Editorials

Spina bifida We can reduce the incidence of this congenital defect with folate fortification of food MJA 1998; 169: 182-183 Each year about 80 babies in Australia are born with spina bifida, a congenital malformation. Spina bifida, including meningocele and meningomyelocele, is one of the spectrum of birth defects known as neural tube defects (NTDs). These defects result from failure of the neural tube to close normally during the first five weeks of embryonic life. The severity of the defect depends on where it occurs and whether nervous tissue or only meninges are involved. At least 80% of people with spina bifida have an Arnold-Chiari malformation and associated hydrocephalus, often requiring a ventricular shunt. Other chronic problems include impaired mobility, bladder and bowel dysfunction, and scoliosis, all of which contribute to high medical and psychosocial morbidity. The incidence of NTDs varies considerably according to geography and ethnicity, ranging from 0.8 to more than 10 per 1000 live births. The incidence in Australia is currently 1.1 per 1000 live births.1 Recurrence risks, which are dependent on the background incidence, reflect this variation. In Australia the recurrence risk for a couple with a previous NTD-affected pregnancy is 3%-4%, and the risk for any first-degree relatives is 1%.2 About 10% of NTDs are caused by chromosomal anomalies, predominantly trisomy 18 and triploidy, or by single-gene disorders. Maternal factors, including diabetes mellitus and exposure to the anticonvulsants valproic acid and carbamazepine, also predispose to NTDs.3 However, most NTDs are isolated malformations and are thought to be multifactorial in origin, caused by an interaction between a genetic predisposition and environmental factors.4 The B group vitamins folic acid (folate) and vitamin B12 appear to be involved in NTDs. These vitamins share metabolic pathways involved in DNA synthesis (Figure), so that a deficiency or metabolic derangement affecting either vitamin may result in impaired cell proliferation and an increased risk of congenital defects. The underlying biology is complex -- several studies have shown that women with NTD-affected pregnancies do not have folate and vitamin B12 levels in the defined deficiency ranges, although some have abnormalities such as hyperhomocysteinaemia, which suggest subtle metabolic defects.5,6 One important genetic influence may be a mutation in the gene for 5,10-methylenetetrahydrofolate reductase, an enzyme involved in folate metabolism (Figure). About 12% of the Caucasian population is homozygous for a mutation which produces a heat-labile form of this enzyme with reduced activity and higher folate requirements.7 This causes higher serum homocysteine levels, and is associated with a greater risk of NTD-affected pregnancies.8 NTDs can be prevented by reducing the incidence in all pregnancies (primary prevention), or by termination of affected pregnancies (secondary prevention). In Australia the rate of spina bifida in live births declined gradually from 7.1 per 10 000 births in 1987 to 2.9 per 10 000 births in 1994. During the same period the number of induced abortions carried out before 20 weeks' gestation for spina bifida increased, although notification of these therapeutic abortions was incomplete.1 These figures indicate that secondary prevention of NTDs is occurring throughout Australia, largely because of improvements in antenatal diagnosis. Antenatal diagnosis of NTDs usually involves maternal serum alpha-fetoprotein (MSAFP) estimation at 15-17 weeks' gestation (raised in NTD-affected pregnancies), followed by targeted ultrasound scanning at 18-19 weeks' gestation.9 The combined sensitivity of these two investigations is greater than 90%. Women at increased risk of an NTD-affected pregnancy may be offered first-trimester vaginal ultrasound and amniotic fluid alpha-fetoprotein and acetylcholinesterase estimation. Alpha-fetoprotein is raised, and acetylcholinesterase detectable, in NTD-affected pregnancies.10 Primary prevention of NTDs is preferable to secondary prevention. Although the mechanisms are not entirely understood, it is well established that periconceptional supplementation with folic acid plays a role in reducing by more than 70% the risk of both the first occurrence11 and the recurrence of NTDs.12 Therefore, current recommendations are that women planning a pregnancy should supplement their diets with 0.5 mg (500 µg) of folic acid daily, starting from at least one month before conception and continuing for the first 12 weeks of pregnancy. Women at increased risk of an NTD-affected pregnancy, including those with a previous NTD-affected pregnancy or a close family history of NTDs, should supplement their diet with 5 mg of folic acid daily.13,14 Despite apparent acceptance of the need for folic acid and the realisation that many Western women do not consume sufficient dietary folate, there has been relatively poor compliance with regimens of periconceptional folic acid supplementation.15,16 One of the main reasons is that at least half of all pregnancies are unplanned. Another reason is that some people cannot afford a folate-rich diet and others are unaware of what constitutes such a diet. There are also indications that obstetricians and general practitioners do not adequately educate and counsel their female patients of reproductive age about the need for periconceptional folic acid supplementation.17 Although education of women and their physicians to ensure consumption of folate-rich foods (such as green leafy vegetables) must continue, the relatively simple and inexpensive strategy of fortification of cereals, breads, pasta and milk would be more efficacious, as it does not involve specific planning or significant alteration of a woman's normal lifestyle or behaviour. This strategy is being applied in the United States -- in January 1998 the Food and Drug Administration, after considerable debate, made fortification of cereals with folic acid mandatory. In Australia, unfortunately, the National Health and Medical Research Council's Food Fortification Panel recommended only voluntary fortification, pending future review.18 Australian companies have not acted; the only folate-fortified breakfast cereals available in Australia are marketed by an American company. Let us hope that local companies will develop the vision to play a role in public health, and adopt voluntary food fortification policies. Debra S Kennedy Staff Specialist in Clinical Genetics Royal Prince Alfred Hospital, Sydney, NSW References Lancaster P, Hurst T, Day P, et al. Congenital Malformations Australia 1993 and 1994. Australian Institute of Health and Welfare National Perinatal Statistics Unit. Birth Defects Series, Number 2, 1997. Harper PS. Practical genetic counselling. 4th ed. Oxford: Butterworth-Heinemann, 1993; 177. Holmes LB. Spina bifida: anticonvulsants and other maternal influences. Ciba Found Symp 1994; 181: 232-238. Hall JG, Friedman JM, Kenna BA, et al. Clinical, genetic, and epidemiological factors in neural tube defects. Am J Hum Genet 1988; 43: 827-837. Mills JL, McPartlin JM, Kirke PN, et al. Homocysteine metabolism in pregnancies complicated by neural-tube defects. Lancet 1995; 345: 149-151. Kirke PN, Molloy AM, et al. Maternal plasma folate and vitamin B12 are independent risk factors for neural tube defects. Q J Med 1993; 86: 703-708. Wilcken DEL. MTHFR 677C®T mutation, folate intake, neural tube defect, and cardiovascular risk [commentary]. Lancet 1997; 350: 603-604. van der Put NMJ, Steegers-Theunissen RPM, Frosst P, et al. Mutated methylene tetrahydrofolate reductase as a risk for spina bifida. Lancet 1995; 346: 1071-1072. Nodel AS, Green NK, Holmes LB, et al. Absence of need for amniocentesis in patients with elevated levels of maternal serum alpha fetoprotein and normal ultrasonographic examinations. N Engl J Med 1990; 323: 557-561. Wald N, Cuckle M, Nanchahal K. Amniotic fluid acetylcholinesterase measurement in the prenatal diagnosis of open neural tube defects. Second report of the Collaborative Acetylcholinesterase Study. Prenat Diagn 1989; 9: 813-829. Czeizel AE, Dudas I. Prevention of the first occurrence on neural-tube defects by periconceptional vitamin supplementation. N Engl J Med 1992; 327: 1832-1835. Medical Research Council Vitamin Study Research Group. Prevention of neural tube defects: results of the Medical Research Council Vitamin Study. Lancet 1991; 338: 131-137. National Health and Medical Research Council. Revised statement on the relationship between dietary folic acid and neural tube defects such as spina bifida. Canberra: NHMRC, 1993. From the Centers for Disease Control and Prevention: recommendations for use of folic acid to reduce the number of spina bifida cases and other neural tube defects. JAMA 1993; 269: 1233-1238. Clark NA, Fisk NM. Minimal compliance with the Department of Health recommendation for routine prophylaxis to prevent fetal neural tube defects. Br J Obstet Gynaecol 1994; 101: 709-710. Marsack CR, Alsop CL, Kurinczuk JJ, Bower C. Pre-pregnancy counselling for the primary prevention of birth defects: rubella vaccination and folate intake. Med J Aust 1995; 162: 403-406. Perelman V, Singal N, Einarson A, et al. Knowledge and practice by Canadian family physicians regarding periconceptional folic acid supplementation for the prevention of neural tube defects. Can J Clin Pharmacol 1996; 3: 145-148. National Health and Medical Research Council. Report of the expert panel on folate fortification. Canberra: NHMRC, 1994. - 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/>

Debra S Kennedy

Matters of life and death: the challenge of CPR decision making How can we improve patient involvement in this complex process? MJA 1998; 169: 124-125 Since its introduction in the 1960s and subsequent widespread dissemination, cardiopulmonary resuscitation (CPR) has saved the lives of many who would otherwise have perished. Today, whenever a patient's heart stops beating, carers are faced with an extraordinary choice. Either they may do nothing and allow the patient to die, or they may use CPR and try to breathe life back into the dying individual. How should this choice be made? Over the past 20 years numerous studies have sought opinions on this dilemma. In this issue of the Journal Kerridge et al report on the first Australian survey into the attitudes of hospital inpatients and staff.1 The authors used a simple cross-sectional design to quiz both patients and healthcare professionals at Newcastle's John Hunter Hospital. They sought attitudes on a range of matters concerning CPR and the decision-making processes that surround its use. Despite the study's shortcomings, such as relatively low response rates and the treatment of the study population as homogeneous, the results contain some interesting and apparently paradoxical findings. Although a large proportion of both patients and healthcare professionals felt that doctors should always ask patients whether they would like CPR, only a very small percentage of patients had actually discussed CPR with their doctors. This perplexing result mirrors the findings of international studies that surveyed far sicker inpatient samples. In two studies, Bedell and co-workers examined patients in Boston who had either required CPR or had been the recipients of do-not-resuscitate orders. Only about 20% of these patients had been involved in their own CPR decisions.2,3 Why is CPR decision making such a difficult issue, and what could be done to improve matters? The hardest thing about CPR decision making is the timing of the decision. Obviously, at the moment a patient requires CPR, he or she is unable to declare a preference about whether resuscitation should occur. Furthermore, patients usually lose their ability to consider CPR options well before the procedure is needed. Only about 20% of patients are competent at the time a do-not-resuscitate order is considered.3,4 Consequently, any patient input into the decision making process must be taken well before the final decision is needed. The patient must declare a position in advance. However, gaining a patient's preferences about CPR, and documenting them, is complicated by a series of other problems. Firstly, the details of advanced CPR and its efficacy are poorly understood by the general public. Providing patients with sufficient information to allow an informed decision is difficult and time consuming. It seems extremely unlikely that any simple method of seeking CPR preferences (upon, say, a patient's admission to hospital) would yield either valid or usable data.5 Secondly, advanced CPR involves a multitude of procedures and many patients may be willing to undergo some of these but not others.6 CPR decisions are not simple "yes or no" choices. Thirdly, although we know that likelihood of survival influences patients' preferences about CPR, it is often difficult to make predictions on the likelihood of benefit for any individual patient.5,7 These predictions become more difficult the longer the period between the prediction and the resuscitation. Fourthly, although people are inclined to believe that they can accurately predict whether they would want CPR in some future situation, this may not be the case. Weighing up risks and benefits hypothetically is quite different to weighing them up in reality. A number of lines of evidence suggest that, in general, the sicker people become the more likely they are to opt for intervention.8 Finally, although there is good evidence that patients find discussion of CPR neither cruel nor insensitive, discussions about death are frequently upsetting for patients and for their doctors.4 When there is no pressure for a CPR decision, it is no surprise that both patients and their doctors are disinclined to bring the matter up. In the face of so many obstacles, how are we to proceed? While guidelines, legislative initiatives, and targeted interventions may all have a role in improving the way CPR decisions are made, there are no simple answers to this dilemma. Generally, patient preferences about CPR must be the most important ingredients in CPR decision making, but these are hard to obtain and may not always be valid in a given situation. Even if one knows the patient's preferences, there can be no doubt that the complex nature of the factors that surround a decision to resuscitate will, on occasion, justify taking a course apparently contrary to the patient's wishes. The best CPR decisions will follow preparations that began long before the patient's heart was stilled. They will involve considered consultation with the patient, family and other healthcare professionals. They will require examination of the evidence relevant to the patient's predicament and they will rest on careful deliberation of all the issues of concern to that patient on that day. They will call forth the finest compassion but, for all of this, they will often fall short of a perfect result. Put simply, the best CPR decisions will involve the best clinical care, and providing that is the challenge for us all. Christopher J Ryan Consultation-Liaison Psychiatrist, University of Sydney, and Department of Psychiatry, Westmead Hospital, Westmead, NSW Kerridge I, Pearson S-A, Rolfe IE, Lowe M. Decision making in CPR: attitudes of hospital patients and healthcare professionals. Med J Aust 1998; 169: 128-131. Bedell SE, Delbanco TL. Choices about cardiopulmonary resuscitation in the hospital. When do physicians talk with patients? N Engl J Med 1984; 310: 1089-1093. Bedell SE, Pelle D, Maher PL, Cleary PD. Do-not-resuscitate orders for critically ill patients in the hospital. How are they used and what is their impact? JAMA 1986; 256: 233-237. Stolman CJ, Gregory OJ, Dunn D, et al. Evaluation of patient, physician, nurse and family attitudes toward do not resuscitate orders. Arch Intern Med 1990; 150: 653-658. Murphy DJ, Burrows D, Santilli S, et al. The influence of the probability of survival on patients' preferences regarding cardiopulmonary resuscitation. N Engl J Med 1994; 330: 545-549. Youngner SJ. Do not resuscitate orders: no longer a secret, but still a problem. Hastings Centre Report 1987; 18: 24-33. Frankl D, Oye RK, Bellamy P. Attitudes of hospitalised patients toward life support: a survey of 200 inpatients. Am J Med 1989; 86: 645-648. Ryan CJ. Betting your life: an argument against certain advance directives. J Med Ethics 1996; 22: 95-99. - 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/>

Christopher J Ryan

Twenty-four hour access to health information and advice An essential component of the healthcare system MJA 1998; 169: 125-126 As the style and funding of healthcare continues to change and evolve, one constant is the need for patients to have access to timely and credible health information. Indeed, it is probable that with the changing nature of the doctor-patient relationship, the doctor's role as the provider of information is becoming more important. Parents, in particular, need information about their children's health,1 and information given in the context of a consultation has been shown to increase patient knowledge,2 decrease anxiety and improve compliance.3 Previously, patients have relied on information and advice being supplied by their healthcare provider, but they now have access to other sources such as the popular media and the Internet.4 However, not all patients have the technical and literacy skills to benefit from written or computer-generated information and, even if they do, it may be difficult for them to extrapolate general information to their own specific problems. Furthermore, because medical problems are often acute and unexpected, it is impossible for patients to predict what information they will need and when they will need it. It is therefore not surprising that the telephone now plays such an important role in healthcare delivery. The provision of around-the-clock telephone advice, especially by hospitals, has been well documented in Australia,5 the United Kingdom6 and North America.7 In this issue of the Journal Fatovich et al8 report the results of their study of telephone advice provided by a hospital emergency department. As well as assessing the usual logistic and demographic data, which can limit the generalisability of findings depending on the particular hospital studied and the community it serves, the authors have attempted to determine the appropriateness of the advice given by hospital staff and the level of patient compliance. The results are not especially striking or surprising, but they raise some important issues for policymakers, hospitals and community-based health providers. There is a huge discrepancy between the amount of attention (and resources) devoted to face-to-face as opposed to telephone consultations. Doctors and nurses undergo extensive supervised training to provide clinical services, there is increasing emphasis on clinical guidelines and evidence-based medicine, good record keeping is considered an important component of quality services -- yet none of these standards has been applied to the provision of telephone advice. Lack of specific funding is also a major issue, especially if, as indicated by the study, emergency departments receive up to 33 phone calls per 100 attendances. The combination of the financial pressure of maintaining a service which is not funded by government, and concern about the medicolegal implications of advice given in an ad hoc manner by relatively junior staff without referring either to medical records or generating any written documentation about the advice given, has led at least one large teaching hospital to discontinue interactive telephone advice and replace it with a recorded information service.9 Presumably general practitioners, community health centres and community nurses also provide telephone advice, although no data are available to estimate the absolute number and proportion of calls relative to the number and proportion received by hospitals. The fact that most calls to hospitals are made after hours may well reflect the unavailability of the patients' usual healthcare provider at this time. Nevertheless, if telephone advice is considered a core part of healthcare services, one might argue that after-hours coverage in the community could be organised in the same way as after-hours locum services. Again, the lack of any remuneration and the potential medicolegal risks are major disincentives. In North America, telephone advice has been accepted as an inevitable part of healthcare services to the extent that individual providers have formally scheduled "call hours", when their patients can call knowing that the doctor or nurse has dedicated this time to the provision of telephone consultations. Furthermore, specific telephone protocols and guidelines have been developed10,11 and evaluated,12 and phone consultation is increasingly becoming part of the training of hospital staff. Twenty-four-hour access to health information and advice has become a service that the community regards as essential. Just as essential is the need for governments and providers to begin to address some of the issues to do with funding, training, quality control and medicolegal responsibility. A possible benefit, which has not been explored systematically, could be the use of hospital telephone advice lines to publicise community-based services and encourage callers to use such services, thus minimising hospital attendances. Furthermore, systematic analyses of calls could provide important information for health promotion efforts and the organisation of health services in a region or community. These are areas that need to be explored if we are serious about developing integrated, cost-effective, "seamless" services and avoiding duplication and fragmentation. Frank Oberklaid Director, Centre for Community Child Health and Ambulatory Paediatrics Royal Children's Hospital, Melbourne, VIC Hall DMB, editor. Health for all children. Oxford: Oxford University Press, 1996. Isaacman DJ, Purvis K, Gyuro J, et al. Standardised instructions: do they improve communication of discharge information from the emergency department? Pediatrics 1992; 89: 1204-1208. Glascoe FP, Oberklaid F, Dworkin PH, Trimm F. Brief approaches to educating patients and parents in primary care. Pediatrics (In press). Vol 101. Also on the American Academy of Pediatrics "web site" <www.pediatrics.org>. Carlile S, Sefton AJ. Healthcare and the information age: implications for medical education. Med J Aust 1998; 168: 340-343. Oberklaid F, Bell J, Duke V. Paediatric telephone consultation -- a neglected area of health service delivery. Aust Paediatr J 1984; 20: 113-114. Crouch R, Patel A, Williams S, Dale J. An analysis of telephone calls to an inner-city accident and emergency department. J Royal Soc Med 1996; 89: 324-328. Perrin EC, Goodman HC. Telephone management of acute pediatric illness. N Engl J Med 1978; 298: 130-135. Fatovich DM, Jacobs IG, McCance JP, et al. Emergency department telephone advice. Med J Aust 1998; 169: 143-146. Royal Children's Hospital, Melbourne. Kid's Health Infoline, 1997. Schmitt BD. Pediatric telephone advice. Boston. Little Brown and Company, 1980. Levy JC, Rosenkrans J, Lamb GA, et al. Developmental and field testing of protocols for the management of pediatric telephone calls: protocol for pediatric telephone calls. Pediatrics 1979; 64: 558-563. Strasser PH, Levy JC, Lamb GA, Rosenkrans J. Controlled clinical trial of pediatric telephone protocols. Pediatrics 1979; 64: 553-557. - 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/>

Frank Oberklaid

General practice stress Winds of change buffet general practitioners MJA 1998; 169: 126-127 The long-running television series GP,1 with its changing cast of "general practitioners" and patients, nicely portrayed the enormous range and diversity of human problems which Australians expect their general practitioners (GPs) to help them solve. The series showed GPs to be ordinary humans, affected like the rest of the community by changing social and political pressures. In recent years, Australian GPs have felt particularly buffeted by their changing roles and feelings of being undervalued in comparison with their specialist colleagues. A national survey of GPs carried out in 19952 showed that, while about two-thirds were satisfied with their current role, 35 per cent indicated that they would leave general practice if they had somewhere else to go, with urban practitioners significantly more likely than their rural colleagues to report this view. The most common sources of dissatisfaction or frustration were a belief that the contribution of GPs is not appreciated by government, apprehensiveness about the changes and reforms in general practice, a belief that government was interfering in the ability to make clinical decisions, pressure to bulk bill patients, and the introduction of "blended" payments (remuneration through a mixture of fee-for-service and non-fee-for-service payments). In this issue of the Journal, Schattner and Coman3 report on a national sample of metropolitan GPs and their perceptions of stress in their work lives. One hundred and fifty-seven of the 296 respondents (53%) had considered leaving general practice because of occupational stress, and 32 (10.8%) claimed that they had experienced severe occupational stress in the past 12 months. Major work stressors (in terms of both frequency and severity) were time pressure to see patients, paperwork in general practice, and too much work to do in a limited time -- factors the authors define as linked to the context (ie, organisation and environment) rather than the content (ie, clinical duties) of general practice. Other frequent stressors were intrusion of work on family life, earning enough money, the pressure to bulk bill, the cost of practice overheads, phone interruptions during consultations, home visits during office hours, and unrealistic community expectations of the medical profession. There were complex relationships between frequency and severity of stressors -- for example, threat of litigation was ranked lowest for frequency but highest for severity. A third of respondents recorded General Health Questionnaire scores of 4 or more, and 12.8% recorded scores of 8 or more, suggesting that significant numbers of GPs are under real psychological strain. How serious is all of this? Should we be alarmed that those who are the first port of call for sick and stressed people are themselves often feeling stressed and unhappy? Or are GPs simply reflecting the fact that we are all being pushed by the pace of change and pressure to be more efficient and effective? Either way, policymakers would be unwise to ignore these findings. We are an affluent society and can afford a system in which GPs and their patients can spend relatively unpressured time together. The clinical decisions made at the first point of contact should not be made in the context of rapid throughput and time constraint. If our system is stressing the doctors, it is almost certainly also stressing their patients. So what are the solutions? The 1998-99 federal Budget4 contains a number of new initiatives in general practice which grew out of two major strategy reviews, the reports of which have recently been released: General practice. Changing the future through partnerships,5 and General practice education: the way forward.6 The Budget papers claim that these reviews mark a "watershed for general practice, providing a vision which will guide and support the work of the profession in the coming years". They argue that the achievement of this vision will depend to a large extent on building strong partnerships based on mutual trust between general practice, the community and government. The Report of the General Practice Strategy Review Group5 contained 174 recommendations, including a number relating to indexation of the GP benefits schedule, additional funding for rural workforce initiatives, incentives to promote microeconomic reform and practice amalgamations, support for expanded use of information technology, a new Practice Incentive Program to replace the unpopular Better Practice Program, and new funds for research. Most of the Review recommendations have been taken up by the Government, as outlined in the ministerial response to the Report, released on 10 June 1998.7 A report should also be available this year on the Relative Value Study, currently being undertaken under the auspices of the Department of Health and Family Services. This study is assessing the relative value of work (beginning with patient attendances) across craft groups within the medical profession, including an assessment of the relative cost structures of those activities. There are also some signs that GP leaders are talking to each other and that there is some mutual give-and-take by them with government. That, itself, is a healthy sign. Whether stress, dissatisfaction, and psychological strain for GPs working in their consulting rooms will diminish as a result of these and the many other changes on the horizon remains to be seen. Robert M Douglas Director Beverly M Sibthorpe Fellow, National Centre for Epidemiology and Population Health The Australian National University, Canberra, ACT GP [television series]. ABC Sydney: screened 1989 and 1994. Bailie R, Sibthorpe B, Douglas B, et al. Mixed feelings: satisfaction and disillusionment among Australian general practitioners. National Centre for Epidemiology and Population Health discussion paper number 12. ANU, Canberra: NCEPH, 1997. Schattner PL, Coman GJ. The stress of metropolitan general practice. Med J Aust 1998; 169: 133-137. Budget 1998-99 fact sheets. No. 4. Canberra: Department of Health and Family Services, 1998. General practice. Changing the future through partnerships. Report of the general practice strategy review group. Canberra: Commonwealth Department of Health and Family Services, 1998. General practice education: the way forward. Report of the ministerial review of general practice training. Canberra: Commonwealth Department of Health and Family Services, 1998. The Government's response to the reviews of general practice: general practice -- foundations for the future. Canberra: Commonwealth Department of Health and Family Services, 1998. - 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/>

