Editorials

Editorial Inaccurate classification of infant deaths in Australia: a persistent and pervasive problem A standardised definition of SIDS and standardised investigative protocols for unexpected infant deaths are needed MJA 2001; 175: 5-7 Australia has an excellent record internationally in the area of sudden infant death syndrome (SIDS). Australian researchers were among the first to provide data linking prone sleeping position to an increased risk of SIDS; Australia was one of the first countries to establish State and national "Reduce the risks" campaigns; and considerable local research has contributed to a greater understanding of this enigmatic disorder. Proof of the efficacy of local preventive activities has been the dramatic and continued decrease in deaths from SIDS, from over 500 in 1988 to 134 in 1999 (Ms Jan Carey, Executive Director, SIDSaustralia [ACT branch] media release, June 2001). There have also been numerous initiatives in Australia and worldwide to improve our ability to distinguish between SIDS and other causes of unexpected infant death. These initiatives include attempts to standardise the definition of SIDS and to introduce uniform guidelines for evaluation of death scenes and autopsy examinations. Unfortunately, significant problems persist. SIDS remains a diagnosis of exclusion, with no pathognomonic features at autopsy. Causes of death such as poisoning, or accidental or deliberate asphyxia, may appear to the pathologist identical to SIDS, and cardiovascular diseases, occult infections and metabolic disorders may be identified only by special dissections or investigations. The confusion that arises with individual pathologists' choosing different definitions is reflected in the recent international literature, where deaths have been accepted as SIDS in the apparent absence of recognised formal definitions. In addition, there is no consistency in the definition of SIDS being used by clinicians, researchers or pathologists in Australia. A number of different definitions of SIDS have been promulgated over the past decade, each emphasising a different aspect: for example, an association with sleep; a requirement for extensive ancillary postmortem investigations (eg, microbiological and toxicological testing); subclassifications based on the presence or absence of minor pathological findings; and specified upper and lower age limits.1-5 There is also an urgent need for a standardising of the investigation of unexpected infant deaths, including guidelines for reviewing the clinical and family history, for carefully examining the death scene and for conducting the autopsy according to established criteria. Established autopsy criteria have included full-body radiological examination and microbiological and toxicological testing. Despite the availability of standard investigative protocols for infant deaths (Box), no protocol is consistently applied in Australia. The usefulness of protocols has been clearly established: more deaths due to unsafe sleeping environments have been identified recently, and each step of the postmortem investigation has been shown to contribute potentially significant information.9,10 Failure to implement a standard approach to unexpected infant deaths may cause distress for families who subsequently discover that significant steps were missed in the autopsy evaluation of their infant. It may also have far-reaching consequences. In the United Kingdom, 42 deaths originally attributed to SIDS were found to be due to homicides.11 The initial failure to diagnose these as homicides would have interfered with police investigations and may have endangered other children in these families and allowed the perpetrators to escape punishment. Australian courts have also reached the same conclusions in similar retrospectively reviewed cases. Recent infant deaths in rural Australia have been accepted as SIDS without proper death scene examinations or autopsies.12 An investigation of autopsy practices in Queensland by a Working Group of the Queensland Council on Obstetric and Paediatric Morbidity and Mortality confirmed that major problems exist, particularly in rural areas.13 The group found that 65% of the reviewed autopsies in infants who died suddenly and unexpectedly failed to attain the minimum acceptable quality score set by the study. They concluded that these autopsies were of "poor quality" and that "a specialist pathologist with appropriate expertise" was required. Similar conclusions were reached in an inquest into a series of infant deaths in South Australia.14 Thus, we have an unacceptable situation: diagnostic guidelines are readily available but are not being used. This is partly because of isolation in rural Australia and underfunding of services. In isolated regions of Australasia infant autopsies have also been performed by non-pathologists. Infant autopsy examination is highly specialised, requiring specific dissection techniques and considerable knowledge of both paediatric and forensic pathology. Expecting non-specialists to perform infant autopsies is neither appropriate nor fair and makes the validity of some of the autopsy conclusions uncertain. It is time to undertake a national initiative to correct these deficiencies. Details of these problems were presented at a national meeting of forensic pathologists in Perth in June this year, with a proposal to convene a National Workshop of Pathologists, in association with SIDSaustralia, to choose an appropriate definition for SIDS and investigative guidelines. It is hoped that these conclusions could be evaluated and endorsed by the Forensic Committee of the Royal College of Pathologists of Australasia and appropriate national "gold standards" agreed upon. Then pathologists' concerns and consensus recommendations for change could be passed on to the respective coronial authorities to ensure proper medicolegal investigation of unexpected infant deaths. Implementing these guidelines would not be easy, requiring financial support by governments, coordinated training programs and local cooperation, and possibly legislative changes in some States. A recently established national coronial database will enable the monitoring of trends in unexpected death in Australia.15 However, idiosyncratic or inexact diagnostic practices among pathologists and failure to follow protocols will result in inaccurate statistics on infant deaths in Australia. This could lead to underdiagnosis of important diseases and conditions, and unreliability of research based on these data. Opportunities to save more lives will be lost, parents will be ill-informed, and coroners will not have a clear picture of problems within their jurisdictions. Over a decade ago, the late John Emery raised the spectre of SIDS becoming a "diagnostic dustbin"16 — unfortunately, he may well have been correct. Roger W Byard Specialist Forensic Pathologist, Forensic Science Centre, Adelaide, SA; Clinical Professor, Departments of Paediatrics and Pathology University of Adelaide, Adelaide, SA byard01ATforensic.sa.gov.au Willinger M, James LS, Catz C. Defining the sudden infant death syndrome (SIDS): deliberations of an expert panel convened by the National Institute of Child Health and Human Development [review]. Pediatr Pathol 1991; 11: 677-684. Cordner SM, Willinger M. The definition of the sudden infant death syndrome. In: Rognum TO, editor. Sudden infant death syndrome. New trends in the nineties. Oslo: Scandinavian University Press, 1995: 18-20. Beckwith JB. A proposed new definition of sudden infant death syndrome. In: Walker AM, McMillen C, editors. Second SIDS International Conference. Ithaca: Perinatology Press, 1993: 418-421. Sturner WO. SIDS redux: is it or isn't it [review]? Am J Forensic Med Pathol 1998; 190: 107-108. Rambaud C, Guilleminault C, Campbell PE. Definition of the sudden infant death syndrome. BMJ 1994; 308: 1439. Cordner SM. Appendix 2: Australasian SIDS autopsy protocol. In: Byard RW, Cohle SD. Sudden death in infancy, childhood and adolescence. Cambridge: Cambridge University Press, 1994: 501-514. Krous H. An international standardised autopsy protocol for sudden unexpected infant death. In: Rognum TO, editor. Sudden infant death syndrome. New trends in the nineties. Oslo: Scandinavian University Press, 1995: 81-95. Centers for Disease Control and Prevention. Guidelines for death scene investigation of sudden unexplained infant deaths. Recommendations of the Interagency Panel on Sudden Infant Death Syndrome. MMWR Morb Mortal Wkly Rep 1996; 45(RR-10): 1-6. Mitchell E, Krous HF, Donald T, Byard RW. An analysis of the usefulness of specific stages in the pathological investigation of sudden infant death. Am J Forensic Med Pathol 2000; 21: 395-400. Mitchell E, Krous HF, Donald T, Byard RW. Changing trends in the diagnosis of sudden infant death. Am J Forensic Med Pathol 2000; 21: 311-314. Meadow R. Unnatural sudden infant death. Arch Dis Child 1999; 80: 7-14. Panaretto K. SIDS and the indigenous community. Plenary presentation at: SIDSaustralia Child and Infant Mortality Matters Conference; March 2001; Canberra. Woodgate P, Colditz P, Brookes K, et al. A review of sudden unexpected deaths in infants autopsies in Queensland 1997-1998. Report from the Sudden Unexpected Deaths in Infancy Working Group of the Queensland Council on Obstetric and Paediatric Morbidity and Mortality. Brisbane: Mater Epidemiology Unit, November 2000. Inquest into the deaths of Deane, Barnard and Nottle. Chivell W, State Coroner, South Australia, 25 August 1995. Monash University National Centre for Coronial Information. National Coroners Information System. <http://www.vifp.monash.edu.au/ncis> Emery JL. Is sudden infant death a diagnosis [editorial]? BMJ 1989; 299: 1240. Make a comment Standard investigative protocols for sudden infant deaths in Australia and overseas National Australasian SIDS autopsy protocol This was formulated in 1992 in a collaboration set up by the Victorian Institute of Forensic Medicine involving the Forensic Committee of the Royal College of Pathologists of Australasia, the ANZ Paediatric Pathology Group and the National SIDS Council of Australia.6 International standardised autopsy protocol This resulted from collaboration between SIDS International and the National Institute of Child Health and Human Development in the United States.7 It (and its instruction manual) has been endorsed by both the Society for Pediatric Pathology and the National Association of Medical Examiners in the United States. Sudden unexplained infant death investigation report form This was formulated by the US Centers for Disease Control and Prevention for the standardisation of death scene examinations.8 Back to text

Roger W Byard

Editorial Appendicectomy — becoming a rare event? Still true: if in doubt, take it out. MJA 2001; 175: 7-8 Appendicitis is now not generally thought to be an interesting subject for research, but it remains an important disease. Appendicitis is the commonest reason for an operation in young adults and is still a cause of mortality, especially at the extremes of life. Fundamental issues such as the possible function of the appendix and the exact causes of appendicitis remain unresolved. Accepted notions that the appendix is vestigial, that appendicitis is usually obstructive and that post-appendicitis adhesions are a significant cause of infertility in females have been challenged.1-3Recent studies reveal an intriguing protective effect of appendicectomy against ulcerative colitis.4 The epidemiology of appendicitis may hold clues to its still-obscure aetiology; this highlights the importance of careful epidemiological studies such as the one by Donnelly et al reported in this issue of the Journal.5 A crucial paper by Fitz (Harvard Medical School) in 1886, in which the term "appendicitis" was first used,6 swept away earlier, unfounded notions of the disease implied by the use of terms such as "perityphlitis". Fitz outlined the clinical diagnosis and suggested early removal of the appendix — but acceptance of this new concept was far from universal or immediate. The first recorded appendicectomy in Australia, done on a kitchen table in Toowoomba, did not occur until 1893.7 Early appendicectomy did not gain wide acceptance in the UK until 1902, when Sir Frederick Treves operated on King Edward VII 12 days before his coronation. The epidemiology of appendicitis poses many unanswered questions. Almost unknown before the 18th century, there was a striking increase in its prevalence from the end of the 19th century, with features suggesting it is a side effect of modern Western life. Rendle Short8 and Burkitt1 summarised the rapid emergence of appendicitis in developed countries in the 20th century, and Burkitt noted its rarity in rural areas and in undeveloped countries. By the mid-1920s, appendicitis was sufficiently common, and the hazards of treating abdominal pain by purgation sufficiently recognised, that life insurance companies took advertisements in magazines warning against the use of laxatives for abdominal pain.9 Dietary theories, notably an inadequate fibre intake, have been advanced to account for the geography of the disease,1,8 but it is clear that diet can not fully explain the epidemiology. An alternative hypothesis, advanced by Barker in 1985,10 proposed that improved hygiene in developed countries reduced the exposure of infants to enteric organisms, modifying the immune response to virus infections, which might then cause appendicitis. Neither the dietary nor hygiene hypothesis adequately explains the significant decline in the frequency of appendicitis in the latter half of the 20th century.11,12 The authors of the Western Australian study have taken advantage of excellent hospital morbidity data collected by the health department in that State.5 They document a striking decline in the age-standardised appendicectomy rate in both sexes from 1981 to 1997. There was a greater decline in women, especially in metropolitan hospitals, where the rate more than halved. Another finding was a decline in the practice of incidental appendicectomy, although this procedure continued at a relatively high rate in non-metropolitan hospitals. How can these data be interpreted? Unfortunately, owing to changes in diagnostic coding practices and a lack of correlation with histology, no firm conclusions can be reached about changes in the frequency of appendicitis in WA. It is likely that the fall in appendicectomy rates is because of more accurate diagnosis, possibly associated with the use of ultrasound examination, computed tomography and laparoscopy, and to a change in surgical attitudes to avoid "unnecessary" operations. Donnelly et al raise the question of whether rural doctors have taken full advantage of these changes, but provide valid reasons why rural approaches to appendicitis appropriately may differ from city practice. An important unresolved question is whether the pendulum of declining appendicectomy rates has swung too far. Incidental appendicectomy was clearly overdone in the past, but it is justifiable in younger patients and should not be abandoned. In patients with acute abdominal pain, reluctance to operate for fear of an "unnecessary" procedure may result in delayed diagnosis of appendicitis, with a consequent increase in morbidity and mortality. Delayed diagnosis of appendicitis is the most common cause of litigation against emergency room physicians.13 One such delayed diagnosis nearly cost the late Sir Donald Bradman his life in 1934, at the peak of his cricketing career; he was so close to death that the cricketing writer Neville Cardus was instructed to prepare his obituary. Although ultrasound examination and computed tomography are valuable aids to diagnosis in equivocal cases, they are not infallible.14 Laparoscopy, although invasive, is more precise and also allows identification and treatment of non-appendiceal causes of pain, especially in females. Further collection of data on appendicitis is important. A rising proportion of perforated or gangrenous cases may indicate an inappropriately conservative approach to appendicectomy or an inadequate use of newer diagnostic methods. In the end, though, the diagnosis of appendicitis remains clinical; in the absence of sophisticated diagnostic tools, the old adage "if in doubt, take it out" is safe. Perhaps, in the laparoscopic era, this might be updated to "if they're crook, take a look". Even though appendicectomy rates may be declining, appendicitis is still a common and sometimes diagnostically challenging problem. Thomas B Hugh Visiting Surgeon, St Vincent's Hospital and St Vincent's Clinic, Sydney NSW thughATdingoblue.net.au Thomas J Hugh Senior Lecturer in Surgery, Royal North Shore Hospital, Sydney, NSW thughATmed.usyd.edu.au Burkitt DP. Appendicitis. London: Norgine Ltd, 1980. Carr NJ. The pathology of acute appendicitis. Ann Diagn Pathol 2000; 4: 46-58. Urbach DG, Cohen MM. Is perforation of the appendix a risk factor for tubal infertility and ectopic pregnancy? An appraisal of the evidence. Can J Surg 1999; 42: 101-108. Andersson RE, Olaison G, Tysk C, et al. Appendectomy and protection against ulcerative colitis. N Engl J Med 2001; 344: 808-814. Donnelly NJ, Semmens JB, Fletcher D, Holman CD'AJ. Appendicectomy in Western Australia. Profile and trends, 1981-1997. Med J Aust 2001; 175: 15-18. Fitz RH. Perforating inflammation of the vermiform appendix with special reference to its early diagnosis and treatment. Trans Assoc Am Physicians 1886; 1: 107. Lee AE. The history of appendicitis in Australia: a window on abdominal surgery. Med J Aust 1944; 26: 653-660. Short AR. The causation of appendicitis. London: John Wright & Sons, 1946. Love RJM. The appendix. London: HK Lewis, 1947. Barker DJP. Acute appendicitis and dietary fibre: an alternative hypothesis. BMJ 1985; 290: 1125-1127. Prunstesta P, Goldace MJ. Appendicectomy for acute appendicitis and for other conditions: an epidemiological study. Int J Epidemiol 1994; 23: 155-160. Walker ARP, Segal I. What causes appendicitis? J Clin Gastroenterol 1990; 12: 127-129. Trautlein JJ, Lambert RL, Miller J. Malpractice in the emergency department — a review of 200 cases. Ann Emerg Med 1984; 13: 709-711. McColl I. More precision in diagnosing appendicitis. N Engl J Med 1998; 338: 190-191. Make a comment

Editorial Safety and quality in Australian healthcare: making progress The newly formed Australian Council for Safety and Quality in Health Care has ambitious plans MJA 2001; 174: 616-617 Australian healthcare is comprehensive and accessible, supported by modern technology and a well trained and motivated workforce. Neverthless, problems occur, typically as a result of a series of systems failures which lead almost inevitably to mishaps by doctors or nurses.1,2In the 21st century, we can, and should, be doing better to identify and manage risks and systemic failures in the healthcare system. There is much that we can learn from industries such as aviation, mining and road safety, and from human-factors engineers and cognitive psychologists, about how to shift to a system that, although inevitably high risk, has high reliability (ie, lessons are learnt from problems, and changes made so that the problems do not recur).3 These industries have seriously tackled these issues and made measurable improvements in safety. Healthcare needs to recognise that safety concerns are real, that the system is prone to error and failure, and that we need to work to reduce the risk in areas that are inherently risky. . . . we need to move beyond a "bad apples" approach, with media sensationalism . . . We need to redesign and simplify many aspects of healthcare. Management of the system needs to change dramatically to allow clinicians and nurses at the frontline to influence management decisions effectively. Otherwise we will fail to engage their active support in improving safety and quality. Management has a necessary focus on improving efficiency, but this alone will not improve safety and quality. Management must also fund, support and encourage redesign of systems, monitor activity reports, feed their results back into the systems, and encourage and reward safety improvements. As well as very significant potential benefits to patients, there are likely to be significant savings through more efficient use of resources. For example, medication error has been estimated to result in at least 80 000 hospital admissions and costs of at least $350 million per year.4 Ultimately, we need to change the culture in healthcare. As part of this change, all who work in or have responsibility for the healthcare system need to be willing to work with their peers to examine more openly and objectively their performances and patient outcomes. In the broader community, we need to move beyond a "bad apples" approach, with media sensationalism, towards a more mature level of understanding and acceptance of the inevitable risks in healthcare. There is much to be done to achieve the desired changes. To promote and facilitate these changes, the Australian Council for Safety and Quality in Health Care was formed in January 2000 by the Federal, State and Territory health ministers. Its role is to lead national efforts to promote systemic improvements in the safety and quality of healthcare in Australia, with a particular focus on minimising the likelihood and effects of error. The Council's first report, Safety first, was presented to health ministers in July 2000. In it, the Council identified the broad areas that it would lead to make "a difference where it counts".5 The health ministers endorsed the Council's terms of reference, agreed in principle to provide $50 million for a five-year national program led by the Council, and required it to report annually on progress and planned action. The Safety first report also highlighted the significant personal and financial costs of adverse events4,6 and noted that existing efforts to improve healthcare safety were valuable but insufficient. After wide consultation, the Council has produced its first national action plan for 2001.7 The major emphasis is on developing and strengthening national standards, with educational support to help healthcare professionals and managers put the standards in place effectively. As no single group can deliver change on its own, a collaborative approach is being taken. Council will work closely with governments, health departments, healthcare funders and management, providers, consumers and educators to ensure that standards developed are put in place and monitored. A key initiative of the Council is to learn lessons through better use of data. Activities to achieve this will include the establishment of national standards for incident monitoring and investigation in healthcare facilities, as well as the design of improved methods to survey and report improvements in healthcare quality. The type of activities that the Council would like to see implemented across the country are exemplified in the report from Wolff and colleagues in this issue of the Journal.8 They present the results of the long-term risk management activities of the Wimmera Health Care group in Horsham, Victoria. Wolff and his colleagues have developed an integrated clinical risk management program, detected adverse events in a variety of ways, analysed both the events and the risks, and taken action to improve care and monitor progress, using a systems approach. Through this systemic approach, they reduced the rate of adverse events from 1.35% of all patients discharged in the first year of the program to 0.74% in the eighth year. In the emergency department, the rate was reduced from 2.71% of all patients attending in the first quarter of monitoring to 0.48% in the eighth quarter. These event rates are very low, but comparison is difficult, as the rate of adverse events found in any study depends not only on standards of care and systems design, but also on study methods and the reporting rate. This allows for wide variability in results. For example, other reported rates of adverse events range from 3.7% in the Harvard study,9 to 16.6% in the Quality in Australian Health Care study,10 30% in a recent study in Victorian hospitals,11 and 45.8% in Florida.12 The study by Wolff and colleagues was prospective and used consistent methods to detect adverse events, thus allowing meaningful comparisons over time. The important finding was a reduction in rates of adverse events, particularly more serious adverse events. The actions taken to reduce their frequency were simple: changes to local protocols, audits, worksheets and supervision practices, as well as the incorporation of feedback, discussion, checklists and assessment tools. All are low-cost activities. Such information about how to improve safety may well be used to inform the development of national standards by the Council. Other priorities of the Council during 2001 are: to address known high-risk areas which contribute significantly to adverse events. These include reducing hospital-acquired infections, promoting safer use of medications and blood products, preventing patient falls and improving patient assessment; to develop national standards for credentialling and performance assessment; to develop specialist and vocational registers; to develop curricula for educational modules in systems safety, human factors and communication; to develop standards for national audits and benchmarking, full disclosure of adverse events and saying "sorry"; and to develop standards for organisational certification, accreditation and licensing, addressing such issues as best practice, structured risk management, teamwork and team training, resource use, skill mix and safety standards. When these priorities have been achieved, the Council will have gone some way towards developing a culture of safety, providing resources for data collection, analysis and feedback, and developing national standards in key areas. It will have a system that is informed by the needs of consumers. There should also be improved morale in healthcare, less unnecessary variation in this care, better performance assessment, more satisfactory outcomes and a reduction in adverse events. The Council will need the willing help of all involved in the system to achieve the benefits available to the community from this ambitious plan. Bruce H Barraclough Chairman, Australian Council for Safety and Quality in Health Care Professor of Cancer Services, University of Sydney, Sydney, NSW Reprints: Professor B H Barraclough, Department of Surgery, Royal North Shore Hospital, Reserve Road, St Leonards, NSW 2065. Berwick DM. Not again! Preventing errors lies in redesign — not exhortation. BMJ 2001; 322: 247-248. Berwick DM, Leape LL. Reducing errors in medicine. BMJ 1999; 219: 136-137. Barach P, Small SD. Reporting and preventing medical mishaps: lessons from non-medical near miss reporting systems. BMJ 2000; 320: 759-763. Roughead EE. The nature and extent of drug-related hospitalisations in Australia, 1999. J Qual Clin Pract 1999; 19: 19-22. Australian Council for Safety and Quality in Health Care. Safety first. Report to the Australian Health Ministers Conference. Canberra: Commonwealth Department of Health and Aged Care, July 2000. Kohn LT, Corrigan JM, Donaldson MS. To err is human: building a safer health system. Committee on Quality of Health Care in America. Institute of Medicine. Washington, DC: National Academy Press, 1999. Australian Council for Safety and Quality in Health Care. National action plan. Canberra: Commonwealth Department of Health and Aged Care, 2001. Wolff AM, Bourke J, Campbell I, Leembruggen D. A clinical risk management program: detecting and reducing hospital adverse events. Med J Aust 2001; 174: 621-625. Brennan TA, Leape LL, Laird NM. Incidence of adverse events and negligence in hospitalized patients: results of the Harvard Medical Practice Study I. N Engl J Med 1991; 324: 370-376. Wilson RM, Runciman WB, Gibberd RW, et al. The Quality in Australian Health Care Study. Med J Aust 1995; 163: 458-471. O'Hara DA, Carson NJ. Reporting of adverse events in hospitals in Victoria, 1994-1995. Med J Aust 1997; 166: 460-463. Krizek TJ. Surgical error. Ethical issues of adverse events. Arch Surg 2000; 135: 1359-1366. Make a comment

