicts account for the magnitude or generality of the changes we noted. Cantor and Coory5 found that Queensland's provincial cities and rural towns of modest size had negligible rate increases compared with metropolitan and major urban areas from 1986 to 1991. They questioned whether there was a rural suicide problem in Queensland. Our study confirms their observations for Queensland cities with populations over 25 000, but notes a massive rate increase in towns with fewer than 4000 people, with substantial numbers supporting this finding. Further, the Queensland picture does not appear to be atypical. There are differences in suicide base rates in the various States. Whether Melbourne's low base rate in 1964 is coincidental, or a result of Victorian coroners showing less willingness to reach a verdict of suicide, requires further investigation. Tasmania's relative isolation, demographically stable population, and easy firearm access may explain its consistently high suicide rates. Suicide methods differ somewhat between States. The high rates for car exhaust suicides in Western Australia may reflect its relative isolation and this method's cultural acceptability. Carbon monoxide sensors, exhaust modifications and changes to catalytic converters may be effective prevention measures.6 High firearm suicide rates among 15-24 year old men in Tasmania and Queensland,7 rising metropolitan firearm suicide rates in those States, and rising rates in small towns (population, <4000) in all States, but especially Victoria and Queensland, probably relate to falling populations in small rural areas with stable or rising suicide numbers, the easy availability of firearms, and the more liberal firearm legislation in Tasmania and Queensland. Applying methods to prevent car exhaust suicide and reducing the availability of guns may reduce suicide rates by these two methods, and possibly total suicide rates.8 While rates for suicide by various methods may differ in different States, residential area trends for firearm and hanging suicides were pronounced in all States. A trend for overall firearm suicide rates to decrease in all States from 1984-1993 conceals substantial firearm rate increases in small rural areas in all mainland States over the 30-year period. Differences in rates between metropolitan and small rural areas, and the fact that the ratio of firearms suicide rates in small rural areas to those in metropolitan areas rose substantially in all mainland States, suggest that particular risk factors (directly and indirectly related to firearms) are operating in small rural areas. Restrictive legislation may differentially affect firearm suicides in metropolitan areas, where availability is lower.9 The rural economic downturn, the strain on small rural communities, and a major population exodus in all States from towns with fewer than 4000 people have meant added health burdens for those communities, with possibly specific risk factors.1 The fact that the equivalent ratio for hanging rates changed little suggests that more general factors are also operating across all areas in relation to suicide in young men. Particular States have local issues which require specific attention, but the fact that all Australian States reflect the national trends in youth suicide in relation to sex and residential area supports a national approach to youth suicide prevention. Effective national approaches will depend in part on acquiring a better understanding of the similarities and differences in health risks faced by metropolitan and rural youth.1 Acknowledgements Thanks are due to Caroline Haski and Margaret Alcock for their painstaking work as research assistants, and to the NSW Institute of Psychiatry, which partly funded this study. References Dudley M, Kelk N, Waters B, et al. Suicide among young rural Australians 1964-1993: a comparison with metropolitan trends. Soc Psychiatry Psychiatr Epidemiol 1997; 32: 251-260. Department of Primary Industries and Energy and Department of Human Services and Health. Rural, remote and metropolitan areas classification, 1991 Census edition. Canberra: AGPS, 1994. Holmes J. In: Jeans D, editor. Space and society. Chapters 2 and 3. Sydney: Sydney University Press, 1988: 24-74. Moller J. An atlas of injury death in Australia 1990-1992. Adelaide: National Injury Surveillance Unit, 1995. Also available online: <www.nisu.flinders.edu.au/data/atlas/atlas.html> Cantor C, Coory M. Is there a rural suicide problem? Aust J Public Health 1993; 17: 382-384. Australian Institute for Suicide Research and Prevention. Access to means of suicide by young Australians; a background report to the Commonwealth Department of Health and Family Services Youth Suicide Prevention Advisory Group. Brisbane: Australian Institute for Suicide Research and Prevention, 1996. Cantor C, Lewin T. Firearms and suicide in Australia. Aust N Z J Psychiatry 1990; 24: 500-509. Cantor C, Baume P. Access to methods of suicide: what impact? Aust N Z J Psychiatry 1998; 32: 8-14. Cantor C, Slater P. The impact of firearm control legislation on suicide in Queensland: preliminary findings. Med J Aust 1995; 162: 583-585. (Received 12 May 1997, accepted 17 Apr 1998) Authors' details University of New South Wales, Sydney, NSW. Michael J Dudley, MB BS, FRANZCP, Lecturer, School of Psychiatry. Norman J Kelk, PhD, Social Worker, School of Community Medicine. Prince of Wales Hospital, Sydney, NSW. Tony M Florio, MPsych, Clinical Psychologist. Macquarie University, Sydney, NSW. John P Howard, PhD, Clinical Psychologist. PO Box 474, Edgecliff, NSW. Brent G H Waters, MD, FRANZCP, Psychiatrist. Reprints will not be available from the authors. Correspondence: Dr M J Dudley, Department of Child and Adolescent Psychiatry, Sydney Children's Hospital, Randwick, NSW 2031. E-mail: m.dudleyATunsw.edu.au - 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/>

Michael J Dudley · Norman J Kelk · Tony M Florio · John P Howard

Ethics Towards a consensual culture in the ethical review of research Donald Chalmers and Philip Pettit, on behalf of the Australian Health Ethics Committee The Report of the Review of the Role and Functioning of Institutional Ethics Committees was submitted to the Minister for Health and Family Services in March 1996.1 It recommended, among other things, that the Statement on Human Experimentation, issued under the name of the National Health and Medical Research Council (NHMRC) in 1992, should be revised. A similar recommendation was made in the report by Dr Margaret Allers in 1994 into the collection, manufacture and injection of human growth hormone.2 The recommendation for a review of the Statement was approved by the Council in November 1996. The Australian Health Ethics Committee, a Principal Committee of the NHMRC, had for some time been discussing various aspects of the Statement on Human Experimentation and independently decided that the Statement should now be revised. The Committee's first consideration was the tone that the Statement should set for the ethical review of research. This article expresses the Committee's views on this matter. MJA 1998; 169: 79-82 Introduction - The goal of ethical review - The path we should be taking - The path we are actually taking - Recommendations for the reform of ethical review - References - Footnote - Authors' details - - More articles on Ethics Introduction The evolution of an ethic among those conducting research on humans has occurred in three stages. First, individual researchers developed a general sense of what was proper behaviour and what was improper behaviour in the pursuit of research goals - in particular, with regard to the treatment of research subjects. Then, professional research bodies (which first appeared in the last century) articulated codes of behaviour for their members. Finally, independent authorities - universities, hospitals, governments - institutionalised the ethical review of research projects that fell within their purview.3,4The forces driving this evolution are complex; we draw attention to one that may easily escape notice. This is a social mechanism that we describe as the "controversy machine". Some research is pursued in an ethically dubious fashion, or with ethically deplorable results. The whistle is blown by an insider, or a newspaper or community group comes to learn by another means what is happening. There is a public scandal, leading to popular demand that something be done to make sure this never happens again. The professional bodies, or other authorities, respond to the demand by taking appropriate action, or at least action accepted as appropriate. Things quieten down, but then, perhaps years later, another scandal is uncovered and the process runs its course once more. The controversy