Robert M Douglas · Beverly M Sibthorpe

How safe is Australian general practice and how can it be made safer? Current systems for preventing or responding to adverse events are inadequate MJA 1998; 169: 67-68 It is common knowledge that adverse events occur regularly in healthcare settings. While many of these events have no long term consequences or reach public attention, serious failures of modern medicine can be mortifying for patients, their loved ones and their healthcare practitioners. The risks and adverse events associated with hospital practice in Australia were documented in the Quality in Australian Health Care Study.1 In this issue of the Journal, Bhasale et al report the incident-monitoring study in Australian general practice2 -- the first reported systematic research of adverse events in general practice. Comparable research in general practice in the United Kingdom has focused on significant event auditing to provide clinical material for facilitated case discussions of specific health issues,3-5 while earlier Australian research considered the educational implications of critical events.6,7 This long-awaited study provides valuable insights into some key quality issues for Australian general practice. The authors report on 805 critical incidents submitted by anonymous, volunteer general practitioners (GPs). Each adverse event was described by the GP, who also estimated its potential for harm, immediate consequences, mitigating and contributing factors, and preventability. The study is based on an incident-monitoring method developed for anaesthetics,8 but is critical incident monitoring appropriate for general practice? We do not know whether some GPs reported only those incidents which they believed had serious potential outcomes and which they thought might be of particular interest to the researchers. Perhaps individual GPs deliberately avoided reporting cases which might have shown them in a bad light; perhaps the reverse is true. Bhasale et al acknowledge some of the methodological issues raised by their study: the non-random sample of GPs and sole reliance on GP selection and self-reporting of critical incidents. The low volunteer rate (42%) and the bias towards relatively experienced GPs may indicate that many GPs are reluctant to be involved in research of this nature. A key feature of general practice is the presentation of undifferentiated medical problems, so diagnostic uncertainty is present in many initial consultations. Vigilance is required to ensure that, where possible, such early symptoms and signs are investigated in an appropriate and timely manner, while the risks and costs of unnecessary investigations are avoided. This is often a very difficult balance to achieve in clinical practice. However, Bhasale et al report errors that arise from basic oversights rather than uncertainty: failure to review the patient's history, inadequate recognition of symptoms and signs, complications arising from drug treatments, poor legibility of prescriptions, and abnormal test results being missed or not acted upon by the practitioner. These problems may relate directly to lapses at the individual practitioner level or at the practice level. Some of these problems may soon be solved by the decision support features of computerised medical record systems and computerised prescribing. Of particular concern in the study is that 4% of the incidents were reported to result in a patient's death and 17% were reported to result in major harm, either organic or psychological. However, there is no clearly demonstrated causal link between the critical events and the deaths reported. The authors state explicitly that this type of study cannot measure the prevalence of potential or actual harmful incidents in general practice. We emphasise that it would be inappropriate to make any such generalisations from the data provided. Bhasale et al highlight key areas for quality improvement in Australian healthcare. Many of these have been alluded to in previous commentaries on hospital care,9,10 and include problems with communication between healthcare professionals and the potential dangers for patients as they move across boundaries in the healthcare system. Failure to provide hospital discharge information to GPs is a longstanding and fundamental flaw in the system. At present, there are no adequate mechanisms for reporting critical incidents or for providing feedback about outcomes, both negative and positive, to all healthcare professionals. It is encouraging to note that integration of general practice into the healthcare sector is currently the focus of considerable research effort in Australia. Problems of communication with patients, particularly the elderly, those with poor English language skills and those with mental health problems, are also highlighted by Bhasale et al. These groups must be deemed populations at particularly high risk of adverse events. General practitioners need support and awareness-raising strategies to enable them to better address the healthcare needs of these groups and other potentially high risk groups, such as people of Aboriginal or Torres Strait Islander origin and people with multiple chronic health problems. There are additional areas where quality improvement initiatives could take place. These include enhancement of the existing process for accreditation of general practices, refinement of the Quality Assurance and Continuing Education program of the Royal Australian College of General Practitioners, and development of systems for reporting critical incidents and negative outcomes to all healthcare professionals. It must be remembered that, even if the best available evidence were applied to every clinical decision made by healthcare workers in this country, critical incidents would still occur. Unfortunately, the current system does not assist individual practitioners to express concerns about errors they witness or make as, in the main, peer support is lacking when adverse events occur in general practice. Clearly, there is a need for processes that allow personal grieving while providing a systematic response to problems. Michael R Kidd Professor of General Practice, University of Sydney and Member of the New South Wales Ministerial Advisory Committee on Quality in Health Care, Sydney, NSW Bronwyn M Veale Senior Research Fellow, Department of Evidence-Based Care and General Practice Flinders University of South Australia, Adelaide, SA Wilson RM, Runciman WB, Gibberd RW, et al. The Quality in Australian Health Care Study. Med J Aust 1995; 163: 458-471. Bhasale AL, Miller GC, Reid SE, Britt HC. Analysing potential harm in Australian general practice: an incident-monitoring study. Med J Aust 1998; 169: 73-76. Pringle M, Bradley CP, Carmichael CM, et al. Significant event auditing. A study of the feasibility and potential of case-based auditing in primary medical care. Occas Pap R Coll Gen Pract 1995; 70: I-VIII. Bradley CP. Turning anecdotes into data -- the critical incident technique. Fam Pract 1992; 9: 98-103. Robinson LA, Stacy R, Spencer JA, Bhopal RS. Use facilitated case discussions for significant event auditing. BMJ 1995; 311: 315-318. Sim MGB, Kamien M, Diamond MR. From novice to proficient general practitioner: a critical incident study. Aust Fam Physician 1996; 25 Suppl 2: S59-S64. Holmwood C. How do general practice registrars learn from their clinical experience? A critical incident study. Aust Fam Physician 1997; 26 Suppl 1: S36-S40. Williamson JA, Mackay P. Incident reporting. Med J Aust 1991; 155: 340-344. McNeil JJ, Leeder SR. How safe are Australian hospitals? Med J Aust 1995; 163: 472-475. Wilson RM, Harrison BT. Are we committed to improving the safety of health care? Med J Aust 1997; 166: 452-453. - 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 R Kidd · Bronwyn M Veale

Prostate-specific antigen testing for prostate cancer: the case for informed consent Informed consent should be obtained before testing asymptomatic men MJA 1998; 169: 9-10 The prostate-specific antigen (PSA) test is only the first step in screening asymptomatic men for prostate cancer. Its lack of specificity usually necessitates transrectal ultrasound-guided multiple biopsies for confirmation of the diagnosis. These procedures will discover a large number of cancers, many of which, viewed from one perspective, will be potentially curable by surgery1 or radiotherapy. However, epidemiological evidence suggests that most cancers localised to the prostate will not cause clinically significant disease for at least 10 years.2 PSA-based screening presents unique difficulties because at present there is no means to distinguish those cancers which will impair health to a degree that justifies the risk of iatrogenic morbidity of investigation (biopsy-related sepsis) and curative treatment (incontinence, impotence, and radiation damage to adjacent organs). This issue of the Journal includes four pertinent articles: the incidence of prostate cancer and the prevalence of PSA testing are described and compared in Western Australia3 (Threlfall et al) and New South Wales4 (Smith & Armstrong); reasons for PSA tests being ordered by general practitioners (GPs) in central Sydney are reported5 (Ward et al); and the prevalence of PSA testing among South Australian men is given, together with findings concerning men's understanding of the immediate consequences of having a PSA test6 (Pinnock et al). PSA tests were the sixth most frequent pathology item ordered by GPs in the June quarter of 1996,5 but their use has fallen since the peak in 1995.3,4 This may indicate that GPs are adopting a more discerning approach, in line with guidelines that recommend against the use of PSA tests to screen for prostate cancer.7 However, in the period 1992-1996, it is clear that GPs and asymptomatic men adopted the test enthusiastically. Medicare data show that one in every four Australian men (27%) aged at least 50 years had a PSA test in 1995 or 19964 and, in a random survey of households in South Australia carried out in 1996, 28% of men aged 50 years or older without prostate cancer reported having a PSA test in the preceding 12 months.6 A high proportion of PSA tests were ordered by GPs for screening ("routine for age") or in response to patient request.5,6 Men over 70 years old have been tested as frequently as younger men4,6 -- but the older the man when prostate cancer is detected, the less likely it is that a benefit from early intervention is possible.8 In South Australia, there was an association between PSA testing and visiting a doctor for urinary symptoms.6 PSA testing is not recommended for men presenting with uncomplicated lower urinary tract symptoms (because such symptoms are unlikely to be indicative of localised prostate cancer),6,9 but it is understandable that GPs may order the test because the question of prostate disease has been raised during the consultation. It is evident that PSA tests have been carried out without the consequences of an abnormal test result being adequately explained.6 GPs need a clear-cut structured framework within which the paucity of good scientific evidence and the potential harms and benefits can be discussed with patients. Most GPs will have had difficulty reconciling the negative evidence relating to the cost-benefit of PSA testing with their natural inclination to detect and treat cancer at an early stage. However, in asymptomatic people the balance of harm versus benefit must demonstrably be more clearly in favour of benefit than in usual clinical practice. In the United States, where enthusiasm for both case-finding by PSA testing and treatment by radical prostatectomy occurred some years earlier than in Australia, there appears to have been a small fall in mortality from prostate cancer in the period 1990-1995.10 Interpretation of this fall is far from clear, but it may be attributable to the dramatic increase in use of radical prostatectomy11 or other therapeutic advances in the 1980s. Conclusive evidence of reduced mortality from prostate cancer as a result of PSA screening must await the completion of randomised controlled trials. From an intention-to-treat analysis of men aged 50-79 years with clinically localised prostate cancer in the population-based US Surveillance, Epidemiology, and End Results (SEER) Program, no advantage in 10-year disease-specific survival was found for either radical prostatectomy or radiotherapy compared with conservative management for men with tumours with a Gleason score of 2-4 (well differentiated).12 For men with tumours with a Gleason score of 5-7 (moderately differentiated) there was an advantage for radical prostatectomy but not for radiotherapy -- this may reflect the fact that patients selected for surgery excluded those whose general health, and therefore prognosis, was already bad when prostate cancer was diagnosed. The 10-year disease-specific survival was better for men with tumours with a Gleason score of 8-10 (poorly differentiated) treated by either radical prostatectomy or radiotherapy compared with conservative management. Because of the way screening for breast and cervical cancers has been promoted, the general public will perceive that finding a cancer earlier is beneficial because treatment is more likely to be effective. However, using the PSA test for detecting prostate cancer in asymptomatic men is not analogous to mammography for early detection of breast cancer in asymptomatic women. Apart from the unproven benefit, there is a need for universally applied guidelines for the management of men with an abnormal test result, comparable with those built into the mammographic screening program. Such guidelines would include counselling and provision for a multidisciplinary approach when a decision is being made about the best course of management. At present, the cascade of events following an abnormal PSA test result proceeds without the man always making an informed choice before the test. Indeed, when men are given prior information about the PSA test and its characteristics, the consequences of having a raised PSA level, follow-up diagnostic procedures, treatment options and side effects, they are less likely to decide to have the test.13 GPs have a professional responsibility to give appropriate advice based on current evidence and, where there is uncertainty, this should be conveyed. Obtaining informed consent is accepted in the context of an invasive procedure. Given the medical uncertainties, the invasive nature of the confirmatory and therapeutic procedures that will be required if the test is positive, and the possibility of doing more harm than good, informed consent should be obtained from asymptomatic men before ordering a PSA test. Margaret McCredie Professorial Research Fellow, Department of Preventive and Social Medicine University of Otago, Dunedin, New Zealand, and Cancer Epidemiology Research Unit, NSW Cancer Council, Woolloomooloo, NSW Brian Cox Senior Research Fellow, Department of Preventive and Social Medicine University of Otago, Dunedin, New Zealand Kaye KW. Prostate cancer: enthusiasm for screening. Med J Aust 1995; 162: 540-541. Johansson J-E, Adami H-O, Andersson S-O, et al. High 10-year survival rate in patients with early, untreated prostatic cancer. JAMA 1992; 267: 2192-2196. Threlfall TJ, English DR, Rouse IL. Prostate cancer in Western Australia: trends in incidence and mortality from 1985 to 1996. Med J Aust 1998; 169: 21-24. Smith DP, Armstrong BK. Prostate-specific antigen testing in Australia and association with prostate cancer incidence in New South Wales. Med J Aust 1998; 169: 17-20. Ward JE, Gupta L, Taylor NJ. Do general practitioners use prostate-specific antigen as a screening test for early prostate cancer? Med J Aust 1998; 169: 29-31. Pinnock CB, Weller DP, Marshall VR. Self-reported prevalence of prostate-specific antigen testing in South Australia: a community study. Med J Aust 1998; 169: 25-28. Australian Health Technology Advisory Committee. Prostate cancer screening. Canberra: AGPS, 1996. Fleming C, Wasson JH, Albertsen PC, et al. A decision analysis of alternative treatment strategies for clinically localized prostate cancer. Prostate Patient Outcomes Research Team. JAMA 1993; 269: 2650-2658. National Health and Medical Research Council. Clinical practice guidelines. The management of uncomplicated lower urinary tract symptoms in men. Canberra: AGPS, 1996. Mettlin CJ, Murphy GP. Why is the prostate cancer death rate declining in the United States? Cancer 1998; 82: 249-251. Lu-Yao GL, Greenberg ER. Changes in prostate cancer incidence and treatment in USA. Lancet 1994; 343: 251-254. Lu-Yao GL, Yao S-L. Population-based study of long-term survival in patients with clinically localised prostate cancer. Lancet 1997; 349: 906-910. Flood AB, Wennberg JE, Nease RF, et al. The importance of patient preference in the decision to screen for prostate cancer. Prostate Patient Outcomes Research Team. J Gen Intern Med 1996; 11: 342-349. 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/>

Margaret McCredie · Brian Cox

Management of localised prostate cancer: state of the art The decision to treat should be based on the age of the patient and the grade of the cancer MJA 1998; 169: 11-12 We know that the incidence of prostate cancer increases with age and that many men "die with, but not from, prostate cancer".1 This has made the medical community concerned that, because of the high prevalence of comorbid illnesses among elderly men, many cancers detected by screening based on prostate-specific antigen (PSA) testing will be clinically insignificant, and that most patients would be overtreated. Unfortunately, we are also faced with the reality that approximately 2500 men succumb to prostate cancer annually, and many, particularly younger men, in fact "die of the disease and not with it".2 Most patients with localised prostate cancer will be given three management options: watchful waiting, radiotherapy, or radical surgery. Watchful waiting is defined as no initial treatment, with regular patient surveillance (which involves frequent consultations, digital rectal examinations and PSA testing) and commencement of androgen ablative therapy when clinical progression occurs. The success of watchful waiting depends on the predicted biological aggression of the cancer (related to the histological grade), as well as on the age and the associated comorbid illnesses of any individual patient. A pooled analysis of 828 patients treated conservatively in six non-randomised studies concluded that histologic grade was an important determinant of outcome. The 10-year cause-specific survival of patients with well or moderately differentiated cancers was 87%, compared with only 36% for those with poorly differentiated disease (who were at high risk of cancer progression and death).3 The cancer had metastasised by 10 years in 19% of men with well differentiated disease and 42% of men with moderately differentiated disease, despite the satisfactory cause-specific survival. Although watchful waiting may be an appropriate treatment choice for men with life expectancy of less than 10 years with well or moderately differentiated cancers, the outcome at 15 years may be less favourable. In another series, among men who survived more than 10 years from their initial diagnosis, prostate cancer was the direct or contributing cause of death in 63%.4 A report from the Connecticut Tumour Registry has shown that in men diagnosed with moderately differentiated cancer there is a modest, but not insignificant, risk of death from prostate cancer (28%) at 15 years with conservative treatment, and a potential loss of 4-5 years of life.5 Both mortality and potential years of life lost were even higher in men diagnosed with poorly differentiated disease. Contemporary radiotherapy offers an alternative to radical surgery for men who prefer not to undergo surgery or who have comorbidities which increase the risks of surgery. It also offers a chance of local tumour control to men with locally advanced cancer deemed unsuitable for curative surgery. There has been debate over the contribution of radiotherapy because surgery achieves higher rates of clinical and biochemical freedom of disease in the long term (although there have been no valid prospective, randomised controlled trials which directly compare these two treatments). However, the apparent advantage of surgery could be a reflection of the use of radiotherapy in patients with more advanced disease than those for whom radical prostatectomy would be contemplated. Success with radiotherapy has been shown to be dependent on both the stage and grade of the cancer. Fifteen-year cause-specific survival rates varied from 84% for low-stage to 52% for high-stage clinically localised cancers, and from 85% for well differentiated to 32% for poorly differentiated cancers.6 Traditional external beam radiotherapy involves a treatment course lasting up to seven or eight weeks. Acute proctitis and cystitis occurs in most patients, and there is a 2%-3% risk of long term rectal morbidity (diarrhoea, rectal bleeding) and a 30%-60% risk of permanent impotence. There are increasingly convincing data to support the hypothesis that local control and disease-free survival rates in patients with apparently localised disease improve with increasing radiation dose.7 Current research strategies are therefore aimed at increasing radiation dose without increasing surrounding normal tissue damage. This may be achieved by three-dimensional conformal therapy or brachytherapy, either alone or in combination with external beam radiotherapy. Another approach is to use androgen ablation to shrink the tumour, and then to deliver radiotherapy to maximise tumour cell kill.8 All these techniques have shown encouraging preliminary results, but follow-up has been relatively short. Improvements in surgical techniques, together with an increased understanding of the anatomy of the prostate, have made radical prostatectomy a popular treatment option for localised prostate cancer since the mid 1980s. A Mayo Clinic review of 3170 men treated by radical prostatectomy for clinically localised disease included 93% of men with clinically palpable disease and 25% with poorly differentiated disease. Cause-specific survival among those with palpable disease at 10 and 15 years was 90% and 82%, respectively, and 82% and 71%, respectively, among those with poorly differentiated cancers.9 The morbidity of radical surgery in an Australian setting has been discussed recently in the Journal.10 Independently administered questionnaires indicated that incontinence requiring daily pads occurred in approximately 10% of men who underwent surgery. Most of those affected required a maximum of one pad per day and the degree of inconvenience was generally low. The nerve-sparing technique may give reasonable postoperative potency rates in selected younger patients,11 but impotence occurs in most older men, and this is the issue that most affects quality of life.10 Nonetheless, men in most series indicated that they would choose to have surgery again,10 suggesting that the patients' desire to be cured of the disease outweighed the disadvantageous side effects. In a comparison of watchful waiting, radiotherapy and surgery, Surveillance, Epidemiology and End Results (SEER) data from the United States have shown that men with well differentiated cancer treated by watchful waiting have 10-year cause-specific survival rates comparable to those treated actively, while in those with moderately or poorly differentiated cancers treatment provides a survival benefit (Table).12 The gap between these groups is likely to widen further at 15 years as more men treated by watchful waiting live long enough to succumb to the disease. In most watchful waiting series, the mean age of the patients is over 70 years, and therefore few patients (5.9%-8.9%) actually survived 15 years.5,13 A recent study comparing 10-year data with 15-year data for men treated conservatively has shown a 15% reduction in cause-specific survival over the additional five years in men with well or moderately differentiated cancer,14 indicating a cumulative increase in prostate cancer mortality even in this cohort with lower grades of cancer. The hypothesis that death rates are declining as a result of increased diagnosis of localised disease treated at an earlier stage is supported by recent National Cancer Institute data showing that prostate cancer mortality in younger white men had declined by 11.7% this decade.15 It is to be hoped that randomised controlled trials currently under way will provide evidence that this is the case. A preliminary report suggests that this may be so.16 However, until the substantive results of these trials are known, men must be thoroughly counselled about the benefits and risks of early detection and treatment of prostate cancer. Aggressive, early therapy should be recommended for patients who are more likely to benefit from treatment -- those with greater than 10-year life expectancy, especially if diagnosed with a higher histological grade of cancer -- while patients less likely to benefit should be spared the morbidity of treatment. Mark Frydenberg Clinical Associate Professor, Department of Surgery, Monash University Head of Urology, Monash Medical Centre, Melbourne, VIC Gillian Duchesne Associate Professor, Department of Urology and Radiation Oncology Peter MacCallum Cancer Institute, Melbourne, VIC Phillip D Stricker Attending Urologist, Department of Urology, St Vincent's Hospital, Sydney, NSW Canstat -- Cancer in Victoria. Melbourne: Anti-Cancer Council of Victoria, 1994. Albertsen PC, Murphy-Setzko MA, Hanley JA, et al. Long term survival following conservative management of localised prostate cancer: fifteen year follow up among men aged 55-75 [abstract]. J Urol 1998; 159: 251. (Abstract No. A963.) Chodak GW, Thisted RA, Gerber GS, et al. Results of conservative treatment of clinically localised prostate cancer. N Engl J Med 1994; 30: 242-248. Aus G, Hugosson J, Norlen L. Long term survival and mortality in prostate cancer treated with non-curative intent. J Urol 1995; 154: 466-469. Albertsen PC, Fryback DG, Storer BE, et al. Long term survival among men with conservatively treated localised prostate cancer. JAMA 1995; 274: 626-631. Bagshaw MA, Cox RS, Hancock SL. Control of prostate cancer with radiotherapy: long term results. J Urol 1994; 152: 1781-1785. Hanks GE, Martz KL, Diamond JJ. The effect of dose on local control of prostate cancer. Int J Radiat Oncol Biol Phys 1988; 15: 1299-1305. Zagars GK, Johnson DE, Von Eschenbach AC, Hussey DH. Adjuvant estrogen following radiation therapy for stage C adenocarcinoma of the prostate: long term results of a prospective randomized study. Int J Radiat Oncol Biol Phys 1988; 14: 1085-1091. Zincke H, Oesterling JE, Blute ML, et al. Long term results after radical prostatectomy for clinically localised prostate cancer. J Urol 1994; 151: 1583-1586. Heathcote PS, Mactaggart PN, Boston RJ, et al. Health related quality of life in Australian men remaining disease free after radical prostatectomy. Med J Aust 1998; 168: 483-486. Quinlan DM, Epstein JI, Carter BS, Walsh PC. Sexual function following radical prostatectomy: influence of preservation of neurovascular bundles. J Urol 1991; 145: 998-1002. Lu-Yao GL, Yao SL. Population based study of long term survival in patients with clinically localised prostate cancer. Lancet 1997; 349: 906-910. Johanssen J-E, Holmberg L, Johansson S, et al. Fifteen year survival in prostate cancer: a prospective population based study in Sweden. JAMA 1997; 277: 467-471. Adolfsson J, Steineck G, Hedlund P-O. Deferred treatment of low grade prostate cancer: actual 10 year and projected 15 year follow up of the Karolinska series [abstract]. J Urol 1998; 159: 252. (Abstract No. A965.) Mettlin CJ, Murphy GP. Why is the prostate cancer death rate declining in the United States? Cancer 1998; 82: 249-251. Charatan FB. Prostate cancer screening reduces death. BMJ 1998; 316: 1626. Reprints: Clinical Associate Professor M Frydenberg, Suite 21, Cabrini Medical Centre, Isabella Street, Malvern, VIC 3144. 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/>