Bruce H Barraclough

CLASS="LinkBox"> Editorial Obesity: definitely a growing concern Time to implement Australia's strategy for preventing overweight and obesity MJA 2001; 174: 553-554 Obesity is increasingly recognised as a health problem by the Australian community, with frequent discussions of obesity-related issues in the media and heavy marketing of weight-loss products. There is abundant evidence to support this view, not least being the 1995 National Nutrition Survey showing that 56% of adult Australians are either overweight or obese.1A casual ...

Louise A Baur

CLASS="LinkBox"> Editorial Priorities in polycystic ovary syndrome A common, multifaceted syndrome for which intervention may help prevent serious long term sequelae MJA 2001; 174: 554-555 The diagnosis of polycystic ovary syndrome (PCOS) has become much more common in recent years. It is now not unusual for women in the United States to come for consultation having self-diagnosed PCOS. This awareness is largely the result of the efforts of two well-organised advocacy groups in the US ...

Rogerio A Lobo

Editorial Indigenous Australian children: educating for health Education and health outcomes for Indigenous Australians are inextricably linked MJA 2001; 174: 488-489 The conference "Learning lessons — approaching Indigenous health through education", held in Darwin in November 2000 under the auspices of the Australian Medical Association, called for pragmatic approaches to reversing deteriorating educational and health outcomes in Aboriginal children. The conference, and the Australian Medical Association,1 unanimously endorsed the 150 recommendations of the landmark review of Indigenous education in the Northern Territory (the Collins Report),2 but particularly emphasised that links between healthcare services and education be built early and maintained throughout a child's development. All levels of government and key Indigenous Australian health and education agencies must ensure that such links are established at the highest level and in the remote communities. Collins also identified practical strategies that need urgent implementation (Box 1). The conference also reignited the call for full implementation of the 1992 Council of Australian Governments Agreement.3 It decried the partial implementation of the Agreement, which endorsed national principles of equity and access to adequate and culturally appropriate service provision. Although there have been significant advances in our medical treatment of Indigenous Australian children, these have had minimal impact on the many conditions that undermine these children's access to learning and literacy. For example, for at least the past 25 years, four to five hundred Indigenous children from remote communities have been admitted annually to the infectious diseases ward at the Royal Darwin Hospital. Associated comorbidities4 included dehydration (50%), malnutrition (60%), hypokalaemia (70%), iron deficiency (90%), anaemia (25%), pneumonia (24%-32%), chronic suppurative otitis media (37%), urinary tract infection (10%), and scabies (25%), often secondarily infected. All too often, chest disease is associated with chronic suppurative lung disease or bronchiectasis.5 Treatable hearing deficiencies in the context of poor general health are the major health-related contributors to poor literacy among Indigenous children.6 Chronic suppurative otitis media (CSOM) affects children's learning ability through temporary and recurring hearing loss, permanent hearing impairment, and language disorders. The World Health Organization indicates that populations with rates of CSOM of greater than 4% have a health emergency. Rates of CSOM are as high as 50% in some Indigenous communities. The Northern Territory Strategic Results Project showed that 79% of children tested had a hearing disability.2 Equally distressing is the fact that educational outcomes for Indigenous Australian children are actually deteriorating.2 For example, in 1998, in the Northern Territory, 14% of Indigenous students progressed from Year 8 to Year 12, compared with 80% of non-Indigenous students. In 1998, 20% of Indigenous students achieved the national reading benchmark in the Northern Territory, compared with 78% of non-Indigenous students. Low educational attainment is also common to other urban and rural Indigenous communities. Failure to achieve literacy affects further ability to learn and to gain employment, and thus later health (see Box 2). International literature indicates that an additional year of education should reduce infant mortality by 7%-10%.7 Caldwell and Caldwell8 identify the importance of level of education on health in Third World countries, pointing to the relationship between increasing mother's education and decreasing child mortality. It appears that better-educated mothers are more likely to prevent accidents or sickness, prevent minor health problems from becoming major, and interact better with health services in obtaining the best outcomes. However, the particular problems of Indigenous Australians living in impoverished conditions within the First World are poorly understood.9 Trudgen outlines the sense of futility felt by Indigenous people who, after obtaining high school education and skills, find that these skills are inappropriate for the needs of their communities.10 Children with hearing problems are subjected to a dominant school culture that does not meet their cultural and language needs, and promotes a sense of failure and lowers self-esteem. This is the result of loss of control by Indigenous people, poor environmental circumstances, poor education, and a communication crisis between the dominant and Indigenous cultures.10 In order that Indigenous Australians regain control of their lives, their own solutions must be sought, heard, and acted upon as directly articulated, and not misinterpreted by policy and a particular economic agenda. We must bridge wide gaps in mutual understanding and develop partnerships between Indigenous Australians, governments, and health and education professionals.10 The major challenge is for the medical profession to acknowledge that health and education are key strategies in improving health outcomes for Indigenous Australians. Although there have been significant advances in our treatment of acutely sick Indigenous Australian children, we have failed to improve health and education outcomes. We have a responsibility, as do all Australians, to ensure that this iniquitous situation is not exacerbated further by the use of solutions that do not work for Indigenous communities. Only when we sit down and really listen — and hear — will we be able to work together to improve Aboriginal health and education. Paul A Bauert Paediatrician, Royal Darwin Hospital, Darwin, NT Ngiare J Brown Executive Officer Australian Indigenous Doctors Association, Sydney, NSW Bob Collins Consultant to the Northern Territory Government on Indigenous Education Darwin, NT Carmel M Martin Director of Health Services Australian Medical Association, Canberra, ACT Australian Medical Association. Position Statement on the links between health and education for Indigenous Australians. Canberra: AMA, 2001. Collins B. Learning lessons. An independent review of Indigenous education in the Northern Territory. Darwin: Northern Territory Department of Education, 1999. National commitment to improved outcomes in the delivery of programs and services for Aboriginal peoples and Torres Strait Islanders. Perth: Council of Australian Governments, 7 December 1992. Ruben AR, Walker A. Malnutrition among rural Aboriginal children in the Top End of the Northern Territory. Med J Aust 1995; 162: 400-403. Maxwell GM. Chronic chest disease in Australian aboriginal children. Arch Dis Child 1972; 47: 897-901. Leach AJ. Otitis media in Australian Aboriginal children: an overview. Int J Pediatr Otorhinolaryngol 1999; 49 Suppl 1: S173-S178. Acheson D. Independent inquiry into inequalities in health report, 1998. <http://www.official-documents.co.uk/document/doh/ih/part2b.htm> (September 1999). Caldwell JC, Caldwell P. The impact of education on health. Proceedings of the conference "Learning lessons -- approaching Indigenous health through education"; Darwin, November 2000. Darwin: Australian Medical Association, NT Branch, 2000. Gray A, Boughton B. Education and health behaviour of Indigenous Australians: evidence from the 1994 National Aboriginal and Torres Strait Islander Survey (NATSIS). Occasional Paper Series Issue No. 3. Casuarina, NT: Cooperative Research Centre for Aboriginal and Tropical Health, 2001. Trudgen RI. Why warriors lie down and die. Adelaide: Openbook Publishers, 2000. Make a comment 1: Key strategies for improving health through education Providing more maternal, baby and early-childhood care; Teacher education to identify and manage hearing and other health issues in classrooms; Accelerating the training of more Aboriginal health workers and providing them with greater support when trained; Improving access to specialist services and health education programs for Indigenous people; Encouraging community efforts to improve nutritional standards through education and community purchasing and cultivation initiatives; and Improving school-based health education. Back to text 2: Roles of education in influencing inequalities in health7 Educational qualifications are a determinant of an individual's labour market position, which in turn influences income, housing, and other material resources, and ultimately health. Education is a traditional route out of poverty for disadvantaged children. Education prepares children for life by ensuring they have the practical, social, and emotional knowledge and skills to achieve a full and healthy life — not just health-related behaviour, but skills in human relationships, dealing with conflict, and practical skills such as budgeting and cooking. Education prepares children to participate fully in society, aware of their democratic and human rights and responsibilities, able to use services, and work with an understanding of other groups in society. The role of the school as part of the local community is crucial. The education system should protect and promote the current health of children by providing an environment and culture which is safe, healthy, and conducive to learning. Back to text

Ngiare J Brown

Editorial How bright is their future? Post-streptococcal glomerulonephritis in Indigenous communities in Australia Streptococcal skin infection may have a major role in the epidemic of chronic renal disease among Indigenous Australians. MJA 2001; 174: 489-490 In 1836, Richard Bright, from Guy's Hospital, London, described the clinical entity of acute glomerulonephritis, later known as Bright's disease. However, it was not until 1907 that streptococci were suggested as a cause of acute glomerulonephritis. At that time, post-streptococcal glomerulonephritis (PSGN) was rife throughout the world, as it remains today in some developing countries. With increasing living standards, Australia has a very low overall incidence of streptococcal infection, but, in contrast, our Indigenous communities have one of the highest incidences in the world, and corresponding high incidences of PSGN and rheumatic heart disease.1-4In this issue of the Journal, White and colleagues highlight anew the problem of the health of our Indigenous communities and provide some ominous insight into the long-term sequelae of PSGN.5 It has been contentious whether PSGN is a relatively benign disease, as traditionally thought, or whether, as suggested 25 years ago, it may lead to progressive renal disease and eventually end-stage renal failure.6 The reported study of albuminuria and haematuria — the harbingers of progressive renal disease — in a remote Aboriginal community suggests that the latter is correct. The study found that people with a history of PSGN in childhood had a risk of overt albuminuria more than six times that in the control group. In fact, the data show that a quarter of cases of overt albuminuria in this population may be attributable to PSGN in childhood. This is alarming, particularly as the Aboriginal population has an incidence of end-stage renal failure 10 times greater than that of the non-Aboriginal population of Australia.1,7,8 It is even more distressing when we realise that streptococcal disease should theoretically be preventable. Proteinuria is increasingly recognised as the best overall indicator of progressive renal disease, whatever the cause. It would thus be very important to follow the study population, preferably over many more years, to determine whether renal damage does indeed progress and lead to end-stage renal failure. Other aspects of epidemic and endemic post-streptococcal infection could also be explored. It has been suggested that, because of the high rate of nephritis in families, a familial trait may be involved, increasing susceptibility to the disease.9 This may have some relevance to the PSGN epidemics in this population. There is no simple treatment for PSGN, and preventing streptococcal infection remains the most important control strategy.10 Penicillin is beneficial in preventing spread of infection during epidemics.2 No vaccine is as yet available. As concluded by White and colleagues, prevention of streptococcal infection through improved economic and living conditions, and particularly control of skin infections, is possible and should reduce the incidence of renal involvement. However, the real tragedy highlighted by this study is that, despite the passage of up to 20 years since these children were infected with streptococci, nothing much has changed to lower the rates of infection among Aboriginal children. Indeed, a very recent report demonstrated that skin infections still occur in up to 70% of Aboriginal children, with the major pathogens being group A streptococci.4 It is imperative that such important results are heeded. Not until fundamental changes take place in the social, economic and living conditions of our Indigenous communities will this streptococcal disease be eliminated, as it has been in all other areas of Australia. We have a bipartisan Federal Government committed to improving the health of Indigenous Australians and an office for Aboriginal and Torres Strait Islander Health in the Commonwealth Department of Health and Aged Care, which is providing a comprehensive funding strategy for Indigenous health issues. The head of the Northern Territory Peak Aboriginal Health Organisation, Pat Andersen, is on record as describing the Primary Health Care Access Programme, now under way, as the most exciting event in Aboriginal affairs since the 1967 referendum. Furthermore, recent studies have shown that Aboriginal people can participate enthusiastically and effectively in chronic disease management, with improvement in their renal disease.11 Thus, the challenge at this time of reconciliation is to restore social equity and health to Indigenous Australians.12 It is to be hoped that this will eliminate post-streptococcal disease in Aboriginal communities. The future should be bright. Robert C Atkins Professor of Medicine and Director of Nephrology Monash Medical Centre, Melbourne, VIC Gogna NK, Nossor V, Walker AC. Epidemic of acute poststreptococcal glomerulonephritis in Aboriginal communities. Med J Aust 1983; 1: 64-66. Streeton CL, Hanna JN, Messer RD, Merianos A. An epidemic of acute post-streptococcal glomerulonephritis among aboriginal children. J Paediatr Child Health 1995; 31: 245-248. Carapetis JR, Currie BJ. Preventing rheumatic heart disease in Australia. Med J Aust 1998; 168: 428-429. Currie BJ, Carapetis JR. Skin infections and infestations in Aboriginal communities in northern Australia. Australas J Dermatol 2000; 41: 139-143. White AV, Hoy WE, McCredie DA. Childhood poststreptococcal glomerulonephritis as a risk factor for chronic renal disease in later life. Med J Aust 2001; 174: 492-496. Baldwin DS. Poststreptococcal glomerulonephritis. A progressive disease? Am J Med 1977; 62: 1-11. Briganti E, McNeil J, Atkins RC, editors. The epidemiology of diseases of the kidney and urinary tract: an Australian perspective. Adelaide: Australian Kidney Foundation Report, 1999. Available at <www.med.monash.edu.au/Epidemiology/general_info/publications.html> Spencer JL, Silva DT, Snelling P, Hoy WE. An epidemic of renal failure among Australian Aboriginals. Med J Aust 1998; 168: 537-541. Rodriguez-Iturbe B. Epidemic poststreptococcal glomerulonephritis. Kidney Int 1984; 25: 129-136. Chadban SJ, Atkins RC. Post-infectious glomerulonephritis. In: Brady HR, Wilcox CS. Therapy in nephrology and hypertension. Philadelphia: WB Saunders, 1998: 115-124. Hoy WE, Baker PR, Kelly AM, Wang Z. Reducing premature death and renal failure in Australian Aboriginals. A community-based cardiovascular and renal protective program. Med J Aust 2000; 172: 473-478. Eades SJ. Reconciliation, social equity and Indigenous health [editorial]. Med J Aust 2000; 172: 468-469. Make a comment