machine played a major role earlier this century in the development of codes of research conduct; these codes were formulated in the first wave of reaction to various scandals in research on humans. It has also played an important part in the last 20 years or so in facilitating the introduction and then the gradual formalising of arrangements for the review of research proposals. With every subsequent scandal made public, ethical surveillance was made more rigorous (Box 1). The controversy machine has been at the origin of many fine achievements in social life, being associated in various countries with the development of a more or less decent civic and public world.9However, the controversy machine does not invariably work for good. In some areas the responses that scandals elicit - and that serve best to satisfy public outrage - are not necessarily the responses that deal most effectively with the underlying problem. For example, the controversy machine may be responsible for the widespread failure of governments to deal humanely and effectively with criminal offenders. Scandals in the criminal justice area - the heinous crime, the offence under parole - tend to generate a get-tough reaction that satisfies public outrage without actually being very effective. Because the controversy machine has been responsible for generating our system of ethical review of research, we who are charged, at whatever level, with running that system should be clear about where exactly we want to get to and whether we are on course for getting there. We need to consider, first, the goal of ethical review; second, the path that we should be taking in pursuit of that goal; and, third, the extent to which we are cleaving to that path. Otherwise, we are in danger of being carried along, unthinkingly, by a process that may do more harm than good. The goal of ethical review One view of the goal of ethical review of human research would be that it is to reduce, as far as possible, the incidence of unethical research. The best way of realising that goal would be to prevent any research whatsoever occurring: no research, ergo no unethical research. But it is important to see that this cannot possibly be right, and no one in the business of ethical review has ever thought that we would have achieved our goal - as distinct from putting ourselves out of a job - if we got rid of research altogether. Any plausible system for ethical review of human research must have as its goal, not only that research should be ethical, but also that research should continue to be pursued. It must be designed, not as a form of ethical inquisition, but, rather, as a system for facilitating and encouraging ethically informed research on humans. There are two models for facilitating ethically informed research. The first is to identify certain ethical standards - inevitably, certain less than fully determinate standards - and, taking scientific value as given, to encourage those projects that in the committee's judgement satisfy the standards. The second is to make a judgement about how scientifically valuable the research is and to encourage research to the extent that (i) it is judged to be both scientifically worthwhile and ethically satisfactory, and (ii) considering the balance between these two aspects, it scores pretty well in the opinion of the committee. The first of these models is more attractive than the second.2 Ethics committees are not necessarily well equipped to determine the scientific quality of the research projects they consider. In fact, it is often quite hard to make a judgement on whether a project is worthwhile or not, and it is clearly wrong for a non-professional group to take on the burden of this judgement. Besides, it would be a source of reasonable resentment and alienation on the part of researchers if a committee that was meant to judge the ethical acceptability of research projects insisted also on making judgements of a methodological character. Of course, ethics committees may require an assurance that any project submitted is of scientific interest. They might, for example, insist on a prior assessment of the risks attendant on the research, as well as the potential benefits to be gained by it. And in difficult cases where special problems arise (e.g., when the research involves the use of placebos with patients who seem certain to die without the drug under trial) they may reasonably seek an assurance that the project really does hold out a firm promise of achieving the alleged benefits. But such assurance should always be sought outside, from an adequately informed authority; otherwise, the committee is going to look like an arbitrary power. The goal we should be pursuing, then, is an arrangement under which ethics committees obtain judgements of scientific merit from elsewhere and work to facilitate all those meritorious projects, and only those, that meet certain ethical standards. The ethical standards will require, among other things, that the subjects are voluntary and suitably informed participants in the enterprise; that the risk of harm to those subjects, or to others affected, is not inappropriate; and that considerations of confidentiality and privacy are reasonably satisfied. Such standards are often going to be difficult to interpret and apply, which is why we mentioned their not fully determinate character. One way in which they will be difficult to apply is that, in judging whether a risk of harm is appropriate, the committee will have to make an assessment of the importance of the benefits promised by the research, according to the scientific assessment: it will have to make a judgement, not on what the potential benefits are, but on how much significance to attach to them. The path we should be taking There are two broadly contrasting approaches that ethics committees might take in pursuing the goal of facilitating ethically informed research. The first is to encourage patterns of ethical self-evaluation among researchers, and to rely on this as the normal means of ensuring ethical conduct. Thus, while routinely overseeing all that happens, and implementing relevant procedures and being available for consultation about them, they would take an interventionist stance only in exceptional cases. The second approach is to adopt an inspectorial and adversarial role in relation to researchers, seeking to articulate an exact code and to make maximum efforts to police that code in every instance. Two facts argue strongly against going the adversarial way.9-11 No system of inspection and policing, no matter how draconian, could hope on its own to achieve a high level of ethical conduct among resistant researchers; there will always be opportunities for researchers to take shortcuts and bend the rules, if they are so inclined. An adversarial system of inspection and policing is likely to make researchers resistant to considerations of ethics; it is likely to put them offside, as they see themselves demeaned and distrusted by the agencies of ethical review. The better prospect for facilitating ethically informed research is the alternative, non-adversarial, approach. This begins from the assumption that most researchers, once they are made aware of ethical concerns, are disposed to take them seriously; only a small minority are likely to ignore them in their enthusiasm for their research goals. The strategy is to build on this strength by generating an awareness of ethical concerns in the research community at large and, without abdicating the position of ultimate authority in ethical matters, by displaying a posture of trust in that community. What would this posture of trust involve? A number of possible initiatives will illustrate the idea; the list offered is meant to be suggestive, not definitive. Invite relevant individuals and bodies to give advice on the ethical problems most prominent in their area, and negotiate about difficulties that individual researchers may find in dealing with their ethics committee. Delegate some degree of responsibility for ethical review to professional departments or agencies; for example, allowing them to review projects coming to the committee, and working towards a situation in which the committee is almost always happy with anything that the professionals approve. Communicate the reservations of the ethics committee to any researcher whose project seems to raise problems and seek to work out ways of getting around those problems, consistent with the aims of the project. Develop a common understanding with the relevant research communities about what is a reasonable period for ethical review and try systematically to complete the review of projects within that period. Seek to devise a system of monitoring that does not