Mark Frydenberg · Gillian Duchesne · Phillip D Stricker

Fundamental reform of hours worked by junior doctors is required It has long been recognised that the rites of passage for junior doctors in public hospitals require extended hours of work with inadequate provision for rest and recovery. Not only are the junior doctors on a very demanding learning curve, but, at the same time, they are required to establish effective working relationships with patients, families and senior colleagues, and deal with the complexity of the modern hospital administration. Add to this a stressful workplace environment and, at times, the necessity to make critical decisions within a limited time frame and you have a situation no other professional group would be prepared to tolerate. Yet the research1 indicates that this is the situation most doctors face at the beginning of their careers. While Olson and Ambrogetti2 in this issue of the Journal present some criticisms of the methods of such research, there is considerable evidence to support the view that junior doctors' hours of work are, at times, excessive.3 The most recent Australian survey, undertaken as part of the current AMA Safe Hours Project, has produced further evidence to support this view.4 Why is this practice, which exerts a very heavy personal toll on the health and work performance of doctors, allowed to persist? No doubt there are respected members of the medical profession who argue that it is an essential component of the "toughening up" process. Clearly the hospital environment and the professional medical work ethic contribute to the excessive hours of work so ingrained in the hospital culture. The depth of this tradition was demonstrated recently in New York, where amendments to the Health Code5 were introduced in 1989 following the death of Libby Zion in a New York hospital. The circumstances of this unfortunate event are outlined by Nocera and Khursandi6 in this issue of the Journal. Libby's father, Sidney Zion, a newspaper columnist, was instrumental in launching a successful campaign restricting the hours of work of junior doctors working in hospital emergency departments. However, recent reports in the New York Times7 indicate there are still a large number of hospitals flouting this law. While legislative reform is one part of the solution, there is clearly a need to look at the attitudes which continue to support the practice. Until recently, little attention was given to the statutory responsibility of the employer to provide a safe system of work for doctors employed in hospitals.8 Currently, under occupational health and safety laws, there is increased emphasis on employers undertaking a hazard identification approach, followed by risk assessment and the application of risk controls. Applying this approach to the work regimen of junior doctors will present particular challenges to hospital administrators. An added consideration is the increasing recognition of the extent to which latent organisational failures may contribute by creating the circumstances leading to mishap.9 A hospital administration which fails to identify hazards and assess risks arising from extended hours of doctors' work could be in breach of a duty of care owed to doctors. Further, permitting a doctor to carry out duties while so fatigued that a patient's safety is endangered could be a breach of duty owed to the patient. The comments of the acting coroner in the recent inquest into the death of a New Zealand woman, the innocent party in a car crash, reinforce the importance of addressing the issue of fatigue.10 The patient survived the accident, but died following a mishap while in hospital. A significant issue for the coroner was the extent to which the fatigue of one of her doctors may have played a part in her demise. The coroner remarked that there was a growing level of concern, both nationally and internationally, over the hours of work of doctors in hospitals, and suggested that the medical professional bodies address the issue of extended periods of work. The hospital work practices of junior doctors appear to be common to many countries. Although the weekly hours worked by doctors in training are variable, it is reasonable to conclude that these routinely exceed 55 hours per week in many European countries.11 While the European Union originally excluded doctors in training from its 1993 Directive on Working Time,12 the Union's Council of Ministers indicated more recently that the directive should also apply to doctors in training.13 In 1990, the United Kingdom adopted an agreement, the New Deal, to phase in reduced hours for junior doctors.14 In March 1996, the AMA Federal Council adopted a policy to promote a safer workplace for junior doctors and patients in public hospitals.15 Part of the strategy involves the development of a national code of practice for the hours of work and rostering arrangements of junior doctors employed in hospitals. The Commonwealth Department of Health and Family Services has provided financial assistance to undertake a number of research projects to support the development of this national code. A draft of the code should be available for public comment in June/July 1998, to be followed by a national symposium in November 1998. Undoubtedly the major challenge is the professional medical culture, which, while it recognises the hazards and risks of excessive hours of work, appears to lack the collective will to resolve the problem. Nocera and Khursandi raise the question "Can the medical profession afford to let the courts decide what is reasonable?". In the absence of the medical profession's commitment to support fundamental reform of hours worked by junior doctors, where else can the victims turn? Gerry Holmes Manager, Occupational Health and Safety University of Wollongong Legal Advisor AMA Steering Committee, Safe Hours Project Swan, N. Juniors' Hours: International Overview. BMJ 1990; 301: 830-832. Olson LG, Ambrogetti A. Working harder -- working dangerously. Fatigue and performance in hospitals. Med J Aust 1998; 168: 614-616. Williamson A. The effects of workload and long hours of work on medical officers. Sydney: National Institute of Occupational Health and Safety (WorkSafe Australia), 1995. Australian Medical Association (AMA). Systems of work and overview of current arrangements. Canberra: Australian Medical Association, 1998. In press. New York State Health Code (10 NYCRR 405.4). New York: Department of Health, 1989. Nocera A, Khursandi DS. Doctors' working hours: can the medical profession afford to let the courts decide what is reasonable? Med J Aust 1998; 168: 616-618. Fein EB. Flouting law, hospitals overwork novice doctors. New York Times, 14 December 1997; 1. Holmes G. Hospital medical officers: hours of work and workloads, A strategic approach to occupational health and safety. Canberra: Australian Medical Association, 1995. Department of Transport. Investigation into the Kings Cross Underground Fire. London: HMSO, 1998. Coroner's Court. In the matter of the death of Patricia Margaret Ross. Rotorua, New Zealand: 15-17 October 1997; 18-20. Permanent Working Group of European Junior Hospital Doctors. Working conditions for doctors in training. Conference Proceedings, Executive Summary. Brussels: European Union Publications Office, December 1995. European Union. Directive on Working Time, 93/104. Brussels: European Union Publications Office, 1993. European Union. Sectors and activities excluded from working time directive. Brussels: European Union Publications Office, 1997. NHS Management Executive. Hours of work of doctors in training: guidance on regional task forces. London: Department of Health; 1991. Federal Council, Australian Medical Association. Executive minutes, 1-2 March 1996. Canberra: Australian Medical Association; 1996. 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 ".

Gerry Holmes

Prescribing heroin: nothing to fear but fear itself? Illicit drug policy based on punitive measures has failed, and it is time to seek a healthcare approach MJA 1998; 168: 590-591 The worsening global problem of illicit drugs will have been under discussion at the United Nations General Assembly Special Session on Drugs (UNGASS) in New York this month (8-10 June), just a few days before this issue of the Journal is published. The international crisis to which the United Nations is responding reflects decades of preferring to view the world as we would like it to be rather than as it is. Despite decades of alarming deterioration in outcomes associated with illicit drugs, the International Day Against Drug Abuse and Illicit Trafficking (26 June) is likely to be marked by yet more grandiloquent pronouncements of unachievable goals. In another editorial in this issue, Manderson describes the evolution of the complex drug control web in which we are now caught.1 Whenever new evidence has emerged of increasing illicit drug production and poorer outcomes, the reflex response of the international community has been to attempt to even more vigorously reduce supply. Genuine efforts to develop evidence-based alternative approaches, such as the proposed Australian Capital Territory heroin trial in 1997, have all too often been resisted by politicians. Senior Australian law enforcement officers have recently begun to question the traditional reliance on efforts to control illicit drug supply, with some calling for greater emphasis on treatment.2 After a recent meeting, Australian police commissioners "formally agreed to consider a range of strategies focusing on rehabilitation and avoiding the criminal justice system".2 Victorian Police Chief Commissioner, Mr Neil Comrie, said commissioners had decided to "almost wipe the slate clean" on current strategies.2 Australian criminal intelligence experts have stated that "law enforcement efforts are having only a limited effect on the amount of heroin offered at street level", and concluded that "it is obvious that current policies are not working".3 Some health interventions against illicit drugs, such as methadone treatment and needle exchange programs, have proved remarkably effective. Pharmacological treatments, of which methadone is by far the most important, attract and retain a substantial proportion of drug users and are strongly supported by evidence of safety and effectiveness.4 As both drug users and the broader community benefit substantially by recruitment and retention of users in treatment, the allocation of additional funding for monitoring and evaluation of trials of new pharmacological treatments in the recent "tough on drugs" statements by the Prime Minister should be warmly welcomed. These treatments include the partial opioid agonist buprenorphine, two opioid agonists (sustained-release oral morphine [SROM] and l-a-acetyl-methadol [LAAM]) and the opioid antagonist naltrexone. Each of these agents has particular advantages compared with methadone: buprenorphine and LAAM are safer and offer less costly alternate-day dispensing; SROM does not accumulate; and naltrexone avoids euphoria or dependence. However, there is no current evidence that these agents are more attractive or effective than methadone. By contrast, some trials have found that treatment retention, which often correlates well with other outcomes, was better for prescribed heroin than for methadone.5-7 There is a long history of pharmacological therapy for illicit drug users. More than 40 government clinics prescribed injectable morphine in the United States between 1919 and 1923.8 Heroin prescribing to treat heroin dependence commenced in the United Kingdom in 1926 and continues today,8 although this practice has been uncommon and rarely evaluated. A surprisingly extensive practice of prescribing amphetamine to amphetamine-dependent patients exists in the United Kingdom (Philip Fleming, Consultant Psychiatrist, Portsmouth Drug and Alcohol Service, Southsea, Hampshire, UK, 1998, personal communication), but is poorly documented and insufficiently evaluated. In this issue of the Journal, Metrebian and colleagues present the results of a UK study of relatively intractable patients allowed to choose treatment with either injectable heroin or injectable methadone.9 This study provides further support for the feasibility of prescribing heroin. The fact that more than one-third of patients chose injectable methadone should reassure those who assume that heroin prescription will prove irresistible to heroin injectors. Diversion of prescribed heroin to others was apparently not a problem, even though some prescriptions were dispensed weekly. Retention in treatment was unimpressive, but these patients had previously proved refractory to multiple treatment modalities. Illicit drug use, injecting risk behaviour, criminal activity, social functioning, health status and psychological adjustment all improved. Although the authors did not compare prescription of injectable drugs with other treatments, this study provides further support for conducting rigorously designed heroin trials. Whether prescribed heroin is suitable only for a heroin-dependent subgroup who do not respond to oral methadone or could be extended successfully to selected treatment-naive heroin users is a question that may also need to be answered one day. Right now, the study by Metrebian et al is also of interest in Australia because the harmful practice of methadone syrup injection is becoming increasingly common, and it is conceivable that parenteral methadone prescription might prove less harmful. The rationale for evaluation of medical prescription of heroin is based mainly on the need for dramatically improved treatment outcomes. The results of the recently completed heroin trial in Switzerland showed impressive health, social and economic gains,7 although the lack of a control arm inevitably limits any conclusions. Patients all had extensive histories of previous unsuccessful attempts at treatment (including methadone treatment). Retention on heroin prescription was considerably better than contemporary national retention rates for oral methadone treatment (although better staffing of the experimental program makes such comparisons problematic). After the Swiss heroin trial, 71% of voters in a national referendum supported continuation of this treatment, with majorities in all 26 cantons. It is hard to think of any new intervention in the illicit drug area in the last quarter-century that has shown such promise. On 6 June this year, the New York Academy of Medicine hosted the first international scientific meeting on heroin trials, reflecting growing international interest. A heroin trial will commence soon in the Netherlands, with trials under consideration in the UK, Germany, Spain, Austria and Canada.10 Interestingly, police chiefs in 10 of the 12 largest cities in Germany have been pressing for such a trial.10 The increasing interest in heroin trials is partly the result of authorities' growing acknowledgement of the failure of current policy. Were responses to illicit drugs to be decided entirely on the basis of evidence rather than fear and rhetoric, Australia would now be awaiting the results of the pilot stage of the ACT heroin trial. Demand for heroin is currently met by adulterated supplies of unknown concentration obtained from criminals. It seems probable that drug users and the general community would be better off if at least part of this demand were met by sterile heroin of known concentration prescribed by medical practitioners. Most doctors faced with a complex, chronic, relapsing-remitting disorder would prefer to choose from a range of effective treatments rather than rely on a single agent. The trials of new pharmacological agents are likely to extend and improve our therapeutic repertoire for treating heroin dependence. And there is still a compelling case for proceeding with a scientifically rigorous Australian heroin trial when political factors allow. Alex Wodak Director, Alcohol and Drug Service St Vincent's Hospital, Sydney, NSW Manderson D. Drug abuse and illicit trafficking. Med J Aust 1998; 168: 588-589. Harris T. Police switch strategies in war on drugs. The Australian 25-26 Apr 1998: 9. Australian Bureau of Criminal Intelligence. Australian illicit drug report 1996-97. Canberra: The Bureau,1997. Ward J, Mattick R, Hall W. Methadone maintenance treatment and other opioid replacement therapies. Amsterdam: Harwood Academic Publishers, 1998. Hartnoll R, Mitcheson M, Battersby A, et al. Evaluation of heroin maintenance in controlled trial. Arch Gen Psychiatry 1980; 37: 877-884. McCusker C, Davies M. Prescribing drug of choice to illicit heroin users: the experience of a UK community drug team. J Substance Abuse Treatment 1996; 13: 521-531. Uchtenhagen A. Summary of the synthesis report. In: Uchtenhagen A, Gutzwiller F, Dobler-Mikola A, editors. Programme for a medical prescription of narcotics: final report of the research representatives. Zurich: Institute for Social and Preventive Medicine, University of Zurich, 1997. Rihs-Middel M, editor. The medical prescription of narcotics. Scientific foundations and practical experiences. Seattle: Hogrefe and Huber. 1997. Metrebian N, Shanahan W, Wells B, Stimson GV. Feasibility of prescribing injectable heroin and methadone to opiate-dependent drug users: associated health gains and harm reductions. Med J Aust 1998; 168: 596-600. Nadelmann E. Commonsense drug policy. Foreign Affairs 1998; Jan/Feb: 111-126. 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/>

Alex Wodak

Kidney disease in Australian Aboriginals: time for decisive action Can governments and healthcare services in northern and central Australia afford not to get organised? MJA 1998; 168: 532-533 The continued alarming rise in incidence of renal failure in Australian Aboriginals living in the Top End of the Northern Territory (NT) is documented in this issue of the Journal by Spencer and coworkers1 from the Royal Darwin Hospital and the Menzies Institute of Health Research. Are their findings an isolated observation, why is it happening, and what should be done to address the problem? The numbers are real. The Darwin incidence and prevalence figures for endstage renal disease (ESRD) in Aboriginals are entirely consistent with figures from other Aboriginal community surveys of the Kimberley, Pilbara and Goldfields regions of Western Australia (WA). The WA Health Services Research Linked Database shows that in the past 8 years there has been a yearly rise in (age-standardised) incidence of dialysis from 67 to 819 per million in Aboriginal men, and from 130 to 758 per million in Aboriginal women. The current rates are, respectively, 12-fold and 20-fold more than the non-Aboriginal rates (Ms K Brameld, Research Officer, Department of Public Health, University of Western Australia, personal communication). Whole-of-Australia incidence data recorded by the Australian and New Zealand Dialysis and Transplant Registry (ANZDATA Registry) also support these findings (Box), with a marked disparity increasing over time between rates for Aboriginals and non-Aboriginals, particularly in the north of Australia. The difference in ESRD rates between Aboriginal and non-Aboriginal populations, described by Spencer et al, increases after age-standardisation and is further accentuated by the non-Aboriginal population in Darwin having a lower ESRD rate (37-47 per million) than the non-Aboriginal population of the rest of Australia (62 per million in the same time period). This lower rate probably reflects the "healthy migrant worker" phenomenon, seen in other isolated cities such as Perth, with relatively low rates of chronic diseases. The increasing number of new cases over time represents a combination of better ascertainment, with the development of the Aboriginal Medical Services, greater acceptance of ESRD therapy by the Aboriginal community, as well as a probable true increase in incidence of renal disease. The trends predate the appointment of a full-time nephrologist in Darwin in 1996. Why is it happening? The problem has multiple causes. An unfortunate mix of racial predisposition is aggravated by multiple adverse environmental and metabolic factors.3 Aboriginal kidney biopsy and autopsy data from the University of Melbourne have shown a range of pathological states (diabetic, hypertensive, and proliferative), underpinned by a remarkable increase in glomerular size of up to threefold normal.4 Whether this unusual glomerular change is entirely genetic or is exacerbated by intrauterine malnutrition followed by subsequent dietary excess has yet to be resolved. The infective insults present in Aboriginal communities have been amply documented,5 with repeated bacterial infections of ears, nose, chest, skin, gut and genitourinary systems, as well as endemic intestinal parasites. Even in the absence of recognised nephritogenic organisms, systemic infection will activate glomerular proliferation, affecting mesangial cells in particular.6 It is probably the development of widespread obesity and "Syndrome X" (raised body mass index, blood pressure, blood glucose, and triglyceride levels; and insulin resistance, and disordered uric acid metabolism) that most closely parallels the renal disease epidemic.7 The background social and legal factors involved are well described:8 loss of employment after voting rights and equal-pay legislation were enacted, access to alcohol, increased welfare benefits, and availability of a high-fat, high-carbohydrate diet. It is ironic that the outstanding success in correcting malnutrition and infective disease in Aboriginal children over the past 30 years should have contributed to creating a cohort of obese adults with hypertension and diabetes.9 Alcohol has several indirect but definite adverse renal effects. Each 10 g of alcohol consumed causes a rise in blood pressure in both white10 and Aboriginal11 populations. The carbohydrate load causes obesity, increasing the risk of diabetes and subsequent diabetic nephropathy. Alcohol both stimulates intestinal production and reduces hepatic clearance of IgA, increasing the risk of IgA nephropathy. (Although this is the commonest form of chronic glomerulonephritis in the non-Aboriginal population, it accounts for only a minority of cases of renal disease in Aboriginals.) Smoking is also recognised in epidemiological surveys as an independent risk factor for renal disease.12 Both these behaviours are very common in Aboriginal communities.13 What can be done about this renal disease epidemic? Remote-area dialysis works. Although renal transplantation usually gives the best rehabilitation at the lowest cost, its application is limited by scarcity of donors (cadaveric or fit live-related), disparate tissue typing between Aboriginal and white populations, and unsuitability of some recipients because of infections or poor medication compliance. The next-best option is self-care dialysis. There is a natural and understandable cultural imperative for patients in kidney failure to wish to return to their families and homes. How to deliver dialysis in remote areas is a challenge that has been successfully met by a number of nephrology units around Australia. In Townsville, Queensland, with a semi-urbanised and relatively sophisticated Aboriginal population, a chronic ambulatory peritoneal dialysis program has been in place for over a decade (Dr P de Jersey, Nephrologist, Townsville Base Hospital, personal communication). In Western Australia, since 1989, both CAPD and self-care haemodialysis have been delivered in areas up to 3500 km away from the parent nephrology unit. This has required some innovative technical approaches (such as inline water coolers, and repressurisation pumps) and training of staff to ensure cultural sensitivity (eg, using photographic rather than written instructions, and showing respect for name avoidance after family deaths).14 These nephrology units have shown that the challenge can be met with complication rates and dialysis survival that approach and occasionally better those observed in metropolitan dialysis units treating white populations.15 While about 25% more expensive than metropolitan self-care dialysis, remote-area dialysis is still half the cost of maintaining dependent, depressed and non-compliant patients against their will in the city. However, there remain patients and areas where self-care dialysis is not practicable. Hospital dialysis units can benefit from the use of Aboriginal liaison officers to improve cultural awareness, and to limit the sense of alienation for patients. Reorganisation of renal referral patterns around geographical proximity rather than along State borders (eg, referring patients from East Kimberley to Darwin, rather than to Perth) would also reduce the extent of dislocation. Screening and intervention programs are a priority. Most of the necessary components of such programs are in place and merely require coordination for maximum efficiency and effectiveness. Chronic disease screening (diabetes, hypertension, obesity) easily lends itself to the incorporation of urinalysis for protein, which, if positive, can be followed by serum creatinine estimation. Given the high rate of medical clinic attendance in Aboriginal communities, such screening can be opportunistic, reserving targeted case finding for a select identified few.16 The prime target remains improved environmental conditions.17 Availability of healthier food choices can reduce renal injury.18 Improvements in lifestyle and medication compliance have been achieved in a sizeable proportion of communities with active programs, particularly where there is Aboriginal "ownership" of the service. Reducing the blood pressure level below 140/90 mmHg (with a target of 125/85 mmHg) can slow the rate of progression of renal disease by up to 50%.19 Further, there is a particular role for angiotensin-converting enzyme inhibitors in proteinuric renal diseases, with or without diabetes.20 The cost-benefit equation is obvious. Every year of dialysis deferred for a single patient could pay the salary of another Aboriginal health worker. Can northern and central Australia healthcare services and governments afford not to get organised? Mark A B Thomas Head, Department of Nephrology Royal Perth Hospital, WA Acknowledgements: The data reported here were supplied by the Australia and New Zealand Dialysis and Transplant Registry. The interpretation and reporting of these data are the responsibility of the author and in no way should be seen as an official policy or interpretation of the Australia and New Zealand Dialysis and Transplant Registry. Spencer J, Silva D, Snelling P, Hoy WE. An epidemic of renal failure among Australian Aboriginals. Med J Aust 1998; 168: 537-541. Disney APS, Russ GR, Walker R, Sheil AGR, editors. Twentieth report of the Australian and New Zealand Dialysis and Transplant Registry 1997. Adelaide: Queen Elizabeth Hospital, 1997. Hoy WE, Mathews JD, McCredie DA, et al. The multidimensional nature of renal disease: findings in a high risk Australian Aboriginal community. Kidney Int 1998. In press. Bertram JF, Young RJ, Seymour AE, et al. Glomerulomegaly in Australian Aborigines. Nephrology 1998. In press. Gracey M, Spargo RM, Smith P, et al. Risk factors for ill-health in a remote desert-dwelling Aboriginal community in Western Australia. Aust N Z J Med 1996; 26: 171-179. Lovett DH, Bursten SL, Gemsa D, et al. Activation of glomerular mesangial cells by gram-negative bacterial cell wall components. Am J Pathol 1988; 133: 472-484. Hoy WE. Markers for cardiovascular and renal morbidity: expectations for an intervention program in an Australian Aboriginal community. Clin Exp Pharmacol Physiol 1996; 23(Suppl 1): S33-S37. Reid J, Trompf P, editors. The health of Aboriginal Australia. Sydney: Harcourt Brace Jovanovich, 1991. O'Dea K, Trainedes K, Hopper JL, Larkins RG. Impaired glucose tolerance, hyperinsulinaemia, and hypertriglyceridaemia in Australian Aborigines from the desert. Diabetes Care 1988; 11: 23-29. Puddey IB, Beilin LJ, Vandongen R, et al. Evidence for a direct effect of alcohol consumption on blood pressure in normotensive men. A randomised controlled trial. Hypertension 1985; 7: 707-713. Smith RM, Spargo RM, King RA, et al. Risk factors for hypertension in Kimberley Aborigines. Med J Aust 1992; 156: 562-566. Orth SR, Ritz E, Schrier RW. The renal risks of smoking. Kidney Int 1997; 51: 1669-1677. Hoy WE, Norman RJ, Hayhurst BG, Pugsley DJ. A health profile of adults in a Northern Territory Aboriginal community, with an emphasis on preventable morbidities. Aust N Z J Public Health 1997; 21: 121-126. Lim C, Matthews M, Whishaw J. Self-care dialysis training for Aboriginal patients. Dial Transplantation 1994; 23: 137-139. Feutrill J, Thomas L, Lazberger J, et al. Determinants of CAPD peritonitis rates in Aboriginal and non-Aboriginal patients. Kidney Int 1996; 50: 1411. Couzos S, Murray RB. Chronic renal failure. In: Aboriginal primary health care -- an evidence-based approach. Melbourne: Oxford University Press, 1999. In press. Gracey M, Williams P, Houston S. Environmental health conditions in remote and rural Aboriginal communities in Western Australia. Aust N Z J Public Health 1997; 21: 511-518. Nath KA, Grande J, Croatt A, et al. Redox regulation of renal DNA synthesis, transforming growth factor-b1 and collagen expression. Kidney Int 1998; 53: 367-381. Zucchelli P, Zuccala A, Borghi M, et al. Long-term comparison between captopril and nifedipine in the progression of renal insufficiency. Kidney Int 1992; 42: 452-458. Ruggenenti P, Remuzzi G. Angiotensin-converting enzyme inhibitor therapy for non-diabetic progressive renal disease. Curr Opin Nephrol Hypertens 1997; 6: 489-495. - 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/>