Robert C Atkins

Editorial Heart failure in older people: the epidemic we had to have Optimal treatment of the increasing number of patients with chronic heart failure will be a major challenge MJA 2001; 174: 432-433 The perception of most Australians of heart disease is the 1960s stereotype: middle-aged men suffering cardiac emergencies such as myocardial infarction, with dramatic symptoms, frantic therapeutic effort and frequently fatal outcome. However, this scenario has become the exception rather than the rule — the age-adjusted incidence of myocardial infarction and of cardiac death is falling in Australia, as in most Western countries,1 although this fall is less clear-cut in lower socioeconomic groups.2 It is possible... that the prescribing habits of GPs are directed towards agents which are likely to produce rapid relief of symptoms Despite these gains, recent evaluations indicate that the prevalence of heart disease in most communities is rising steadily, and that this is reflected in costs of hospitalisation if not in mortality data.1 This rise suggests that the strategies directed at reducing risk of ischaemic heart disease (such as cessation of smoking and lowering of serum cholesterol level) should be regarded as means of postponing disease onset rather than as "vaccines" against eventual ischaemia. Therapies such as thrombolytic agents3 and coronary angioplasty4 for patients with acute myocardial infarction, and β-adrenoceptor antagonists5 and angiotensin-converting enzyme (ACE) inhibitors6 for those with symptomatic heart failure, have led to increased survival rates, and thus more individuals with chronic heart disease. In addition, in older people, increasing rates of atrial fibrillation and aortic stenosis also contribute to cardiac disability. The Cardiac Awareness Survey and Evaluation (CASE) Study examined the current contributions of general practitioners to the diagnosis and management of chronic heart failure (CHF) in patients over the age of 60 years. The results, published in this issue of the Journal,7 shed considerable light on the magnitude of this emerging problem in Australia. One of the most complex questions in cardiology is the diagnosis of CHF. In the vast majority of controlled clinical trials to date, the diagnosis of CHF has been predicated on objective evidence of left ventricular systolic dysfunction, documented by echocardiography or radionuclide ventriculography. Most intervention studies have only included patients with severe systolic dysfunction, in order to maximise the frequency of end-points. Yet, this is just the tip of the CHF iceberg in the general population. For patients with predominantly diastolic, or mild degrees of systolic, left ventricular (LV) dysfunction, estimation of LV ejection fraction alone provides little diagnostic information, and the diagnosis of CHF becomes somewhat arbitrary. This was so in some patients in the CASE study: it is clear that GPs do not use echocardiography widely to assess patients with possible CHF. This blurring around the edges of the diagnosis (especially in patients with mild dysfunction) is regrettable, but there is no easy solution. Conversely, however, it is impossible to exclude from the CASE study design a number of patients with LV dysfunction but minimal symptoms, a group which may benefit from appropriate pharmacotherapy. Overall, one recommendation from the CASE study, which resulted in new diagnosis of CHF in 2% of the study population, is that widespread access to echocardiography by GPs for people older than 60 years is likely to be cost effective. The major stimulus to the diagnosis of CHF is the institution of appropriate therapy. It is here that the CASE study is most revealing. There have been dramatic advances in the management of CHF in the past 15 years, resulting in considerable improvement in outcomes for this patient population,8 although there is clearly scope for further reductions in both morbidity and mortality.9 ACE inhibitors (preferably in the largest tolerated dose),6 spironolactone10 and β-adrenoceptor antagonists5 all reduce mortality and morbidity in patients with LV systolic dysfunction. There is also evidence for the use of angiotensin-receptor antagonists or hydralazine/nitrates in patients intolerant of ACE inhibitors. Digoxin, in patients in sinus rhythm, has no major effect on mortality but slightly reduces hospitalisation risk.11 Conversely, some agents, notably calcium antagonists12 and the COX-1 (and possibly the COX-2)13 inhibitors, should be used with caution in patients with CHF, and the role of diuretic therapy is probably limited to the prevention of peripheral and/or pulmonary oedema. It is therefore an important finding of the CASE study that, even in the hands of an "interested" cohort of GPs, ACE inhibitors were used in little more than half of the patients, and usually with low-dose regimens. In contrast, use of diuretics and digoxin was surprisingly high. This makes it clear that in Australia, as in other countries,14 CHF is largely under-treated, and the price we pay is increased risk of deterioration, hospitalisation and death. It is possible, although not specifically examined by the CASE study, that the prescribing habits of GPs are directed towards agents which are likely to produce rapid relief of symptoms rather than agents with prognostic benefits. The epidemic of CHF in older people has its counterpart in an explosion of recent relevant clinical trial information. The HOPE study results suggest that all patients at high risk of ischaemia should be considered for treatment with ACE inhibitors, irrespective of the presence or absence of CHF.15 The data on the beneficial effect of spironolactone are quite recent, as are some of the β-adrenoceptor antagonist data. It is also clear that community-based outreach services for CHF patients may improve outcomes.16 Identification of and optimal therapy for these patients constitutes a major challenge for the new millennium. John D Horowitz Professor of Cardiology University of Adelaide, and Director Cardiology Unit North Western Adelaide Health Service, Adelaide, SA Simon Stewart Ralph Reader Postdoctoral Fellow Department of Public Health University of Glasgow, Glasgow, UK Tunstall-Pedoe H, Kuulasmaa K, Mahonen M, et al. Contribution of trends in survival and coronary-event rates to changes in coronary heart disease mortality: 10-year results from 37 WHO MONICA project populations. Monitoring trends and determinants in cardiovascular disease. Lancet 1999; 353: 1547-1557. Morrison C, Woodward M, Leslie W, Tunstall-Pedoe H. Effect of socioeconomic group on the incidence of, management of, and survival after myocardial infarction and coronary death: analysis of community coronary event register. BMJ 1997; 314: 541-546. Indications for fibrinolytic therapy in suspected acute myocardial infarction: collaborative overview of early mortality and major morbidity results from all randomised trials of more than 1000 patients. Fibrinolytic Therapy Trialists' (FTT) Collaborative Group. Lancet 1994; 343: 311-322. A clinical trial comparing primary coronary angioplasty with tissue plasminogen activator for acute myocardial infarction. The Global Use of Strategies to Open Occluded Coronary Arteries in Acute Coronary Syndromes (GUSTO IIb) Angioplasty Substudy Investigators. N Engl J Med 1997; 336: 1621-1628. Effect of metoprolol CR/XL in chronic heart failure: Metoprolol CR/XL Randomised Intervention Trial in Congestive Heart Failure (MERIT-HF). Lancet 1999; 353: 2001-2007. Packer M, Poole-Wilson PA, Armstrong PW, et al. Comparative effects of low and high doses of the angiotensin-converting enzyme inhibitor, lisinopril, on morbidity and mortality in chronic heart failure. Circulation 1999; 100: 2312-2318. Krum H, Tonkin AM, Currie R, et al. Chronic heart failure in Australian general practice. The Cardiac Awareness Survey and Evaluation (CASE) Study. Med J Aust 2001; 174: 439-444. MacIntyre K, Capewell S, Stewart S, et al. Evidence of improving prognosis in heart failure: trends in case-fatality in 66,547 patients hospitalised between 1986 and 1995. Circulation 2000; 102: 1126-1131. Stewart S, MacIntyre K, MacLeod MM, et al. Trends in hospitalisation for heart failure in Scotland, 1990-1996. An epidemic that has reached its peak? Eur Heart J 2001; 22: 209-217. Pitt B, Zannad F, Remme WJ, et al. The effect of spironolactone on morbidity and mortality in patients with severe heart failure. Randomized Aldactone Evaluation Study Investigators. N Engl J Med 1999; 341: 709-717. The effect of digoxin on mortality and morbidity in patients with heart failure. The Digitalis Investigation Group. N Engl J Med 1997; 336: 525-533. O'Connor CM, Carson PE, Miller AB, et al. Effect of amlodipine on mode of death among patients with advanced heart failure in the PRAISE trial. Prospective Randomized Amlodipine Survival Evaluation. Am J Cardiol 1998; 82: 881-887. Dzau VJ, Packer M, Lilly LS, et al. Prostaglandins in severe congestive heart failure. Relation to activation of the renin-angiotensin system and hyponatremia. N Engl J Med 1984; 310: 347-352. Edep ME, Shah NB, Tateo IM, Massie BM. Differences between primary care physicians and cardiologists in management of congestive heart failure: relation to practice guidelines. J Am Coll Cardiol 1997; 30: 518-526. Yusuf S, Sleight P, Pogue J, et al. Effects of an angiotensin-converting-enzyme inhibitor, ramipril, on cardiovascular events in high risk patients. The Heart Outcomes Prevention Evaluation Study Investigators. N Engl J Med 2000; 342: 145-153. Stewart S, Marley JE, Horowitz JD. Effects of a multidisciplinary, home-based intervention on unplanned readmissions and survival among patients with chronic congestive heart failure: a randomised controlled study. Lancet 1999; 354: 1077-1083. Make a comment

John D Horowitz · Simon Stewart

Large initiatives are under way, but, as individual doctors, we can begin to identify the silent two-thirds majority who are too frightened to seek help MJA 2001; 174: 436-437 Urinary incontinence is a distressing and debilitating condition which will become more prevalent as our population ages. The personal suffering of those who find urine running down their legs is difficult to measure, but we know that quality of life is severely impaired. It is disturbing that only about a third of those affected actually seek medical help, because of lack of knowledge (on the part of the patient or the provider) about available treatments,1 as well as patients' embarrassment about revealing their "lack of control". For patients with urinary incontinence, the cost of buying pads and other appliances is a major burden. Indeed, some women are forced to reuse their commercial pads by opening them and restuffing them with toilet paper, or to dry their urine-soaked disposable pads on a heater for later use to reduce costs.2 The "cost" of a disease or condition is not adequately described by the dollars spent in the healthcare system. Nonetheless, in the current climate of economic healthcare rationalisation, it is still useful to calculate the measurable costs of a condition, as least to justify expenditure on this rather than upon some other medical problem. The cost of an illness comprises three components:3 "direct costs", which include personal costs (eg, pads and replacement of urine-soaked clothes), and treatment costs (met by patients and by several government subsidies); "indirect costs", which include lost productivity both in the home and in outside employment; and "intangible costs", which are most difficult to measure financially, but include psychological distress and impaired physical or mental health. The costs of urinary incontinence, for the sufferer and for the Australian healthcare system, have not been previously ascertained. The report by Doran and colleagues in this issue of the Journal4 represents the first attempt to estimate the direct costs of incontinence for all community-dwelling Australian women. Their calculations were made possible by two recent events. Firstly, the Women's Health Australia (WHA) project, a large, ongoing national longitudinal epidemiological survey, has made it possible to gain an accurate picture of the prevalence of incontinence in 41 724 young (18-23 years), middle-aged (45-50 years) and older (70-75 years) women.5 It also identified women who did and did not seek help. Secondly, an Australian group devised and validated a test instrument to measure the direct personal and treatment costs of incontinence in 100 community-dwelling women.2 Doran et al have extrapolated from the WHA prevalence data, using Australian Bureau of Statistics population figures, to deduce the total number of incontinent women in this country. They then used estimates from the second study to calculate the personal costs for all affected women, and added the treatment costs of those who sought help, to derive an annual cost for incontinence of $387 per incontinent woman, or $710 million (in 1998 prices). As the authors indicate, these figures do not include indirect or intangible costs. Equally important in terms of human suffering is the high prevalence of incontinence among Australian nursing home residents, and this also imposes a huge financial burden. One report found that urinary incontinence affected 77% of a sample of 1659 such residents, and that up to 25% of nursing staff time was spent dealing with urinary leakage.6 The long term care of each incontinent nursing home resident was estimated to cost $45 000 per annum, or $450 million a year (1991 prices). Many incontinent nursing home residents are not provided basic management, such as being taken to the toilet at regular intervals, owing to a lack of trained nurses in such facilities. Cost-effective strategies, such as applying continence pads instead of changing wet beds (with laundry savings of $40 per incontinent resident per month),7 are not routinely employed. So, what are we doing about the problem of incontinence and its great financial cost? There is hope on the horizon. The World Health Organization (WHO) has recently focused on the problem. At the first international WHO consultation on incontinence, in June 1998, a team of 24 committees (including five Australian clinicians and scientists) considered the best way to eradicate incontinence. The issue of cost, and our poor knowledge of the magnitude of the problem, was a major concern.3 The proceedings have been widely disseminated, and the second Consensus Meeting will be held in July 2001. The WHO concluded that incontinence should be considered a disease rather than a condition, in view of its debilitating effects upon health and wellbeing. In Australia, the Commonwealth Department of Health and Aged Care has recently provided $15 million over five years to fund a National Continence Management Strategy.8 Its expert advisory committee, which includes nurse continence advisors and representatives from general practice, urology, urogynaecology, colorectal surgery, physiotherapy and geriatric medicine, first met in September 1998. Funds are allocated to ensure more education of healthcare providers, wider dissemination of information about treatment to the public, and to develop a national management framework. As a first step, a Continence Helpline has been established (see Box). Three pilot projects about new ways to increase the uptake of continence treatment are under way in Perth, Wangaratta and the Hunter region. Recently, over one million dollars was allocated to testing innovative treatments. A project to measure all costs of incontinence for patients and for the tiers of funding subsidy is currently being assessed. The efforts of WHO and the Australian Government are laudable, but we must rise to the challenge of helping those with incontinence as individual doctors. By tactful enquiries of patients with known risk factors,9 we may begin to identify the silent two-thirds majority of affected patients who are frightened to seek help. By starting conservative treatment and, where appropriate, initiating a full investigation at an early stage, we can render help quickly before the problem has become entrenched, refractory and even more costly. Telephone number of the Continence Helpline: 1800 330 066 Back to text Kate H Moore Associate Professor of Obstetrics and Gynaecology Department of Urogynaecology, St George Hospital University of New South Wales, Sydney, NSW Holst K, Wilson PD. The prevalence of female urinary incontinence and reasons for not seeking treatment. N Z Med J 1988; 101: 756-758. Dowell CJ, Bryant CM, Moore KH, Simons AM. Calculating the direct costs of urinary incontinence: a new test instrument. Br J Urol 1999; 83: 596-606. Versi E, Defever M, Hu TW, et al. Socio-economic considerations in urinary incontinence. In: Abrams P, Khoury S, Wein A. Incontinence. Report of the World Health Organisation Consensus Conference. Plymouth, UK: Health Publications Ltd, 1999: 869-929. Doran CM, Chiarelli P, Cockburn J. Economic costs of urinary incontinence in community-dwelling Australian women. Med J Aust 2001; 74: 456-458. Chiarelli P, Brown W, McElduff P. Leaking urine: prevalence and associated factors in Australian women. Neurourol Urodynam 1999; 18: 567-577. Steel J, Fonda D. Minimising the cost of urinary incontinence in nursing homes. PharmacoEconomics 1995; 7: 191-197. Szonyi G, Pang S. Use of continence pads to reduce laundry costs in a nursing home. Aust Continence J 1998; 4: 34-37. Fonda D. National continence management strategy. Aust Continence J 1998; 4: 100-101. Millard RJ, Moore KH. Urinary incontinence: the cinderella subject. Med J Aust 1996; 165: 124-125. Make a comment

Kate H Moore

Editorial Vocational part-time training: jobs for the girls and boys There is a clear demand from many levels of the medical profession that part-time training be available, viable and valuable MJA 2001; 174: 376-377 Medicine is different today — isn't it? Changing knowledge, changing technology, changing disease patterns, changing service delivery, changing consumer expectations — and a changing medical workforce. The medical workforce is changing in terms of gender balance, expectations regarding lifestyle, working conditions, ethnic/cultural background and age of entry to medical school. Medicine is the same as ever — isn't it? The same hierarchical structure, with men dominating at senior levels; the same culture of heroic individualism; the same male-female inequalities with selection/promotion/retention procedures; the same difficulties for women to reach their professional potential. Women are clustered in the lower-status areas of medicine, earn less money on average, make less contribution to the profession outside direct medical care, experience higher levels of stress, have many more family responsibilities, and are much more likely to modify their careers to accommodate the needs of their partners and families.1 One outcome is very clear — part-time trainees report satisfaction with their job and lifestyle. Less clear is the training outcome. Medicine, like society in general, is both different and the same. What is clear is that our younger colleagues, both women and men, are demanding real change in the structure, organisation and practice of medicine to allow them to have a more balanced lifestyle. One very important structural and organisational issue is the availability of part-time training during the long and demanding medical vocational pathway. Two articles2,3 in this issue of the Journal discuss job-sharing, which is one way of achieving part-time training. Job-sharing often involves more than one sharing arrangement — for example, alternating periods of a week or a fortnight, or splitting the week. Whitelaw and Nash2 note that job-sharers in paediatric training are more likely to share work on a weekly basis while raising children, but to share in longer blocks if preparing for exams. Gun3 found a job-sharing colleague with similar needs that meshed over some, but not all, of her training years. Whitelaw and Nash note that the perceptions of hospital managers and doctors-in-training differ on the availability of particular units for job-sharing; they also note that there are different eligibility requirements between hospitals, implying judgement about what are "acceptable" and "unacceptable" reasons for job-sharing.2 Whether a reason is "acceptable" may depend on the sex of the trainee, but, increasingly, men as well as women are beginning to request part-time training to give them the opportunity to combine training with care of children, study, and hobbies. There has been a gradual increase in the number of part-time trainees in recent years (especially in emergency medicine, paediatrics and psychiatry) — in 1999, part-time trainees made up 6.5% of the total.4 Interestingly, in general practice, traditionally considered a very flexible training area, there was a 50% drop in part-time training over the period 1995-2000. The specialties with minimal numbers of part-time trainees include anaesthetics, dermatology, obstetrics and gynaecology, radiology and surgery. The two articles illustrate a major difficulty in assessing part-time training: while Gun states that there were 17 part-time paediatric trainees in 1998 (a figure quoted from a report of the Medical Training Review Panel),3Whitelaw and Nash's survey identified 34 such trainees in the same year.2 The true proportion of trainees working part-time remains unclear, with differing periods of time per year spent in part-time training, and differing information provided by institutions and Colleges. More accurate collection of data and a clear definition of "part-time" training that differentiates it from "interrupted" training (eg, three months on and three off) are required. Perceived problems continue to be canvassed: Whom do you share with? Will the College agree (in practice as well as in principle)? Is your reason "good enough"? Are your colleagues resentful ("Why should s(he) have 'time off'? "What if I have to do extra to cover?")? Are your consultants cautious ("What about continuity of care?" "What about continuity of meeting the needs of my busy lifestyle?")? Will the hospital bear potential extra costs? Can you and your childcare arrangements cope with converting to full-time work to cover your partner's leave or sickness? Can you get to the 7 am ward round or journal club? Will you miss that special clinic or unit meeting that is always on your day off? Should you refuse secondment? What will happen next year? One outcome is very clear — part-time trainees report satisfaction with their job and lifestyle.2,3 Less clear is the training outcome. There is no intrinsic reason why part-time training, if appropriately balanced, should be less effective than full-time training. However, institutional satisfaction with part-time training is hard to measure given the barriers to implementation, the variable number of trainees from year to year, the different specialties and consultants involved, and the rapid, concurrent changes to service delivery and the organisation of the junior medical workforce (including changes associated with implementing "safe hours" policies). Obvious benefits to the hospital of part-time work include having a potential pool of trainees to cover each other for illness or holidays, and improving the work contribution of trainees.2 There is a clear demand from many levels of the profession that part-time training be available, viable and valuable. The reality is that availability is highly variable, viability often still depends on the trainees "proving themselves", but value is clear. The need for part-time training is part of a much wider debate about vocational medical training. We continue to grapple with the traditional needs of training organisations versus the personal and professional needs of trainees, the conflict between education and service in a tight fiscal environment, and the overall size, setting, distribution and safety of the junior medical workforce. Cultural change is required; a change of core values and norms "from within" to achieve commitment to new organisational structures5 so that the medical profession better meets the needs of, and thus reaps the most benefit from, its entire medical workforce. Jillian R Sewell President, Paediatrics and Child Health Division, Royal Australasian College of Physicians Member, Australian Medical Workforce Advisory Committee Working Party — Career Choice and Workforce Participation Dennerstein L. Roles and achievements: a survey of medical graduates. Melbourne: Key Centre for Women's Health in Society, 1989. Whitelaw CM, Nash MC. Job-sharing in paediatric training in Australia: availability and trainee perception. Med J Aust 2001; 174: 407-409. Gun MT. Part-time specialty training — my experience. Med J Aust 2001; 174: 410-412. Medical Training Review Panel. Fourth report. Canberra : MTRP and Commonwealth Department of Health and Aged Care, August 2000. Sinclair A. Doing leadership differently: gender power and sexuality in a changing business culture. Melbourne: Melbourne University Press, 1998. Make a comment