communicate a sense of being under surveillance and suspicion to researchers. Encourage the relevant professional bodies to assume responsibility for keeping their members informed about ethical issues and for organising discussion of those issues. The path we are actually taking These considerations about the goal of ethical review, and about the best means of pursuing it, are not entirely uncontroversial. Still, they are likely to attract a broad consensus among those concerned with the ethics of human research, in particular among those with some sense of the difficulties associated with regulation, and of the possibility of regulation becoming counterproductive. They lead us now to ask whether the path we are actually taking in ethical review - the path on which the controversy machine has set us - is likely to prove adversarial or non-adversarial in character. Unfortunately, it doesn't require much reflection to see that the controversy machine has left us with a system of ethical review that is in danger of becoming extremely adversarial. The fact that the system orginated in reaction to scandal, and is legitimated as a protection against further scandal, projects two assumptions of an adversarial character. Researchers are regarded as the source of ethical problems: they are cast in the role of potential offenders. And reviewers are regarded as those with the unique responsibility, and the unique power, to prevent those problems arising: they are cast in the role of protectors and police. Under this interpretation of the two sides - and it is not yet a reality, only a threatening scenario - researchers get to be seen as one-sidedly interested in research goals, reviewers as equally one-sidedly interested in ethical standards. The review process is presented as a struggle between those of a single scientific mind, who want to pursue their research ambitions at any cost, and those of a single ethical mind, who have to try to keep the researchers honest. There is no room left in the scenario for the possibility of the two sides coming to a common mind on relevant matters. Not only does the origin of the system in the controversy machine project assumptions of an adversarial character, but also the possibility of the machine being called into action serves to reinforce an adversarial relationship between reviewers and researchers. The system we have at present puts reviewers under threat of being themselves exposed to public censure in the event of approving a research project that gives rise, fairly or unfairly, to a scandal of some sort; that is, it imposes a heavy penalty on a positive mistake: a mistake in approving what perhaps should not have been approved. However, the system in place imposes no such penalty on a negative mistake: a mistake in not approving what should have been approved. Thus, the system creates a conflict of interest between reviewers and researchers; it gives the reviewers a special incentive for taking the cautious line that goes against the interests of the researchers. These effects of the controversy machine on our system of ethical review have the potential to be very damaging. Here is a list of some possible consequences. We stress that these are possible consequences, not results that have actually been documented; what they constitute is a "watch-list" for those who have a responsibility for ethical review. Ethical reviewers see research as the concern of researchers, ethics as their own concern, and so do not worry about the effects of their reviewing on research activity. In particular: they may have no hesitation in refusing to approve research projects that raise any difficult questions; they may delay and obstruct research projects that they approve, through being excessively procedural and legalistic; and they may be willing to see the traditional agenda of research being seriously cut back, if that is where their deliberation leads. Ethical reviewers are unwilling to contemplate a "steady state", in which research generally satisfies the accepted ethical standards and ethics committees play an ever more passive role. In particular: as research projects meet accepted standards, reviewers begin to make those standards more demanding, exploiting the indeterminacy mentioned earlier: they become tougher on questions to do with what is an acceptable risk of harm, on what is adequate information for research subjects to be given, and so on; and ethical reviewers begin to look for further ways of monitoring the extent to which researchers stick to ethical guidelines: they begin to assume a greater surveillance and policing role. Researchers respond to this indifference, and this incremental creep, by adopting a resistant posture. In particular: they become alienated from the process of ethical evaluation, as they come to think of ethics as the reviewers' business, not their own; they see it as perfectly legitimate to do whatever is necessary in order to bypass the standards imposed on them; they may even take positive pleasure in defying and defeating the reviewers; and they develop a collective mentality of this resistant kind and become disposed to close ranks under any scrutiny from outside; whistle-blowers are a thing of the past. Recommendations for the reform of ethical review It would be a great tragedy if our system of ethical review became adversarial under the pressure of the controversy machine that helped to spawn it. We do not believe that the system has yet assumed a fully adversarial profile, but there is a danger that it may be headed in that direction. It is therefore important at this juncture to try to reshape it. We conclude with some broad-gauge suggestions about the steps that need to be taken. Before offering those recommendations it may be useful to stress that they are all compatible, in our view, with the fundamental role of the ethics committee in protecting the interests of those affected by research and the interests of the community as a whole. While it is important that ethical review should not have an adversarial cast and should not assume an obstructive role, it is even more important that its role should not be compromised in any way. We believe that our suggestions (Box 2) do not threaten any compromise; on the contrary, we think, for reasons already indicated, that their implementation should help to further the ends of ethical review. These proposals are certainly not exhaustive of the things that might be done to make sure that the course of ethical review, despite its origins in the controversy machine, does not assume an adversarial direction. A widespread discussion among reviewers and researchers would be necessary to generate a full sense of the initiatives available. We hope that such a discussion will materialise and that the adversarial trajectory will not win out by default. References Report of the Review of the Role and Functioning of Institutional Ethics Committees. Canberra: AGPS, 1996. Allers M. Inquiry into the use of pituitary drug hormones in Australia and the Creutzfeldt-Jakob Disease. Canberra: AGPS, 1994. Gillespie R. Research on human subjects: an historical overview. Bioethics News 1989; 8 Suppl: 4-15. McNeil P. The ethics and politics of human experimentation. Cambridge: Cambridge University Press, 1993: 15-84. The Nuremberg Code. JAMA 1996; 276: 1691. Beecher H. Ethics and clinical research. N Engl J Med 1996; 274: 1354. Furrow B. Health law. New York: West Publishing, 1995: 839-841. Pettit P. Institutionalising a research ethic: chilling and cautionary tales. Bioethics 1992; 6: 89-112. MacDonagh O. A pattern of government growth 1800-60. London: Macgibbon and Kee, 1961. Ayres I, Braithwaite J. Reponsive regulation. New York: Oxford University Press, 1992. Grabosky P. Counterproductive regulation. Int J Sociol Law 1955; 24: 347-369. Sunstein CR. Paradoxes of the regulatory state. University of Chicago Law Review 1990; 57: 407-441. Footnote This paper represents the consensual view of the Australian Health Ethics Committee as that view was developed over the triennium 1994-1996. It was revised in the light of discussions in the Committee itself, and at a number of workshops throughout Australia in 1995, and was approved for publication by the Committee. Authors' details Law Faculty, University of Tasmania, Hobart, TAS. Donald Chalmers, LLM, Chair, Australian Health Ethics Committee 1994-. Research School of Social Sciences, Australian National University, Canberra, ACT. Philip Pettit, LPh, PhD, member, Australian Health Ethics Committee, 1994-1996. No reprints will be available from the authors. Correspondence: Professor P Pettit, Research School of Social Sciences, Australian National University, Canberra, ACT 0200. E-mail: pnpATcoombs.anu.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/>