Wernicke's encephalopathy and thiamine fortification of food: time for a new direction? We should be fortifying beer to target the people who develop this disorder MJA 1998; 168: 534-535 Wernicke's encephalopathy (WE) usually occurs in people who have been drinking alcohol heavily and not eating, but can also occur after persistent vomiting or during hunger strikes. It is characterised by an acute global confusional-apathetic state with ophthalmoplegia or nystagmus. The ophthalmoplegia and confusion respond to thiamine treatment. Korsakoff's amnesic psychosis is associated with WE. Typically, it is recognised when the confusion clears in response to treatment with thiamine. While Korsakoff's psychosis (KP) sometimes responds slowly to thiamine, it is often persistent. Wernicke's encephalopathy is not easy to differentiate from other impairments of mental function in alcohol abusers. There is no rapid confirmatory special investigation. A patient with WE can die before being brought to hospital, and, in hospital, if the condition is not quickly recognised it is likely to lead to permanent memory damage in the form of Korsakoff's psychosis.1 Australia appears to have had both a higher incidence of WE than other comparable countries, and more people requiring long term care because of KP.2 In the 1980s, our national incidences of acute WE and of KP were estimated at about 6.5 cases/100 000 adults per year,3 and 22 cases/100 000 adults per year, respectively. As WE is not easily differentiated (as mentioned above) and as KP does not usually respond to thiamine treatment, this is evidently a disease complex more suitable for prevention than treatment. Public health measures have been under active discussion by Commonwealth health authorities since the problem was set out in a 1979 conference.4 In 1987, the National Health and Medical Research Council (NHMRC) recommended addition of thiamine to beer and flagon wine.5 However, nutrification of alcoholic beverages was unprecedented and was opposed by both brewers and anti-alcohol groups. After more discussion the NHMRC adopted the compromise suggested by its Nutrition Committee, that thiamine be added to bread flour as a first measure.6 Thiamine fortification of white bread is common in other industrial countries, introduced to restore losses of this vitamin from wheat by the refining process. Addition of thiamine to bread flour (at 6.4 mg/kg) was made mandatory in Australia on 1 January 1991. The Federal Government did not set up a system to monitor the effect of bread fortification, but information is accumulating that there has been some effect. A retrospective survey of records from the 17 major public health hospitals in greater Sydney for cases of Wernicke-Korsakoff syndrome (WKS) over the 10 years to 1993 showed that numbers of acute cases of WE or KP were lower in 1992 and 1993 than for any of the years preceding fortification.7 In this issue of the Journal, Harper and colleagues report on neuropathological postmortem examination of over 2000 brains at the NSW Institute of Forensic Medicine in 1996 and 1997.8 WKS can be identified by its effects on the mammillary bodies and walls of the third ventricle, and needs to be distinguished from changes caused by Alzheimer's disease, infarction, hypoxia and head injury. With the use of standardised techniques and special stains, 25 cases of WKS were identified, giving a prevalence of 1.1%. This is less than half the rate of 2.8% that Harper found in 4677 people (1783 postmortem brain examinations and 2894 hospital patients) in Western Australia between 1973 and 1978.1 Only two of the 25 NSW cases reported in this issue had been diagnosed at autopsy as acute WKS; six were diagnosed as acute-on-chronic and 17 as chronic. No note of ophthalmoplegia or nystagmus was found in hospital records for the 18 cases for which these were available.8 The neuropathology survey is thus showing a different end of the Wernicke-Korsakoff spectrum than the hospital record survey,7 which specifically sought new, acute cases. Both report from the Sydney area. A third look at WKS trends across Australia is afforded by comparing national mortality data obtainable from the Australian Bureau of Statistics for 1984 and 1989 (before fortification) with data for 1993 and 1996 (after fortification). Deaths from "other thiamine deficiency", "Korsakov's alcoholic psychosis" and "alcoholic cardiomyopathy" (some of which were presumably the result of thiamine deficiency) declined 22% from a combined two-year total of 329 to 255. By contrast, combined deaths from "other alcoholic dementia", "alcohol dependence syndrome" and "non dependent use of alcohol" increased somewhat from 452 to 493. A continuation of the survey of inpatient records in Sydney's 17 public general hospitals7 now includes data to 1996.9 Disregarding 1991, as it was the transition year, the average incidence of acute cases of WE or KP in the five years since fortification (1992-1996) was 40% lower than in the five years before fortification (1986-1990). This difference was statistically significant (P < 0.002),9 but the downward trend is not continuing -- the average of 41 acute cases per year for 1995 and 1996 was no lower than the 40 cases per year in 1992 and 1993.9 Increased thiamine intake from bread seems the most likely explanation for the apparent reductions of Wernicke-Korsakoff syndrome in Australia in the 1990s. Clinical diagnosis is subject to error, and postmortem diagnosis is based on morphological, and not chemical, characteristics. However, the decline, determined by different methods in three different studies,7-9 appears to be consistent over several years. Although the occurrence of Wernicke-Korsakoff syndrome in Australia appears to have been reduced by thiamine fortification of bread, it has not been eliminated. As nearly all cases occur in heavy alcohol drinkers, beer is probably a more appropriate vehicle for thiamine nutrification than bread. Prominent psychiatrist Eric Dax first suggested this 30 years ago.2 Beer is the preferred beverage of patients presenting with Wernicke's encephalopathy;7,10 the taste of thiamine hydrochloride can merge with the flavour of beer11 (but not with that of table wine); and it has been estimated that addition of thiamine to beer would be much more cost-effective than adding it to bread.12 It is clearly time for Commonwealth and State health authorities, the brewers and the NHMRC to seriously reconsider trialling the addition of thiamine to Australian beers -- to make them nutritionally the best in the world. Leslie R Drew Senior Lecturer, Department of Psychiatry A Stewart Truswell Professor of Human Nutrition University of Sydney, Sydney, NSW Victor M, Adams RD, Collins GH. The Wernicke-Korsakoff syndrome and related neurologic disorders due to alcoholism and malnutrition. 2nd ed. Philadelphia: FA Davis, 1989. Yellowlees PM. Thiamin deficiency and prevention of Wernicke-Korsakoff syndrome. A major public health problem. Med J Aust 1986; 145: 216-219. Gold J, Perdices M, Lardnet K, et al. The Wernicke-Korsakoff Project. Final report to the NH&MRC. Sydney: School of Public Health and Tropical Medicine, 1986. Prevention of alcohol-related brain damage. The report of a national workshop, Canberra 5-6 April 1979. Canberra: Commonwealth Department of Health, 1979. National Health and Medical Research Council. Report of 104th Session, November 1987. Canberra: NHMRC. 1988. National Health and Medical Research Council. Report of 108th Session, November 1989. Canberra: NHMRC, 1990. Ma JJ, Truswell AS. Wernicke-Korsakoff syndrome in Sydney hospitals: before and after thiamine enrichment of flour. Med J Aust 1995; 163: 531-534. Harper C, Sheedy D, Lara A, et al. Prevalence of Wernicke's encephalopathy in Australia: has thiamine fortification of flour made a difference? Med J Aust 1998; 168: 542-545. Rolland S, Truswell AS. Wernicke-Korsakoff syndrome in Sydney hospitals after six years' thiamin enrichment of bread. Public Health Nutrition 1998. In press. Price J. The Wernicke-Korsakoff syndrome in Queensland, Australia: antecedents and prevention. Alcohol Alcoholism 1985; 20: 233-242. Price J, Theodoros MT. The supplementation of alcoholic beverages with thiamine -- a necessary preventive measure in Queensland? Aust N Z J Psychiatry 1979; 13: 315-320. Connelly L, Price J. Preventing the Wernicke-Korsakoff syndrome in Australia: cost-effectiveness of thiamin-supplementation alternatives. Aust N Z J Public Health 1996; 20: 181-187. - 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/>

Leslie R Drew

Children are currently being denied vaccines for inappropriate reasons The most recent edition of the National Health and Medical Research Council's Australian immunisation handbook gives very clear guidelines about the contraindications to vaccination with pertussis vaccine and measles-mumps-rubella vaccine (MMR).1 This was necessary because many children have been denied these vaccines for inappropriate reasons, such as previous reactions at the injection site, fever or irritability after pertussis vaccine, or a history of egg allergy (for ruling out measles vaccine).2 The guidelines now recommend only two absolute contraindications to pertussis-containing vaccines -- encephalopathy or severe allergic reaction following a previous dose. However, over the past two years the Australian Childhood Immunisation Register has recorded that more than 32 000 doses of combined diphtheria-tetanus vaccine (CDT) have been administered to children in place of diphtheria- tetanus-pertussis vaccine (DTP), suggesting that doctors are not following this advice. In addition, based on substantial local and overseas evidence, the guidelines also recommend that "egg allergy, even anaphylactic egg allergy, is NOT a contraindication to immunisation with measles vaccine or MMR".1,3 The previous concept that egg allergy contraindicated MMR came from the manufacturers' product insert and was based on the incorrect assumption that, as it was cultured in chick fibroblasts, it could contain egg antigens. It is likely that inappropriate caution about vaccinating children with previous reactions to pertussis vaccine has been partly responsible for the re-emergence of pertussis over the past four years.4 There were more than 10 000 notified pertussis cases in Australia in 1997, and nine deaths between October 1996 and November 1997.5 Similarly, unnecessary caution about children with egg allergy may have contributed to our measles outbreaks.6 In this issue of the Journal, Andrews and colleagues show how children with previous severe reactions to pertussis vaccine (convulsions, apnoea, hypotonic-hyporesponsive episodes, high fever and persistent screaming) were safely vaccinated in a special clinic at The Canberra Hospital.7 This clinic was the first of a number of similar services now operating or about to begin operating in other centres, including Sydney, Melbourne, and Adelaide. Information about these services is available from State and Territory health departments, which have encouraged their establishment. These clinics plan to collaborate and share expertise nationally. What does this mean for the doctors and nurses who provide routine vaccinations? It means that they should be confident about the guidelines in the Immunisation handbook.1 Children with previous mild to moderate non-anaphylactic reactions (including persistent screaming and high fever) can be vaccinated (with routine precautions) by their usual vaccine provider. Paracetamol should be given prophylactically (15 mg/kg body weight for each oral dose1) to reduce the rate of local and systemic reactions to vaccines containing the whole-cell pertussis component. Children who have had severe reactions (prolonged hypotonic-hyporesponsive episodes and seizures, each seen about once every 2000 doses of whole-cell pertussis vaccine) can also be vaccinated safely,8,9 but may need to be assessed and vaccinated at (or, for rural families, in consultation with) a special clinic. The few children with a history of anaphylaxis following vaccination -- said to occur in about 1/50 000 doses of DTPw (diphtheria-tetanus-whole-cell pertussis vaccine)10 -- and children with underlying medical conditions who may be at special risk (eg, severe neurological disorders) should also be referred for assessment and advice. A new vaccine containing acellular pertussis components (DTPa -- diphtheria-tetanus-acellular-pertussis) is now approved in Australia for use in infants and children. It is funded nationally for the doses given to children aged 18 months and 4 to 5 years, and by some States and Territories (at present South Australia and the Northern Territory) for the three infant doses. Acellular vaccines are associated with a significantly lower rate of reactions at the injection site, hypotonic-hyporesponsive episodes, convulsions and screaming.11 For this reason they are recommended for infants who have had a previous severe reaction to DTPw. Acellular vaccines were not available when The Canberra Hospital clinic was established, so DTPw was used and found satisfactory. Since the use of acellular vaccines for the fourth and fifth doses (at 18 months and 4 to 5 years) in the United States, the rate of serious side effects after vaccination has been reduced by 60% to 70%.12 The availability of acellular pertussis vaccine should remove any need for general practitioners to use CDT vaccine. In Australia, as in many other countries, the States and Territories have established a formal reporting system for vaccine adverse events. Providers report vaccine reactions either to their local public health units or to central disease control units of State or Territory health departments. This information is then supplied to the national Serious Adverse Events Following Vaccination Surveillance Scheme (SAEFVSS), which commenced in March 1995 and is run by the National Centre for Disease Control in Canberra.13 Many vaccine providers do not realise that they should be reporting serious reactions -- so, for example, the number of hypotonic-hyporesponsive episodes being reported is less than would be expected from vaccine trials in which there is active follow-up.11 Other forms of adverse event surveillance should now be used to supplement the SAEFVSS. This would include transmission of data to the SAEFVSS from the special clinics and from hospital admissions, or active surveillance, through such initiatives as the Australian Paediatric Surveillance System, of specific rare serious events. These measures would help make the system more sensitive,14,15 and this would further reassure both providers and the public about the good safety record of the vaccines used in the current childhood immunisation schedule. We must conclude from The Canberra Hospital clinic report that most children with previous severe reactions can be safely vaccinated and that no child should be deprived of pertussis or MMR vaccines without consultation with a specialist advisory service. Margaret A Burgess Director Peter B McIntyre Deputy Director Timothy C Heath Research Fellow National Centre for Immunisation Research and Surveillance of Vaccine Preventable Diseases, Royal Alexandra Hospital for Children Westmead, and The University of Sydney, Sydney, NSW National Health and Medical Research Council. The Australian immunisation handbook. 6th ed. Canberra: AGPS, 1997. MacIntyre CR, Nolan T. Attitudes of Victorian immunisation providers to pertussis vaccine. Med J Aust 1994; 161: 293-294. Aickin R, Hill D, Kemp A. Measles immunisation in children with allergy to egg. BMJ 1994; 309: 223-225. Burgess MA, McIntyre PB, Heath TC. Pertussis re-emerging: who is responsible? Aust N Z J Public Health 1998; 22: 9-10. Communicable Diseases Surveillance. Pertussis epidemic continues. Commun Dis Intell 1997; 21: 359-360. Communicable Diseases Surveillance. Measles. Commun Dis Intell 1995; 19: 562-563. Andrews RM, Kempe AE, Sinn KK, Herceg A. Vaccinating children with a history of serious reactions after vaccination or of egg allergy. Med J Aust 1998; 168:491-494. Miller E. Collapse reactions after whole cell pertussis vaccination. Pertussis remains a bigger risk than collapse after vaccination [editorial]. BMJ 1998; 316: 876-877. Vermeer-de Bondt PE, Labadie J, RŸmke HC. Rate of recurrent collapse after vaccination with whole cell pertussis vaccine: follow up study. BMJ 1998; 316: 902-903. Peter G, editor. Pertussis. In: 1997 Red Book: Report of the Committee on Infectious Diseases. 24th ed. Elk Grove Village, Ill: American Academy of Pediatrics, 1997: 401. Cherry JD. Comparative efficacy of acellular pertussis vaccines: an analysis of recent trials. Pediatr Infect Dis J 1997; 16 (4 suppl): S90-S96. Committee on Infectious Diseases. American Academy of Pediatrics. Acellular pertussis vaccine: recommendation for its use as the initial series in infants and children. Pediatrics 1997; 99: 282-288. Communicable Diseases Surveillance. Surveillance of serious adverse events following vaccination. Commun Dis Intell 1995; 19: 273-274. Farrington P, Pugh S, Colville A, et al. A new method for active surveillance of adverse events from diphtheria/tetanus/pertussis and measles/mumps/rubella vaccines. Lancet 1995; 345: 567-569. Chen RT, Glasser JW, Rhodes PH, et al. Vaccine Safety Datalink Project: a new tool for improving vaccine safety monitoring in the United States. Pediatrics 1997; 99: 765-773. 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 ".

Margaret A Burgess · Peter B McIntyre · Timothy C Heath

Despite the risk of incontinence and impotence, most patients would choose surgery again to improve their chances of long term survival Prostate cancer is a major public health issue in all Western countries, including Australia. It is now the most commonly diagnosed cancer in men, and second only to lung cancer as the leading cause of cancer death in men. The age-standardised incidence of prostate cancer remained steady at 40 per 100 000 men until 1990, when there was a dramatic increase, associated with the introduction of early detection and screening programs based on measurement of prostate-specific antigen (PSA) levels (Anti-Cancer Council of Victoria Epidemiology Centre, personal communication). The incidence peaked by 1994 and has subsequently fallen to about 120 per 100 000 men. In the United States the incidence peak occurred several years earlier, in 1990-1991, and has fallen 1% per year since then.1 The decision by a patient, in consultation with his treating physician, to undergo active therapy for localised prostate cancer is complex and severely hampered by a lack of randomised controlled trials comparing different treatment methods with each other and with an untreated control group. Trials that may clarify the situation are under way in both the United States and Europe, but definitive results are many years away because of the relatively slow growth and progression of many prostate cancers. In the meantime, many variables need to be considered when making a treatment decision; these include the patient's age, associated co-morbid illnesses, stage and grade of the disease, and pretreatment PSA levels. Data from the Surveillance, Epidemiology, and End Results (SEER) program in the United States have demonstrated that for some men prostate cancer may be well managed with close surveillance ("watchful waiting") over a 10-year period.2 However, the data provide little security for healthy men in the age group 50-60 years who are diagnosed with the disease -- especially if diagnosed with cancer of higher histological grades, for which radical prostatectomy was shown to provide a survival benefit at 10 years.2 Thus, younger men diagnosed with localised prostate cancer have a strong desire to eradicate the disease and to maximise their chances of improved long term survival. Unfortunately, therapy of localised prostate cancer is associated with side effects that may alter quality of life. Watchful waiting, on the other hand, has no adverse effects until progression occurs, and the patient is placed on androgen ablative therapy, with its attendant side effects, such as hot flushes and impotence. Owing to the incidence of postoperative impotence and incontinence, most of the scrutiny of side effects of therapy has focused on radical prostatectomy. Early studies from single institutions in the United States reported very low complication rates. Catalona et al, in 1993, reported a 94% continence rate, and that, depending on whether a bilateral or unilateral nerve-sparing procedure was performed, 41%-63% of men regained potency after the operation.3 Another group reported a 92% continence rate and a 68% potency rate.4,5 However, these analyses were based on review of patient records and direct physician interview of the patient. This method may not accurately reflect the true morbidity because of patients' reluctance to directly report adverse events to their surgeon. In this issue of the Journal, Heathcote et al present the results of an independently administered questionnaire to determine patients' perception of the incidence and significance of side effects following surgery.6 The authors are to be commended for the study, which provides local results, experiences and attitudes. They found that postoperative urinary incontinence occurred in 20% of patients, with 11% of patients requiring pads at least once a week, 8% requiring one pad daily, and only 1% requiring two or more pads daily. Only 12% of men were truly potent after prostatectomy, but, despite this, 75% were happy or coping with the situation. Nevertheless, impotence was the treatment-related problem most affecting quality of life. Although the authors did not use a formal validated instrument to measure quality of life (eg, CaPSURE7), an appropriate modification specifically assessing continence and potency issues was used. This study is consistent with other international studies in which independent questionnaires were used. It is clear that the early publications may have under-reported the incidence of complications (see Box, below). Independent questionnaires, including that of Heathcote et al, have detected a higher incidence of complications. Despite this, patients reported that they were generally happy with treatment and would choose to have surgery again. Only eight of the 112 patients surveyed by Heathcote et al were not satisfied with treatment, and only 14 were reluctant to have the same treatment again. The results suggest that, in almost all patients, the desire to be cured of the disease may outweigh any adverse effects of radical prostatectomy. It is important for surgeons to know that patients can successfully adapt to these side effects, but this adaptation does not mean that the side effects are unimportant to patients. In most studies of quality of life with prostate cancer, less than 10% of patients required pads on a daily basis (although up to 30% may leak on occasions but not require pads). Most required only one pad per day and found this of minimal concern. The 1%-2% who required two or more pads each day generally found the side effect troublesome. Impotence was a larger concern in most series, including that of Heathcote et al, but, surprisingly, only 10%-30% of patients found it to be a serious problem, and usually not enough of an issue that they would not choose surgery again. It is crucial that patients understand and agree to these compromises, having been fully informed of the controversies regarding the benefits of aggressive treatment of localised prostate cancer. Mark Frydenberg Clinical Associate Professor, Department of Surgery, and Chairman Department of Urology, Monash Medical Centre, Melbourne, VIC Wingo PA, Riel LAG, Rosenberg HM, et al. Cancer incidence and mortality, 1973-1995: a report card for the US. Cancer 1998; 82: 1197-1207. Lu-Yao GL, Yao S-L. Population based study of long term survival in patients with clinically localised prostate cancer. Lancet 1997; 349: 906-910. Catalona WJ, Basler JW. Return of erections and urinary continence following nerve sparing radical retropubic prostatectomy. J Urol 1993; 150: 905-907. Steiner MS, Morton RA, Walsh PC. Impact of anatomical radical prostatectomy on urinary continence. J Urol 1991; 145: 512-515. Quinlan DM, Epstein JI, Carter BS, Walsh PC. Sexual function following radical prostatectomy: influence of preservation of neurovascular bundles. J Urol 1991; 145: 998-1002. Heathcote PS, Mactaggart P, Boston RJ, et al. Health-related quality of life in Australian men remaining disease-free after radical prostatectomy. Med J Aust 1998; 168: 483-486. Lubeck DP, Litwin MS, Henning JM, Carroll PR. Measurement of health-related quality of life in men with prostate cancer: the CaPSURE database. Qual Life Res 1997; 6: 385-392. Bates TS, Wright MPJ, Gillatt DA. Prevalence and impact of incontinence and impotence following total prostatectomy assessed anonymously by the ICS-Male questionnaire. Eur Urol 1998; 33: 165-169. Fowler FJ Jr, Barry MJ, Lu-Yao G, et al. Effect of radical prostatectomy for prostate cancer on patient quality of life: results from a Medicare survey. Urology 1995; 45: 1007-1015. Kaye KW, Creed KE, Wilson GJ, et al. Urinary continence after radical retropubic prostatectomy. Analysis and synthesis of contributing factors: a unified concept. Br J Urol 1997; 80: 444-451. 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 ".