Jillian R Sewell

Editorial Can hepatitis C transmission be reduced in Australian prisons? Strategies to reduce the number of people who inject drugs and to minimise harm should help, but the cooperation of correctional authorities is essential MJA 2001; 174: 378-379 Approximately 20 000 people were incarcerated in Australia at the end of 1999.1 Another 20 000 had cycled through our prison systems in that year, but had been released by December 1999. This dynamic movement of people in and out of prisons not only increases the possibilities for transmission of infections such as hepatitis C virus (HCV) and HIV, but also makes it very difficult to detect transmission. Hepatitis C infection is endemic among Australian prisoners. In New South Wales prisons, approximately a third of male and two-thirds of female inmates are infected. Corrections Health Service had the second-highest number of hepatitis C notifications for an Area Health region in NSW in its debut report.2 HCV incidence is likely to be high in prison, but to date there have been few cases reported.3 Nevertheless, several studies have found that a history of imprisonment is associated with HCV infection.4 These findings, from both Australia3 and overseas,4 raise two questions: What is the incidence of HCV for various transmission modes in prison?; and Can HCV transmission be reduced in prison? Despite gaps in our knowledge, there is sufficient evidence to address the two most frequent modes of transmission: injecting drug use and tattooing. About a quarter of prisoners inject drugs while incarcerated.3 Virtually all drug injecting occurs with used injecting equipment shared among numerous partners. Therefore, the primary goal has to be to reduce drug injecting in prison. One way to achieve this is to reduce the number of drug injectors in prison.5 There is abundant evidence that community-based methadone treatment reduces injecting, crime and the subsequent incarceration of drug users,6 yet only a third of the demand for methadone treatment is met in the community.6 Another way to reduce the level of drug injecting in prison is to provide methadone maintenance treatment for prisoners. In one study, prisoners maintained on methadone injected half as often as those out of treatment, but only when doses reached 60 mg and treatment was provided for the entire term of the prison sentence.7 The NSW prison methadone program started in 1987, but meets only a quarter of the potential demand for treatment.5 Prison methadone programs have been recently introduced or expanded in Queensland, South Australia, Victoria, Tasmania and the Australian Capital Territory. Drug injecting in prison is also likely to be reduced if prisoners receive lesser punishment for the use of non-injectable drugs compared with injectable drugs. Yet prisoners receive the same penalty whether they test positive on urinalysis for cannabis or for heroin. Research into mandatory drug screening in United Kingdom prisons found that inmates moved from smoking cannabis (detectable in urine for weeks) to injecting heroin (detectable in urine for only a day or two) after mandatory drug testing was introduced.8 South Australia and Tasmania have introduced differential penalties for different drugs, with the aim of reducing drug injecting in prison. Victoria is considering a similar system. Another way to reduce drug injecting is to facilitate non-injecting routes of administration among injecting drug users. Preliminary results from a cognitive behavioural trial indicated that some injecting drug users will shift to non-injecting methods of use (A Wodak, Director, Alcohol and Drug Service, St Vincent's Hospital, Sydney, personal communication). Prisons, where injecting is so risky and common, are ideal settings for a trial of this intervention. Without doubt, the most controversial strategy is prison needle and syringe exchange programs. These programs have been successfully implemented in Switzerland, Germany and Spain in 17 different prisons.9 However, they reduce sharing of injecting equipment rather than drug injecting itself, and the problems of fatal overdose, abscesses, and inmates' involvement in the prison drug trade may persist. If prison needle and syringe exchange programs are unacceptable, then much more effort must be directed towards meeting the demand for drug treatment by prisoners. HCV transmission in prison may also occur through tattooing. One way to reduce tattoo-related hepatitis C transmission is to train select inmates in infection control procedures and to provide them with autoclaves and single-use ampoules of ink. Penalties for tattooing in prison should be removed. Allowing professional tattooists to visit prison is likely to be too expensive for inmates. So how can these strategies be implemented? The first step would have to be increasing the number of general practitioners who prescribe methadone both in the community and in prison. Less than 1% of GPs prescribe methadone in NSW.10 The opportunities for improvement here are enormous. Almost all other strategies listed above require the cooperation of prison authorities. Yet, correctional services administrators (comprising prison commissioners from each jurisdiction) have signalled their resistance to examining hepatitis C infection in prison by declining to even discuss recommendations made in the Review of the Third National HIV/AIDS Strategy.11 Until prison authorities are made to recognise that prisons play a significant role in the hepatitis C epidemic, it is unlikely that hepatitis C transmission will be reduced in Australian prisons. Kate A Dolan Senior Lecturer National Drug and Alcohol Research Centre University of New South Wales, Sydney, NSW Corrective Services, Australia. Canberra: Australian Bureau of Statistics, December 1999. (Catalogue no. 4512.0.) NSW Department of Health. Healthy people 2005: new directions for public health in NSW. NSW Public Health Bull 2000; 11: 198. Dolan K. The epidemiology of hepatitis C infection in prison populations [discussion paper]. Canberra: Commonwealth Department of Health and Aged Care, 2000. MacDonald M, Crofts N, Kaldor J. Transmission of hepatitis C virus: rates, routes and cofactors. Epidemiol Rev 1996; 18: 137-148. Dolan K. Surveillance and prevention of hepatitis C infection in Australian prisons. A discussion paper. Technical Report No. 95. Sydney: National Drug and Alcohol Research Centre, 2000. Ward J, Mattick R, Hall W. Methadone maintenance treatment and other opioid replacement therapies. Amsterdam: Harwood Academic Press, 1998. Dolan KA, Hall W, Wodak A. Methadone maintenance reduces injecting in prison. BMJ 1996; 312: 1162. Gore SM, Bird AG. Mandatory drug tests in prisons. BMJ 1995; 310: 595. Rutter S, Dolan K, Wodak A, Heilpern H. Prison syringe exchange: a review of international research and program development. Technical Report No. 112. Sydney: National Drug and Alcohol Research Centre, 2001. NSW Health Department. The NSW drug treatment services plan, 2000-2005: better health good health care. Sydney: NSW Health Department, 2000. Proving partnership. Review of the National HIV/AIDS Strategy 1996-97 to 1998-99. Canberra: Australian National Council on AIDS and Related Diseases, 1999. Make a comment

Kate A Dolan

Editorial The mental health of young Australians Are we as a nation taking seriously enough the task of preventing and treating mental illness in the young? MJA 2001; 174: 380-381 The United States Surgeon General recently warned that "The burden of suffering experienced by children with mental health needs and their families has created a health crisis in this country [USA]. Growing numbers of children are suffering needlessly because their emotional, behavioural, and developmental needs are not being met by those very institutions which were explicitly created to take care of them. It is time that we as a Nation took seriously the task of preventing mental health problems and treating mental illnesses in youth."1 What is Australia's scorecard in the area of children's mental health? In 1995, as part of the National Mental Health Strategy, the Federal Government funded a national survey to establish the prevalence of mental disorders, disability and service use in the Australian population. The adult component (ie, people over 17 years) was conducted in 19972 and the child and adolescent survey (people aged 4-17 years) in 1998. Findings of the latter survey were released recently3 and are summarised in the Box. The strength of the child and adolescent survey was that it considered mental health problems in a variety of ways, including psychiatric diagnosis, service use, and the impact of mental disorders on quality of life. Limitations of the survey were that diagnoses were based solely on information from parents (some questionnaire data were obtained from adolescents but no information was sought from teachers), and only three conditions were examined. These shortcomings may explain, among others, the high rates of attention deficit hyperactivity disorder found — as many as 19.3% of boys aged 6-12 years were found to be suffering from this condition. Some findings are worth highlighting. First, the prevalence of mental health problems among the young (14%) is high and not much different from that found in adults (18%).2 That is, half a million Australians aged 4-17 years have serious emotional and behavioural problems.3 Second, these conditions impair their functioning and quality of life. Disturbed young people also behave in ways injurious to health much more often than their healthy counterparts. Third, only a quarter of those who need help receive it. Mental disorders impose a heavy burden on children, families and communities1,2,4 and often persist into adulthood. The cost to society in human and economic terms is great.1 There is broad agreement that we need to detect these problems early, provide effective treatment and attempt prevention.1,4 A four-pronged approach is necessary: Increase awareness that mental health problems are a major issue in child health and try to prevent them. This will help give children the chance for a healthy start in life.1 Improve the use of resources and access to services. For example, general practitioners could, with appropriate training, play a central role identifying and treating children with mental health problems. GPs (after schools, the second most common source of help) are well placed to take on this role, especially as disorders are often chronic, and contact with specialist services is likely to be only episodic.5 To do this, GPs will need better support — for example, rapid access to specialist telephone advice and to psychiatric assessment, and good liaison with child and adolescent community teams.5 Psychiatrists, psychologists and other mental health professionals need to be more accessible and responsive, particularly in crises.6 It is poignant that, while Australia prides itself on providing universal access to free healthcare, half of the parents needing help believe it is too expensive.3 Increase funding for mental health services for young people. In 1997-98, the last year for which data are available, State and Territory governments spent $1.4 billion on mental health services ($74 per capita).7 Of this sum, only $107 million (7%) was spent on the young, who make up a quarter of the Australian population — this amounts to an average of $23 per child, compared with $95 per adult.7 Increase the number of specialists in mental health and carry out more research. The shortage and maldistribution of specialists7,8 is well documented, and it is important to establish which treatments and service-delivery models work and which do not.1,4 We must ask ourselves whether we as a nation take seriously enough the task of preventing and treating mental illnesses in the young. The recent proliferation of programs8 promoting mental health suggests we are moving in the right direction, but it remains to be seen whether this is a measure of real commitment or just window dressing. The findings of the latest survey of mental disorders in young people3 will at least give us a baseline for comparison when the next national survey is conducted. Joseph M Rey Professor, Department of Psychological Medicine, University of Sydney Director, Child and Adolescent Mental Health Services Northern Sydney Health, Sydney, NSW Report of the Surgeon General's Conference on Children's Mental Health: a national action agenda. Washington, DC: US Public Health Service, 2000. Australian Bureau of Statistics. Mental health and wellbeing profile of adults, Australia 1997. Canberra: AGPS, 1998. Sawyer MG, Arney FM, Baghurst PA, et al. The mental health of young people in Australia. Canberra: AGPS, 2000. Raphael B. Promoting the mental health and wellbeing of children and young people. Discussion paper: key principles and directions. Canberra, AGPS, 2000. Garralda ME. Child and adolescent psychiatry in general practice. Aust N Z J Psychiatry (in press). Australian Medical Workforce Advisory Committee. The specialist psychiatry workforce in Australia. Sydney: AMWAC, 1999. (AMWAC Report 1999.7.) Commonwealth Department of Health and Aged Care. National mental health report 2000. Canberra, AGPS, 2000. National action plan for promotion, prevention and early intervention for mental health. Canberra: Commonwealth Department of Health and Aged Care, 2000. Make a comment Main findings of the 1998 Australian Federal Government survey on the mental health of young people3 From interviews with a representative sample of 4509 parents and questionnaires returned by 1490 adolescents aged 13-17 years, the following information was obtained: 14.1% of 4-17-year-olds had experienced mental health problems in the previous six months. The prevalence of three specific mental disorders during the previous year had been — Depressive disorder 3.7% — Conduct disorder 3.0% — ADHD 11.2% (Inattentive subtype, 5.8%; hyperactive-impulsive subtype, 2.0%; combined subtype, 3.3%) Young people living in sole-parent and low-income families had higher rates of problems. In adolescents, rates of suicidal ideation, suicide attempts, cigarette smoking, and alcohol and cannabis use increased steeply with increasing emotional and behavioural problems. Twenty-five per cent of children and adolescents with problems had used at least one service (broadly defined) in the previous six months. The three services attended most often were counselling at school or in a special class, GPs and paediatricians. Half of the parents reported that help was too expensive, and almost half did not know where to seek help. Only 6% reported that social stigma was a barrier to seeking help. Among the adolescents, 38% preferred to manage the problems themselves, 18% believed nothing could help, 17% did not know where to get help, and 14% were worried about the social stigma. ADHD = attention deficit hyperactivity disorder. Back to text

Joseph M Rey

Editorial Heart Week 2001: "Get active"! A call to action Include physical activity advice in consultations, especially for those at risk of heart disease MJA 2001; 174: 381-382 The focus of the National Heart Foundation Heart Week, the first week of May, is physical activity and heart disease. This is timely given recent evidence that inactivity is a major risk factor for coronary heart disease (CHD), and that the population risk attributable to inactivity appears to be similar to the risk posed by smoking, raised lipid levels or hypertension.1,2The evidence Much of the epidemiological evidence relates to primary prevention and comes from good-quality observational (cohort) studies. The better-designed studies show stronger relationships and a dose-response relationship between inactivity and CHD; the benefits of increasing activity levels accrue particularly for people who have been inactive.1 Evidence from meta-analyses suggests that people who remain sedentary have about twice the risk of CHD of those who participate in regular activity.3 Replication studies in diverse populations since 1990 have reinforced this evidence. There is consistent evidence that women benefit almost as much as men from regular, moderate-intensity physical activity, as do older adults.4,5 It appears that only recent or current physical activity is beneficial, rather than athleticism in earlier life.6 For all age groups, adopting physical activity reduces the risk of CHD deaths, leading to the maxim that "it is never too late to start being active".5,7 Some of this cardiovascular benefit occurs even at levels of physical activity below those required for aerobic (fitness or cardiorespiratory) training, at levels as low as 50% of the maximal predicted heart rates for age.1,8 However, for the general population, more vigorous activity results in additional benefits. There is also evidence that physical activity may prevent ischaemic stroke.9 The mechanism may be through reducing the risk of thrombus formation, or the effects of physical activity may be mediated through reducing blood pressure levels. These protective effects reducing the incidence and mortality from CHD are independent of the influence of physical activity on other cardiovascular risk factors. Nonetheless, there are direct benefits on other risk factors, with moderate activity contributing to lowered blood pressure, increased high density lipoprotein (HDL) cholesterol level, and improvements to the fibrinolytic system.1,8 More sustained physical activity may also help with weight loss. Physical activity has similar benefits for many patients with established coronary artery disease. In those who become active, these benefits include increased fitness, improved oxygen consumption, and decreases in ischaemic responses.8Biological mechanisms: Researchers have begun to explore the biological mechanisms to explain the benefits of physical activity in preventing CHD. There is controlled-trial evidence that sustained vigorous activity can lead to some regression of atherosclerosis.8,10 Exercise may improve coronary endothelial-dependent vasodilatation responses, possibly leading to recruitment of collateral vessels in ischaemic heart disease.11 However, further work is needed to define the exact biological mechanisms. For patients with CHD, there is clinical evidence of increased functional capacity and improved myocardial perfusion after exercise training, and there may even be some benefits for those with uncomplicated heart failure.8 Cardiac rehabilitation: Although the benefits of cardiac rehabilitation are generally accepted,12 these are multifaceted programs, and the individual benefits of the exercise component are difficult to disentangle from the overall program benefit. The key issue here is that, after myocardial infarction, a much higher proportion of patients in Australia need to complete supervised rehabilitation programs than is currently the case. Risk of acute cardiac events: One well-known paradox is the issue of the increased risk of acute cardiac events in unfit sedentary people who embark on vigorous exercise regimens.13 Although the risk of sudden cardiac events is transiently increased (during and for a half hour after strenuous exertion), this acute increment in risk is much reduced for moderate activity. Overall, even among CHD patients, the long term benefits of activity vastly outweigh the short term risks. Furthermore, it has been shown that the overall risk for primary cardiac arrest is much lower among those who are moderately active.14 Thus, among cardiac patients, vigorous activity should be started with caution and in supervised settings, whereas moderate physical activity should be easier to initiate. In conclusion, almost half of Australian adults do not achieve the health goal of moderate participation in physical activity. Recent trends have shown that physical activity levels are declining (as obesity rates are increasing), and that women, those least advantaged and non-English speakers are more likely to be inactive.15 There is a clear mandate to include physical activity advice in consultations, especially for those at risk of heart disease. Brief advice about activity, delivered in the surgery, can positively influence physical activity levels.16 Adherence to structured activity programs is poor, so that constant reinforcement is useful, as well as recommending types of activity which can become part of everyday life. Some patients will be very active, but still develop CHD. However, on balance, increasing activity is a worthwhile investment of medical practitioners' time. For Heartweek 2001, go for a regular walk, and recommend it to almost every patient! Recommendations for physical activity* Recommendations for the general community are that every Australian adult should accumulate half an hour of moderate-intensity activity on most days of the week. Examples of moderate-intensity activities include regular walking at 4km/hour energetic gardening or lawn mowing swimming doubles tennis, and, possibly golf. These are achievable by most people. *Commonwealth Department of Health and Aged Care. National physical activity guidelines for Australians. Canberra: AGPS, 1999. Adrian E Bauman Professor of Public Health and Epidemiology School of Community Medicine University of New South Wales, Sydney, NSW Terry J Campbell Professor of Medicine University of New South Wales (St Vincent's Hospital), Sydney, NSW United States Department of Health and Human Services. The Surgeon General's report on physical activity and health. Washington, DC: US Government Printing Office, 1996. Bauman A. The use of population attributable risk (PAR) in understanding the health benefits of physical activity. Br J Sports Med 1998; 32: 279-280. Berlin JA, Colditz GA. The meta-analysis of physical activity in the prevention of coronary heart disease. Am J Epidemiol 1990; 132: 612-627. Manson J, Hu FB, Rich-Edwards JW, et al. A prospective study of walking as compared with vigorous exercise in the prevention of coronary heart disease in women. N Engl J Med 1999; 341: 650-658. Wannamethee SG, Shaper AG, Walker M. Physical activity and mortality in older men with diagnosed coronary heart disease. Circulation 2000; 102: 1358. Sherman SE, D'Agostino RB, Silbershatz H, Kannel WB. Comparison of past versus recent physical activity in the prevention of premature death and coronary artery disease. Am Heart J 1999; 138: 900-907. Blair SN, Kohl H, Barlow CE, et al. Changes in physical fitness and all-cause mortality. A prospective study of healthy and unhealthy men. JAMA 1995; 273: 1093-1098. Shephard RJ, Balady GJ. Exercise as cardiovascular therapy. Circulation 1999; 99: 963-972. Shinton R, Sagar G. Lifelong exercise and stroke. BMJ 1993; 307: 231-234. Hambrecht R, Niebauer J, Marburger C. Various intensities of leisure time physical activity in patients with coronary heart disease: effects on cardiorespiratory fitness and progress of coronary atherosclerotic lesions. J Am Coll Cardiol 1993; 22: 468-477. Hambrecht R, Wolf A, Gielen S, et al. Effect of exercise upon coronary endothelial function in patients with coronary artery disease. N Engl J Med 2000; 342: 454-460. O'Connor GT, Buring JE, Yusuf S, et al. An overview of randomized trials of rehabilitation with exercise after myocardial infarction. Circulation 1989; 80: 234-244. Albert CM, Mittleman MA, Chae CU, et al. Triggering of sudden death from cardiac causes by vigorous exertion. N Engl J Med 2000; 343: 1355-1361. Lemaitre RN, Siscovick DS, Raghunathan TE, et al. Leisure-time physical activity and the risk of primary cardiac arrest. Arch Intern Med 1999; 159: 686-690. Armstrong T, Bauman A, Davies J. Physical activity patterns of Australian adults: results of the 1999 National Physical Activity Survey. Canberra: Australian Institute of Health and Welfare, 2000. (AIHW Catalogue No. CVD 10.) Halbert JA, Silagy CA, Finucane PM, et al. Physical activity and cardiovascular risk factors: effect of advice from an exercise specialist in Australian general practice. Med J Aust 2000; 173: 84-87. Make a comment