Gestational diabetes mellitus -- management guidelines The Australasian Diabetes in Pregnancy Society Linda Hoffman, Chris Nolan, J Dennis Wilson, Jeremy J N Oats and David Simmons MJA 1998; 169: 93-97 Synopsis - Screening - Diagnosis - Management of GDM - Patient education - Fetal surveillance - Timing of delivery - Delivery - Neonatal management - Maternal follow-up - Directions for future research - Acknowledgements - References - Authors' details - - ©MJA1998 Synopsis GDM is defined as carbohydrate intolerance of variable severity with onset or first recognition during pregnancy. Universal screening is recommended. If selective screening is considered more appropriate (because of limited resources or known low GDM incidence), screening may be reserved for those at higher risk. Risk factors include glycosuria, age over 30 years, obesity, family history of diabetes, past history of GDM or glucose intolerance, previous adverse pregnancy outcome and belonging to a high risk ethnic group. The recommended screening test for GDM is performed at 26-28 weeks' gestation and positive results are: 1 hour venous plasma glucose level ≥7.8 mmol/L after a 50 g glucose load (morning, non-fasting); or 1 hour venous plasma glucose level ≥8.0 mmol/L after a 75 g glucose load (morning, non-fasting). Confirmation of diagnosis after a positive screening test: a 75 g oral glucose tolerance test (fasting) with a venous plasma glucose level at 0 hours of ≥5.5 mmol/L and/or at 2 hours of ≥8.0 mmol/L.* Patient education is very important and a team approach, if available, is beneficial. Dietary therapy is the primary therapeutic strategy, with insulin added where required to achieve the minimum goals for glycaemic control: fasting blood glucose <5.5 mmol/L, 1 hour postprandial <8.0 mmol/L or 2 hour postprandial <7.0 mmol/L. Careful antepartum fetal surveillance is essential. Continuation of the pregnancy in uncomplicated GDM to 10 days beyond term is acceptable provided that indications from fetal monitoring are reassuring. Close neonatal monitoring is important, particularly for the detection of hypoglycaemia. Maternal follow-up, with an oral glucose tolerance test, should be performed 6-8 weeks postpartum, then at least every 2 years, because of the increased risk of developing permanent diabetes. Prospective trials are needed to clarify whether universal screening is justified, and to determine the degree of maternal hyperglycaemia that causes an adverse outcome for the offspring. The management strategies in this article have been the subject of widespread discussion with the ADIPS membership between 1991 and 1998 at annual scientific meetings, annual general meetings, and in ADIPS newsletters. They represent the majority opinion. * Cut-off point for Australia; cut-off point in New Zealand ≥9.0 mmol/L. Introduction Gestational diabetes mellitus (GDM) is defined as carbohydrate intolerance of variable severity with onset or first recognition during pregnancy.1 Women with GDM are a heterogeneous group and may include those with unrecognised pre-existing non-insulin-dependent diabetes (type 2) and also a small number with insulin-dependent diabetes. The presence of GDM has implications for both the baby and the mother. Although there is no evidence that perinatal mortality is increased in pregnancies with treated GDM, some studies have shown perinatal mortality to be increased in untreated GDM.2-4 GDM is associated with increased perinatal morbidity, the characteristics of which are the same as for infants of mothers with overt diabetes (eg, macrosomia, neonatal hypoglycaemia, hyperbilirubinaemia, respiratory distress syndrome).5 In considering longer term outcomes for the baby, evidence is gradually mounting that GDM adds an intrauterine environmental risk factor to an already increased genetic risk for the development of obesity and/or diabetes.6-8 In one follow-up study insulin therapy for GDM was associated with less adiposity in the offspring.9 For the mother, GDM is a very strong risk factor for the development of permanent diabetes later in life (49.9% with up to 28 years' follow-up).10 Screening There has been much debate about whether universal or selective screening of pregnant women for GDM is more appropriate.11-13 Moses and Colagiuri recently estimated that, between 1991 and 1994, 50% of pregnant women in New South Wales were not screened for gestational diabetes.14The Australasian Diabetes in Pregnancy Society (ADIPS) recommends that screening for GDM should be considered in all pregnant women. However, if resources are limited, screening may be reserved for those at highest risk. Risk factors include: Glycosuria; Age over 30 years; Obesity; Family history of diabetes; Past history of GDM or glucose intolerance; Previous adverse pregnancy outcome; and Belonging to an ethnic group with a high risk for GDM. Ethnicity is a particularly important factor determining incidence of GDM (eg, very high risk -- Australian Indigenous, Polynesian and South Asian [Indian] groups; moderate high risk -- Middle Eastern and other Asian groups).15 Most Australian centres report a GDM incidence of 5.5%-8.8%.16-19 When selective screening is deemed more appropriate because of known low GDM incidence, the ADIPS criteria are similar to those recommended by the American "Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus".20 A recent article by Naylor et al21 derived a risk factor scoring system that excluded the need for screening up to a third of pregnant women. However, complex criteria for selective screening may cause difficulties in busy clinical practice. A summary of the screening and diagnostic procedures recommended by ADIPS is given in the Table. Diagnosis The guidelines for diagnosing GDM in Australia are essentially unchanged from those recommended for use in Australasia in 1991.22 Although there are no uniform international criteria for the diagnosis of GDM, commonly used criteria are those of O'Sullivan and Mahan23 and the World Health Organization (WHO).24 One problem with the development of absolute diagnostic criteria is the lack of evidence that perinatal mortality is increased in pregnancies associated with mild degrees of hyperglycaemia. The commonly used diagnostic criteria were not formulated to assess the risk of adverse perinatal outcomes, although this was a factor taken into account in the diagnostic criteria at the Mercy Hospital for Women, Melbourne.4 The existence of different methods of performing glucose tolerance tests has also hindered the development of uniform diagnostic criteria for GDM. After consensus, ADIPS has endorsed the diagnostic criteria developed by the working party chaired by Dr F I R Martin in 1991, which are modified WHO criteria.22 In New Zealand, the 2 hour oral glucose tolerance test (OGTT) cut-off value for a positive diagnosis is a venous plasma glucose level of 9.0 mmol/L. This figure was chosen by a majority decision of specialists at the 1992 meeting of the New Zealand Society for the Study of Diabetes. They chose the higher figure to reduce the worry and inconvenience for women of being given a false positive diagnosis and to reduce the strain on stretched specialist resources in many centres. ADIPS recognises the importance of working towards an Australasian consensus on this issue. If the clinical suspicion of GDM is high, a diagnostic OGTT is indicated, irrespective of the stage of pregnancy. In such circumstances, if an OGTT gives normal results early in pregnancy the test should be repeated between 26 and 30 weeks' gestation. A 75 g OGTT should use 75 g of anhydrous glucose or the equivalent, and preferably should also be performed after a high carbohydrate diet of at least 150 g of carbohydrate for three days. Management of GDM A team approach is ideal for managing women with GDM and, if available, should be used. The team would usually comprise an obstetrician, diabetes physician, a diabetes educator (diabetes midwifery educator), dietitian, midwife and paediatrician. In practice, however, the team approach is not always possible due to limited resources. In such circumstances, management by an obstetrician or obstetric general practitioner knowledgeable in GDM management, often with the assistance of an appropriately skilled dietitian, diabetes educator or midwife, is acceptable. Patient education The importance of educating women with GDM (and their partners) about the condition and its management cannot be overemphasised. Compliance with the treatment plan depends on the patient's understanding of: The implications of GDM for her baby and herself; The dietary and exercise recommendations; and The how and when as well as the goals of self monitoring of blood glucose level. Care