Mark Frydenberg

Problem-based learning: does it prepare medical students to become better doctors? Some evidence shows that it does, but the jury is still out MJA 1998; 168: 429-430 Problem-based learning (PBL) is an approach to medical education in which students learn collaboratively by confronting clinical problems. Courses are usually organised thematically rather than by discipline, often by a small team of teachers with different disciplinary backgrounds. The group problem-analysis and independent self-directed study -- rather than teacher- or examination-driven education -- in PBL may encourage students to become more thoughtful problem-solvers and life-long learners.1 PBL is now the instructional method of choice in an increasing number of medical schools around the globe. Introduced in 1969 at McMaster Faculty of Health Sciences, Canada, PBL is now used in about 150 (of 1400) medical schools worldwide.2 In Australia, PBL was introduced quite early, in 1978, through the pioneering efforts of the late David Maddison and staff at the University of Newcastle. Other medical schools in Australia, such as the University of Sydney, Flinders University of South Australia, the University of Queensland and Monash University, have since followed. Why has PBL recently become popular in medical education? Clearly, the approach matches current efforts to involve students more actively in their own education, which does improve learning.3 In addition, students prefer PBL to other methods and spend more time on self-directed learning activities, using more information resources.4 In this issue of the Journal Finucane et al discuss these and other issues in PBL.5 Do students trained through PBL become better doctors? This question is not easy to answer, partly because there are few comparative studies of actual behaviour in professional practice and partly because it is difficult to attribute differences (or their lack) to specific features of the curricula being compared. In a recent study, final-year medical students from Maastricht University (which has a PBL-based curriculum) had a much higher level of proficiency in most of the professional skills tested than students from another Dutch medical school with a conventional curriculum.6 But is this effect attributable to the Maastricht PBL curriculum, or is it the result of the more extensive skills training also provided by that curriculum? Another possible confounding factor is that admission policies in some medical schools with PBL differ from those of conventional medical schools; the fact that students have different characteristics to begin with may itself explain differences in knowledge and skills shown both during the course and after graduation. With these reservations in mind, I will summarise what is known about the impact of PBL curricula on students, confining myself to studies that compared graduates or final-year students from medical schools with conventional, lecture-based programs and schools with PBL programs. Do students from PBL institutions become life-long learners? Some believe that PBL encourages the acquisition of independent study skills. Such skills would help a practitioner to keep up-to-date. Primary care physicians who graduated from McMaster University displayed more up-to-date knowledge of an important clinical concept (hypertension),7 but graduates from the same institution did not participate in more continuing education activities.8 Are there any differences in practice patterns? Studies in the United States9 and Finland10 have shown that graduates from schools with innovative curricula are more likely to choose a career in primary care than their counterparts from more traditional schools; these students also report their education to be more relevant to their present practice. These findings have not been replicated in other countries. It seems that career choice is more a matter of the explicitly stated mission of a school than its instructional approach. However, McMaster graduates in general practice, compared with matched controls from other Ontario medical schools, billed the healthcare system less, had fewer patients and spent more time with them, and referred less to psychotherapeutic services, suggesting that they were more comfortable with providing the services themselves.11 Are there differences in medical knowledge? In the US, the source of most of these comparisons, graduates from PBL schools acquire less knowledge of the basic sciences, but compensate with slightly more clinical knowledge.12 Overall, there are no differences in medical knowledge; PBL is just as good (or poor) in this respect as conventional medical education.13 Does PBL increase diagnostic competence? Small-scale studies have had mixed results. Patel et al asked 54 students from two medical schools -- one with a PBL-based curriculum and the other conventional -- to diagnose a clinical case and explain their diagnosis, and then examined their reasoning processes. The PBL students explained the causes more extensively, using the relevant biomedical knowledge, but made more diagnostic errors.14 Other investigators, using a similar task, found that PBL students also showed more extensive causal reasoning, but made fewer diagnostic errors.15,16 As these studies presented only one or two cases to be solved, the findings may reflect the specific cases rather than resulting from the instructional formats compared. In a large-scale study, in which 612 students were presented with 30 epidemiologically representative cases and provided a diagnosis for each of them,17 Maastricht final-year students17 performed better than the group from the medical school with the conventional curriculum, with the mean difference between the two groups being 1.5 cases out of 30. If we extrapolate these findings to actual practice (under the perhaps questionable assumptions that these students, in the future, will actually see about 30 patients per day, and that these paper-and-pencil test findings do signify a difference in actual diagnostic expertise between students from the two schools), the results imply that for each month (20 working days) in practice a graduate from the conventional medical school would miss 20 x 1.5 cases (ie, about 30 diagnoses) that would be accurately made by a Maastricht graduate. These findings suggest that even relatively small effects of curriculum type, when extrapolated, may affect the quality of everyday diagnostic performance in non-trivial ways. There is some evidence that PBL at least contributes to the making of better doctors. The evidence, though scarce, seems to suggest that students trained through the confrontation with clinical problems become more accomplished diagnosticians. In addition, after these students graduate, they appear to have better self-directed learning and other professionally relevant skills. Much more research, of course, is mandatory. This will be an interesting challenge for the new Australian PBL medical curricula. Henk G Schmidt Professor of Psychology and Health Professions Education Faculty of Psychology, Maastricht University, the Netherlands Barrows HS. Problem-based, self-directed learning. JAMA 1983; 250: 3077-3080. Schmidt HG, Neufeld VR, Nooman ZM, Ogunbode T. Network of community-oriented educational institutions for the health sciences. Acad Med 1991; 65: 259-263. Norman GR, Schmidt HG. The psychological basis of problem-based learning: A review of the evidence. Acad Med 1992; 67: 557-565. Vernon DT, Blake RL. Does problem-based learning work? A meta-analysis of evaluative research. Acad Med 1993; 68: 550-563. Finucane PM, Johnson SM, Prideaux DJ. Problem-based learning: its rationale and efficacy. Med J Aust 1998; 168: 445-448. Scherpbier AJJA. Kwaliteit van vaardigheidsonderwijs gemeten (Measuring the quality of skills instruction). PhD Thesis. Maastricht: Universitaire Pers Maastricht, 1997. Shin JH, Haynes RB, Johnston ME. Effect of problem-based, self-directed undergraduate education on life-long learning [see comments]. Can Med Assoc J 1993; 148: 969-976. Tolnai S. Lifelong learning habits of physicians trained at an innovative medical school and a more traditional one. Acad Med 1991; 66: 425-426. Mennin SP, Kalishman S, Friedman M, et al. A survey of graduates in practice from the University of New Mexico's conventional and community-oriented, problem-based tracks. Acad Med 1996; 71: 1079-1089. Kumpusalo E, Neittaanmaki L, Virjo I, et al. Relevance of medical education to professional needs of doctors in community-oriented and traditional medical schools. Educ Health 1996; 9: 167-178. Woodward CA, Ferrier BM, Cohen M, Goldsmith A. A comparison of the practice patterns of general practitioners and family physicians graduating from McMaster and other Ontario medical schools. Teaching Learning Med 1990; 2: 79-88. Mennin SP, Friedman M, Skipper B, et al. Performances on the NBME I, II, and III by medical students in the problem-based learning and conventional tracks at the University of New Mexico. Acad Med 1993; 68: 616-624. Albanese MA, Mitchell S. Problem-based learning: A review of literature on its outcomes and implementation issues. Acad Med 1993; 68: 52-81. Patel VL, Groen GJ, Norman GR. Effects of conventional and problem-based medical curricula on problem solving. Acad Med 1991; 66: 380-389. Boshuizen HPA, Schmidt HG, Wassmer L. Curriculum style and the integration of biomedical and clinical knowledge. In: Bouhuijs PAJ, Schmidt HG, van Berkel HJM, editors. Problem-based learning as an educational strategy. Maastricht, the Netherlands: Network Publications, 1994: 33-42. Hmelo CE. Development of independent learning and thinking: A study of medical problem solving and problem-based learning. PhD Thesis. Nashville TN: Vanderbilt University, 1994. Schmidt HG, Machiels Bongaerts M, Hermans H, ten Cate TJ, et al. The development of diagnostic competence: Comparison of a problem-based, an integrated, and a conventional medical curriculum. Acad Med 1996; 71: 658-664. ©MJA 1998 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/> © 1998 Medical Journal of Australia.

Henk G Schmidt

At the end of the 20th century, the good news about rheumatic fever is that it has become so rare in most of Australia that many medical practitioners will never see a case. This is a dramatic change from the first half of the century; in Melbourne during the 1930s, more than 50% of paediatric hospital medical beds were occupied by children with acute rheumatic fever or acute poststreptococcal glomerulonephritis, with rheumatic fever patients outnumbering those with glomerulonephritis (Dr Howard E Williams, previously In-Patient Physician, Royal Children's Hospital, Melbourne, personal communication). The decline of rheumatic fever in affluent populations occurred largely as a result of economic development and improved living conditions, with perhaps a small contribution from antibiotics and the possibly altered virulence of circulating group A streptococcal strains.1 The bad news is that socially and economically disadvantaged populations worldwide, including some indigenous and minority populations living in affluent countries, continue to have high rates of rheumatic fever and rheumatic heart disease. The highest published incidence of acute rheumatic fever in the world is in Aboriginal people living in the "Top End" of the Northern Territory.2 In this population the annual incidence of acute rheumatic fever (1989-1993) is between two and seven cases for every 1000 children aged 5 to 14 years, while up to three per cent of all people in some of the remote Aboriginal communities have established rheumatic heart disease. In contrast, the prevalence of rheumatic heart disease in the non-Aboriginal population is 0.014 per cent, and no non-Aboriginal children had acute rheumatic fever over this five-year period.2 While rheumatic fever appears to occur in only a subset of any given population, there are no data to support any major predisposition based on ethnicity. Similar high rates were documented in non-Aboriginal people in Melbourne during the 1930s and 1940s.3 The current high rates of rheumatic fever in the Aboriginal population are not related to ethnicity, but are likely to reflect high levels of exposure to group A streptococci, which, in turn, are related to overcrowding and continuing poor living conditions.4,5 The World Health Organization has promoted the use of rheumatic fever registers in developing countries,6 with the major aims of coordinating individual patient management and improving adherence to secondary prophylaxis to prevent recurrent rheumatic fever and the associated cumul ative valve damage. Registers are useful not only for developing countries: a register-based program in New Zealand, with acute rheumatic fever as a notifiable disease, helped reduce from 22% to 6% the proportion of hospitalised cases of rheumatic fever which were recurrences.7 The Commonwealth Department of Health and Family Services, together with the Australian Institute of Health and Welfare, has taken the commendable step of funding a register-based control program in the Top End of the Northern Territory (Dr Vicki Krause, Director, Centre for Disease Control, Territory Health Services, Darwin, personal communication). This program will also involve new health promotion strategies in Aboriginal communities -- directed at both health and education staff and at people with rheumatic fever and rheumatic heart disease and their families. Videos, booklets and treatment charts have been developed by indigenous educators and researchers.8 The program will attempt to create a partnership for change, involving indigenous and non-indigenous health professionals and government and non-government health services. Secondary prophylaxis will reduce the number of people developing rheumatic heart disease or requiring intervention for worsening valvular damage, but it will not stop initial episodes of acute rheumatic fever. This is where rheumatic fever control becomes difficult. While efforts to address social and economic inequities, particularly living conditions and overcrowding in Aboriginal communities, cannot be overemphasised,4,5 in some remote communities substantial change in these areas has not been evident over the past two decades and, in the current economic climate, is unlikely, we believe, to occur for some time. Conventionally, primary prevention relies on the accurate diagnosis and timely treatment with penicillin of group A streptococcal pharyngitis. However, most developing countries do not have the finances, skilled staff or laboratory facilities to do this well. Furthermore, more than two-thirds of cases of acute rheumatic fever may not follow symptomatic pharyngitis,9 so concentrating only on sore throats probably will not prevent most cases of rheumatic fever. Important progress is being made towards the development of a group A streptococcal vaccine, including current Australian initiatives,10 but in the shorter term other approaches are needed. In one such approach, a program of regular throat swabbing and treatment of streptococcal carriers in one Aboriginal community appeared to coincide with fewer cases of rheumatic fever,11 although the program was not sustained over the long term.12 This program appears to be the sole published effort to improve primary prevention of acute rheumatic fever in an Aboriginal community. While an association between streptococcal skin sores and acute rheumatic fever remains speculative, clues to further primary prevention strategies may come from understanding the epidemiology of group A streptococcal diseases in Aboriginal communities -- where the prevalence of streptococcal pyoderma (skin sores) may be up to 70% in children, but throat carriage rates of group A streptococci are often low.13 The ongoing epidemic of scabies in Aboriginal communities must underlie much of the streptococcal skin disease. More research is needed to better understand the epidemiology and best management of sore throats, streptococcal pharyngitis and skin sores in Aboriginal communities, as well as the relationship between streptococcal throat and skin infections and rheumatic fever. In the meantime, primary prevention strategies should include measures to reduce the reservoir of circulating streptococci found in skin sores; coordinated programs to control skin sores and underlying scabies can be effective in Aboriginal communities.13 Successful primary prevention strategies developed in Australia could have global implications for rheumatic fever control. Rheumatic heart disease in Aboriginal communities can be controlled in the short term through the use of comprehensive strategies to improve adherence to secondary prophylaxis regimens and to reduce exposure to group A streptococci, and possibly, in the longer term, with a vaccine. However, the ultimate aim must be improved living conditions for Aboriginal people, including emphasis on water supply, taps and showers, the disposal of sewage and solid waste, and resources to support better hygiene.

Jonathan R Carapetis · Bart J Currie

Rugby and spinal injury: what can be done? We cannot be complacent -- we must continue an expanding injury database MJA 1998; 168: 372-373 In the early 1980s, staff in Australian hospital spinal units became aware of a serious increase in the incidence of young football players in both codes of rugby -- union and league -- admitted with serious or permanent cervical spinal cord injury. By 1983 the two spinal units in Sydney were admitting 10 or more young players in a season.1 By 1984, I had introduced the Spinal Awareness and Prevention Program at the Royal North Shore Hospital, Sydney, for audiovisual presentation to schoolchildren in independent and public schools in New South Wales. Lecturers in this program, themselves disabled from spinal cord injury, highlighted how spinal cord injury could occur. By 1987, documentation from injured players had been presented in a report to the International Rugby Board, and changes to the scrum formation had been recommended. In 1987, in a review of 107 footballers in Australia who had suffered a spinal cord injury between 1960 and 1985, scrummaging in rugby union was identified as particularly dangerous, with illegal tackles (eg, "spear tackling" -- with a player being driven head-first into the ground, or a "stiff-arm" impact to a player's head and neck) identified as the most serious problem in rugby league.2 Administrators of both codes had already acknowledged these problems, particularly in "schoolboy" football. There were also lectures by sports medicine specialists to coaches and selectors of teams, with identification of the particular danger for young players in their mid teens beginning to participate in a contact sport. During the second half of the 1980s, coaches for both schoolboy and more senior grades of rugby union and rugby league were emphasising adequate preparation for the game and careful selection of players for particular positions of play, and encouraging the reporting of injuries. Some heads of independent schools in Sydney were initially reluctant to accept that many boys are genetically and psychologically destined to be unsuitable for participation in competitive contact sport! Some administrators were reluctant to consider changes of rules necessary to reduce the forces generated on the necks and shoulders of players involved in scrums and mauls and to ensure the absolute necessity of playing according to the rules. In 1997, Armour et al confirmed an increased frequency of serious spinal cord injuries in rugby union and league players over the 20-year period 1976 to 1995 in New Zealand.3 One hundred and forty-one players were admitted to New Zealand's two spinal injury units, and 47 remained permanently paralysed. The authors noted that, although studies of cervical spinal cord injury in rugby football had been presented to medical and rugby authorities within the previous five years, no action appeared to have been taken to reduce the unacceptable incidence of this grave injury. Professor Timothy Noakes, from Cape Town, South Africa, lamented in an editorial in the British Medical Journal in 1995 that "nearly 20 years after the BMJ first drew attention to the issue, we still do not know the true incidence of either spinal cord or cervical injuries in rugby players in any rugby-playing country".4 He emphasised that changes in rules of the game and player preparation could not be supported without sufficient accurate epidemiological data. More recently, Scher reported that the incidence of serious rugby spinal injuries in South Africa had not decreased over the past 10 years, with an average of 5.4 players per year admitted to one of the world's largest spinal cord injury centres, in Cape Town.5 Of interest, therefore, is the finding of Rotem et al, reported in this issue of the Journal, of a "small but significant decline in the number and approximate incidence of cases [of permanent neurological deficits leading to tetraplegia] associated with rugby union but no change in rugby league", from their survey of the spinal units at Royal North Shore Hospital and Prince Henry's Hospital.6 Further collection of data will allow a more detailed study of the statistics and will, one hopes, confirm the apparent trend towards reduction in injury incidence. In the 18 months since the New Zealand Rugby Union instituted compulsory nationwide safety seminars for coaches early in 1996, no cases of spinal cord injury from scrums have been reported in that country, although one player sustained tetraplegia in a tackle.3 During 1997, the spinal unit at Royal North Shore Hospital had no admissions of patients with serious cervical spinal cord injury from playing either rugby union or league (Dr Sue Rutkowski, Medical Director, personal communication), although this encouraging statistic could be a continuation of the variability seen in Rotem et al's study. In 1995, the National Health and Medical Research Council released a handbook7 with Guidelines for prevention and management of head and neck injuries in football. Compiled by medical specialists with knowledge and interest in neurotrauma from sporting injuries, this useful guide should be in the hands of all referees, umpires, coaches and players. The handbook highlights important first-aid principles and assessment of injured players before returning them to play, to prevent aggravation of a potentially serious injury. The laws for under-19 players, with the 1993 variations (such as rules eliminating "crotch binding" in scrums) introduced to rugby union in New South Wales, must also be maintained. The cost to the community of spinal cord injuries cannot be overemphasised. In Australia, 300 new patients with spinal cord injuries are expected every year; the lifetime cost is one million dollars for each paraplegic casualty and five million dollars for a tetraplegic casualty, as confirmed by awards in Australian courts. Our pessimism should be balanced by remembering Davidson's 1987 findings that, among 1444 schoolboys injured in interschool rugby from 1969 to 1986, there were two clinically "serious" injuries -- a skull fracture and a fracture dislocation of the cervical spine. The "severe" injury rate was 14 per 10 000 player-hours, or 0.12 per 100 player-games.8 Rotem et al have confirmed the impression of a reduction in the incidence of spinal cord injury in some contact sports following rule changes, as well as increasing our understanding of how cervical spinal cord injury occurs. Further epidemiological studies are essential for the adequate re-assessment of rule changes and of techniques to prepare players for contact sports. We must also further our knowledge of how injuries occur, and remain in close consultation with physicists, sports medicine clinicians and biomedical engineers. There must be no complacency in the future. Continuing vigilance is imperative to avoid the devastating personal and societal costs. John D Yeo, AO Associate Professor, and Consultant in Spinal Injuries Royal North Shore Hospital, Sydney, NSW Yeo JD, Walsh J. Prevention of spinal cord injuries in Australia. Paraplegia 1987; 25: 221-224. Taylor TKF, Coolican MRJ. Spinal cord injuries in Australian footballers, 1960-1985. Med J Aust 1987; 147: 112-118. Armour KS, Clatworthy BJ, Bean AR, et al. Spinal injuries in New Zealand rugby and rugby league -- a 20-year survey. N Z Med J 1997; 110: 462-465 . Noakes T, Jakoet I. Spinal cord injuries in rugby union players. BMJ 1995; 310: 1345-1346. Scher AT. Rugby injuries to the cervical spine and spinal cord -- a 10-year review. Clin Sports Med 1998; 17: 195-206. Rotem T, Lawson JS, Wilson SF, et al. Severe cervical spinal cord injuries related to rugby union and league football in New South Wales, 1984-1986. Med J Aust 1998; 168: 379-381. Newcombe R, et al. Football injuries of the head and neck. National Health and Medical Research Council Report, January 1995. Canberra: AGPS, 1995. Davidson RM. Schoolboy rugby injuries, 1969-1986. Med J Aust 1987; 147: 119-120. Lewis CS. The problem of pain. London: Collins Fontana Books, 1940: 141. - 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/>