Adrian E Bauman · Terry J Campbell

Editorial Testicular cancer management We have to keep our eye on the ball MJA 2001; 174: 320-321 Almost 600 young Australian men are diagnosed with testicular cancer each year. It is the second most common malignancy in men aged 18-35 years, behind melanoma, and its incidence has more than doubled over the past 30 years.1 Fortunately, this disease is one of the major successes of modern oncology, and almost all of these men can now expect to be cured. With the advances in the management of the disease over the past 25 years, most men with metastatic testicular cancer are now curable with combination chemotherapy. During the same time, patients with earlier stages of the disease have benefited from changes that reduce the toxicity of treatment. These changes include: a reduction in the number of cycles of chemotherapy required for treatment of good-prognosis metastatic disease, a reduction in the radiation dose and field size for the treatment of early-stage seminoma, and the introduction of active surveillance (close, structured follow-up to detect and treat relapse) for Stage I non-seminomatous tumours. ... there is much variability in the care of these men, and this may affect the extent and toxicity of their treatment These advances are the outcomes of oncologists' long term commitment to high quality clinical trials, and Australian research has contributed substantially to this evidence base.1-3In this issue of the Journal, Toner et al provide, for the first time, Australian population-based data on the management of testicular cancer.4 They retrospectively surveyed doctors who were involved in the management of more than 600 patients in Victoria with testicular cancer between 1988 and 1993. Their survey included information on the location of care, investigations performed, treatment and survival. The men were treated at a large number of hospitals, most of which treated fewer than two patients with testicular cancer each year. How did this dispersion of care and expertise affect management and outcomes? Staging and surveillance were often inadequate. There was a low rate of completion of staging and follow-up investigations in the first year for patients with early-stage disease undergoing active surveillance, and no patients underwent primary retroperitoneal lymph node dissection. Furthermore, more than 10% of patients with Stage I seminoma were managed with surveillance (often poorly implemented), which at the time (and arguably even today) was not a proven treatment. There are no data about the delivery or adverse effects of treatment. Despite some of the shortcomings in management, there was an excellent overall relative five-year survival of 95%, a figure that is similar to those obtained elsewhere in Australia,5,6 and internationally.7 However, these findings offer only partial reassurance, since differences in outcomes between groups may be hard to establish with so few adverse events. This has been noted previously in similar studies. For example, no differences in outcome based on location of care were identified for Scandinavian men with testicular cancer when all patients were considered. However, when the patients with the earliest stage of disease (and hence the best prognosis) were excluded, differences became apparent, with better survival for patients cared for in centres that treated large numbers of patients.8 This is reinforced by better outcomes for patients managed in centres treating large numbers of patients in reports from the United States9 and the United Kingdom.10 The data also suggest better outcomes for men treated in centres recruiting the largest numbers of patients to randomised clinical trials.11 Indeed, management of patients in small centres without the necessary expertise may limit access to some treatments. The failure by Toner et al to demonstrate differences in outcome between the centres treating many patients and those treating few may also reflect imbalances in prognostic factors. For example, patients with the worst prognostic features seen at smaller centres are likely to be referred to larger centres, making outcomes appear to be better at the former and worse at the latter. Furthermore, in a disease with such effective salvage treatment, the main disadvantage of inadequate surveillance may be the need for more intensive therapy, with the associated problems of increased toxicity and cost, rather than worse overall survival. These aspects were not assessed in the Victorian study. The apparent shortcomings in care must also be considered in the light of the study's limitations. The data are based on a questionnaire completed three to eight years after the patients were treated. Although the response rate was high (with information obtained for 95% of cases), there was no independent verification of the data provided by the respondents. The answers reflect both the quality of the practitioners' medical records and their knowledge of the purpose and expectations of the investigators. In addition, although many hospitals each treated a small number of patients, it is not clear how many individual doctors were involved — potentially more important in terms of clinical experience and expertise. Outcomes for men with testicular cancer in Victoria are excellent. However, there is much variability in the care of these men, and this may affect the extent and toxicity of their treatment. Optimal management is demanding on patients, doctors and support staff. Men with testicular cancer should be treated in centres with multidisciplinary expertise, experience and access to all treatment options — there is too much at stake for it not to be done right. Michael J Boyer Head, Department of Medical Oncology Martin R Stockler Senior Lecturer in Cancer Medicine and Clinical Epidemiology Sydney Cancer Centre, Royal Prince Alfred Hospital and University of Sydney, Sydney, NSW Levi JA, Thomson D, Sandeman T, et al. A prospective study of cisplatin-based combination chemotherapy in advanced germ cell malignancy: role of maintenance and long-term follow-up. J Clin Oncol 1988; 6: 1154-1160. Levi JA, Raghavan D, Harvey V, et al. The importance of bleomycin in combination chemotherapy for good-prognosis germ cell carcinoma. Australasian Germ Cell Trial Group. J Clin Oncol 1993; 11: 1300-1305. Boyer MJ, Cox K, Tattersall MH, et al. Active surveillance after orchiectomy for nonseminomatous testicular germ cell tumors: late relapse may occur. Urology 1997; 50: 588-592. Toner GC, Neerhut GJ, Schwarz MA, et al. The management of testicular cancer in Victoria, 1988-1993. Med J Aust 2001; 174: 328-331. Supramanian R, Smith D, Coates M, Armstrong B. Survival from cancer in New South Wales in 1980 to 1995. Sydney: NSW Cancer Council, 1999. South Australian Cancer Registry. Epidemiology of cancer in South Australia. Adelaide: South Australian Cancer Registry, 2000. Ries LAG, Kosary CL, Hankey BF, et al. SEER cancer statistics review, 1973-1996. Bethesda: National Cancer Institute, 1999. Aass N, Klepp O, Cavallin-Stahl E, et al. Prognostic factors in unselected patients with nonseminomatous metastatic testicular cancer: a multicenter experience. J Clin Oncol 1991; 9: 818-826. Feuer EJ, Frey CM, Brawley OW, et al. After a treatment breakthrough: a comparison of trial and population-based data for advanced testicular cancer. J Clin Oncol 1994; 12: 368-377. Harding MJ, Paul J, Gillis CR, Kaye SB. Management of malignant teratoma: does referral to a specialist unit matter? Lancet 1993; 341: 999-1002. Collette L, Sylvester RJ, Stenning SP, et al. Impact of the treating institution on survival of patients with "poor-prognosis" metastatic nonseminoma. European Organization for Research and Treatment of Cancer Genito-Urinary Tract Cancer Collaborative Group and the Medical Research Council Testicular Cancer Working Party. J Natl Cancer Inst 1999; 91: 839-846. Make a comment

Michael J Boyer · Martin R Stockler

Editorial White coats and the medical profession Time to rediscover the symbol of our purpose and our pride? MJA 2001; 174: 324-325 Ask doctors to nominate the symbols of their profession and many will select the Hippocratic Oath or the serpented staff of Aesculapius. Ask the same question of a person in the street and the stethoscope or the doctor's black bag are common responses. However, the most recognisable symbol of the profession is the white coat.1 Indeed, media portrayal of doctors in Marcus Welby MD or ER showcases the obligatory white coat and dangling stethoscope. Doctors first wore white coats in the late 19th century when science began to make significant inroads into medicine and physicians adopted the laboratory coat as their own.1 Its initial purpose was to protect the patient and physician from cross-contamination, but, as the partnership between science and medicine2 transformed hospitals from institutions for the dying to centres for curing the sick, the white coat became a potent symbol of the authority of science and the art of healing. Superimpose on this metamorphosis Western cultural connotations of whiteness — "life, purity, innocence, superhuman power, goodness — and it is easy to see how the white coat became the favored garment for physicians".1,3 However, as the 20th century advanced, and sociologists turned their attention to medicine4,5 and the dynamics of the patient-doctor relationship, the white coat was seen increasingly as a barrier to effective communication. In an attempt to dispel this perception, paediatricians, psychiatrists and doctors in private practice shed the white coat. Furthermore, the changes in society and healthcare that turned doctors into "healthcare providers" and patients into "clients, consumers or customers" also witnessed the extinction of the white-coated doctor. Today, doctors in our hospitals have become a hidden species, virtually indistinguishable from other hospital personnel or even patients' visitors. But what do Australian patients want doctors to wear? In this issue of the Journal, Harnett explores this question.6 Among patients attending oncology clinics, a clear majority preferred junior doctors to wear white coats "for identification purposes" or because "it looked more professional". For senior doctors, the issue was not as clear-cut, but many of the patients still preferred these doctors to wear white coats. These findings are not surprising. There is now substantive information that adult patients prefer doctors in clinics and hospitals to be traditionally, or at least smartly, dressed;7-12 to wear a necktie;7-9,11,12 to have short hair;8,10,12 and to wear white coats with a name tag.7,8,10-12 Does all this foreshadow a rebirth of doctors in white coats? Probably not. Most of the current information on patients' preferences for doctors' attire is derived from limited cross-sectional surveys. In the current era of evidence-based healthcare, any return of the white coat awaits the outcome of a randomised controlled trial to settle the question: to be or not to be in a white coat! And yet, the practice of medicine involves more than its subservience to evidence or science. It also involves issues such as the meaning of service and feelings of professional pride. In this context, the white coat has become a symbol for the humane face of medicine and its professionalism in the newly discovered white coat ceremonies.13 To date a uniquely North American phenomenon, these ceremonies are performed each year for students entering US medical schools. The students (accompanied by friends and families) are welcomed into the profession by the assembled faculty of the medical school. After an address by an eminent member of the profession, each student is presented with, and helped into, his or her white coat by the dean and other faculty members. This robing ceremony is followed by a public proclamation by the students of their professional commitment akin to the Hippocratic Oath. Inaugurated in 1993 by the Arnold P Gold Foundation, the white coat ceremony had already been adopted by 93 US medical schools some five years later,14 suggesting a groundswell in the search for meaning in service to the community in medicine and in professionalism. The Foundation has identified six components of the ceremony to "help create an environment which fosters a psychological contract for professionalism and empathy in medicine".13 These include The presence of friends and families "representing the support and value system closest to the student"; The welcome by the dean and faculty of the school and its hospitals "representing the value system of the school and the new profession they are about to enter"; An inspiring address by a physician role-model; The personal robing with the white coat through which senior doctors "demonstrate their belief in the student's ability to carry on the noble tradition of doctoring"; A public proclamation by the students of the Hippocratic Oath or a similar declaration representing their "willingness to assume the obligations and responsibilities of the medical profession"; and A reception celebrating the students' new professional status "to reinforce an important and memorable moment". The white coat ceremony is not without its critics who question its appropriateness and perceive a darker symbolism;3 nor are there comparable exercises in Australian medical schools. In these troubled times of uncertainty and confusion in medicine, might not the time be right to rediscover the white coat as a symbol of our purpose and our pride as a profession? Martin B Van Der Weyden Editor Medical Journal of Australia Blumhagen DW. The doctor's white coat. The image of the physician in modern America. Ann Intern Med 1979; 91: 95-119. Weatheral D. Science and the quiet art. Medical research and patient care. Oxford: Oxford University Press. 1995: 55-88. Wear D. On white coats and professional development: the formal and the hidden curricula. Ann Intern Med 1998; 129: 734-737. Annandale E. The sociology of health and medicine. A critical introduction. Cambridge: Polity Press, 1998: 4-32. Freidson E. Profession of medicine. New York: Harper and Rowe, 1970. Harnett PR. Should doctors wear white coats ? Med J Aust 2001; 174: 343-344. Dunn JJ, Lee TH, Percelay JM, et al. Patient and house officer attitudes on physician attire and etiquette. JAMA 1987; 257: 65-68. Gjerdingen DW, Simpson DE, Titus SL. Patients' and physicians' attitudes regarding the physician's professional appearance. Arch Intern Med 1987; 147: 1209-1212. McKinstry B, Wang J-X. Putting on the style: what patients think of the way their doctor dresses. Br J Gen Pract 1991; 41: 275-278. Hennessy N, Harrison DA, Aitkenhead AR. The effect of the anaesthetist's attire on patient attitudes. Anaesthesia 1993; 48: 219-222. Gledhill JA, Warner JP, King M. Psychiatrists and their patients: views on forms of dress and address. Br J Psychiatry 1997; 171: 228-232. Menahem S, Shvartzman P. Is our appearance important to our patients? Fam Pract 1998; 15: 391-397. Gillon R. White coat ceremonies for new medical students. J Med Ethics 2000; 26: 83-84. Branch WT Jr. Deconstructing the white coat. Ann Intern Med 1998; 129: 740-742. Make a comment

Editorial Economy class syndrome A misnomer for a syndrome for which the evidence is, as yet, missing MJA 2001; 174: 264-265 Two unexpected and widely reported deaths from pulmonary embolism (PE) after flights between Australia and the United Kingdom — one of a 28-year-old woman arriving in London, the other a 68-year-old man after landing in Melbourne — have provoked four months of worldwide media interest in air-travel-related PE and deep-vein thrombosis (DVT). News headlines and editorials have reported on its supposed incidence, causes and prevention. Now the Federal Government has launched an enquiry into the risks of long-haul flying. And there is inevitable talk of litigation. Air travellers are rightly concerned to know the level of risk, who is likely to be affected, and what precautions they should take. Answers are, however, constrained by a serious lack of definitive information, as the evidence is limited to case series of DVT or PE discovered during or soon after air travel, and a few case-control studies with limited power and contradictory results. Air travellers are rightly concerned to know the level of risk, who is likely to be affected, and what precautions they should take. Venous thromboembolism (VTE) during or soon after prolonged flight or travel by motor car has been recorded since 19541 and was labelled "economy class syndrome" in 1988 (two of the six cases were authors of that report, and paradoxically, one of the authors with DVT had travelled in business class).2 Case series have come from the Paris airports (Orly and Roissy, where the airport emergency medical service diagnosed PE in 70 incoming passengers during the 24 years to 19983), Heathrow Airport (where 11 of 61 inflight deaths reported to the coroner between 1979 and 1982 were caused by PE4), the island of Martinique (40 cases of flight-related VTE in six years5) and Réunion island (six cases in one year6). Lastly, in the Hawaiian Islands, 17%-25% of patients with VTE admitted to two Honolulu hospitals had a recent history of air travel.7,8 Others have extended this association to prolonged travel by bus, car, truck or train.9 Prolonged travel in a seated position can cause venous stasis, so that an association of VTE with travel would be consistent with Virchow's classic postulate that venous stasis contributes to VTE. However, the present evidence regarding air travel as a cause of VTE is circumstantial and could be misleading. VTE is a common disorder with an annual incidence of about one per 1000 population for DVT and 0.5 per 1000 for PE.10 Its incidence is age-dependent and rises to nearly 1% per annum in the elderly.11 Given the high community prevalence of VTE and exponential growth in worldwide air travel by all age groups, the reports of flight-related VTE from isolated islands and at busy airports could therefore be mere coincidence. Clinical suspicion of VTE is notoriously misleading, so that retrospective reports might be contaminated by diagnostic bias, and recall bias could influence surveys of predisposing air travel. Prospective case-control studies seek to minimise bias and estimate risk by obtaining a history of travel from patients with VTE and also from contemporary age-matched and sex-matched controls. Two recent studies from cities with busy international airports have given opposing results. In Nice, 39 of 160 patients with VTE (24.4%) had travelled during the previous four weeks (nine by plane, 28 by motorcar and two by train), compared with 7.5% of 160 age-matched but not sex-matched controls visiting a cardiology outpatient clinic. In this study, recent travel raised the odds ratio (OR) for VTE to 4.0 (95% confidence interval, 1.9-8.4; P < 0.0001).12 By contrast, when 788 patients with a clinically suspected DVT were interviewed in Amsterdam before diagnostic testing, recent travel was no more prevalent in the 186 patients who had DVT than in the 602 where tests excluded DVT (the OR for DVT after any recent travel, prolonged travel, or air travel was 1.0; 95% CI, 0.3-1.4).13 These case-control studies do not decide the issue, as the control groups were suboptimal12,13 or the study was too small to exclude an important effect of prolonged air travel.13 In the absence of good evidence to the contrary, it is prudent to assume that air travel can provoke VTE, although the absolute risk remains uncertain and is probably quite small in most people. This conclusion derives from the Paris airports emergency medical service report.3 By relating the number of people with PE detected during or immediately after a flight to the total number of arrivals, the report derived an overall incidence of about one PE per 3 000 000 arriving travellers3 ("true" risk is likely to be somewhat higher, as about two-thirds of travel-related VTE presents after patients leave the airport14). The Paris airports report also observed an obviously greater incidence when travel times were longer than 12 hours.3 As 10 of the 11 inflight deaths from PE recorded in the Heathrow report occurred during prolonged flights,4 it is likely that travel duration will prove to be important. It is essential that this still-isolated information is verified and extended with further studies. Advice on prevention is based on assumptions about pathogenesis. In addition to the presumption of venous stasis, there are studies of aircrew or volunteers during prolonged real or simulated flights that suggest dehydration,15,16 stress and climatic change,15 and early activation of the blood-clotting system17 might also contribute. Business and first class passengers are not immune, so more generous seating space is unlikely to be the answer (and "economy class syndrome" is most likely a misnomer). The following general advice has no direct supporting evidence but is common sense, harmless, inexpensive, and likely to be appropriate, particularly for flights longer than 6-8 hours.18,19 These general precautions are directed at preventing venous stasis and include regular foot exercises to activate the plantar and calf muscle pumps, a generous fluid intake, avoiding excessive alcohol (especially when combined with the use of hypnotics), and wearing loose clothing while travelling. Prolonged movement about the cabin during flight is discouraged because this may bring other hazards, including from unexpected clear air turbulence. Travellers with an above-average risk of thrombosis should seek specific medical advice on additional preventive measures before travelling. Case series suggest that people with previous VTE, chronic venous insufficiency, recent surgery, chronic heart and lung disease, cancer, old age and those who are overweight are all at greater than average risk. Oral contraceptives, hormone replacement and inherited thrombophilia (including factor V Leiden) may predispose, but there is no good published evidence for this. Screening for factor V Leiden (activated protein C resistance) is not recommended in this or any other context if there is no personal or family history of VTE, as about 5% of people of European descent have this polymorphism, and most will never develop thrombosis.11 As a generalisation, it usually takes two or three risk factors acting together to provoke VTE,11 and, as this is likely to apply also in travellers, it is people with several concurrent risk factors who are most likely to require specific prophylaxis. Aspirin alone is not likely to be appropriate, as the evidence that aspirin prevents DVT or PE is highly controversial and the plausible level of risk reduction is small.20,21 Prescribing aspirin for all travellers may also cause sufficient excess bleeding to negate any benefit. Graded pressure support stockings to be worn during flight must be carefully fitted: too tight and they become a tourniquet, too loose and they are ineffective. And they are contraindicated in some people with advanced peripheral vascular disease. People at highest risk (including those with previous VTE) should consider self-injecting a low molecular weight heparin before and perhaps for some days after travel. Few people die of PE without some warning from unexpected breathlessness, chest pain, or leg symptoms. Information kits about DVT and PE, predisposing factors and various clinical presentations should therefore be widely distributed to travellers before they leave home. People should know that, although symptoms of VTE may arise during flight, they are more often first noticed some time after landing. More importantly, we need better evidence. If the present media crisis and federal inquiry brings a greater awareness that VTE may develop during or soon after prolonged travel, and if it triggers a productive collaboration of airlines with investigators to measure the real risk and evaluate preventive measures, then it will have served a useful purpose. Alex S Gallus Professor of Haematology and Director of Pathology Services Flinders Medical Centre and Repatriation General Hospital Adelaide, SA Ross I Baker Director, Thrombosis and Haemophilia Service, Royal Perth Hospital and Clinical Senior Lecturer in Medicine, University of Western Australia Perth, WA Homans J. Thrombosis of the deep leg veins due to prolonged sitting. N Engl J Med 1954; 250: 148-149. Cruikshank JM, Gorlin J, Jennett B. Air travel and thrombotic episodes: the economy class syndrome. Lancet 1988; 2: 497-498. Clerel M, Caillard G. Thromboembolic syndrome from prolonged sitting and flights of long duration: experience of the Emergency Medical Service of the Paris Airports. Bull Acad Natl Med 1999; 183: 985-997. Sarvesvaran R. Sudden natural deaths associated with commercial air travel. Med Sci Law 1986; 26: 35-38. Ribier G, Zizka V, Cysique J, et al. Venous thromboembolic complications following air travel. Retrospective study of 40 cases recorded in Martinique. Rev Med Interne 1997; 18: 601-604. Paganin F, Laurent Y, Gaüzere BA, et al. Pulmonary embolism on non-stop flights between France and Reunion Island [letter]. Lancet 1996; 347: 1195-1196. Eklof B, Kistner RL, Masuda EM, et al. Venous thromboembolism in association with prolonged air travel. Dermatol Surg 1996; 22: 637-641. Mercer A, Brown JD. Venous thromboembolism associated with air travel. Aviat Space Environ Med 1998; 69: 154-157. Tardy B, Page Y, Zeni F, et al. Phlebitis following travel. Presse Medicale 1993; 22: 811-814. Van Beek ER, BŸller HR, ten Cate JW. Epidemiology of venous thromboembolism. In: Tooke JE, Lowe GDO, editors. A textbook of vascular medicine. London: Arnold, 1996: 471-488. Rosendaal FR. Venous thrombosis: a multicausal disease. Lancet 1999; 353: 1167-1173. Ferrari E, Chevallier T, Chapelier A, Baudouy M. Travel as a risk factor for venous thromboembolic disease: a case-control study. Chest 1999; 115: 440-444. Kraaijenhagen RA, Haverkamp D, Koopman MMW, et al. Travel and risk of venous thrombosis. Lancet 2000; 356: 1492-1493. Bounameaux H. Thromboembolism and air travel [letter]. Lancet 1988; 2: 797. Carruthers M, Arguelles AE, Mosovich A. Man in transit: biochemical and physiological changes during intercontinental flights. Lancet 1976; 1: 977-981. Simons R, Krol R. Jet lag, pulmonary embolism, and hypoxia. Lancet 1996; 348: 416. Bendz B, Rostrup M, Sevre K, et al. Association between acute hypobaric hypoxia and activation of coagulation in human beings. Lancet 2000; 356: 1657-1658. Kesteven PL. Traveller's thrombosis. Thorax 2000; 55 (Suppl 1): S32-S36. Ferriman A. Travellers should be warned of thrombosis risk. BMJ 2000; 321: 1310. Sors H, Meyer G. Place of aspirin in prophylaxis of venous thromboembolism. Lancet 2000; 355: 1288-1289. Cohen A, Quinlan D. PEP trial [letter]. Lancet 2000; 356: 247. Make a comment