should be taken to minimise the anxiety of the women. Glycaemic control Dietary therapy: Dietary therapy is the primary therapeutic strategy for the achievement of acceptable glycaemic control in GDM. All women should receive nutritional advice, preferably from an appropriately skilled dietitian. However, it is important to avoid a severe calorie-restricted diet, as this can predispose to ketonuria, and also to infants that are small for their gestational age, which carries an increased risk of diabetes in later life.25 The diet needs to: Conform with the principles of dietary management of diabetes in general; Meet the nutritional requirements of pregnancy; Be individualised for each patient, depending on maternal weight and body mass index; and Be culturally appropriate. Moderate exercise has recently been recognised as an adjunct therapy, with potential benefits when used together with diet, or diet and insulin therapy, in the management of gestational diabetes in women without a medical or obstetric contraindication.26 Monitoring: Glycaemic control needs to be monitored. Self monitoring of blood glucose level is the optimal method and is well tolerated by most women. On commencement of self monitoring, at least one fasting and one 1 or 2 hour postprandial glucose level should be obtained daily. The frequency may be decreased or increased depending on the results of the blood glucose monitoring and the progress of the pregnancy. If self monitoring is not possible, fasting and 1 or 2 hour postprandial laboratory capillary blood or venous plasma glucose levels should be performed regularly (at 1 to 2 weekly intervals). In pregnancies complicated by GDM, the value of self monitoring of blood glucose and appropriate insulin therapy in the prevention of macrosomia and its associated perinatal complications has previously been demonstrated.27,28 The minimum goals for glycaemic control are: a fasting capillary (venous plasma) blood glucose level <5.5 mmol/L a 1 hour postprandial capillary (venous plasma) blood glucose level <8.0 mmol/L a 2 hour postprandial capillary (venous plasma) blood glucose level <7.0 mmol/L. These minimum goals have been set on the basis of informed consensus opinion in Australasia and vary little from those of the American Diabetes Association clinical practice recommendations on gestational diabetes (fasting glucose ≤5.8 mmol/L and 2 hour postprandial plasma glucose ≤6.7 mmol/L).29 The setting of minimal goals for glycaemic control is controversial, however, as some, but not all, studies show benefit from tight glycaemic control in women with GDM.27,28,30-32 The reasons for the variance in results between studies may relate to differences in the underlying rates of GDM complications from one study population to another. The recommended fasting glycaemia goal of <5.5 mmol/L is supported by Langer et al, who have shown that rates of large-for-gestational-age (LGA) infants are increased in diet-treated GDM pregnancies if the fasting glucose level is between 5.3 and 5.8 mmol/L (28.6% LGA) compared with ≤5.3 mmol/L (5.35% LGA).32 Insulin treatment was shown to reduce the rates of LGA infants to 10.3% in GDM pregnancies with fasting glucose levels between 5.3 and 5.8 mmol/L.32 In support of the 1 and 2 hour postprandial glycaemic goals of <8.0 and <7.0 mmol/L, respectively, it has been shown that glycohaemoglobin (HbA1c) levels, birth weight, and rates of macrosomia, neonatal hypoglycaemia and caesarean section (for cephalopelvic disproportion) can all be significantly reduced in insulin-treated GDM subjects if insulin therapy is adjusted according to 1 hour postprandial, rather than preprandial, glucose measurements, aiming for <7.8 mmol/L.27 HbA1c levels may be used as an ancillary test, as assurance that the self monitored blood glucose results are appropriate. Fructosamine levels are reduced during pregnancy because of the dilutional effect of pregnancy on plasma proteins. HbA1c and fructosamine are not reliable substitutes for self monitoring of blood glucose level. Insulin therapy: Insulin therapy should be considered if the blood glucose goals are exceeded on two or more occasions within a 1 to 2 week interval, particularly in association with clinical or investigational suspicion of macrosomia. However, the benefit of instituting insulin therapy after 38 weeks' gestation is unproven. Human insulin should be used. No insulin preparations have a pregnancy category listing, except for the new, rapidly acting insulin analogue lispro, which is Category B2 (Australian medicines in pregnancy category). Two cases of congenital malformations were recently noted in women with insulin-dependent diabetes treated in pregnancy with lispro.33 The number of women treated with lispro in pregnancy is small to date, but no causative relationship between lispro and teratogenicity has been documented. In general, the insulin preparations and dosage schedules should be tailored to the abnormalities present in the glycaemic profile (eg, postprandial and/or fasting hyperglycaemia) and patient acceptability. The doses may be higher than those required in non-pregnant subjects and should be reviewed frequently so that adequate glycaemic control is achieved rapidly. Care should be taken to minimise the risk of hypoglycaemia, especially nocturnal episodes. Oral hypoglycaemic agents have no place in treatment of GDM under normal circumstances. Fetal surveillance The timing of commencement and the frequency of fetal monitoring in pregnancies complicated by GDM depend on the presence of other pregnancy complications such as pre-eclampsia, hypertension, antepartum haemorrhage and intrauterine growth retardation. The regimen chosen should be dictated by the severity of the obstetric complication. Monitoring may be by either Doppler umbilical bloodflow measurement or cardiotocograph (CTG). Although CTG surveillance is commonly undertaken routinely from around 36 weeks' gestation, there is no objective evidence that fetal monitoring in uncomplicated GDM affects fetal outcome.34 Common practice in the United States is to commence CTG monitoring after 40 weeks' gestation, while awaiting spontaneous onset of labour in uncomplicated GDM pregnancies,35 but again there is no evidence-based medicine to support or refute this practice. Ultrasonography should be considered at around 34 weeks' gestation to detect abnormalities of fetal growth and polyhydramnios. It may be indicated earlier in some women, for example for women unsure of their dates, or those with morbid obesity or suspected undiagnosed non-insulin-dependent diabetes. Ultrasonography may need to be repeated if any abnormality is detected. Timing of delivery The possibility that diagnosis of GDM may lead to increased obstetric intervention, including induction of labour and caesarean section,36 is a concern. Delivery before full term is not indicated unless there is evidence of macrosomia, polyhydramnios, poor metabolic control or other obstetric indications (eg, pre-eclampsia or intrauterine growth retardation).37 Continuation of the pregnancy in uncomplicated GDM to 10 days beyond term is acceptable provided that indications from fetal monitoring are reassuring. Delivery During labour, good glycaemic control needs to be maintained while avoiding hypoglycaemia. Lower insulin requirements are common during labour (often no insulin is necessary). Fetal surveillance is needed, as it is for any high risk pregnancy. A paediatrician should be present at the delivery if significant neonatal morbidity is suspected. The maternal blood glucose level should be monitored for 24 hours postpartum and, if indicated, continued for longer. Neonatal management The neonates of mothers with GDM are at risk of all the complications of infants born to mothers with overt diabetes, particularly those infants born macrosomic (birth weight >4000 g).38 The neonates should be observed closely after delivery for respiratory distress. Capillary blood glucose should be monitored at 1 hour of age and before the first four feeds (and for up to 24 hours in high risk neonates). Currently, some amperometric blood glucose meters are acceptable for use in neonates, provided that suitable quality control procedures and operator training are in place. A neonatal blood glucose level <2.0 mmol/L needs to be verified by repeat testing (laboratory verification is preferred but should not delay the initiation of treatment). Levels <2.0 mmol/L should be considered abnormal and treated. If the baby is obviously macrosomic, calcium and magnesium levels should be checked on Day 2. Breastfeeding is actively encouraged. Maternal follow-up It is important that women with GDM be counselled with regard to their increased risk of developing permanent