John D Yeo

Panic disorder and coronary artery spasm Whatever the causative mechanism, prolonged chest pain during panic attacks requires investigation MJA 1998; 168: 376-377 The three cases reported by Mansour et al1 in this issue of the Journal add to the evidence for increased risk of adverse cardiovascular events in people with severe anxiety. The existing evidence derives from both prospective epidemiological studies2,3 and controlled longitudinal clinical studies.4 In the latter, mortality was related to severity of emotional arousal; panic disorder patients were at greater risk of sudden cardiac death than patients with lesser forms of anxiety, such as generalised anxiety disorder. Two of the cases reported by Mansour et al (Patients 1 and 3) showed a close temporal association between panic attacks and ischaemic chest pain. In the absence of severe obstructive coronary disease, might the ischaemia be due to coronary artery spasm? Patient 1 presented with severe chest pain accompanying episodes of panic. An electrocardiogram (ECG) showed mild tachycardia and ST-segment depression, but no cardiac enzymes were released, and the coronary angiogram was normal. With subsequent panic attacks, the patient continued to experience anginal pain, which resolved completely after prescription of amlodipine (a potent dihydropyridine calcium antagonist known to prevent epicardial coronary spasm). Patient 3 had long-standing panic disorder and mild hypertension. He had acute ischaemic chest pain during a panic attack; cardiac enzyme levels were raised, and infarction was diagnosed. Angiography showed no underlying atherosclerosis. Angina-like chest pain occurred during subsequent panic attacks, but once again resolved completely after amlodipine therapy. The other patient (Patient 2) experienced an infarct associated with exercise rather than with an acute panic attack. Coronary angiography during the acute stage showed that the infarct-related artery was occluded, while the other coronary arteries were normal. The patient had a nine-year history of panic disorder, and previous panic attacks had been accompanied by chest pain. However, no chest pain occurred during post-infarction panic attacks, and there was no temporal relationship between panic attacks and the major ischaemic episode. Although coronary artery spasm is one of the plausible mechanisms for the cardiac ischaemia, none of these patients had convincing evidence of spasm during panic attacks. Spasm of an epicardial coronary artery usually results in ST-segment elevation, which accompanies transmural ischaemia. A definitive diagnosis of coronary spasm requires demonstration of ST-segment elevation, or spasm at angiography, during spontaneous angina or after provocation with ergonovine, acetylcholine or hyperventilation. In Patient 1, the ECG during chest pain showed ST-segment depression, while in Patient 3 no ECG changes were seen. While coronary spasm with ST-segment depression or even no ST changes has been reported, this is very uncommon. In Patient 1, the presence of tachycardia along with ST-segment depression raises the possibility of Syndrome X (angina-like chest pain with ST-segment depression, no demonstrable myocardial ischaemia and normal coronary arteries,5 which is not to be confused with the endocrinological Syndrome X, or insulin resistance metabolic syndrome6 ). Another possible explanation is the coronary "slow flow" phenomenon, which may be caused by microvascular spasm, although slow flow was not mentioned in the angiography report. Nevertheless, the complete resolution of angina in Patients 1 and 3 after treatment with amlodipine provides circumstantial evidence that spasm was involved. Radionuclide studies shed some light on a possible link between mental stress and coronary vasoconstriction. Subjects exposed to minor experimental stress have been shown to develop significantly reduced coronary perfusion and ischaemic abnormalities of left ventricular wall motion. These abnormalities are due to coronary vasoconstriction, but are limited to subjects with at least minor degrees of underlying coronary artery disease, and are more pronounced when this disease is more severe. Subjects with normal arteries do not show such changes.7 Similarly, coronary spasm in the setting of emotional problems was described in nine women with normal or near-normal arteries,8 but it was likely that most had at least minor atherosclerosis (ie, <25% narrowing). In two of the patients reported by Mansour et al, coronary vessels were normal (and possibly also in Patient 2 before occlusion), so induction of spasm or vasoconstriction with ischaemia seems inconsistent with the experimental studies. However, angiographically "normal" arteries may harbour minor atherosclerotic lesions that do not encroach on the lumen. In addition, the severe and overwhelming emotional stress and arousal typical of panic, which these patients doubtless experienced, contrasts with the relatively minor tasks with minimal emotional responses to which the experimental subjects were exposed. The coronary vascular responses to severe and minor stress may be quite different. For example, extreme rage induced myocardial infarction in dogs, although after a critical stenosis had been created in a coronary artery.9 Severe emotional arousal deserves further investigation. Wilkinson et al showed that patients with panic disorder have dramatic increases in epinephrine secretion and cardiac epinephrine spillover during panic, but that baseline levels and responses to mild experimental stress differ little from those of control subjects.10 Cardiac perfusion and functional studies during panic would be of interest, but would require panic attacks to be artificially induced in the laboratory. The absence of ECG changes in Patient 3, despite severe chest pain and significantly raised cardiac enzyme levels, raises an important issue about myocardial ischaemia. In the radionuclide studies mentioned above, significant decreases in perfusion or abnormalities in wall motion often occurred without ischaemic pain or ECG changes. Ischaemia can be electrocardiographically "silent", particularly in certain vascular distributions, such as that of the left circumflex coronary artery. Nevertheless, it must be unusual that ischaemia sufficient to produce necrosis should produce no ECG changes. These cases should raise clinician awareness of the potential association between severe anxiety and myocardial ischaemia, so that patients with chest discomfort and panic disorder are appropriately investigated. All patients with severe panic accompanied by prolonged chest pain should have cardiac enzyme levels measured, irrespective of ECG findings. While epicardial coronary artery spasm is a plausible explanation, further investigations are needed into the mechanisms of ischaemia in panic disorder. S Ben Freedman Professor, and Head, Department of Cardiology Concord Repatriation General Hospital, University of Sydney, NSW Christopher C Tennant Professor and Head, Department of Academic Psychiatry Royal North Shore Hospital, University of Sydney, Sydney, NSW Mansour VM, Dominic JC, Jennings GL, et al. Panic disorder: coronary spasm as a basis for cardiac risk? Med J Aust 1997; 168: 390-392. Kawachi I, Sparrow D, Vokonas PS, Weiss ST. Symptoms of anxiety and risk of coronary heart disease. Circulation 1994; 90: 2225-2229. Kawachi I, Colditz GA, Ascherio A, et al. Prospective study of phobic anxiety and risk of coronary heart disease in men. Circulation 1994; 89: 1992-1997. Coryell W, Noyes R, Clancy J. Excess mortality in panic disorder. A comparison with primary unipolar depression. Arch Gen Psychiatry 1982; 39: 701-703. Cannon RO. Does coronary endothelial dysfunction cause myocardial ischemia in the absence of obstructive coronary artery disease? Circulation 1997; 96: 3251-3254. Alford FP. Syndrome X (insulin resistance metabolic syndrome): a deadly quartet or an awesome foursome? Med J Aust 1996; 164: 4-5. Tennant C. Experimental stress and cardiac function. J Psychosom Res 1996; 40: 569-583. Bashour T, Hakim O, Cheng TO. Coronary spastic angina in middle-aged women: a psychosomatic disorder? Am Heart J 1983; 106: 609-613. Verrier RL, Hagestad EL, Lown B. Delayed myocardial ischemia induced by anger. Circulation 1987; 75: 249-254. Wilkinson DJC, Thompson JM, Lambert GW, et al. Sympathetic activity in patients with panic disorders at rest, under laboratory mental stress and during panic attacks. Arch Gen Psychiatry 1998. In press. Reprints: Professor S Ben Freedman, Department of Cardiology, Concord Repatriation General Hospital, Hospital Road, Concord, Sydney, 2137. - 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/>

Christopher C Tennant

Prescriptions, practitioners and pharmacists Better communication and teamwork for improved patient outcomes MJA 1998; 168: 317-318 Medicines are clearly an important component of healthcare. In Australia, prescriptions are written in 63.8% of general practitioner consultations,1 and in 1996 approximately 178 million prescriptions were dispensed. With the potential for adverse reactions and reported suboptimal use of drugs,2-5 it is important to work towards the best possible use of medicines. There are a number of indicators of inappropriate drug use in Australia, including the large quantities of unused medicines collected in the Return of Unwanted Medicines campaign,6 and studies showing that between 5.7% and 16.6% of all hospital admissions are drug-related events.7,8 Further, a recent report of the South Australian Community Pharmacy Model Practices Project showed that, at entry to the project, 90% of patients at high risk of medication misadventure (usually those taking more than four medications) had unresolved health or medication problems, two-thirds of which were medication related.3 Medication care can be improved by enhancing communication between doctors, pharmacists, other health professionals and consumers. Indeed, a number of intervention studies have found that quality of medication care can be improved through further building of the healthcare team, academic detailing (promotion of rational prescribing through detailing visits from pharmacists), medication review by pharmacists and doctors and feedback of prescribing patterns to doctors.2-5,9 In this vein, the Royal Australian College of General Practitioners (RACGP) and the Pharmaceutical Society of Australia (PSA), in their draft joint statement about communication between GPs and pharmacists,10 proposed a range of conventions and abbreviations aimed at improving the prescription as a communication medium. In this issue of the Journal Liddell and Goldman report the findings of the pilot study11 on which the final version of the joint statement, published in 1996, was based.12 In their study, Liddell and Goldman11 trialled the use of certain prescription notations by GPs as a means of providing the pharmacist with information for enhancing patient understanding and medication care. A modified prescription form was preprinted with the abbreviations recommended in the draft RACGP-PSA joint statement.10 These abbreviations were intended to alert the pharmacist to patient needs for counselling and assistance, and to the existence of written instructions given to the patient by the GP to enable the pharmacist to label the medicine accordingly and reinforce the patient's understanding. The prescription conventions trialled were (i) writing the general purpose for which a medication was prescribed on the form, (ii) indicating when this should not be written on the label, (iii) underlining and initialling unusual dosages, (iv) indicating that an unusual pack size was intended, and (v) noting that therapy with an ongoing medication had been stopped. Liddell and Goldman11 examined the use of and attitudes towards these new notations and found that at least one of the new notations was used on 45% of the 3464 prescription items, and that one in particular -- the general purpose of the medication -- was noted on 35%. Some preprinted notations were used so rarely that they were excluded from the final joint statement,12 and the "cease" notation was also so rarely used (14 times) that it was relatively ineffective. However, consumers felt that writing the purpose of a medication on its label was generally appropriate and helpful. Participating GPs and pharmacists were positive about the notations, especially the indication of a medication's purpose. Effective communication and collaboration between specialists, GPs and pharmacists, beyond simply changing the way prescriptions are written, are likely to result in advances in medication care. A range of collaborative interdisciplinary primary care models have been developed and trialled both here3,5,13 and in the United Kingdom.14 In the Community Pharmacy Model Practices Project (mentioned above), protocols were defined by pharmacists, with input from GPs and consumers, to optimise quality pharmaceutical services for patients with a high risk of medication misadventure; more than 80% of consumers felt that the pharmacists' service had made a significant contribution to their health and there was an estimated net societal saving to the health system of $110 per patient.3 The Commonwealth Department of Veterans' Affairs has attempted to facilitate communication in its medication management program through written referrals between specialists, general practitioners and pharmacists, with the consent of veterans, and through education programs.13 In the UK, models of pharmacists' input to primary care include (i) review of repeat prescriptions, (ii) total medication review, (iii) drug use evaluation, (iv) development of drug formularies (or drug lists) for general practices, (v) development of prescribing policy, and (vi) audit of prescribing by disease or condition.14 Not surprisingly, it was found that rational and cost-effective prescribing was best achieved when pharmacists and general practitioners worked together.14 Successful models of interdisciplinary collaboration need to be implemented cautiously, as rapid imposed change can create conflict and resistance. Relationship building, stakeholder involvement (at both "grass roots" and organisational levels) and communication between the professions have been key components associated with Australian studies of medication care.3-5,9 There are dangers in ignoring these components and other recommendations in translating trials into practice. For example, selective implementation of recommendations in providing consultant pharmacist services to nursing homes without the recommended involvement of and support to GPs,4 has resulted in some justifiable concern by GPs (personal, unpublished data). Clearly, any national effort to facilitate optimal medication care should mandate the involvement of all key stakeholders. Communication and relationships are the keys to balancing collaboration and optimal patient care with autonomy and privacy issues. Effective communication depends both on its being a two-way process, and on how the relationship between the two parties influences the interpretation of "messages" by each. Trust, confidence, involvement and a mutual respect for each professional's role and competence are therefore essential in any functioning team. The development of these elements should start during interdisciplinary undergraduate (and postgraduate) clinical education of doctors, pharmacists and other health professionals.15 Interdisciplinary clinical teaching, recognition of emerging practice models and the need for interprofessional student interaction are sadly lacking in Australia. With the introduction of the four-year pharmacy course and the graduate medical courses nationally, now is the time to grasp the opportunity offered for interdisciplinary development. Further, electronic prescribing links16 and newer avenues of interprofessional communication, such as regular joint medication reviews,9 consumer medicine information and the National Prescribing Service, are opportunities for overcoming the barriers to communication and information sharing, and to nurturing professional relationships. Facilitating information sharing between specialists, medical practitioners and pharmacists through interprofessional collaboration and better communication (including through the prescription form10-12) should lead to improved patient care and outcomes, easier and more effective communication between health professionals, and high quality, cost-effective use of medicines. The Australian healthcare system must build and maintain relationships between professionals and with consumers if it is to improve. Michael S Roberts NHMRC Senior Principal Research Fellow, and Professor Julie A Stokes Research Scholar Department of Medicine, University of Queensland, Princess Alexandra Hospital Brisbane, QLD Bridges-Webb C, Britt H, Miles D, et al. Morbidity and treatment in general practice in Australia 1990-1991. Med J Aust 1992; 157 Suppl Oct 19: S1-S56. Parkes AJ, Coper L. Inappropriate use of medications in the veteran community. How much do doctors and pharmacists contribute? Aust N Z J Public Health 1997; 21: 469-476. Gilbert A. Final report of the Community Pharmacy Model Practice Project. Canberra: Federal Department of Health and Family Services, 1997. Roberts MS, Stokes J, Bonner C, et al. Clinical pharmacy intervention and resident outcomes in Australian nursing homes. Proc Austral Soc Clin Exp Pharmacol Toxicol 1995; 2: 158. McNeece J. The drug and therapeutics information service. Aust J Hosp Pharm 1994; 24: 28-31. Goodman M, Lazzarini R. Examination of the feasibility of an ongoing strategy for disposal of unwanted and outdated medicines [abstract]. The Pharmaceutical Education Program 1995 Work in Progress Conference; Sydney Aug 24-26. Canberra: Commonwealth Department of Health and Family Services, 1995. Dartnell JG, Anderson RP, Chohan V, et al. Hospitalisation for adverse events related to drug therapy: incidence, avoidability and costs. Med J Aust 1996; 164: 659-662. Blackbourn J. Readmission to Fremantle Hospital. Part 2. Drug-related readmissions. Fremantle Hosp Drug Bull 1991; 15: 13. ACT Division of General Practice. Managing medication in nursing homes -- GP involvement in medication reviews. A report of the outcomes of the "Aged Care Assessment Project". Canberra: ACT Division of General Practice, 1998. In press. Ruth R, Constable V, Dammery D, et al. General practitioners' and pharmacists' interprofessional communication. Aust Fam Physician 1994; 23: 1544-1546. Liddell MJ, Goldman SP. Attitudes to and use of a modified precription form by general practitioners and pharmacists. Med J Aust 1998; 168: 322-355. Bollen M. Improving communication between general practitioners and pharmacists. Aust Fam Physician 1996; 25: 1011-1013. Coper L. Pharmaceutical Management Program. Canberra: Commonwealth Department of Veterans' Affairs, 1997. Bradley CP, Taylor RJ, Blenkinsopp A. Developing prescribing in primary care. BMJ 1997; 314: 744-747. Greene RJ, Cave I, Jackson SMD. Interprofessional clinical education of medical and pharmacy students. Med Educ 1996; 30: 129-133. Getting connected. Newslet Nat Pharm Intranet Demonst 1997; 1: 1-8. - 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 S Roberts · Julie A Stokes

Medical informatics meets medical education There's more to understanding information than technology MJA 1998; 168: 319-320 The decades-long predicted arrival of the information revolution in healthcare has taken perhaps no more than four years to go from a matter of minority opinion to one of general consensus.1,2 Not long ago, medical journals rarely discussed information technology, but now most carry regular articles on the subject. Indeed, all the major journals are now available in electronic form on the Web, and some argue that the paper journal is a dinosaur at the end of its time.3 Evidence grows for the value of using the computer to assist in routine tasks like prescribing4 and reminding general practitioners to carry out screening procedures.5 It is conceivable that, in the future, failure to use such tools could come to be regarded as negligent practice. Change such as this can often be abrupt and distressing, no matter how beneficial it may ultimately be. Existing skills become redundant and the young, who have time and energy to learn, have the advantage over those who may be more experienced but are constrained by existing clinical responsibilities. Clinicians with years of experience might thus be forgiven for throwing up their hands in despair at the sudden enthusiasm for computers and telemedicine, apparently at the expense of hard-won clinical skill and human empathy. However, if the scenarios that Carlile and Sefton paint in this issue of the Journal come to pass, then our dependence on information and communication technology can only deepen over the years.6 They draw our attention to the need to prepare medical graduates for work in a world where the inability to use this technology would be as debilitating as the inability to read or write is today. The ambitious new graduate medical program they describe at the University of Sydney is almost entirely structured around teaching material in the form of multimedia documents on the Web. Whether this move to a computer-based and problem-oriented curriculum will produce better-prepared graduates will no doubt become clearer with time. Certainly, all students in this program should graduate with proficiency in using the technology. In comparison, at the beginning of this decade only 25% of medical students at a comparable institution felt they could use computers well.7 While such an educational program is to be lauded, there is probably a greater educational challenge within the community of practising clinicians, most of whom have never had any formal training in information technology (IT). Nevertheless, they will be expected to work for many decades in an environment in which IT illiteracy will become increasingly burdensome. It is for these individuals that the immediate urgency lies. Certainly there is a case to be argued for basic postgraduate education in the use of IT in patient care, and if some medical colleges do not consider IT literacy a core component of their continuing education programs then perhaps they need to think again. Just how much training is needed depends on the systems clinicians need or want to use, and their current skills in doing so. If we are optimistic, these barriers for working clinicians will diminish over time as the technology becomes easier to use, and progressively develops into a commonplace and natural part of the clinical environment. However, we have no guarantees that such optimism is warranted. There is at least one major caveat in this rush to master the new technologies -- we must not forget that basic computer skills are not the same as being skilled in the management of information. Simply teaching practising clinicians or medical students to use IT is not enough. Just as the ability to suture doesn't make one a surgeon, the ability to surf the Web does not imply that one understands the principled use of information. With the current emphasis on evidence-based practice highlighting the skills needed to collate, distil and apply clinical research, we have a powerful example of the broader information and communication skills needed in healthcare. Information skills are basic to good medical practice. Every clinician needs to understand the principles of data interpretation, the logical foundations of the diagnostic process, and the management of uncertainty in clinical knowledge.8 The problem-oriented medical record is just an information instrument, and clinicians need to know when it is appropriate, and when indeed other formulations might be better choices. The dynamics of communicating with patients and with colleagues are altered when the exchange moves from a face-to-face interaction to the telephone, e-mail, voicemail or video.9 Understanding the implications of using one medium rather than another is central to developing effective communication skills as these communication options become commonplace in the community. Medical informatics is the name now given to the study of clinical information and communication processes. It is the rational study of the way we think about patients, and the way that treatments are defined, selected and developed. It is the study of how medical knowledge is created, shaped, shared and applied. Ultimately, it is the study of how we organise ourselves to create and run healthcare organisations.10 Understanding how to use information technology appropriately can only ever be one small component of this wider discipline. Where once these disparate elements of informatics were taught piecemeal, there is now growing consensus about the essential information skills needed by clinicians, and medical informatics is now appearing on more curricula as a distinct entity.11 A proposal for 10 essential clinical informatics skills is provided to give flesh to these ideas, and to stimulate debate about the role of informatics in medical education. So, the computer, the telephone, the Web, video -- these, and all that is still to come, are unquestionably powerful tools. Used badly, they do indeed waste time and money, create inefficiency, and dehumanise our interactions with each other. Used well, they are neither to be feared, loved nor loathed. They are simply to be used. And in the next century, the study of informatics will become as fundamental to the practice of medicine as anatomy has been to the last. Enrico Coiera Senior Project Manager Hewlett-Packard Laboratories, Bristol, UK E-mail: ewc AT pobox.com Coiera E. Medical Informatics. Med J Aust 1994; 160: 438-440. House of Representatives Standing Committee on Family and Community Affairs. Health on line: a report on health information management and telemedicine. Commonwealth of Australia. Canberra: The Committee, 1997. LaPorte RE, Marler E, Akazawa S, et al. The death of biomedical journals. BMJ 1995; 310: 1387-1389. Walton RT, Gierl C, Yudkin P, et al. Evaluation of computer support for prescribing (CAPSULE) using simulated cases. BMJ 1997; 315: 791-794. Shea S, Du Mouchel W, Bahamonde L. A Meta-analysis of 16 randomised controlled trials to evaluate computer-based clinical reminders for preventative care in the ambulatory setting. J Am Med Informatics Assoc 1996; 3: 399-409. Carlile S, Sefton AJ. Healthcare and the information age: implications for medical education. Med J Aust 1998; 168: 340-343. Kidd MR, Connoley GL, Cesnik B, McPhee W. What do medical students know about computers? Med J Aust 1993; 158: 283-284. Haynes RB, Ramsden M, McKibbon KA, et al. A review of medical education and medical informatics. Acad Med 1989; 64: 207-212. Coiera E, Tombs V. Communication behaviours in a hospital setting -- an observational study. BMJ 1998; 316: 673-677. Coiera E. Guide to medical informatics, the Internet and telemedicine. London: Chapman and Hall, 1997 ( see also http://www.coiera.com). Greenes RA, Shortliffe EH. Medical informatics -- an emerging academic discipline and institutional priority. JAMA 1990; 263: 1114-1120. - 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/>