Alex S Gallus · Ross I Baker

Editorial Helping older people to remain in their own homes Community assistance should emphasise preventing and ameliorating disabilty rather than simply compensating for it MJA 2001; 174: 266-267 Australia is ageing rapidly. It is projected that between 1996 and 2016 the general population will increase by 21% or 3.1 million, the number of people over the age of 65 years will increase by 59% or 1.3 million, and those over the age of 80 years will increase by 76% or 368 000.1It is this last statistic which best represents the growing need for services for older people, as people aged over 80 years are disproportionate consumers of the major support systems — 68% of people in nursing homes are aged over 80 years.1 Despite the use of federal targets for residential care based on population ratios and increased funding for home support services, there is pressure on all parts of the aged care system, including residential care.2 What measures can the Australian community initiate to both increase the quality of life for older Australians and decrease the expenditure requirement for the more costly items of care? Over the past 15 years the policy of the State and Federal governments has been to provide services to allow individuals to remain in their own homes for as long as possible. This policy of support for home care has intrinsic appeal and there have been substantial real increases in funding. Federal expenditure on Home and Community Care (HACC) has increased in inflation-adjusted terms from 561 million dollars in 1991-92 to 799 million dollars in 1997-98.1 In addition, the Federal Government spent $2.8 billion dollars, or approximately 0.5% of GDP, on residential care in 1997-98.1 So, if expenditure has grown, why do we have increasing numbers of older people in acute hospital beds awaiting residential care placement, and long waiting times for community care?2 Answers to these questions lie in the interplay of the total health and welfare systems. Over the past 15 years there has been a relative decrease in the number of beds in the nursing home sector and a small increase in hostel beds, which is almost entirely consumed by people who have been assessed as requiring high-level care.2 Also, because the provision of residential care is based on the number of people aged over 70 years, and an increasing proportion of these will be aged over 80 years, there is an expected decrease in the number of beds relative to the number of people who need them the most. More insidiously, State governments have effectively capped their expenditure on assessment and rehabilitation services, as well as opting out of the residential care sector (the public nursing home sector frequently supplied special-needs residential care as well as slow-stream rehabilitation beds). Thus, the availability of assessment, rehabilitation and specialised residential care beds has decreased at a time when it is needed most. It has been suggested that there should be more emphasis on home-based rehabilitation, as a broad range of rehabilitation services in the home can be streamlined and individualised, based on the individual's abilities and condition, and using the family to supplement care.3,4 Rehabilitation attempts to help individuals regain freedom of movement and functional independence, and to reintegrate as fully as possible into community life. Although different settings for individuals will be appropriate at certain stages, the development of community-based rehabilitation by multidisciplinary teams can be effective in promoting the independence of patients and reducing their demand for other community services.5 Home rehabilitation programs can emphasise a task-and-context-oriented approach, educate patients, and apply information in practical situations to solve problems in the home. These programs are usually short-term, providing interventions to individuals who are experiencing or at risk of some degree of functional decline. In this issue of the Journal, Wang and colleagues identify factors that are associated with an increased risk for needing nursing home care in the future.6 With each five-year increase in age there is a doubling of the likelihood of admission to nursing home care. This risk reaches a peak of 35% in the group aged 85 and over. The doubling of risk every five years is similar to the changes in incidence of a number of important conditions known to produce high rates of disability, such as dementia and hip fracture. Although dementia is the commonest condition found in people in residential care,7 cognition was not measured at baseline in the study of Wang et al. However, other disabilities, such as special sensory impairment, arthritis and walking difficulty, were strongly associated with subsequent nursing home admission. As Wang et al point out, these factors are often modifiable, and older people may benefit from community-based rehabilitation programs to improve mobility and independence. Falls may contribute to the need for nursing home admissions, and research has suggested that most are potentially preventable,8 although the effects of intervention are not as dramatic as might be expected.9 Falls-prevention programs with a multi-intervention approach, either clinic-based or through home visits, are effective in meeting the needs of a large number of older people at risk of falls.9 Specific other problems associated with nursing home placement, such as undernutrition and incontinence, are also potentially remediable. Directing further funds to a plethora of HACC agencies providing untargeted maintenance services for some of the personal-care needs of frail older people is unlikely to markedly decrease the need for residential care. Revolutionary changes in either information technology10 or biotechnology11 may produce dramatic benefits, although this can only be speculative at this stage. For now, a focus on targeted assessment and rehabilitation strategies may both give older people a better quality of life and reduce the demand for residential care. An example of this would be providing home-based physiotherapy to an older person who was experiencing decreased mobility and falls, rather than just delivering meals and providing home help. Community rehabilitation teams that work with the acute care sector, HACC services and primary care offer some prospect of improvement in services for older people. R Arthur Criddle Physician, Department of Geriatric Services Sir Charles Gairdner Hospital, Nedlands, WA Leon Flicker Professor, Department of Medicine — Geriatric Medicine University of Western Australia, Royal Perth Hospital, Perth, WA Acknowledgements: The authors would like to thank Caroline Reberger for helpful comments and criticism. Gibson D, Benham C, Racic L, editors. Older Australia at a glance. Canberra: Australian Institute of Health and Welfare, 1999 (Catalogue no. AGE 12). Flicker L. Health care for older people in residential care — who cares? Med J Aust 2000; 173: 77-79. Brocklehurst JC, Morris P, Andrews K, et al. Social effects of stroke. Soc Sci Med 1981; 15: 35-39. Young J. Rehabilitation and older people. BMJ 1996; 313: 677-681. Evans RL, Connis RT, Hendricks RD, Haselkorn JK. Multidisciplinary rehabilitation versus medical care: a meta-analysis. Soc Sci Med 1995; 40: 1699-1706. Wang JJ, Mitchell P, Smith W, et al. Incidence of nursing home placement in a defined community. Med J Aust 2001; 174: 271-275. Rosewarne R, Opie J, Bruce A, et al. Care needs of people with dementia and challenging behaviour living in residential facilities. Canberra: AGPS, 1997. Clemson L, Cumming RG, Roland M. Case-control study of hazards in the home and risk of falls and hip fractures. Age Ageing 1996; 25: 97-101. Gillespie LD, Gillespie WJ, Cumming R, et al. Interventions for preventing falls in the elderly (Cochrane Review). In: The Cochrane Library, Issue 4. Oxford: Update Software, 2000. Celler BG, Lovell NH, Chan DKY. The potential impact of home telecare on clinical practice. Med J Aust 1999; 171: 518-521. Schenk D, Barbour R, Dunn W, et al. Immunization with amyloid-beta attenuates Alzheimer-disease-like pathology in the PDAPP mouse. Nature 1999; 400: 173-177. Make a comment

Leon Flicker

Editorial Changes to the Pharmaceutical Benefits Advisory Committee Any proposed change in the Committee's role should be communicated widely MJA 2001; 174: 209-210 On 31 December 2000, the Pharmaceutical Benefits Advisory Committee (PBAC) and its Economics and Drug Utilisation subcommittees were dissolved under legislation passed precipitately through the Federal Senate. PBAC members, the media and some politicians were surprised by this legislative haste;1,2 such urgency and resolve appeared incongruous for legislation of an apparently routine nature. A review group (including PBAC representatives), convened by the Parliamentary Secretary for Health to review aspects of the Committee's operations, had recommended that PBAC members should come from a broader range of constituencies, and that membership tenure should be limited. To ensure the continued effectiveness of the Committee, they also recommended a transitional phase for implementing the changes. Thus, the legislative amendment appeared innocuous and the principles had been agreed to. ... advisory bodies such as the PBAC need the strong and unambiguous support of government, and a guarantee of independence. The legislation initially proposed clauses setting maximum terms of membership, and making this retrospective. This was a key issue -- it had the effect of making some members ineligible for further membership, including the chairs of the PBAC and its two subcommittees. These amendments were withdrawn after opposition in the Senate. Unexpectedly, the Government used the surviving amendment concerning membership to spill the committees. In the weeks that followed, the Government appointed a pharmaceutical industry lobbyist to the PBAC. So what is going on? Why would a government move against its own advisory committee in this way? Had the committees not been performing their legislated functions satisfactorily? No one has claimed that the committees did not perform adequately. The PBAC received a supportive review by the Australian National Audit Office, and international commentaries have been generally favourable.3-5 A recent independent review, part-funded by the pharmaceutical industry, commented positively on the general approach to the operation of the Pharmaceutical Benefits Scheme (PBS).6 A striking feature of the relationship between the present Government and the PBAC has been the Government's ambiguity. The committee chairs have been informed that the Government is concerned about the rising costs of the PBS ($3.2 billion in the 1999-2000 financial year, a 14% rise over the previous year7), but, at the same time, wishes to support the pharmaceutical industry. The roles of the PBAC are spelled out in the National Health Act 1953 (Cwlth) (amended 1987).8 The principal task of the committee is to make recommendations regarding the listing of new drugs on the PBS. The PBAC is required by law to consider both "the effectiveness and cost of therapy involving the use of the drug"; the committee can not list a pharmaceutical product that is substantially more costly than alternatives unless it provides "a significant improvement in efficacy or reduction of toxicity over the alternative therapy". The current interpretation of the Act by the Federal Court allows a role for the PBAC in considering total costs to the community, including the financial impact of "leakage" (wide prescribing for patients not covered by the listed indications).9 The Act does not provide a mechanism for companies to appeal the substance of PBAC decisions, but they may seek a judicial review of the decision (as in the case brought by Pfizer Pty Ltd when sildenafil [Viagra] was not listed).9 Importantly, the PBAC places no limits on the number of resubmissions that it will consider. The evaluation methodology developed by the committees, with the strong support of the Department of Health and Aged Care, is rigorous in its evidentiary demands, and has withstood both administrative scrutiny and legal challenge.3,9 Why has the Government sent mixed messages to the PBAC? A possible explanation is that it was under pressure from the international pharmaceutical manufacturers lobbying to have their products listed at higher prices on the PBS.10 Perhaps the PBAC is viewed as being too demanding, making recommendations that result in prices that set "undesirable" international precedents? It is difficult to get accurate information on the level of contact between the present Government and the pharmaceutical industry. However, in 1998, a Pharmaceutical Industry Working Group was formed, comprising the ministers of Health and Aged Care, and Industry, Science and Resources, and senior staff from the Australian Pharmaceutical Manufacturers' Association. This group has met regularly and been responsible for initiating reviews of PBAC activities. Worldwide, the pharmaceutical industry has enjoyed a period of unparalleled profitability and influence. It has been among the best performers in the share market. Unlike other products of technology-based industries (eg, computers), the medicinal drug market has become a "sellers' market", with some new products offering only marginal clinical benefits at much higher prices than the agents they replace. It may be difficult for the industry to sustain recent levels of growth in the face of increasingly critical purchasers around the world. Pharmaceutical benefits schemes like the one in Australia are being considered, or have been adopted, in other countries, including Canada, United Kingdom, Netherlands, Italy, Portugal, Sweden, Norway and Finland.12,13 In response, some sections of the pharmaceutical industry have aggressively defended their positions, with tactics that have been widely criticised.14-17 These have included legal challenges and threats to governments, advisory bodies and individuals in Canada, United States, United Kingdom and Australia.9,18-23 In developing countries, the relentless pursuit of intellectual property rights has denied the rights of local manufacturers to produce much-needed drugs.11,15-17,24,25 The health needs of these countries receive scant attention, as companies prefer the more secure business of developing "me too" drugs, fixed combinations of existing agents, or drugs for the "problems" of affluent societies, such as hair loss or obesity.11,14,24,25 It is significant that criticism has come, not from radical sources, but from conservative journals, such as The Wall Street Journal and the New England Journal of Medicine.11,14 These are not judgements on the morals of the individuals who work for the companies, but rather the corporate culture that develops when there is widespread market failure and weak intervention by governments.26 When faced with the lobbying powers of pharmaceutical companies with market values of hundreds of billions of dollars, advisory bodies such as the PBAC need the strong and unambiguous support of government, and a guarantee of independence. The Department of Industry, Science and Resources has a degree of responsibility to support the pharmaceutical industry, but many would consider that the Department of Health and Aged Care does not. The members of the PBAC deserve and need the Health Minister's support, even though their recommendations may sometimes be unpopular with the pharmaceutical industry. But the Government can do even more. The reasons for the PBAC's decisions (positive and negative) should be available to everyone. Information that is truly sensitive, such as manufacturing details, should be protected, but a summary of data forming the clinical and economic case for listing, or not listing, a drug (with the arguments and reasoning behind the PBAC's final recommendation) should be placed on the PBS website.27 Interested parties should be free to criticise these decisions, and the PBAC should be able to respond publicly and, if justified, to modify its recommendations. Presently, such openness is prevented by secrecy provisions in the National Health Act and has been opposed by industry. Where should the medical profession stand on these issues? The PBAC committees' roles and activities need to be better communicated to health professionals and consumers. Doctors should be well represented on the "new" PBAC through nominations from the Colleges, the Australian Medical Association and the Doctors' Reform Society. Doctors, particularly specialists, sometimes lobby the PBAC to have new drugs listed. When unsolicited and motivated by concern for patients such approaches are welcome, particularly if they contain arguments based on evidence and experience. However, some letters appear to have ghost authors; this is inappropriate, particularly if the issue is a dispute over pricing rather than interpretation of clinical data. Some doctors may perceive their responsibility to patients as consistent with a close relationship with industry, for instance through membership of "advisory panels". In reality these roles are often in conflict. In the past decade the medical profession has become enmeshed to an unprecedented extent in the affairs of the drug manufacturers. This was exemplified by the difficulty experienced recently by the New England Journal of Medicine in locating an independent editorialist to comment on a therapeutic trial.28 Perhaps the time has come for a searching review of the ethics of relationships between the medical profession and the health industry in Australia. Perhaps, if the profession develops a different view of its responsibilities to the community, we may read letters from doctors criticising the inordinate prices requested by drug companies, rather than complaining when the PBAC does not accede immediately to their demands for a drug's listing on the PBS. Considering the recent imbroglios accompanying the changes to the PBAC, the Government might wish to more fully inform the medical profession and the community on the reasons for these changes and whether it wants a fundamental change in the Committee's role. David A Henry Past Chair Economics Sub-Committee of the Pharmaceutical Benefits Advisory Committee Professor of Clinical Pharmacology, University of Newcastle, NSW Donald J Birkett Past Chair, Pharmaceutical Benefits Advisory Committee Professor of Clinical Pharmacology Flinders University of South Australia, SA Meddling with drugs [editorial]. The Sydney Morning Herald 2000; 2 Dec. Drugs scheme has its benefits [editorial]. Australian Financial Review 2000; 13 Dec. The Auditor-General Audit Report No. 12, 1997-98: Peformance Audit -- Pharmaceutical Benefits Scheme, Department of Health and Family Services. <http://www.anao.gov.au> (accessed February 2001). Cookson R. ASTEC non-EU case study on Australia. London: LSE Health, London School of Economics, 2000 <http://www.lse.ac.uk/Depts/lse_health/res_ projects/oz.pdf> (accessed February 2001) Witcher SK. In the land down under, a model for national drug insurance. The Wall Street Journal 2000; 6 Sept. M-TAG Pty Ltd. Report on the Australian System of Pharmaceutical Financing and Delivery. Vol 1: Efficiency and equity implications of public versus private funding of pharmaceuticals. Chatswood, NSW: Medical Technology Assessment Group, Nov 1999. PBS expenditure and prescriptions. <www.health.gov.au/haf/docs/ pbbexp/index.htm> (accessed February 2001). National Health Act (1953, amended 1987). <http://www.austlii.edu.au> (accessed February 2001). Pfizer Pty Ltd v Birkett. Federal Court of Australia 20 March 2000. <http://www.fedcourt.gov.au/judgments/judgmts.html> (accessed February 2001). Moynihan R. A dose of drama in debate on drugs. Australian Financial Review 2000; 8 Dec. Angell M. The Pharmaceutical Industry -- to whom is it accountable? N Engl J Med 2000; 342: 1902-1904. Mullins CD, Ogilvie S. Emerging standardization in pharmaco-economics. Clin Ther 1998; 20: 1194-1202. Yamey G. NICE to rule on influenza flu drug zanamivir. BMJ 1999; 319: 937. Harris G. Drug firms, stymied in the lab, become marketing machines. The Wall Street Journal 2000; 6 July. le CarrŽ J. The biggest pushers of all. The Spectator (London) 2000; 16 Dec. Schoofs M. Glaxo attempts to block access to generic AIDS drugs in Ghana. The Wall Street Journal 2000; 1 Dec. Gellman G. A turning point that left millions behind. Washington Post 2000; 28 Dec. Korcok M. Cheap prescription drugs creating new brand of US tourist in Canada, Mexico. CMAJ 2000; 162: 1869-1870. Silverman E. Drug makers on attack in Maine. The Star Ledger (New Jersey) 2000; 24 Sep. Shuchman M. Drug company threatens legal action over Canadian guidelines. BMJ 1999; 319: 1388. Nathan DG, Weatherall DJ. Academia and industry: lessons from the unfortunate events in Toronto. Lancet 1999; 353: 771-772. Rennie D. Thyroid storm. JAMA 1997; 277: 1238-1243. Dyer C. Viagra guidance declared unlawful. BMJ 1999; 318: 1509. McNeil DG. Drug companies and the Third World: a case study in neglect. The New York Times; 2000: 21 May. Silverstein K. Millions for Viagra. Pennies for the poor. The Toronto Star 1999; 13 Aug. Mansfield P. Sickening sales pitch of the drug marketers. The Sydney Morning Herald 2000; 3 July. Department of Health and Aged Care. Pharmaceutical Benefits Branch. <http://www.health.gov.au/haf/docs/pbacrec.htm> (accessed February 2001). Angell M. Is academic medicine for sale? N Engl J Med 2000; 342: 1516-1518.