diabetes. They should be made aware of the symptoms of hyperglycaemia. Advice should be given about the importance of healthy eating and exercise patterns. Contraceptive advice should be given in the puerperium, and women should be advised to plan future pregnancies and be reviewed medically by their general practitioner before conception (a pre-conception OGTT should be considered). An OGTT, using WHO criteria for the non-pregnant population, should be performed at 6-8 weeks' postpartum to exclude permanent diabetes. Repeat OGTTs should be performed at least every two years (possibly at the same time as the cervical cancer screening). Impaired glucose tolerance merits careful follow-up, which should include at least twice-yearly checks for frank diabetes in addition to assessment of other risk factors for macrovascular disease. The rates of development of permanent diabetes are much higher in several non-European ethnic groups. For example, the prevalence of type 2 diabetes in Polynesian women having a postpartum OGTT has been reported to be 30%.39 Life-table analysis in a cohort of Latino women shown to have normal glucose tolerance in the postpartum period after pregnancy complicated by GDM revealed a 47% cumulative incidence of type 2 diabetes 5 years after delivery.40 Similarly, 62% of women in Trinidad have been reported to develop type 2 diabetes after 3.6-6.5 years of follow-up.41 Follow-up OGTTs, therefore, should be more frequent than every two years in those groups at highest risk. Directions for future research ADIPS emphasises that, due to a lack of good quality randomised controlled clinical trials in the area of GDM, these guidelines are based on what is a reasonable consensus of informed opinion in Australasia. They are designed as a guide to practical management rather than a strict protocol. It is expected that the guidelines will not be static but will evolve as the results of clinical trials become available. Carefully designed, randomised controlled clinical trials are needed in order to determine: Whether universal screening programs are warranted; The optimal criteria for diagnosis of GDM; The costs v. benefits of the team approach; Optimal management (eg, clarification of the indications for insulin therapy); The role of follow-up programs for affected mothers and babies; and Possible interventions to reduce the rates of development of permanent diabetes in the mother. One such trial is the prospective Australasian Carbohydrate Intolerance Study in Pregnancy (ACHOIS), which aims to clarify what degree of maternal hyperglycaemia results in specific adverse outcome. In the design of these trials consideration needs to be given not only to perinatal outcome, but also to the potential long term benefits of diagnosis and treatment for both the baby and the mother. Acknowledgements The assistance of all members of ADIPS who contributed to the consensus statement is gratefully acknowledged. Valerie Arnol's assistance is also gratefully acknowledged. References Metzger BE, editor. Proceedings of the third international workshop-conference on gestational diabetes mellitus. Diabetes 1991; 40 Suppl 2: 1-201. O'Sullivan JB, Charles D, Mahan CM, Dandrow RV. Gestational diabetes and perinatal mortality rate. Am J Obstet Gynecol 1973; 136: 901-904. Pettitt DJ, Knowler WC, Baird HR, Bennett PH. Gestational diabetes: infant and maternal complications of pregnancy in relation to third trimester glucose tolerance in Pima Indians. Diabetes Care 1980; 3: 458-464. Oats JN, Beischer NA. Gestational diabetes. Aust N Z J Obstet Gynaecol 1986; 26: 2-10. Hod M, Merlob P, Friedman S, et al. Gestational diabetes mellitus: a survey of perinatal complications in the 1980s. Diabetes 1991; 40 (Suppl 2): 74-78. Van Asche FA, Aerts L, Holemans K. The effects of maternal diabetes on the offspring. Baillieres Clin Obstet Gynaecol 1991; 5: 485-492. Silverman BL, Metzger BE, Cho NH, Loeb CA. Impaired glucose tolerance in adolescent offspring of diabetic mothers: relationship to fetal hyperinsulinism. Diabetes Care 1995; 18: 611-617. Pettitt DJ. Diabetes in subsequent generations. In: Dornhurst A, Hadden DR, editors. Diabetes and pregnancy: an international approach. Chichester: J Wiley and Sons, 1996: 367-376. Simmons D, Robertson S. Influence of maternal insulin treatment on the infants of women with gestational diabetes. Diabet Med 1997; 14: 762-765. O'Sullivan JB. The Boston Gestational Diabetes Studies: review and perspectives. In: Sutherland HW, Stowers JM, Pearson DWM, editors. Carbohydrate metabolism in pregnancy and the newborn. London: Springer-Verlag, 1989: 287-294. Greene MF. Screening for gestational diabetes. N Engl J Med 1997; 337: 1625-1626. Jarrett RJ. Should we screen for gestational diabetes? BMJ 1997; 315: 736-737. Soares J de AC, Dornhurst A, Beard RW. The case for screening for gestational diabetes. BMJ 1997; 315: 737-739. Moses RG, Colagiuri S. The extent of undiagnosed gestational diabetes mellitus in New South Wales. Med J Aust 1997; 167: 14-16. Beischer NA, Oats JN, Henry OA, et al. Incidence and severity of gestational diabetes mellitus according to country of birth in women living in Australia. Diabetes 1991; 40: 35-38. Beischer NA, Wein P, Sheedy MT, Steffen B. Identification and treatment of women with hyperglycaemia diagnosed during pregnancy can significantly reduce perinatal mortality rate. Aust N Z J Obstet Gynaecol 1996; 36: 239-247. Moses R, Griffiths R, McPherson S. The incidence of gestational diabetes in the Illawarra area of New South Wales. Aust N Z Obstet Gynaecol 1994; 34: 425-427. Martin FIR, Ratnaike S, Wootton A, et al. The 75 g oral glucose tolerance in pregnancy. Diabetes Res Clin Pract 1995; 27: 147-151. Yue DK, Molyneau LM, Ross GP, et al. Why does ethnicity affect prevalence of gestational diabetes? The underwater volcano theory. Diabet Med 1996; 13: 748-752. Report of the expert committee on the diagnosis and classification of diabetes mellitus. Diabetes Care 1997; 20: 1183-1197. Naylor CD, Sermer M, Chen E, Farine D. Selective screening for gestational diabetes mellitus. N Engl J Med 1997; 337: 1591-1596. Martin FIR. The diagnosis of gestational diabetes. Med J Aust 1991; 155: 112. O'Sullivan JB, Mahan CM. Criteria for the oral glucose tolerance test in pregnancy. Diabetes 1964; 13: 278-285. World Health Organization Study Group, Diabetes Mellitus. World Health Organ Tech Rep Ser 1985; 727: 13-14. McCance DR, Pettitt DJ, Hanson RL, et al. Birth weight in non insulin dependent diabetes. Thrifty genotype, thrifty phenotype or surviving small baby genotype? BMJ 1994; 308: 942-945. Jovenovic-Peterson L, Peterson CM. Is exercise safe or useful for gestational diabetic women? Diabetes 1991; 40 Suppl 2: 179-181. De Veciana M, Major CA, Morgan MA, et al. Postprandial versus preprandial blood glucose monitoring in women with gestational diabetes mellitus requiring insulin therapy. N Engl J Med 1995; 333: 1237-1241. Langer O, Rodriguez DA, Xenakis EMJ, et al. Intensified versus conventional management of gestational diabetes. Am J Obstet Gynecol 1994; 170: 1036-1047. American Diabetes Association: clinical practice recommendations 1997. Diabetes Care 1997; 20 Suppl 1: S1-S70. Hare JW. Gestational diabetes mellitus. Levels of glycemia as management goals. Diabetes 1991; 40 Suppl 2: 193-196. Garner P, Okun N, Keely E, et al. A randomized controlled trial of strict glycemic control and tertiary level obstetric care versus routine obstetric care in the management of gestational diabetes: a pilot study. Am J Obstet Gynecol 1997; 177: 190-195. Langer O, Berkus M, Brustman L, et al. Rationale for insulin management in gestational diabetes mellitus. Diabetes 1991; 40 Suppl 2: 186-190. Diamond T, Kormas N. Possible adverse effect of insulin lispro. N Engl J Med 1997; 337: 1009-1010. Landon MB, Langer O, Gabbe SG, et al. Fetal surveillance in pregnancies complicated by insulin-dependent diabetes mellitus. Am J Obstet Gynecol 1992; 167: 617-621. Carr DB, Gabbe S. Gestational diabetes: detection, management and implications. Clin Diabetes 1998; 16: 4-11. Hunter DJS, Keirse MJNC. Gestational diabetes. In: Chalmers I, Enkin M, Keirse MJ NC, editors. Effective care in pregnancy and childbirth. Vol 1. Oxford: Oxford University Press, 1989: 403-410. Rasmussen MJ, Firth R, Roley M, Stronge JM. The timing of delivery in diabetic pregnancy: a 10-year review. Aust N Z J Obstet Gynaecol 1992; 32: 313-317. Maresh M, Beard RW, Bray CS, et al. Factors predisposing to and outcome of gestational diabetes. Obstet Gynaecol 1989; 74: 542-546. Simmons D, Conroy C, Thompson C. Diabetes in pregnancy in South Auckland. Proceedings of the Australasian Diabetes in Pregnancy Society Annual Scientific Meeting, Melbourne, 1995. Melbourne: ADIPS, 1995: 55. Kjos SL, Peters RK, Xiang A, et al. Predicting future diabetes in Latino women with gestational diabetes. Utility of early postpartum glucose tolerance testing. Diabetes 1995; 44: 586-591. Ali Z, Alexis SD. Occurrence of diabetes mellitus after gestational diabetes mellitus in Trinidad. Diabetes Care 1990; 13: 527-529. Authors' details Department of Diabetes and Endocrinology, Royal Hobart Hospital, Hobart, TAS. Linda Hoffman, MD, FRACP, Visiting Specialist. School of Nutrition and Public Health, Deakin University, and Geelong Hospital, Geelong, VIC. Chris Nolan, PhD, FRACP, Postdoctoral Research Fellow, and Visiting Specialist. Department of Endocrinology, The Canberra Hospital, Canberra, ACT. J Dennis Wilson, MD, FRACP, Director of Endocrinology. Master Misericordiae Mothers' Hospital, South Brisbane, QLD. Jeremy J N Oats, DM, FRACOG, Director, and Clinical Professor of Obstetrics and Gynaecology. Department of Medicine, Middlemore Hospital, University of Auckland, Auckland, New Zealand. David Simmons, MD, FRACP, Senior Lecturer in Medicine. Reprints: Associate Professor L Hoffman, Department of Diabetes and Endocrinology, Royal Hobart Hospital, 48 Liverpool Street, Hobart, TAS 7001. - 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/>