Enrico Coiera

Disseminating and applying best evidence Does use of systematic reviews equal evidence-based medicine? MJA 1998; 168: 260-261 There are two purposes to medical research: one abstract -- the pursuit of knowledge for its own sake -- the other practical -- to improve health outcomes. To achieve the latter, research results must be disseminated and implemented, but this process may be slow, inaccurate and incomplete, resulting in varying clinical practice and outcomes. This is not through wilful disregard of medical advances; no active clinician expects to practise without needing new information and skills as health advances occur. Yet it is not humanly possible to keep up with all advances in all areas of medical research. Medical practitioners may use different forms of evidence to enlighten decisions but, until recently, were not taught how to ask the relevant questions about the new knowledge needed, how to sieve the medical literature and access information efficiently, nor how to assess success in applying new knowledge. Recognition of these deficiencies led to the discipline of evidence-based medicine (EBM). However, the recently emerged centres and departments of EBM are distrusted by some, perhaps because of visions of "cookbook" medicine, or the implied deficiencies in existing knowledge and practice, but often through misunderstanding of the nature of EBM. EBM is "a process of lifelong, self directed learning in which caring for our own patients creates the need for clinically important information about diagnosis, prognosis, therapy and other clinical and health care issues, and in which we: Convert these information needs into answerable questions; Track down with maximum efficiency the best evidence with which to answer them (whether from the clinical examination, the diagnostic laboratory, from research evidence or other sources); Critically appraise that evidence for its validity (closeness to the truth) and usefulness (clinical applicability); Apply the results of this appraisal in our clinical practice; Evaluate our performance."1 EBM is a structured process through which all available evidence is used to support clinical decision-making. Most active clinicians would support this philosophy, and data show that much clinical decision-making is in keeping with current knowledge.2-4 In this issue of the Journal, Jordens et al5 address the issue of how well Australian neonatologists and obstetricians access and use one such source of information -- systematic reviews, which aim to review all available clinical trial data in a structured way, often including meta-analyses. It is implicit in the research of Jordens et al that use of systematic reviews is "a good thing" and should be encouraged. They found that 72% of Australian neonatologists and 44% of their sample of Australian obstetricians reported using systematic reviews on average once per month. Is this a "good" result? Or should it be expressed as 28% of neonatologists and 56% of obstetricians report not using systematic reviews, with the implication that systematic reviews should be used by more? I believe neither is the issue. It remained unclear from the study whether using systematic reviews objectively improved practice, or whether respondents who used systematic reviews more also practised better, as judged by external benchmarks. Furthermore, Jordens et al found that, for keeping abreast with new clinical developments, respondents relied primarily on journals, followed (in decreasing order) by conferences and meetings, colleagues, and MEDLINE, with systematic reviews last. For clinical problem-solving, respondents relied on colleagues, MEDLINE, journals and other printed medical literature, again above systematic reviews. Does this mean that systematic reviews are not valuable? Of course not. It merely identifies them as one of many sources of information. Choice of sources will depend on the existing skills and knowledge of the individual practitioner. Although systematic reviews undoubtedly have a place in continuing medical education and may be more informative than traditional opinion-based, narrative reviews,6 we rarely acknowledge their flaws. As with any summary, they have a finite life span and must be updated obsessively and regularly. Systematic reviews on the same topic may be inconsistent.7 They are often based on meta-analyses, which may be flawed in design8 or incorrect.9 In 35% of instances, meta-analysis results are not corroborated by subsequent large scale randomised clinical trials.9 For these reasons, systematic reviews must be seen as one source of information, and not as the only or best source. They are merely a structured way of reviewing other investigators' data. Documenting and disseminating the evidence is only the beginning of continuing medical education. It does not matter how advances are disseminated, as long as it is done accurately and efficiently. More importantly, it is not the dissemination per se that is crucial, but the appropriate application and use of the information. Effective strategies for changing clinical practice include use of reminders, academic visits, opinion leaders and combinations of these.10 Other sources of information known to be important include university-sponsored continuing medical education, hospital rounds, and pharmaceutical representatives.11 Conferences and lectures are in general least effective, while colleagues and journals consistently score highly.10,11 Different strategies will work for different clinicians in different environments12 and must be adapted to the specific practice change desired, the target, setting, and obstacles to change. A series of staged alterations will usually be needed, including review of whether practice has changed and appropriate further alterations as necessary. Unfortunately, it is clear that there are still major problems with dissemination and application of evidence. For example, only 36%-42% of patients in the United States may be receiving b -blockers after myocardial infarction,13 despite their well known benefits. Systematic reviews certainly have a place in improving the dissemination and application of current best knowledge, but it is worrying when it is implied that these reviews equal EBM and that if practitioners do not use them routinely their knowledge base or clinical practice is flawed. Jordens et al have shown that systematic reviews are accessed as one source of clinical information and may alter clinical practice. However, whether or not clinicians use a particular source of information is not the important issue. The challenge is to improve further the application of best knowledge. Paddy A Phillips Professor, and Head of Medicine, Flinders University of South Australia Flinders Medical Centre, Adelaide, SA Sackett DL, Richardson WS, Rosenberg W, Haynes RB. Evidence based medicine: how to practice and teach EBM. New York: Churchill Livingstone, 1997. Ellis J, Mulligan I, Rowe J, Sackett DL. Inpatient general medicine is evidence based. Lancet 1995; 346: 407-409. Geddes JR, Game D, Jenkins NE, et al. What proportion of primary psychiatric interventions are based on evidence from randomised controlled trials? Qual Health Care 1996; 5: 215-217. Gill P, Dowell AC, Neal RD, et al. Evidence based general practice: a retrospective study of interventions in one training practice. BMJ 1996; 312: 819-821. Jordens CFC, Haw P, Irwig LM, et al. Use of systematic reviews of randomised trials by Australian neonatologists and obstetricians. Med J Aust 1998; 168: 267-270. Cook DJ, Mulrow CD, Haynes RB. Systematic reviews: synthesis of best evidence for clinical decisions. Ann Intern Med 1997; 126: 376-380. Jadad AR, Cook DJ, Browman GP. A guide to interpreting discordant systematic reviews. Can Med Assoc J 1997; 156: 1411-1416. Bailar JC. The promise and problems of meta-analysis. N Engl J Med 1997; 337: 559-601. LeLorier J, Gregoire G, Benhaddad A, et al. Discrepancies between meta-analyses and subsequent large randomized, controlled trials. N Engl J Med 1997; 337: 536-542. David DA, Thomson MA, Oxman AD, Haynes B. Changing physician performance: a systematic review of the effect of continuing medical education strategies. JAMA 1995; 274: 700-705. Felch WC, Scanlon DM. Bridging the gap between research and practice: the role of continuing medical education. JAMA 1997; 277: 155-156. Grol R. Beliefs and evidence in changing clinical practice. BMJ 1997; 315: 418-421. Rogers WJ, Bowlby LJ, Chandra NC. Treatment of myocardial infarction in the United States (1990 to 1993): observations from the National Registry of Myocardial Infarction. Circulation 1994; 92: 2103-2114. - 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/>

Paddy A Phillips

Smoking -- time to ring the alarm bells again 1998 offers a golden opportunity for evolutionary tobacco control legislation MJA 1998; 168: 204-205 The mortality rate from tobacco-related disease remains inordinately high, with one Australian death every 30 minutes.1Hill, White and Scollo, in this issue of the Journal, report smoking rates of Australian adults for 1995 and look at trends in smoking prevalence over time.2 The 1995 figures show that, compared with the previous uniformly downward trend in smoking prevalence in Australia, there has been a disturbing stabilising in prevalence of smoking in both men and women. For other countries, comparative 1995 data are sparse, and, high mortality rates notwithstanding, Australian (and New Zealand) smoking rates are among the lowest on the international ladder, together with those of Sweden, Finland, the United Kingdom, the United States (especially California), and a small number of other exemplar countries or States. The average smoking rate for this group is about 25%-30% or less,3 and consistently measured data are available over a considerable period. Despite their similar smoking patterns, the countries and environments in which lower smoking rates have been achieved differ remarkably, making generalisation about the most effective tobacco control policies perilous. Australia began with health warnings in the early 1970s, and a patchwork quilt of State and federal laws to control advertising, which evolved (amid much controversy) into good, but not perfect, comprehensive federal legislation in 1992, with final implementation achieved only in 1996. We also have good research-based education programs. Finland and Sweden have had comprehensive legislation in place for two decades (which cannot, of course, prevent cross-border advertising) and have backed this up with competent education programs. California has spent very large amounts of money in recent years on well researched antismoking campaigns, which have been competing with vigorous and clever tobacco advertising (only radio and TV advertising is banned). At present, antismoking campaigns are being conducted amid enormous public debate.4 Mean smoking prevalence in 1995 was 16.7%.5 The United Kingdom can be best classified as having modest advertising controls and modest education programs. Although implementation of tobacco control policy has been somewhat erratic, there is historical and international agreement6 on the necessity for a comprehensive approach (including comprehensive legislation) which prohibits all forms of tobacco promotion, conducts public education campaigns, implements programs to help smokers to quit, restricts smoking in public places and sales to minors, and regularly increases prices. More recently, the emphasis has been on smoke-free workplaces, generic packaging and banning point-of-sale promotions. Probably the only generalisations possible are that no country has been successful in shielding its population from all tobacco advertising and that no country has consistently spent commercially large amounts of money on education over a significant period of time (such as amounts spent by Coca-Cola -- $30-$35 million nationally in Australia7 -- or the Victorian Traffic Accident Commission -- $24 million8). Meanwhile, the resilient and resourceful tobacco industry has responded to tobacco control by focusing increasingly on cross-border and global advertising and global brands. A topical example of global advertising -- Formula One car racing -- is illustrative. Excluded from the Australian prohibition on television and radio advertising in 1975 by a last-minute amendment9 which opened a suitable loophole, Grand Prix racing is still favoured by specific exclusion in 1998. Winfield, which otherwise may be advertised only at point of sale in Australia, is to be launched as a global brand in 1998 through Formula One, and will therefore be advertised back into Australia, as well as globally, by this means. One can only marvel at the tobacco industry's advertising ingenuity10 in using the kangaroo symbol, placing it on the red background of the new packet, and incidentally turning Qantas tailplanes into surrogate Winfield advertisements. Continued broadcasting of the tobacco-sponsored Grand Prix from the United Kingdom will occur until the year 2006. This decision was preceded by a controversial pre-election gift of £1 million to the British Labour Party by the key promoter of the Formula One Grand Prix,11 a feat which the public health fraternity will have difficulty matching. The Australian situation is indeed serious, and, as with the other developed industrialised countries mentioned, prevalence averages conceal both the better and the worse aspects of smoking habits -- all these countries have the same education and occupation gradients. Regardless of how impressive the low smoking prevalence of 18.7% (16.7% for women) is among the highest occupational level of Australian households, it is profoundly depressing to observe the prevalences of 40.9% and 31.8%, respectively, for the lowest occupational level, even though these blue collar levels have seen quite large falls over time. Clearly more effort is needed. Hill et al collated data on smoking prevalences and antismoking campaigns and found that the levelling off in previously declining prevalences is related to lower per capita expenditure on antismoking campaigns. The solution, in essence, requires renewed action on two major interrelated fronts. One is money; the other is legislation. Money need not be a problem. The popular principle of allocation of tobacco tax for health promotion purposes was established by the Victorian Tobacco Act 1987 (a world first), which established the Victorian Health Promotion Foundation (VicHealth). Similar Acts followed in Western Australia and South Australia. The original mandate of VicHealth included spending 30% of its then $28 million budget on sport, plus significant amounts on arts sponsorship and outdoor advertising, to buy out and replace the vested interests then advertising tobacco. This is no longer necessary, as federal legislation now consolidates advertising prohibition in these fields. As a consequence, in 1997, the Victorian Quit campaign received 10% of VicHealth's $23 million. Australian tobacco tax is low by UK and Scandinavian standards and should be increased. Lifting the Victorian Quit allocation from under $3 million to $12 million would equal about $3 per head of population, and would cost less than a packet of cigarettes per head. If followed by other States and matched by 1997 level federal expenditure a serious national campaign could be mounted. State (and possibly federal) tobacco legislation now requires rewriting, both because State tobacco licence fees have been declared unconstitutional and because national competition policy requires it.12 So, 1998 offers a golden opportunity to rewrite the prescription, and some evolutionary legislation is indeed timely: Generic packaging should be introduced; Sales to minors should be more effectively restricted and the restrictions implemented; Point-of-sale advertising should disappear; and Exemptions for international sporting events should be phased out over time, preferably in conjunction with similar action in the United States and Europe. Finally, enough is now known about nicotine-driven compensatory smoking13 and differential carcinogen levels in cigarette brands14 to legislate for control of nicotine content and to introduce, and progressively reduce, upper limits for specific carcinogens. New tobacco legislation is needed in 1998-99. It should be about tobacco, its control and the proper funding of programs to reduce its use and effects. Smoking prevalence and tobacco disease should then continue to decline. Nigel J Gray Consultant European Institute of Oncology, Milan, Italy English DR, Holman CDJ, Milne E, et al. The quantification of drug caused morbidity and mortality in Australia. 1995 edition. Canberra: Commonwealth Department of Human Services and Health, 1995. Hill DJ, White VM, Scollo MM. Smoking behaviours of Australian adults in 1995: trends and concerns. Med J Aust 1998; 168: 209-213. Tobacco or health: a global status report. Geneva: World Health Organization, 1997. Gray N. The global settlement -- a global view [editorial]. J Surg Oncol 1997; 66: 79-80. Glantz SA. Tobacco control in Australia: it's time to get back on top down under. Health Promot J Aust 1997; 7(1): 72-73. Gray NJ, editor. Lung cancer prevention: guidelines for smoking control. Geneva: Union International Contre le Cancer, 1997. Business Review Weekly 1997; Feb 7: 73. Victorian Traffic Accident Commission, Annual Report, Melbourne: VTAC, 1997. Gray NJ. Forty years of plotting for public health. Med J Aust 1997; 176: 587-589. Toy M-A. Outrage as Rothmans plans kangaroo label on cigarettes. The Age (Melbourne) 1998; Jan 17: 1. Morrison J. Row blights Blair's honeymoon. The Sunday Age (Melbourne) 1997; Nov 16: 15. Colebatch T. States' $5b tax rescue plan. The Age (Melbourne) 1997; Aug 6: A.1. Kozlowski LT, Ricket WS, Pope MA, et al. Estimating the yields to smokers of tar, nicotine and carbon monoxide from the lowest yield ventilated filter cigarettes. Br J Addict 1982; 77: 159-165. Hoffmann D, Hoffmann I. Tobacco consumption and lung cancer. In: Hansen HH, editor. Lung cancer. Advances in basic and clinical research. Dortrecht: Kluwer Academic Publications, 1994: 1-42. o - 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/>

Nigel J Gray

Hyperparathyroidism: what does surgery have to offer? Even asymptomatic patients should be considered for surgery MJA 1998; 168: 148-149 The report by Delbridge et al in this issue of the Journal1 describes the changing clinical picture of primary hyperparathyroidism (PHPT) in patients referred for surgical treatment at Royal North Shore Hospital, Sydney, over the past 30 years. The most common presentation in the 1990s is in women over the age of 50 years with bone loss indistinguishable from that of postmenopausal or senile osteoporosis (31%). Patients with kidney stones still constitute 15%, and those with subtle but distressing symptoms of fatigue, depression or altered cognitive function constitute 20%. Delbridge et al have also observed an "exponential" increase in the number of cases referred for surgery over the past decade, reflecting contemporary epidemiological studies which have unearthed a virtual epidemic of PHPT among postmenopausal women -- it affects 2% to 3% of women in this age group.2,3 Even so, the absolute number of patients undergoing operation at Royal North Shore Hospital each year remains small when compared with the number expected by extrapolation from this prevalence. Presumably, this is due in part to underdiagnosis of PHPT, as well as continuing reluctance among physicians to refer patients for surgery unless they have marked hypercalcaemia or overt "bone or stone" disease. Modern surgical treatment of PHPT is very safe, with a hospital stay of two days or less. As documented by Delbridge et al, a primary neck exploration for PHPT by experienced surgeons is successful in 95% to 98% of cases. Most authorities would agree with these authors that preoperative tumour-localising studies are not cost effective because of the significant number of both false positive and false negative results.4 The limitations of these tests are not universally appreciated by physicians, many of whom still consider a positive tumour-localising study to be a prerequisite for surgical referral. In an attempt to discourage this, John Doppman (Chief, Department of Diagnostic Radiology, United States National Institutes of Health [NIH]) stated at the NIH Consensus Development Conference on PHPT that "the only localisation study needed by a patient undergoing initial parathyroid surgery is to locate an experienced parathyroid surgeon".5 A parathyroid neck exploration is often so easy that the uninitiated surgeon may wonder what all the fuss is about. However, the operation has many potential pitfalls which can lead to failure, with the result that the patient then has to undergo further irksome and costly investigations and a potentially hazardous reoperation. There is thus a high premium on succeeding at the first try. In this regard there is no substitute for experience on the part of the surgeon, who must be able to recognise a parathyroid gland, know the distribution of the glands, where they can be hidden, and how to distinguish between normal and abnormal glands with the naked eye. To acquire this expertise requires a dedicated training in a specialised centre by an experienced preceptor.4 Which patients with PHPT should have surgery? The NIH Consensus Development Conference agreed on criteria for surgery in patients with PHPT.5 These include any one of the following: Serum calcium above 2.99 mmol/L; Marked hypercalciuria (> 9.98 mmol/day); Any overt manifestation of PHPT (nephrolithiasis, osteitis fibrosa cystica, or classic neuromuscular disease); Markedly reduced cortical bone density; Reduced creatinine clearance in the absence of another cause; and Age less than 50 years. The recent demonstration by Silverberg et al6 that parathyroidectomy markedly improves cancellous (ie, lumbar spine) bone density in patients with PHPT has added vertebral osteopenia to the list of indications for surgery. There is also increasing evidence, including a recent prospective case-control study,7 attesting to the beneficial effect of parathyroidectomy on symptoms of hypercalcaemia, such as muscle weakness, fatigue, lethargy, depression, and memory loss. Patients with such symptoms now comprise 20% of those undergoing surgery for PHPT at Royal North Shore Hospital. As for patients who are truly asymptomatic with uncomplicated (or "biochemical") PHPT, the NIH Consensus Development Conference concluded that such patients should also be considered for surgery.5 The natural history of biochemical PHPT is unpredictable, and the costs of long term surveillance are not inconsiderable.8 Given the safety and efficacy of modern parathyroid surgery, it presents an attractive alternative to indefinite follow-up. The trend toward liberalising the indications for surgical treatment of PHPT has been given added impetus recently by several Scandinavian population-based studies indicating that patients with untreated PHPT have an increased risk of dying from cardiovascular disease and malignancy when compared with age- and sex-matched controls in the normal population.9 This increased risk of death can be reduced, if not eliminated, by parathyroid surgery.10 In this context, it is particularly relevant that the earlier the disease is recognised the more rapidly the mortality risk returns to normal after surgery. What is the future of parathyroid surgery? Delbridge et al have described the latest enthusiasm for endoscopic parathyroidectomy as "a passing interest", but this may be prematurely dismissive. Rightly or wrongly, endoscopic parathyroidectomy is already being done, and workshops teaching the technique are now conducted regularly at more than one European centre. In my opinion, it would be unfortunate if this procedure were to become the province of self-proclaimed "experts" in endosurgery who have little experience of the vagaries and nuances of parathyroid anatomy and pathology -- they could have difficulty in exploring the neck if the parathyroid tumour is not found endoscopically and conversion to open operation is required. Theoretically, endoscopic parathyroid surgery may offer advantages to patients through less postoperative pain, shorter hospital stay and smaller, more aesthetically pleasing scars. It is therefore appropriate to evaluate critically the efficacy, safety and cost of this procedure relative to those of a competently performed open parathyroidectomy, by way of a prospective controlled trial.11 Anthony J Edis Surgeon, Mount Hospital, Perth, WA Delbridge L, Younes N, Guinea A, et al. Surgery for primary hyperparathyroidism 1962-1996: indications and outcomes. Med J Aust 1998; 168: 153-156. Palmer M, Jakobson S, Akerstrom G, et al. Prevalence of hypercalcemia in a health survey: a 14-year follow-up study of serum calcium values. Eur J Clin Invest 1988; 18: 39-46. Lundgren E, Ridefelt P, Akerstrom G, et al. Parathyroid tissue in normocalcemic and hypercalcemic primary hyperparathyroidism recruited by health screening. World J Surg 1996; 20: 727-735. Edis A. Primary hyperparathyroidism in 1992: questions and answers. RACS Bull Nov 1992: 2-4. NIH Consensus Development Conference Panel. Diagnosis and management of asymptomatic primary hyperparathyroidism. Consensus development statement. Ann Int Med 1991; 114: 593-597. Silverberg S, Locker F, Bilezikian J. Vertebral osteopenia: a new indication for surgery in primary hyperparathyroidism. J Clin Endocrinol Metab 1996; 81: 4007-4012. Chan A, Duh Q, Catz M, et al. Clinical manifestations of primary hyperparathyroidism before and after parathyroidectomy: a case-control study. Ann Surg 1995; 222: 402-414. Heath H III, Hodgson S, Kennedy M. Primary hyperparathyroidism, incidence, morbidity and potential impact in a community. N Engl J Med 1980; 302: 189-193. Palmer M, Adami H-O, Bergstrom R, et al. Survival and renal function in persons with untreated hypercalcemia: a population-based cohort study with 14 years of follow-up. Lancet 1987; 1: 59-62. Hedback G, Oden A, Tisell L-E. The influence of surgery on the risk of death in patients with primary hyperparathyroidism. World J Surg 1991; 15: 399-407. Edis A, Sheiner H. Laparoscopic surgery: an ethical dilemma. Aust N Z J Surg 1996; 66: 201. 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/>