David A Henry · Donald J Birkett

Editorials Awareness during general anaesthesia: is it worth worrying about? Bispectral index monitoring may be a solution to the problem MJA 2001; 174: 212-213 Patients rightfully expect that they will have no memory of their surgery when it is performed under general anaesthesia. However, the incidence of postoperative recall of intraoperative events ("awareness") is about 1 in 1000 in patients undergoing non-cardiac surgery and greater than 3 in 1000 in cardiac surgical patients.1 As about two million general anaesthetics are performed each year in Australia, about 2000 patients will suffer an episode of awareness. This makes awareness one of the most common serious complications of anaesthesia.1-7Chilling accounts of intraoperative awareness abound in the medical literature and lay press.3,8,9 Patients who have experienced awareness during anaesthesia report the perception of paralysis, conversations, and surgical manipulations, accompanied by feelings of helplessness, fear and pain. While patients usually recognise the event as real, few are willing to report the experience to their anaesthetist for fear of being disbelieved or ridiculed. Post-traumatic stress disorder may develop as a devastating sequel of awareness.9 Why does awareness occur? Anaesthetic requirement is a balance between the amount of anaesthetic administered and the state of arousal of the patient. During any operation, the intensity of stimulation varies markedly, with the most potent noxious stimulus, endotracheal intubation, occurring at the beginning of the procedure. At the same time, the haemodynamic effects of the anaesthetic drugs may limit the amount that can be safely given. Thus, critical imbalances between anaesthetic requirement and delivery may occur. Marked interindividual variation in anaesthetic requirement, the use of muscle relaxants, and lack of a proven monitor for awareness compound the problem. In addition, awareness may occur as a result of anaesthetist error or technical mishaps.10 In an era of sophisticated intraoperative monitoring, it may surprise many non-anaesthetists (and our patients) that we are unable to guarantee loss of consciousness during surgery. A definitive monitor for awareness has been described as the "Holy Grail" of anaesthesia.11 Clinical signs of somatic or autonomic responsiveness have always been the mainstay of anaesthetic depth monitoring, but they lack proven utility in detecting awareness.5 Other techniques (the isolated forearm technique,12 frontalis electromyogram13 and lower-oesophageal contractility14) have similarly been unreliable. Promising technologies such as auditory evoked potential15 and heart-rate variability16 monitoring await wide availability and acceptance into clinical practice. Many attempts have been made to produce a simplified interpretation of the electroencephalograph (EEG) that predicts anaesthetic depth,11 but, in most cases, these were unsatisfactory.17 Recently, sophisticated pattern recognition systems that assess multiple features of the EEG have been developed. One such monitor, the bispectral index (BIS) (Aspect Medical Systems Inc, MA, USA), displays a single number derived from bispectral analysis of the EEG. The BIS ranges from 0 to 100, values below 60 being associated with unconsciousness. It has been shown to be a reliable indicator of level of consciousness18,19 and to improve operating room utilisation and reduce costs (by allowing faster patient turnover and reducing the use of drugs).18 Is BIS monitoring a reliable method of detecting and preventing awareness during anaesthesia? According to Aspect Medical Systems' product information, more than 1.2 million patients have been monitored with BIS and only 41 have reported awareness. Many of those experiencing awareness recorded a BIS value of greater than 65. This low reporting rate either represents an underestimate of the true incidence of awareness or reflects the effectiveness of BIS monitoring in preventing awareness. A suitably designed randomised trial could help to answer this clinically important question,20 although it has been argued that the low incidence of awareness under anaesthesia would necessitate a prohibitively large trial (about 50 000 patients).7,21 However, if a high-risk group could be identified, adequate power could be achieved with a much smaller sample size.20 Obstetric, cardiac and trauma patients are among those who are more likely to report awareness during anaesthesia.2 A study of 2300 patients in this group would be sufficient to reliably detect a decrease in incidence of awareness from 1% to 0.1% resulting from a more effective monitor (a = 0.05; b = 0.2). This large treatment effect is realistic for two reasons: (i) the acceptance of a monitor into routine anaesthetic practice would require a convincing demonstration of benefit; and (ii) the rate of awareness during BIS monitoring is thought to be extremely low. We are currently undertaking such a trial in Australia, New Zealand and Hong Kong (for further details, see our website at <http://www.b-aware-trial.org>). While widespread use of BIS would certainly incur considerable cost for acquisition and ongoing expenses, this should be balanced against the ability of BIS monitoring to improve anaesthetic drug titration (thereby decreasing drug and recovery-room costs18), the potential to prevent costly litigation, and the possibility of reducing the level of patient anxiety about awareness (up to 54% of patients due to undergo surgery are concerned about awareness6). We believe that if a monitor was proven to decrease the incidence of awareness in an appropriately designed and conducted trial, the costs would be justified. Our patients expect nothing less. Kate Leslie Anaesthetist, Royal Melbourne Hospital, Melbourne, VIC Honorary Senior Fellow, Department of Pharmacology, University of Melbourne kate.leslieATmh.org.au Paul S Myles Head of Anaesthesia Research Alfred Hospital, Melbourne, VIC Associate Professor Department of Epidemiology and Preventative Medicine, Monash University Competing interests: Aspect Medical Systems Inc have provided some funding for a multicentre awareness monitoring trial (the B-Aware Trial), designed and independently conducted by us. Dowd M, Cheng D, Karski J, et al. Intraoperative awareness in fast-track cardiac anaesthesia. Anesthesiology 1998; 89: 1068-1073. Liu W, Thorp T, Graham S, et al. Incidence of awareness with recall during general anaesthesia. Anaesthesia 1991; 46: 435-437. Lyons G, Macdonald R. Awareness during Caesarean section. Anaesthesia 1991; 46: 62-64. Ranta S, Ranta V, Aromaa U. The claims for compensation for awareness with recall during general anaesthesia in Finland. Acta Anaesthesiol Scand 1997; 41: 356-359. Phillips A, McLean R, Devitt J, et al. Recall of intraoperative events after general anaesthesia and cardiopulmonary bypass. Can J Anaesth 1993; 40: 922-926. Myles P, Williams D, Hendrata M, et al. Patient satisfaction after anaesthesia and surgery: results of a prospective survey of 10,811 patients. Br J Anaesth 2000; 84: 6-10. Sandin R, Enlund G, Samuelsson P, et al. Awareness during anaesthesia: a prospective case study. Lancet 2000; 355: 707-711. Macleod AD, Maycock E. Awareness during anaesthesia and post traumatic stress disorder. Anaesth Intensive Care 1992; 20: 378-382. Cobcroft M, Forsdick C. Awareness under anaesthesia: the patients' point of view. Anaesth Intensive Care 1993; 21: 837-843. Domino K, Posner K, Caplan R, et al. Awareness during anesthesia: a closed claims analysis. Anesthesiology 1999; 90: 1053-1061. Todd M. EEGs, EEG processing, and the bispectral index. Anesthesiology 1998; 89: 815-817. Bogod D, Orton J, Oh T. Detecting awareness during general anaesthetic caesarian section. Anaesthesia 1990; 45: 279-284. Edmonds HL. Anesthetic adequacy, surface EMG, and quantitated EEG. Acta Anaesthesiol Scand 1993; 37(Suppl 100): 102-104. Raftery S, Enever G, Prys RC. Oesophageal contractility during total i.v. anaesthesia with and without glycopyrronium. Br J Anaesth 1991; 66: 566-571. Thornton C, Konieczko K, Jones JG, et al. Effect of surgical stimulation on the auditory evoked response. Br J Anaesth 1988; 60: 372-378. Sleigh J, Donovan J. Comparison of bispectral index, 95% spectral edge frequency and approximate entropy of the EEG, with changes in heart rate variability during induction of general anaesthesia. Br J Anaesth 1999; 82: 666-671. Sigl JC, Chamoun NG. An introduction to bispectral analysis for the electroencephalogram. J Clin Monit 1994; 10: 392-404. Gan T, Glass P, Windsor A, et al. Bispectral Index monitoring allows faster emergence and improved recovery from propofol, alfentanil, and nitrous oxide anesthesia. Anesthesiology 1997; 87: 808-815. Leslie K, Sessler DI, Schroeder M, et al. Propofol blood concentration and the Bispectral Index predict suppression of learning during propofol/epidural anesthesia in volunteers. Anesth Analg 1995; 81: 1269-1274. Myles P. Why we need large randomized studies in anaesthesia. Br J Anaesth 1999; 83: 833-834. Simini B. Awareness of awareness during general anaesthesia. Lancet 2000; 355: 672-674.

Kate Leslie · Paul S Myles

Editorial The emerging European epidemic of variant Creutzfeldt-Jakob disease and bovine spongiform encephalopathy: lessons for Australia Australia needs to ensure that all reasonably practical precautions for risk minimisation are implemented and communicated to the public MJA 2001; 174: 160-161 Creutzfeldt-Jakob disease (CJD) and kuru are the human disease forms of a spectrum of infectious animal diseases (eg, scrapie in sheep, and bovine spongiform encephalopathy [BSE]) which currently feature on the front pages of most daily newspapers in Europe. In the 1950s, Australia played a pivotal role in describing kuru in Papua New Guinea.1 This devastating illness was caused by transmission of infectivity from human-to-human through cannibalistic mourning rituals involving infected brain tissue. At the peak of the kuru epidemic, more than 5% of the population practising these rituals died each year. The more recent agricultural practice of supplementing ruminant feeds with protein derived from bovine meat and bone meal (a practice differing in no substantial way from cannibalism) has resulted in the bovine-to-bovine cycle of transmission of BSE, a particularly virulent strain of this infectious protein. It is now clear that BSE has crossed the bovine-human species barrier, and that the result is the variant form of CJD (vCJD) in humans.2 The next year or so may be crucial in estimating the likely extent of the epidemic of vCJD in Europe. Last year, the number of new cases in the United Kingdom grew at the disturbing rate of 30%3 (yielding a total of more than 90 cases since the epidemic commenced in 1995), and there were approximately 20 deaths from vCJD. The source of this human pathogen has been convincingly linked to the preceding outbreak of BSE, with transmission occurring orally. Unlike the classical forms of sporadic CJD, the vCJD strain has a propensity for replication in peripheral lymphoreticular tissue. Although the UK outbreak of BSE is now almost under control, the same can not be said for the rest of Europe, where recent evidence suggests that increasing numbers (albeit from a low base) of affected cattle are to be expected in France, Germany, Switzerland, Portugal and the Republic of Ireland (Box).4 As more sensitive biochemical assays become available for the detection of the disease-associated forms of the prion protein (PrPSc), it is likely that subclinical forms of BSE will be detected. Australia's monitoring program includes examination of diseased cattle, but there is as yet no random sampling. Ruminant protein is prohibited from entering the feed of ruminants. In the United Kingdom, the regulatory authorities have taken unprecedented steps to reduce the risks of transmission of BSE from cattle. These include severe restrictions on all feeding of mammalian proteins to ruminants, severe restrictions on specified bovine and ovine offals entering the human food chain, and a ban on cattle over 30 months of age entering the human food chain. Further measures will be introduced to minimise the risks of establishing a reservoir of self-sustaining human-to-human infectivity, including: universal leukodepletion of all blood donations; cessation of use of UK-sourced plasma for the preparation of licensed blood products (eg, coagulation factors, albumin); increased levels of decontamination of surgical instruments, especially those used for neurosurgery and ophthalmic surgery; increased use of disposable surgical instruments, initially for tonsillectomies, but possibly extending to other equipment which comes into direct contact with tissues of known high infectivity (central nervous system, ophthalmic tissues, lymphoreticular system). The Australian responses to this new threat have been cumulative and consistent with measures that have been progressively introduced in other countries that remain BSE-free. Surveillance mechanisms are in place to monitor the occurrence of classical forms of CJD, and to rapidly identify any cases of vCJD which might occur in people in Australia who were exposed to the disease in Europe. This is being achieved through the National CJD Case Registry (based at the Department of Pathology, University of Melbourne, and funded by the Commonwealth Department of Health and Aged Care). The CJD Case Registry also provides a diagnostic service for interpretation of brain tissue samples and a western blot test of the 14-3-3 phosphoprotein, which is present in all nerve cells and released into the extracellular space when the cells degenerate. It is measured in cerebral spinal fluid and has proven utility in the clinical diagnosis of classical forms of CJD.5 The CJD Case Registry is also able to examine tonsil and other lymphoid tissues, which may be biopsied for the diagnosis of vCJD, and to provide genetic tests for mutations and susceptibility for the PrPSc-related gene. Of paramount importance is safety of the Australian blood supply. Concern about the risk of transmitting vCJD through blood and blood products has been rising steadily, culminating with the disclosure of infectivity in the blood of a sheep, which occurred halfway through the incubation period after it had been experimentally infected with BSE.6 Although no case of either classical or variant CJD has yet been linked to contamination of blood or blood product,7 the propensity for PrPSc to accumulate in the lymphoreticular system, coupled with the experimental demonstration of infectivity in blood,8 was sufficient to convince the Australian regulatory authorities to introduce a deferral of donations of blood from people who have lived in the United Kingdom for more than six months between 1980 and 1996. Six months was chosen by US authorities as an arbitrary interval calculated to balance reduction in risk and preserving sufficient blood donors so as not to jeopardise the blood supply. Currently, questions have been raised about extending the donor deferral to residents of other European countries with an emerging BSE problem. The physicochemical inactivation profile of vCJD differs significantly from classical CJD. While in both types of diseases the infectious agent is likely to consist entirely of the PrPSc protein, the differing conformations of the protein may be the reason why the vCJD agent is more resistant to heat inactivation. As further tests on this are carried out, it may become necessary to modify current recommendations for decontamination of surgical instruments. Combining heat (134ºC) with some form of chemical inactivation (1 mol/L NaOH) may prove to be the only effective measure to assure complete sterilisation. These measures are likely to be introduced into the United Kingdom for instruments used at critical sites (brain, eyes, lymphoid tissue), together with increased use of disposable instruments. Australian authorities will need to make an independent assessment of this risk, and then implement appropriate measures. To assist in this process, a National Health and Medical Research Council Expert Committee has been formed, and one of its immediate tasks is an analysis of risk associated with imported European beef products (eg, canned corned beef). Concurrently, the federal Chief Medical Officer has announced that these products have been suspended from importation and are to be removed from the food supply pending an analysis of any BSE-related risk. The risk from non-food items such as cosmetics and pharmaceuticals will be carefully re-evaluated. Another lesson from the past comes from the largest outbreak of scrapie in sheep in the 1940s, which was caused by contamination of a vaccine (for louping-ill virus -- a tick-borne flavivirus causing encephalomyelitis, principally in sheep).9 It would therefore be prudent to monitor carefully the quality of vaccines prepared for both bovine and human use in the event that they might contain trace amounts of the infectious BSE agent. The recent recall in Ireland of a batch of oral poliovirus vaccine, in which human plasma albumin had been sourced from a pool including a donor who subsequently developed vCJD, highlights the sensitivity of this issue.10 Although the risks must have been incalculably small, it is clear that the UK regulatory authorities were not prepared to declare the risk negligible. This situation epitomises the difficulties in risk management when the absolute levels of risk are unknown, and are likely to remain unknown for the foreseeable future. A decade or more from now, we will be able to look back with hindsight and determine whether the correct decisions were made. A judicial inquiry into the BSE epidemic in the United Kingdom has now been through this exercise, and delivered a valuable appraisal of how government, its advisory committees, and the scientific research community conducted the process of risk assessment, management and communication.11 To their credit, veterinary researchers rapidly identified the nature and probable causes of the BSE epidemic within a year of its recognition, and the UK government acted swiftly to break the cycle of bovine-to-bovine transmission. However, serious deficits were identified in the way that government managed the process of assessment, management and communication of the risk to human health. In the 10-year interval between the identification of BSE and the realisation of the emergence of vCJD, the repeated warnings of medical scientific advice were not adequately managed or communicated to the general public.12 The disastrous consequences of these failures (loss of public confidence in the beef industry, heightened suspicion of all matters related to biotechnological manipulation of foods) will resonate for at least the next decade. The most pressing need for Australia right now is to ensure that all reasonably practical precautions for risk minimisation are implemented and adequately communicated to the public. Research into better methods of diagnosis and therapeutic strategies should be encouraged. Vigilant surveillance for all forms of CJD should be continued in the expectation that epidemiological risk factors will be elucidated. Australia, once again geographically remote from the epicentre of a major infectious calamity, may be in a prime position to answer critical questions such as cumulative dose effects and incubation periods within members of its population who have been exposed to BSE. We can learn a great deal from the hard lessons which have been visited upon our European colleagues. Colin L Masters Department of Pathology, University of Melbourne Melbourne, VIC and the Mental Health Research Institute of Victoria c.mastersATunimelb.edu.au Farquhar J, Gajdusek DC, editors. Kuru: early letters and field-notes from the collection of D Carleton Gajdusek. New York: Raven Press, 1981: 338 pp. Will RG, Zeidler M, Stewart GE, et al. Diagnosis of new variant Creutzfeldt-Jakob disease. Ann Neurol 2000; 47: 575-582. Andrews NJ, Farrington CP, Cousens SN, et al. Incidence of variant Creutzfeldt-Jakob disease in the UK. Lancet 2000; 356: 481-482. Donnelly CA. Likely size of the French BSE epidemic. Epidemiological analysis helps in evaluating the potential risks of eating French beef. Nature 2000; 408: 787-788. Zerr I, Pocchiari M, Collins S, et al. Analysis of EEG and CSF 14-3-3 proteins as aids to the diagnosis of Creutzfeldt-Jakob disease. Neurology 2000; 55: 811-815. Houston F, Foster JD, Chong A, et al. Transmission of BSE by blood transfusion in sheep. Lancet 2000; 356: 999-1000. Wilson K, Code C, Ricketts MN. Risk of acquiring Creutzfeldt-Jakob disease from blood transfusions: systematic review of case-control studies. BMJ 2000; 321: 17-19. Kuroda Y, Gibbs J, Amyx HL, Gajdusek DC. Creutzfeldt-Jakob disease in mice: persistent viraemia and preferential replication of virus in low-density lymphocytes. Infect Immun 1983; 41: 154-161. Gordon WS. Advances in veterinary research. Louping-ill, tick-borne fever and scrapie. Vet Rec 1946; 58: 516-520. Birchard K. Concern over vCJD donor in polio-vaccine pool in Ireland. Lancet 2000; 356: 2167. Phillips [Lord], Bridgeman J, Ferguson-Smith M. The BSE Inquiry: report, evidence and supporting papers of the Inquiry into the emergence and identification of bovine spongiform encephalopathy (BSE) and variant Creutzfeldt-Jakob Disease (vCJD) and the action taken in response to it up to 20 March 1996. Vol 1: Findings and conclusions. London: The House of Commons. The Stationery Office, 2000: 308 pp. (HC 887-I.) Aldhous P. Inquiry blames missed warnings for scale of Britain's BSE crisis. Nature 2000; 408: 3-5. Back to text