Linda Hoffman · Chris Nolan · David Simmons

Preventing suicide: what will work and what will not Stephen J Rosenman Population, not individual, approaches to suicide prevention MJA 1998; 169: 100-102 See also Dudley et al Suicide is the second most common cause of death among young men in the Western world.1 The emotional impact of suicide, especially of young people, on the community has produced a "do something, do anything" flurry of preventive activity, directed mostly at identifying and intervening with people at high risk.2,3 Much of the activity is ineffective4 and some may even make things worse.5-7 Here, I argue that focusing on people at "high risk" squanders resources, and that we may have to abandon this approach to suicide prevention as an immediate health target. Can we identify and assist high-risk individuals? Focusing prevention on people at "high risk" of suicide appears efficient because it seems to concentrate on those most likely to benefit. But can we identify high-risk individuals? Dimensional risk factors, such as hypertension or depression, have a linear relationship to mortality; only an arbitrary cut-off separates high risk from low risk.8 For conditions with multiple risk factors, such as coronary heart disease and also suicide, each factor adds a little to the risk, but often only when it interacts with other factors. No single predictor or combination of predictors is present in every individual, and membership of the high-risk group changes from moment to moment. Half a bottle of whisky may create a high suicide risk within an hour. As we learn to specify risk more precisely, the identified high-risk group gets smaller and -- while the individual risk of each member increases -- as a group they contribute a diminishing proportion of all suicides. Many more suicides come from the very much larger low-risk population. In a hypothetical population of 100 000, we may identify 500 people with a high suicide risk of, say, 10% (the 10-year suicide risk in schizophrenia, for example) and the remaining 99 500 with a low risk of, say, 0.1% (the approximate 10-year suicide risk in the population). The high-risk group will produce 50 suicides, while 100 will come from the low-risk group -- prevention targeted at high-risk people will miss most of the suicides. Another problem appears once we identify high-risk individuals. They then need advice and treatment that is effective, available and acceptable to them. How do we measure effectiveness if we can count only the failures? If we look at population suicide rates, agencies such as telephone suicide crisis services seem ineffective.4 Intervention after suicide attempts has not only been of little effect,9 but is also irregular in its availability, and frequently ignored by those it is intended to benefit.10,11 Those deemed at high risk, such as those discharged from hospital after a suicide attempt, already receive intensive follow-up, and further improvements will show diminishing returns of people saved.12 However, the insuperable problem in the high-risk approach arises when we try to use common characteristics of history and personality to identify individuals at risk of events that are uncommon in statistical terms. For events as infrequent as suicide, even highly specific and sensitive predictions will have high error rates.13 Theoretically, suicide predictions with 99% specificity will predict 1000 suicides in a population of 100 000; but the current suicide rate of around 15 per 100 000 population means that, in a year, fewer than 20 will be correct predictions. In the real world, where 85% is "good" specificity, those who will ultimately die are hidden in a haystack of people "at risk". If a high-risk approach is ineffective, is any other strategy better? Newer approaches and paradigms for prevention in public health have not fully penetrated policymaking for mental disorders. William Haddon, a former Director of the United States National Highway Safety Bureau, propounded principles for injury prevention which widened the focus from the victim to the array of environmental interactions amenable to change (see below).14 More radically, Geoffrey Rose, an epidemiologist at the London School of Hygiene, switched the spotlight away from individuals at high risk of suicide and turned it onto whole populations.15 He argued that mortality falls more if we reduce the whole population's exposure to factors related to suicide than if we identify and treat high-risk people. Time to consider a population-based approach? The principle of the "population-based" approach is to apply preventive strategies to the whole population or subpopulation in order to shift the distribution of risk, so that at any time fewer people are over the threshold that leads to completed suicide16 (see Figure). We do not have to identify the individuals within the population to save them. This is demonstrated by the successful reduction in mortality from road trauma and from cardiovascular disease. These successes should now be models for suicide prevention. Road trauma deaths in Australia decreased after the apparently inexorable rise seen in the 1960s,17 and this decline clearly followed the introduction of measures that applied to the whole population. These measures -- seat belts, random breath tests for alcohol, speed-limit enforcement, and improvements to roads and cars -- succeeded where strategies to identify the "high-risk" individual -- the dangerous driver, "the nut holding the steering wheel" -- had failed or aggravated the problem. Each measure, ranging from those most proximate to the crash (seat belts, collapsible steering columns) through the antecedent conditions (alcohol, speed) to the most nebulous antecedents, such as public attitudes to road safety,18 contributed its bit to the sum of prevention, and mortality fell without anyone identifying a high-risk individual or tackling the chain of causes which explain an individual death. Indeed, by 1968, Haddon had already challenged myths of accident prevention: ". . . because drivers cause most accidents [we assume that] programs correspondingly must be concerned with drivers. In the real world there is no basis for making this assumption [which] leads to demonstrably false conclusions."19 The decline in cardiovascular disease mortality is not explained by the vigorous treatment of high-risk people. Established risk habits such as smoking and diet were strikingly resistant to change in high-risk individuals.20 More importantly, most cardiac deaths occur among the large numbers of lower-risk people. Overall cardiovascular mortality fell with the change in community-wide attitudes to cigarettes, diet, inactivity and stress.21 At first sight, suicide prevention in these terms seems much more difficult because the antecedents of suicide appear harder to discern and change. However, if we take what we do know about suicide risk and apply it to the population rather than to defining the individual at risk, reducing suicide may become feasible.4,12 How do we put a population-based approach into practice? Restricting access to the means of suicide (eg, by detoxification of domestic and vehicle exhaust gases, gun regulation, control of dangerous medication) will tackle the most proximate antecedents. Close antecedents susceptible to reduction include drug and alcohol abuse; the population load of mood disturbances, including clinical and subclinical depression;22-24 conduct disorders;22 and media modelling of suicide.25 The more