Anthony J Edis

Short-stay carotid endarterectomy Does the risk of complications warrant more than overnight stay? MJA 1998; 168: 149-150 Each year an estimated 32 000 Australians suffer a first-ever stroke1 (about 80% of which are ischaemic2 ), and a similar number are affected by transient ischaemic attacks (TIAs).3 About 40% of patients with ischaemic stroke syndromes have extracranial arterial lesions accessible to surgery,4 most commonly carotid stenosis. Significant carotid stenosis is present in an estimated 80 000 Australians aged 50-74 years.2 For many with this condition, carotid endarterectomy is the treatment of choice.2 The operation of carotid endarterectomy is more or less standardised, although controversies persist over technical issues (eg, local versus general anaesthesia, need for monitoring of cerebral perfusion or brain function, indications for shunting to maintain carotid flow during carotid clamping, and closure of the arteriotomy directly versus with a patch).5 Nevertheless, for most patients, the operation is straightforward. In this issue of the Journal, Bourke and Crimmins report 59 patients who underwent carotid endarterectomy with short hospital stay.6 Patients were admitted on the morning of the operation (performed under local anaesthesia) and discharged the next day. Before admission, patients were counselled about possible complications and how to respond. Six were excluded from overnight hospital stay for good reasons. No strokes or major complications occurred among the 59, although one developed the reperfusion syndrome which threatened a haemorrhagic stroke, another developed headaches severe enough to prolong hospital stay, and a third was returned to the operating theatre because of complications in the groin wound. The major conclusion of the report is that patients can safely undergo carotid endarterectomy with only an overnight stay. Short-stay carotid endarterectomy is practised in some other Australian institutions, notably Victorian teaching hospitals, probably in response to management efficiencies driven by casemix funding. In the United States, overnight carotid endarterectomy has been usual for several years, with some groups even advocating same-day carotid endarterectomy (with discharge the afternoon or evening of the operation). What are the main disadvantages of overnight carotid endarterectomy? Apart from inconvenience, there is the possibility that longer hospital stay might allow the complications of the surgery to be prevented or better treated. Firstly, stroke may follow carotid endarterectomy. The North American Symptomatic Carotid Endarterectomy Trial (NASCET) found perioperative stroke rates of 1%-5%,7 while rates are considerably higher in many institutions.8 The neurologic deficit may be evident on conclusion of the operation, but more often there is a latent period during which the patient is awake and neurologically intact. For example, unpublished data from the European Carotid Surgery Trial (ECST) show that, among 1807 patients who underwent carotid endarterectomy, 85 had a perioperative stroke or died within the first 24 hours after surgery, 14 on the second day, five on the third day, eight on the fourth day, and 13 from the fifth day onwards (Dr Graeme J Hankey, Neurologist, Royal Perth Hospital, Perth, WA, personal communication, 1997). Most delayed strokes are caused by thrombotic occlusion of the internal carotid artery or by embolism of thrombus formed at the site of the reconstruction. 9 Stroke progression will be halted, and about half the patients returned to normal, by urgent repeat disobliteration of the carotid reconstruction.9 Therefore, based on the ECST data, remaining in hospital a second night might mitigate or prevent perhaps 5% of perioperative strokes. Cerebral haemorrhage occurs in about one per 400 patients, typically from the fifth day onwards.10 Often there is preceding hypertension, headaches, and sometimes epileptiform convulsions. These are attributed to cerebral hyperperfusion, and treated by reduction of blood pressure to normal, bedrest, and pain relief. If a late stroke occurs, urgent cerebral computed tomography is needed to distinguish cerebral haemorrhage from infarction, as treatment otherwise usually includes heparin and perhaps redo carotid reconstruction. A second complication after carotid endarterectomy is temporary instability in control of blood pressure and heart rate, which occurs in a little over half of patients.11 In 60% of these, hypertension (presumably due to interference with carotid baroreceptors) persists and may lead to cerebral oedema and stroke. The other 40% develop hypotension and/or bradycardia and may require heparin to minimise the chance of carotid thrombosis, although fluid replacement and atropine are usually effective. The cardiovascular instability usually resolves within 24 hours of surgery, and patients may be discharged when their blood pressure has returned to the usual preoperative level. A third early hazard after carotid endarterectomy is bleeding into the neck wound. At St Vincent's Hospital, Sydney, haemorrhage from the carotid suture line or other vessels needs to be corrected urgently in the operating theatre after about one per 200 operations (unpublished data), while at the Cleveland Clinic, United States, cervical haematoma requiring drainage developed after 1.5% of operations.12 Although most developed within the first 24 hours after surgery, some were delayed to the second or third day. A neck haematoma can rapidly obstruct the airway, and, as laryngeal oedema makes endotracheal intubation difficult, an expert anaesthetist and facilities for urgent tracheotomy should be available. Sudden disruption of the arterial suture line with heavy bleeding can be fatal or lead to a stroke through impaired carotid flow. None of these complications affected the patients reported by Bourke and Crimmins, although one patient was urgently readmitted for the reperfusion syndrome. The authors also had the advantage of treating local patients, facilitating postdischarge supervision and care. However, complications do occur for other surgeons, and, in general, patients should remain in hospital while complications are a real risk. Same-day carotid endarterectomy is inappropriate for most Australian institutions, as most patients return home on discharge from hospital rather than transfer to a nearby hospital-affiliated domiciliary service, as in the United States. Bourke and Crimmins also reported using duplex ultrasonography routinely instead of cerebral angiography to assess carotid stenosis before surgery. Duplex ultrasonography of the cervical vessels is indicated when carotid stenosis is suspected or the significance of a neck bruit is uncertain. It accurately confirms the presence of carotid stenosis, and measures its degree, but caveats apply. It cannot directly assess the arteries within the chest or cranial cavity, its accuracy depends on operator experience, and it is less reliable when the carotid arteries are tortuous or rotated or when the internal carotid artery is completely, or apparently completely, occluded. Angiography is more comprehensive, allowing visualisation of the intrathoracic and intracranial vessels, as well as the neck vessels, and nowadays can be performed on outpatients using a fine catheter introduced into the brachial or femoral artery by percutaneous puncture. Further, intra-arterial digital subtraction angiography reduces the volume of contrast medium, but, even so, angiography is invasive and potentially dangerous, causing stroke in about one per 200 patients, even in good centres,11 and more in less-skilled hands.13 Magnetic resonance angiography is a safer alternative, but current Federal Government policies restrict its availability. The cost of a carotid endarterectomy in Australia has been variously estimated as $56002 and $7000.5 This can be reduced by eliminating unnecessary investigations and by shortening hospital stay. Nevertheless, safety demands that patients are properly advised and their suitability assessed before they enter an overnight program. Short hospital stay is not appropriate if patients cannot be accommodated close to the hospital after discharge. It is also inadvisable when patients have persisting cardiovascular instability, questionable neurologic status or will be returning to unsupervised solitary accommodation. Short-stay policies must be designed to provide ongoing supervision by the clinical team, including domiciliary nurses during convalescence. Further, short-stay policies from institutions with demonstrated excellent outcomes and well organised postdischarge supervision and care cannot be translated to others with inferior or uncertain standards. In the case of carotid endarterectomy, most of the postoperative hazards needing urgent intervention are unlikely after 48 hours. Therefore, hospital discharge two days after the operation is a reasonable compromise and, in my opinion, safer than discharge a day earlier. Reginald S A Lord Professor of Surgery University of New South Wales, and St Vincent's Hospital, Sydney, NSW Reprints: Professor RSA Lord, Surgical Professorial Unit, Level 17, O'Brien Building, St Vincent's Hospital, Darlinghurst, NSW 2010. Anderson CS, Jamrozik KD, Burvill PB, et al. Ascertaining the true incidence of stroke: experience from the Perth Community Stroke Study, 1989-1990. Med J Aust 1993; 188: 80-84. National Health and Medical Research Council. Clinical practice guidelines: prevention of stroke. Canberra: NHMRC, 1996. Dennis MS, Bamford J, Sandercock P, Warlow C. Incidence of transient ischaemic attacks in the Oxford Shire, England. Stroke 1989; 20: 333-339. Robins M, Baum HM. The national survey of stroke. Incidence. Stroke 1981; 12 (2 Pt 2 Suppl 1): I45-I57. Lord RSA. Carotid endarterectomy: options and outcomes. Aust N Z J Surg 1995; 65: 151-159. Bourke BM, Crimmins DC. Overnight stay for carotid endarterectomy. Med J Aust 1998; 168: 157-160. North American Symptomatic Carotid Endarterectomy Trial (NASCET) collaborators. Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. N Engl J Med 1991; 325: 445-453. Rothwell PM, Slattery J, Warlow CP. A systematic review of the risk of stroke and death due to endarterectomy for symptomatic carotid stenosis. Stroke 1996; 27: 260-265. Lord RSA, Chao A. Urgent carotid reconstruction for the neurologically unstable patient. Proceedings of Seminar on Acute Carotid Interventions, Rome, Italy, 12 December 1997. Hafner DH, Smith RB, King OW, et al. Massive intracerebral hemorrhage following carotid endarterectomy. Arch Surg 1987; 122: 305-310. Lord RSA. Surgery of occlusive cerebrovascular disease. St Louis, Mo: CV Mosby, 1986. Hertzer NR, Bevan EG, O'Hara PJ, Krajewski LP. A prospective study of vein patch angioplasty during carotid endarterectomy. Three-year results for 801 patients and 917 operations. Ann Surg 1987; 206: 628-635. Hankey GJ, Warlow CP, Sellar AG. Cerebral angiographic risk in mild cerebrovascular disease. Stroke 1990; 21: 209-222. 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/>

Tuberculosis in the young: focusing on those at risk Recognition and workable strategies for children at risk are needed MJA 1998; 168: 100-101 Tuberculosis (TB) is curable and preventable, yet causes more deaths worldwide than any other infectious disease -- three million yearly, with 450 000 involving children. Australia has one of the lowest rates of TB in the world, and multidrug-resistant TB has not emerged as a problem here.1,2 None the less, people born overseas, Aboriginal people, those infected with HIV, the elderly (especially men over 65), and the homeless experience much higher than average rates of disease. Children up to the age of 14 years account for only 3%-6% of all Australian notifications. Children are also much less likely to transmit infection than adults. However, they have a high risk of developing active disease -- 23%-43% for those infected in the first year of life, 8%-25% for those infected between one and 10 years of age, and 16% for those infected when aged 11-15 years.3 Thus, it is important to identify infected children for preventive therapy (i.e., usually isoniazid for six months) to prevent progression to disease. Children born overseas, child contacts of infectious (usually adult) patients and Aboriginal children have much higher than average rates of infection and disease and deserve specific TB control strategies. The primary strategy for TB control is to stop transmission by timely diagnosis and curative treatment of infectious patients. The next priority, especially in children, is to identify by Mantoux testing those infected and to initiate preventive therapy where appropriate. Screening of at-risk groups and contact tracing of cases are important for both these strategies. It is also important that the skills and resources for diagnosing and curing TB are available to health care providers serving those at risk, such as general practitioners working in high risk migrant communities, Aboriginal medical services and regional chest clinics or public health units. The overall age-specific rates in Australia in 1995 were highest in overseas-born children aged 0-4 years (approximately 44, compared with 1 per 100 000 in Australian-born children of the same age).4 By contrast, 5-14-year-olds, whether born in Australia or overseas, have the lowest specific rates of any age groups, a finding that is consistent worldwide. In this issue of the Journal, the Consensus Statement5 on strategies for TB control in children in Australia from two paediatric special interest groups recommends Mantoux screening of immigrant children from high prevalence countries. This recommendation is long overdue, but needs a workable strategy. Issuing a Tuberculosis Undertaking (as is done for any adult migrant considered to be at increased risk of TB) to all children under five years of age emigrating from countries of high TB prevalence (> 25 per 100,000) would obligate a parent or guardian to contact the Health Assessment Service of the Department of Immigration and Multicultural Affairs within a specific period for direction to the nearest centre for Mantoux testing. The Health Assessment Service is currently investigating the feasibility of such a proposal. Findings from the Melbourne study by Johnson and colleagues6 on the prevalence of asymptomatic Mycobacterium tuberculosis infection in secondary school students add to earlier studies from Sydney,7,8 the Northern Territory9 (NT) and South Australia10 (SA) in supporting targeted school screening. Clearly, there is no current evidence to support mass school screening, and efforts should be directed towards students from countries of high TB prevalence to identify those at risk of developing active, contagious TB in adulthood and to offer them preventive therapy. TB is detected in around 1% of contacts of active cases. While contact tracing finds up to 10% of notified cases of TB overall, this percentage is much higher in children. In 0-14-year-olds, 65% of all cases11 and 78% of intrathoracic cases12 were identified by contact tracing. TB in a child which is not found by contact tracing usually signals recent transmission within the family, providing an opportunity to diagnose adult TB and stop further transmission. Alternatively, it may indicate inadequacies in current control methods, such as failure to trace contacts or to promote successful preventive therapy in identified infected children. The forthcoming National Health and Medical Research Council (NHMRC) publication Towards elimination of tuberculosis II emphasises the importance of contact tracing and provides detailed guidelines for contact screening.3 Limited national data are available on TB in Aboriginal children, but reports from Queensland, SA and the NT confirm they are at increased risk of infection and disease. In the NT from 1989 to 1997, Aboriginal children represented 25 of the 28 notified TB cases aged 0-14 years. Twelve of these 25 cases were nodal TB, consistent with the high rate of extrapulmonary disease seen in children; in contrast, only two cases of non-tuberculous (atypical mycobacteria) nodal disease were found. Suspected mycobacterial disease of lymph nodes always requires culture and susceptibility testing, and in Aboriginal as in migrant children should be considered as TB until proved otherwise. This is in contrast to the 1989 NHMRC statement "that in children born in Australia, mycobacterial disease of lymph nodes is almost invariably due to atypical mycobacterial disease".13 Strategies for TB control among Aboriginal children include diligent contact tracing, which may extend to community screening due to sociocultural interactions and overcrowded housing,3 and targeted school Mantoux testing, education and preventive therapy in regions of high TB incidence.9 The Consensus Statement lists BCG vaccination as an important control strategy, and recommends extending this beyond Aboriginal and Torres Strait Islander neonates in regions of high incidence, neonates born to parents with leprosy, and children under the age of five years living or travelling in countries of high TB prevalence for more than three months, as recommended by the NHMRC TB Working Party.3 While BCG vaccination protects against disseminated TB in the young, it has not played a large role in reducing transmission and controlling TB worldwide. Children born in Australia with one or both parents born overseas are at no higher risk of infection than those with Australian-born parents.6,7,8,9,10 Present evidence therefore supports continuing BCG vaccination according to the three recommendations above. Comprehensive information about the actual TB cases notified in all Australian-born children would be useful to further evaluate this issue. The recommendation that specialised State and Territory TB control programs be maintained in a climate of economic rationalism for a disease with low national rates and low rates in children5 is appropriate. However, an international focus is also required. To this end, it is encouraging that TB has been recognised as a priority issue by the Advisory Group on International Health of AusAID. With 75% of cases being in the migrant population, and Australia's location between two regions which the World Health Organization estimates account for two-thirds of the world's 8-9 million cases, we can not work alone towards eliminating TB. Australia needs to be a partner in the region as well as a contributor to global TB-control strategies. Vicki L Krause Director, Centre for Disease Control Territory Health Services, Casuarina, NT Dawson DJ, Cheah DF, Chew WK, et al. Tuberculosis in Australia 1989-1992. Bacteriologically confirmed cases and drug resistance. Med J Aust 1995; 162: 287-290. Dawson D. Tuberculosis in Australia: bacteriologically confirmed cases and drug resistance, 1994 and 1995. Commun Dis Intell 1997; 21: 245. Towards elimination of tuberculosis II -- guidelines and protocols for controlling tuberculosis in Australia. Draft prepared by NHMRC Tuberculosis Working Party -- 2nd stage public consultation. Canberra: NHMRC, June 1996. Oliver G, Harvey B. Tuberculosis notifications in Australia, 1995. Commun Dis Intell 1997; 21: 261-269. Isaacs D, Mellis CM. Tuberculosis in children in Australia: strategies for control. Med J Aust 1998; 168: 121-124. Johnson PDR, Carlin JB, Bennett CM, et al. The prevalence of asymptomatic tuberculosis infection in Melbourne secondary school students. Med J Aust 1998; 168: 106-110. Alperstein G, Fett MJ, Reznik R, et al. The prevalence of tuberculosis infections among Year 8 school children in inner Sydney in 1992. Med J Aust 1994; 160: 197-201. Alperstein G, Morgan K, Fett MJ, et al. Prevalence of tuberculosis infection among primary school entry children in Sydney. Aust J Pub Health 1996; 20: 123-128 . Wright J, Krause V. Outcomes of the NT School Mantoux Program 1991-1994 [abstract]. Program and abstracts. The 2nd National Tuberculosis Conference: Australia's regional role in tuberculosis control. 1997 Nov 17-18: 38. Sydney: The Public Health Association of Australia, 1997. Broomell K, Antic R, Stapledon R. A decade of tuberculosis control in SA. Abst. Program and Abstracts. The 2nd National Tuberculosis Conference: Australia's regional role in tuberculosis control. 1997 Nov 17-18: 38. Sydney: The Public Health Association of Australia, 1997. Goldman JM, Teale C, Cundall DB, Pearson SB. Childhood tuberculosis in Leeds, 1982-90: social and ethnic factors and the role of the contact clinic in diagnosis. Thorax 1994; 49: 184-185. Pineda PR, Leung A, Muller NL, et al. Intrathoracic paediatric tuberculosis: a report of 202 cases. Tubercl Lung Dis 1993; 74: 261-266. National Health and Medical Research Council. Tuberculosis in Australia and New Zealand into the 1990s. Canberra: AGPS, 1989. 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/>

Vicki L Krause

General internal medicine in Australia and New Zealand -- a renaissance A new society challenges potentially excessive subspecialisation MJA 1998; 168: 104-105 Last year in Auckland the Internal Medicine Society of Australia and New Zealand (IMSANZ) arose from the merger of the Australian Society of Consultant Physicians in General Medicine and the Internal Medicine Society of New Zealand. The new society, with 400 Australian and 100 New Zealand members, is now the regional voice of consultative general medicine. Its birth coincides with the renaissance of this discipline in Canada, the United States and Europe. Hospitals, health care managers and funders are reconsidering the likely benefits to both quality and efficiency of health care when medical services are provided by a team in which the "breadth" skills of generalists complement the "depth" skills of subspecialists.1 Outcomes of care Who achieves better outcomes -- general or subspecialty physicians? There are two relevant Australian studies, both in tertiary hospitals. One was not completed because of lack of enthusiasm by busy clinicians and doubts about the value of consensus evaluation following case note audit.2 The second, a randomised study, showed no differences between general medical and specialist geriatric care in acutely ill patients older than 70.3 Although comparisons with the US are problematic because "general" in the US includes primary care as well as consultative general medicine, US subspecialists have better outcomes for the care of rheumatoid disease and myocardial infarction,1 while for hypertension and non-insulin-dependent diabetes outcomes for generalists and specialists are similar.4 However, specialists consume more resources.5 Health care costs In the US, swelling numbers of physician subspecialists reportedly increase health care costs, unmatched by proportional outcome benefits.6 Excessive subspecialisation may lead to economic blow-out, especially in the uncapped, fee-for-service private sector. With "managed care" to contain costs, there is a resurgence of training and career opportunities for generalists.7,8 Is there too much subspecialisation in Australia and New Zealand? In Australian capital cities, subspecialisation, especially in procedural subspecialties, may be excessive. Of 2611 Australian consultant physicians in adult medicine in 1995, only 399 described themselves as "general", compared with 371 cardiologists and 286 gastroenterologists.9 In State capitals in the period 1988-1995 physician numbers (excluding paediatricians) increased from 1729 to 2146, while general physician numbers dropped from 412 to 281.9 In 1996, of 552 Australian advanced trainees of the Royal Australasian College of Physicians (excluding those in paediatrics), only 42 (8%) were in general medicine, with 84 in cardiology and 51 in gastroenterology. However, in New Zealand, 25% of the trainees were generalists. Despite the subspecialisation in Australia's biggest cities, there are shortages of consultant physicians in country areas. Up to 50 additional consultant physicians are needed in provincial and rural Queensland alone.10 Most would need to be generalists. Why do tertiary hospitals need general medical units? Tertiary practice, now dominated by technology and procedures, is becoming organisationally and financially based on discrete episodes of care involving single diagnoses. In this climate, the general medical unit may be seen by some as unnecessary; three teaching hospitals in Sydney as well as the Canberra Hospital, ACT, now have no such units. Compartmentalisation of care by medical specialty means that significant comorbidities and patient concerns unrelated to the particular specialty are easily overlooked, misdiagnosed or inappropriately managed. Gains in efficiency through greater throughput of patients with similar problems may be offset by more consultations and unnecessary investigation. Further, the continuity of care is disrupted. Generalists, with skills in managing undifferentiated problems and conditions that cross subspecialty barriers and an awareness of both the psychosocial and the biological aspects of illness, offer "whole person" patient care and can act as advocates for the patient.11 While many subspecialists practise in a similar way, general units are needed to provide training positions and role models for both basic and advanced training in general medicine. The generalists' integrated view of patients is an absolute requirement for undergraduate and early postgraduate education in a setting where illness is not arbitrarily framed by such overlapping criteria as age (e.g., geriatrics), organ system (e.g., cardiology), pathological process (e.g., oncology), aetiology (e.g., infectious disease) and treatment goal (e.g., palliative care). New agenda for general internal medicine General internal medicine has the breadth and the capacity to embrace new challenges. Generalists can continue to learn from experienced subspecialists and can acquire both the knowledge and procedural skills that might be necessary in particular city or rural, hospital or office settings. They can also lead the way, as in North America,12 in clinical epidemiology and decision-making, ethics, clinical informatics, health technology assessment, clinical audit, and health service research. General physicians can act with other colleagues (e.g., in general practice, surgery, emergency medicine, psychiatry, geriatrics) to help integrate medical care and provide an overview of medical management that may be lost with exclusive specialty care.13 Barriers to the realisation of this new agenda include negative perceptions of generalists by some influential subspecialists in hospitals, by professional societies and by patient support groups; difficulties faced by general trainees in competing for coveted subspecialty training positions;14 and competition among institutional units for limited resources under casemix funding. Lack of confidence and leadership among generalists themselves may set up internal barriers. While the need for subspecialisation in consultative physician practice is recognised and supported, it seems the pendulum has swung too far. Our health care systems stand to benefit from a more vigorous contribution by well-trained and committed general physicians. For a winning team, we need outstanding players -- some with specialised talents and others who are versatile.1 Ian A Scott Director General Medicine Princess Alexandra Hospital, Brisbane, QLD Peter B Greenberg Director General Medical Services North Western Health Care Network, Melbourne, VIC Nash DB, Nash IS. Building the best team. Ann Intern Med 1997; 127: 72-73. Douglas RM, Blood A. Evaluation and peer review of the role of specialist and general medical units in a teaching hospital. Aust N Z J Med 1978; 8: 337-343. Harris RD, Henschke PJ, Popplewell PY, et al. A randomised study of outcomes in a defined group of ill elderly patients managed in a geriatric assessment unit or a general medical unit. Aust N Z J Med 1991; 21: 230-234. Greenfield S, Rogers W, Mangotich M, et al. Outcomes of patients with hypertension and non-insulin-dependent diabetes mellitus treated by different systems and specialties. Results from the medical outcomes study. JAMA 1995; 274: 1436-1444. Welch WP, Miller ME, Welch HG, et al. Geographic variation in expenditures for physician services in the United States. N Engl J Med 1993; 328: 621-627. Schroeder SA, Sandy LG. Specialty distribution of US physicians -- the invisible driver of health care costs. N Engl J Med 1993; 328: 961-963. Wartman SA. Managed care and its effect on residency training in internal medicine. Arch Intern Med 1994; 154: 2539-2544. Weiner JP. Forecasting the effects of health reform on US physician workforce requirement. Evidence from HMO staffing patterns. JAMA 1994; 272: 220-230. Dent O. The Royal Australasian College of Physicians Clinical Workforce in Internal Medicine and Paediatrics in Australia 1988 and 1995. Fellowship Affairs 1989; 8: 9-20, and 1997; 16: 17-30. Hadfield C. Rural manpower in Queensland -- a start to tackling the problem? IMSANZ Newsletter June 1997: 6-7. Guidelines for members and advanced trainees in general medicine, 1997. Sydney: Internal Medicine Society of Australia and New Zealand, 1997. Greenbeck MR. Educating physicians for the 21st century. Acad Med 1995; 70: 179-185. Ward JD. The hospital general physician in the 1990s. J R Coll Physicians Lond 1996; 30: 209-210. Smith BJ, Darzins P, Heller RF. RACP Survey of advanced trainees' job aspirations: the fate of those who pass the clinical exam of the RACP. Fellowship Affairs 1993; 12: 31-33. 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/>

Ian A Scott · Peter B Greenberg