remote antecedents in all age groups include socioeconomic deprivation26 and, to a surprisingly uncertain degree, unemployment.4,27 In younger populations, family breakdown and alienation, relationship losses, school failure and suspension may portend suicide,28 while in older populations loneliness and physical morbidity may do so.29 In Aboriginal populations, suicide is prefigured by substance abuse and high incarceration rates, which are problems for the whole community to address, not just the problems of high-risk individuals.30,31 What to do and where to start? Haddon and Baker14 assert that we should first do those things we can, rather than struggling with things we cannot define or alter. Attacks on access to means of suicide, such as firearms32 and car exhausts,33 are within our present reach. By a large margin, they will have the strongest and most immediate effect in reducing suicide rates,4 even though such measures may not strike at what might seem the most "important" emotional antecedents. The problem with social antecedents, such as alienation or drug abuse, is that they demand difficult social engineering. It is unpromising to try to reconstruct families after they have broken down. Reducing the incidence of family breakdown and other such antecedents in the community may not be easier, but may be more profitable34 in terms of prevention, and for this medical efforts must harmonise with other social and educational initiatives. Of course, these antecedent problems (and others such as mental illness) warrant action on their own merits, not just as targets in suicide prevention initiatives. We cannot comfortably assume that education campaigns will always help, and there are good arguments against tackling prevention through "suicide prevention" or "education" campaigns. In the past, school-based driver education in the United States was associated with unexpectedly higher road accidents and deaths.35 Suicide education campaigns in schools not only miss excluded students, but have also shown complex and possibly harmful effects on attitudes to suicide6,10 and on completed suicide.7 The final analysis Firstly, identifying and treating high-risk individuals is unlikely to result in lower suicide rates. The refinement of individual assessment has passed the point of diminishing returns, and the obsessive study of suicidal individuals will not uncover the Holy Grail of perfect prediction. Clearly, we will not stop doing our best for distressed and suicidal people, even though this will not reduce population suicide rates. But this is not prevention. Secondly, pessimism about suicide may not be justified, despite the rising rates. The turnaround in the rising road toll and in cardiovascular disease teaches what can be done. The lesson is that measures which reduce overall risk in the whole population will reduce the number of people above the fatal threshold, and we do not need to identify the high-risk people individually. Consequently, we may have to abandon the frontal assault on suicide. We cannot justify prevention campaigns driven by the suicidal risk of individuals, despite the intuitive and political appeal of such measures. Indeed, to the degree that they drive resources into ineffective strategies, current approaches to "suicide prevention" may impede suicide prevention. Instead, we must "bite the bullet" in restricting access to means of suicide, the most proximate factor. Beyond that, we need the diligent, unspectacular work in the population which mitigates those factors which lead, among other things, to suicide. For medicine, it is to treat the ill,36 whether or not they are suicidal, and, from a public health pulpit, to address the social ills which produce morbidity, whether or not they lead to suicide. References Pritchard C. New patterns of suicide by age and gender in the United Kingdom and the Western World 1974-1992; an indicator of social change? Soc Psychiatry Psychiatr Epidemiol 1996; 31: 227-234. CDC. From the Centers for Disease Control and Prevention. Suicide among children, adolescents and young adults -- United States 1980-1992. JAMA 1995; 274: 451-452. Commonwealth Department of Health and Family Services (Australia). Youth suicide in Australia: the National Youth Suicide Prevention Strategy. Canberra: Australian Government Printing Service, 1997. Gunnell D, Frankel S. Prevention of suicide: aspirations and evidence. BMJ 1994; 308: 1227-1233. Shaffer D, Garland A, Vieland V, et al. The impact of curriculum-based suicide prevention programs for teenagers. J Am Acad Child Adolesc Psychiatry 1191; 30: 588-596. Hazell P, King R. Arguments for and against teaching suicide prevention in schools. Aust N Z J Psychiatry 1996; 30: 633-642. Lester D. State initiatives in addressing youth suicide: evidence for their effectiveness. Soc Psychiatry Psychiatr Epidemiol 1992; 27: 75-77. Patton GC, Harris R, Carlin JB, et al. Adolescent suicidal behaviours: a population based study of risk. Psychol Med 1997; 27: 715-724. Deykin E, Chung-Chen H, Joshi N. Adolescent suicidal and self-destructive behaviours: results of an intervention study. J Adolesc Health Care 1986; 7: 88-95. Shaffer D, Garland A, Gould MS, et al. Preventing teenage suicide: A critical review. J Am Acad Child Adolesc Psychiatry 1988; 27: 675-687. Goldney RD. Out-patient follow-up of those who have attempted suicide: fact or fantasy? Aust N Z J Psychiatry 1975; 9: 111-113. Lewis G, Hawton K, Jones P. Strategies for preventing suicide. Br J Psychiatry 1997; 171: 351-354. Pokorny AD. Prediction of suicide in psychiatric patients. Arch Gen Psychiatry 1983; 40: 249-257. Haddon W, Baker SP. Injury control. In: Clark DW, McMahon B. Preventive and community medicine. Boston: Little Brown, 1981. Rose G. The strategy of preventive medicine. Oxford: Oxford University Press, 1985. Rose G. Mental disorder and the strategies of prevention. Psychol Med 1993; 23: 553-555. Federal Office of Road Safety (FORS). Trends in road safety. Monograph No 1. Canberra: FORS, 1997. Graham JD. Injuries from traffic accidents: Meeting the challenge. Annu Rev Public Health 1993; 14: 515-543. Haddon W. The changing approach to the epidemiology, prevention and amelioration of trauma: the transition to approaches etiologically rather than descriptively based. Am J Public Health 1968; 58: 1431-1438. Susser M. The tribulations of trials: Intervention in communities [editorial]. Am J Public Health 1995; 85: 156-158. Epstein FH. Cardiovascular disease epidemiology: a journey from the past into the future. Circulation 1996; 93: 1755-1764. Shaffer D, Gould MS, Fisher P, et al. Psychiatric diagnosis in child and adolescent suicide. Arch Gen Psychiatry 1996; 53: 339-348. Depression and suicide: are they preventable [editorial]? Lancet 1992; 340: 700-701. Brent DA, Perper JA, Goldstein CE, et al. Risk factors for adolescent suicide. Arch Gen Psychiatry 1988; 45: 581-585. Phillips DP, Carstensen MS. Clustering of teenage suicides after television news stories about suicide. New Engl J Med 1986; 315: 685-689. Gunnell DJ, Peters TJ, Kammerling RM, Brooks J. Relation between parasuicide, suicide psychiatric admissions and socioeconomic deprivation. BMJ 1995; 311: 226-230. Platt S. Unemployment and suicidal behaviour: a review of the literature. Soc Sci Med 1984: 19; 93-115. Gould MS, Fisher P, Parides M, et al. Psychosocial risk factors of child and adolescent completed suicide. Arch Gen Psychiatry 1996; 53: 1155-1162. Draper BM. Prevention of suicide in old age. Med J Aust 1995; 162: 533-534. Royal Commission into Aboriginal Deaths in Custody. National Report. Canberra: Australian Government Publishing Service, 1991. Hunter E. An examination of recent suicides in remote Australia: Further information from the Kimberley. Aust N Z J Psychiatry 1991; 25: 197-202. Kellerman AL, Rivara F, Somes G, et al. Suicide in the home in relation to gun ownership. New Engl J Med 1992; 327: 467-472. Rosenman SJ. Car exhaust suicide. Med J Aust 1997; 166: 288-289. Zigler EF, Taussig C, Black K. Early childhood intervention: a promising preventative for juvenile delinquency. Am J Psychol 1992; 47: 997-1006. Robertson LS. Crash involvement of teenaged drivers when driver education is eliminated from high school. Am J Public Health 1980; 70: 599-603. Wilkinson G. Can suicide be prevented? Better treatment of mental illness is more appropriate aim. BMJ 1994; 309: 860-861. Authors' details Canberra Psychiatry Group, and National Health and Medical Research Council Psychiatric Epidemiology Research Centre, Canberra, ACT Stephen J Rosenman, MD, FRANZCP, Psychiatrist. Reprints: Dr Stephen J Rosenman, GPO Box 610, Canberra, ACT 2601. E-mail: sjrATatrax.net.au - 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/>

Stephen J Rosenman