Colin L Masters

Editorial Iron deficiency in children: food for thought Many Australian children are at risk of iron deficiency and long term neurocognitive impairment MJA 2001; 174: 162-163 Iron deficiency is the most common nutritional deficiency worldwide. Iron depletion and deficiency and, less commonly, iron-deficiency anaemia (defined in the Box) are prevalent in all age groups, but particularly in infants, the elderly and women after the onset of menses, and also in socioeconomically deprived populations, such as refugees and recent migrants. Infancy is the critical period for brain growth, and nutrient deficiencies during this time may affect psychomotor development and neurocognition. Iron-deficient infants are often apathetic, listless, irritable and anorexic. These symptoms resolve rapidly with iron supplementation, but less well known is the fact that long term neurocognitive impairment may persist.1,2 Young children with iron-deficiency anaemia have been found to score 12 to 15 points lower on the Bayley infant development scale than their iron-sufficient peers.3 Prolonged iron supplementation improved these scores and other performance parameters, such as fine motor and discriminative skills, but did not produce complete resolution despite an excellent haematological response.4Persisting deficits in a variety of psychometric tests have also been shown both in five-year-olds in Chile and 10-year-olds in Costa Rica who were iron deficient in infancy,1,5 but there are no convincing data on long term outcome in adult life. In older children with iron deficiency (eg, teenage girls), iron supplementation can also improve neurocognitive performance.6 Therefore, although no studies have established a direct causal relationship between iron deficiency and performance, it is prudent to prevent iron depletion and, if present, to treat it until iron status is normal. Australian paediatricians have long been aware that populations who have recently migrated, such as the Vietnamese, as well as refugees from most of the world's troublespots and Indigenous populations, have a high prevalence of iron deficiency. In this issue of the Journal, Karr and colleagues report on the iron status of a group of Sydney children whose mothers were born in an Arabic-speaking country.7 In this group of 403 children aged 12-38 months, prevalence of iron-deficiency anaemia was 6%, iron deficiency without anaemia 9%, and iron depletion 23%. These levels are disturbing. Similar results have been found among children of South East Asian descent in Adelaide, South Australia.8 Although most children with iron depletion will suffer no long term harm, they should be viewed as part of a continuum, with children with iron-deficiency anaemia at greatest risk of not achieving their full intellectual potential. Most of these children have no other nutritional deficiency and, indeed, are often obese. The risk factors for impaired iron status identified by Karr and colleagues were similar to those seen in other countries, and include prematurity, excessive consumption of cows' milk and recent maternal immigration. However, the mechanisms by which these risk factors contribute to iron depletion are explored only superficially by Karr and colleagues, and no convincing strategies to correct iron depletion were espoused other than provision of Arabic interpreters at early childhood health centres. Some of the reasons the identified risk factors contribute to iron depletion are as follows. Prematurity results in inadequate iron accrual. Cows' milk is deficient in iron and in young infants causes occult microscopic blood loss from the colon. Recent maternal immigration may be linked to poverty, and these children may consume excessive amounts of cows' milk because it is cheap and readily available. Recent immigrant mothers may also have inadequate iron stores, resulting in diminished iron stores in their babies. Once children become iron deficient, they become very restricted in the range of foods they will accept. Appetite and tolerance of new or previously discarded foods improves with iron repletion.9 Furthermore, maternal iron deficiency results in large placental size and small babies whose iron stores are insufficient to sustain them through rapid early growth.10 The currently fashionable "Barker hypothesis" states that health outcomes in later life are programmed by intrauterine events. Infants who are small for gestational age tend to have worse adult outcomes and are more likely to develop insulin resistance and hypertension. Maternal iron deficiency may conceivably result in yet to be recognised consequences in adult life. Medical practitioners should try to ensure that children and women of childbearing age are iron replete. Commonsense dictates that, because of the concern over persisting neurocognitive deficits, it is much better to prevent iron deficiency in the community than to treat it case by case. Although it is tempting to view iron depletion as a problem of disadvantage, many other children are at risk. We therefore recommend that: Young children of high-risk ethnic groups, survivors of prematurity and children with excessive cows' milk consumption or prolonged breast-feeding (breast milk is very low in iron) should have a full blood examination and iron studies, including measurement of ferritin levels. Any developmentally delayed child should be screened for iron status. In addition, children with breath holding may be iron deficient, and breath holding may improve substantially following iron supplementation.11 Iron-depleted children should receive full supplementation of elemental iron at a dose of 6 mg/kg per day for about two to three months, when the iron studies should be repeated. Commercial iron preparations are relatively unpalatable, and it is often difficult to enforce prolonged therapy. Iron absorption is enhanced if supplements are administered with a vitamin C source, such as orange juice. Parents should be warned that bowel motions are often black and that this does not denote ill-health. Dietary advice about iron-rich foods should also be offered. Protocol advice for iron deficiency should be incorporated into the early years program currently being promoted by the Commonwealth Department of Health and Aged Care and the Royal Australasian College of Physicians, which concentrates on optimising intellectual and social outcomes with interventions aimed at infants. Some countries, not including Australia, recommend iron supplementation in infancy. The most effective measure on a global scale to prevent iron deficiency has been fortification of infant formula with iron, and currently all breast-milk substitute formulas in Australia are iron fortified. This intervention is most effective in the first year of life, but does not address the problem of infants who are exclusively breastfed and children with a large intake of cows' milk. All infants should have iron-rich foods, particularly red meat, introduced shortly after six months of age. A dietary program aimed at improving iron status in Australian mothers and children would benefit both individuals and society as a whole. The high incidence of iron-deficiency anaemia in this cohort of Australian children of Arabic background and its known association with persisting neurocognitive deficits should provide Australian health planners with food for thought. Richard T L Couper Senior Paediatric Gastroenterologist University of Adelaide, Women's and Children's Hospital, Adelaide, SA Karen N Simmer Associate Professor and Staff Neonatologist Flinders University and Flinders Medical Centre, Adelaide, SA Lozoff B, Jimenez E, Wolf A. Long-term developmental outcome of infants with iron deficiency. N Engl J Med 1991; 325: 687-694. De Andraca I, Walter T, Castillo M, et al. Iron deficiency anaemia and its effects upon psychological development at preschool age: a longitudinal study. Nestlé Foundation Nutritional Annual Report. Lausanne: Nestlé Foundation, 1990; 53-62. Oski FA, Honig AS. The effects of therapy on the developmental scores of iron deficient infants. J Pediatr 1978; 92: 21-25. Lozoff B, Wolf AW, Jimenez E. Iron deficiency anaemia and infant development: effects of extended oral iron therapy. J Pediatr 1996; 129: 382-385. Lozoff B, Jimenez E, Hagen J, et al. Poorer behavioural and developmental outcome more than 10 years after treatment for iron deficiency in infancy. Pediatrics 2000; 105: ES1. Bruner AB, Joffe A, Duggan AK, et al. Randomized study of cognitive effects of iron supplementation in non-anaemic iron deficient adolescent girls. Lancet 1996; 348: 992-996. Karr MA, Mira M, Alperstein G, et al. Iron deficiency in Australian-born children of Arabic background in central Sydney. Med J Aust 2001; 174: 165-168. Oti-Boateng P, SeshadTi R, Petrick S, Gibson RA, Simmer K. Iron status and dietary iron intake of 6-24 month old children in Adelaide. J Paediatr Child Health 1998; 34: 250-253. Stockman JA. Microcytic anaemias. In: Behram RE, editor. Nelson textbook of paediatrics. 14th ed. Philadelphia: WB Saunders, 1992; 1239-1241. Hindmarsh PC, Geary NIPP, Rodeck CH, et al. Effects of early maternal iron stores on placental weight and structure. Lancet 2000; 356: 719-723. Mocan H, Yildiran A, Orhan F, Erduran E. Breath holding spells in 91 children and response to treatment with iron. Arch Dis Child 1999; 81: 361-362. Definitions of impaired iron statusIron depletion: Low iron stores but no change in haematological parameters. Iron deficiency: Low iron stores and reduced mean cell volume but normal haemoglobin concentration. Iron-deficiency anaemia: Low iron stores, reduced mean cell volume and reduced haemoglobin concentration. Back to text

Karen N Simmer

Editorial Gestational diabetes: universal or selective screening? Gestational diabetes and its outcomes need to be better defined before we can tackle this question MJA 2001; 174: 113-114 Gestational diabetes mellitus (GDM) is defined as carbohydrate intolerance of variable severity with onset or first recognition during pregnancy.1 The first recorded case was described in Berlin in 1823,2 but the term gestational diabetes did not appear in the medical literature until 1961.3 The initial studies in the 1960s developed diagnostic criteria which identified mothers likely to develop type 2 diabetes later in life. However, as late as the mid-1990s, GDM was not widely accepted as a risk factor for type 2 diabetes in Australia. That situation has now changed, and the Federal Government has established a committee to advise on the significance of GDM. This is particularly relevant given that preliminary results from the Australian Diabetes, Obesity and Lifestyle Study indicate that 7.2% of Australians over the age of 25 years have diabetes, with 50% being undiagnosed.4 The individual, societal and healthcare costs of this diabetes epidemic are significant, particularly as many individuals have complications such as retinopathy by the time of diagnosis.5 As intervention in high-risk groups, with advice on diet, exercise and weight control, may delay the onset of type 2 diabetes and its complications,6 any opportunities for such intervention should not be missed. Preliminary results from the Australian Diabetes, Obesity and Lifestyle Study indicate that 7.2% of Australians over the age of 25 years have diabetes The initial diagnostic criteria for GDM were subsequently used to identify risks of complications during the index pregnancy, such as macrosomia and associated birth trauma. Nevertheless, whether these diagnostic criteria can be used for predicting both later diabetes and pregnancy outcome is contentious. These issues will be largely settled by the Hyperglycaemia and Adverse Pregnancy Outcome (HAPO) study, which is now under way. This study, funded by the United States National Institutes of Health, will test 25 000 women in 16 field centres around the world. Two centres are in Australia — at the John Hunter Hospital, Newcastle, and the Mater Mothers' Hospital, Brisbane. Results are expected to become public in June 2004 and, it is hoped, will answer current questions about the association between various levels of glucose intolerance during pregnancy and adverse outcomes. Evidence-based criteria for GDM to prevent or minimise adverse pregnancy outcomes can then be developed. The longer-term outcomes for the baby also need to be remembered, as evidence is accumulating that raised glucose levels in utero are a risk factor for later development of obesity and diabetes.7 Given these considerations, and given that GDM is mostly asymptomatic and that it is not practical to perform glucose tolerance tests on all pregnant women, a systematic screening program is a necessary first step for detecting GDM. This raises three obvious questions: whom to screen, how to screen and when to screen? When to screen? There is general agreement on this issue, as abnormal carbohydrate tolerance is likely to be seen from the beginning of the third trimester. Screening should be carried out between 24 and 28 weeks' gestation, or earlier in women from high-risk ethnic groups or with a previous history of GDM. How to screen? This question remains controversial. The most validated method is plasma glucose measurement one hour after a random 50 g glucose load.1 Many other suggested methods have not gained wide acceptance. Whom to screen? This question is also controversial and is addressed by Davey and Hamblin8 in this issue of the Journal. They investigated 6032 Melbourne women who had undergone universal screening for GDM, concluding that selective screening on the basis of risk factors for GDM is practicable. Selecting out women aged under 25 years who had a body mass index less than 27 kg/m2 and no family history of diabetes, and who did not belong to a high-risk ethnic group (eg, Indigenous Australian, Pacific Islander, Asian or Middle Eastern background), would have missed only two of 313 women diagnosed with GDM (0.6%) and could have avoided up to 17% of screening tests. The concept of selective screening is not new. It has been suggested by both the American Diabetes Association and, in circumstances of limited workforce resources, by the Australasian Diabetes in Pregnancy Society.9Davey and Hamblin point out that their proposed form of selective screening requires rigorous questioning about racial and family history and accurate measurement of weight and height. Whether this would be done in routine clinical practice is questionable. At least their proposal is less onerous than that of Naylor and colleagues, who developed a complicated scheme to exclude women from screening that reduces screening tests by a third, but which most agree is not practical.10 The other important issue is how many women with GDM would be missed by this selective screening. Davey and Hamblin claim only 0.6% of potential cases would be missed. This is at variance with the studies of Moses and colleagues in another Australian population,11 which found that prevalence of GDM in a similar low-risk group of women was 2.8%. Excluding this low-risk group from screening would still leave 80% of women requiring tests, but would miss nearly 10% of all cases of GDM. Both these estimates of the number who would be missed by selective screening are based on current criteria for diagnosis of GDM, which, as indicated earlier, are not based on studies of pregnancy outcome. It is perhaps wise at this time to wait for the development of evidence-based criteria for pregnancy outcome before making further recommendations on screening for GDM. If possible, universal screening should continue for the present. To fail to diagnose this condition denies the opportunity for intervention to improve pregnancy outcome and the long-term health prospects of both the baby and the mother. J Dennis Wilson Clinical Associate Professor Endocrinology Department, Canberra Hospital Canberra, ACT dennis.wilsonATact.gov.au Metzger BE, editor. Proceedings of the Third International Workshop-Conference on Gestational Diabetes Mellitus. Diabetes 1991; 40 Suppl 2: 1-201. Williams JW. The clinical significance of glycosuria in pregnant women. Am J Med Sci 1909; 137: 1-26. O'Sullivan JB. Gestational diabetes. Unsuspected, asymptomatic diabetes in pregnancy. N Engl J Med 1961; 264: 1082-1085. Dunstan D, deCourten M, Welbourn T, et al. The Australian Diabetes, Obesity and Lifestyle study (AUSDIAB) B preliminary results. Abstracts of the Annual Scientific Meeting of the Australian Diabetes Society and Australian Diabetes Educators Association. Cairns, QLD; 2000. Abstr OR601. UK Prospective Diabetes Study V1. Complications in newly diagnosed type 2 diabetic patients and their association with different clinical and biochemical risk factors. Diabetes Res 1990; 13: 1-11. Pan XR, Li GW, Hu YH, et al. Effects of diet and exercise in preventing NIDDM in people with impaired glucose tolerance. The Da Qing IGT and Diabetes Study. Diabetes Care 1997; 20: 537-544. Silverman BL, Metzger BE, Cho CH, Loeb CA. Impaired glucose tolerance in adolescent offspring of diabetes mothers: relationship to fetal hyperinsulinism. Diabetes Care 1995; 18: 611-617. Davey RX, Hamblin PS. Selective versus universal screening for gestational diabetes mellitus: an evaluation of predictive risk factors, Med J Aust 2001; 174: 118-121. Hoffman L, Nolan C, Wilson JD, et al, for the Australasian Diabetes in Pregnancy Society. Gestational diabetes mellitus — management guidelines. Med J Aust 1998; 169: 93-97. Greene MF. Screening for gestational diabetes mellitus [editorial]. N Engl J Med 1997; 337: 1625-1626. Moses RG, Moses J, Davis WS. Gestational diabetes: do lean young Caucasian women need to be tested? Diabetes Care 1998; 21: 1803-1806. Make a comment

Editorial Male infertility: the case for continued research Even with modern assisted-reproduction technologies, clinical assessment and basic research on male infertility are essential MJA 2001; 174: 116-117 In Australia, male infertility affects one man in 20, contributes to half of all infertility problems in relationships, and is the underlying reason for 40% of infertile couples using assisted-reproduction technologies (ARTs). It is a major health problem, placing a heavy psychosocial burden on affected men and their partners and a financial burden on the community. Intracytoplasmic sperm injection (ICSI) has revolutionised infertility practice. Any man with viable sperm found at any point in the genital tract can now father his own children. Erroneously, the media reported this development as signalling that male infertility was "cured". Such pronouncements may result in failure to assess men for infertility and encourage the view that further research on male infertility can be scaled back. We strongly disagree. For all men presenting with an infertility problem, a medical history should be taken, and an examination and appropriate investigations carried out. Accurate diagnosis may prompt alternative, less expensive treatments that do not expose the female partner to the risks associated with ART (such as ovarian hyperstimulation syndrome). For example, infertility related to a pituitary prolactinoma is best managed with a dopamine agonist rather than ICSI. A diagnosis will also satisfy the man's legitimate desire to understand the reason for his infertility. Testicular examination is mandatory: a Prader orchidometer is used for volume estimation and careful palpation is performed. A past history of cryptorchidism is common in infertile men. Moreover, this condition and infertility are primary risk factors for testicular cancer.1 It is also important to detect and treat androgen deficiency, which is more common in infertile men, to improve quality of life and prevent long-term sequelae such as osteoporosis. Erectile dysfunction and infrequent or poorly timed intercourse may be remediable with specific therapy or counselling. Deficiency of pituitary gonadotropins, although rare (occurring in less than 1% of infertile men), must be considered in the diagnostic work-up, as infertility resulting from this condition is amenable to gonadotropin therapy. Of the identifiable causes of male infertility, obstruction is the most common. Obstruction is increasingly managed with ICSI because surgery is either impossible or compares poorly. Examples include bilateral congenital absence of the vas (BCAV), epididymal or ejaculatory duct obstruction, and vasectomy-related infertility (the largest single group). Surgical reversal of vasectomy offers only a 50% prospect of restoring fertility. As men rarely store sperm before vasectomy, couples who are infertile as a result of the procedure now generally opt for ART with testicular or epididymal sperm (particularly since the removal of the Medicare rebate for vas reversal2). Sperm autoimmunity affecting sperm motility, vitality or function is now managed by ICSI rather than immunosuppressive drug therapy. In about 60% of infertile men no cause is found for low sperm counts or inadequate production of sperm with normal motility, morphology and function. Such conditions, collectively termed "seminiferous tubule failure" (STF), include a number of distinct disorders characterised by poor semen quality. Varicoceles are certainly more common in men with STF (25%-35%) than men in the general population (10%-15%), but there is no firm evidence that semen quality or fertility is improved by varicocele removal. In 6%-10% of men with azoospermia or severe oligospermia (ie, sperm densities of <5 million/mL; normal, >20 million/mL), there are microdeletions in the long arm (Yq) of the Y chromosome, suggesting a genetic basis for STF. The Yq11 region includes a number of testis-specific genes and gene families thought to be important in spermatogenesis. The detection of Yq11 deletions provides a definitive diagnosis of STF, and the demonstration that these deletions are passed on to male offspring conceived by ICSI has emphasised the importance of genetic evaluations in men considering the use of ICSI.3,4 In the majority of remaining men with STF, other genetic lesions are likely. An autosomal-recessive pattern of transmission is a possibility in families with a history of involuntary infertility.5 Mutations of the androgen receptor gene (on the X chromosome) may be associated with male infertility and poor spermatogenesis. There are numerous animal models of single-gene defects associated with specific impairment of spermatogenesis, and, although such evidence is lacking in humans, it seems extremely likely that single-gene and polygene defects will be found to be an important cause of infertility. Severely infertile men with STF are known to have an increased incidence of chromosomal aneuploidy (sex-chromosome mosaicism or autosomal translocations).6 These abnormalities may affect the health of offspring conceived with the use of ICSI. Although male karyotyping is routine before ICSI, there is accumulating evidence that, even when karyotype is normal, there is a roughly threefold increased risk of Klinefelter's syndrome and autosomal translocations in the offspring of these men.7 As mutations of the cystic fibrosis gene are the most common cause of BCAV, routine screening of female partners before ICSI is essential to avoid the possibility of cystic fibrosis in offspring.8 Such examples show the added complexities of clinical practice with ICSI and the important role of genetic counselling in the management of couples in which the male partner is infertile. The alleged decline in sperm counts over the past 40 years and differences in sperm counts between geographical regions have led to speculation that environmental factors may adversely affect male reproductive potential. However, Australian data do not support the contention that sperm counts are falling.9 Environmental oestrogens are often cited as male reproductive toxicants, but it is notable that in the large number of males exposed to high levels of diethylstilboestrol during gestation fertility appears unaffected, although there is an increased incidence of epididymal cysts and abnormalities.10 A great deal of research is needed to identify other possible toxic substances — a daunting task when one considers the enormous number of chemicals in industry and the environment. ICSI is a "bypass" procedure, not a treatment — it can help some, but by no means all, infertile men. The ICSI revolution must not distract practitioners (particularly gynaecologists lacking training in clinical andrology) from the appropriate clinical management of male infertility or obscure the need for continued basic and clinical research that may ultimately provide specific treatment or prevention strategies. Robert I McLachlan Principal Research Fellow Prince Henry's Institute of Medical Research David M de Kretser Professor, Monash Institute of Reproduction and Development Australian Centre for Excellence in Male Reproductive Health Monash University, Melbourne, VIC rob.mclachlanATmed.monash.edu.au Moller H, Skakkebaek NE. Risk of testicular cancer in subfertile men: case-control study. BMJ 1999; 318: 559-562. Jequier AM. Vasectomy related infertility: a major and costly medical problem. Hum Reprod 1998; 13: 1757-1759. Krausz C, Quintana-Murci L, McElreavey K. What is the clinical prognostic value of Y chromosome microdeletion analysis? Hum Reprod 2000; 15: 1431-1434. Cram D, Ma K, Bhasin S, et al. Y chromosome analysis of infertile men and their sons conceived through intracytoplasmic sperm injection: vertical transmission of deletions and rarity of de novo deletions. Fertil Steril 2000; 74: 909-915. Lilford R, Jones AM, Bishop DT, et al. Case-control study of whether subfertility in men is familial. BMJ 1994; 309: 570-573. Peschka B, Leygraaf J, Van der Ven K, et al. Type and frequency of chromosome aberrations in 781 couples undergoing intracytoplasmic sperm injection. Hum Reprod 1999; 14: 2257-2263. Bonduelle M, Camus M, De Vos A, et al. Seven years of intracytoplasmic sperm injection and follow-up of 1987 subsequent children. Hum Reprod 1999; 14: 243-264. Lissens W, Mercier B, Tournaye H, et al. Cystic fibrosis and infertility caused by congenital bilateral absence of the vas deferens and related clinical entities. Hum Reprod 1996; 11(Suppl 4): 55-78. Handelsman DJ. Sperm output of healthy men in Australia: magnitude of bias due to self-selected volunteers. Hum Reprod 1997; 12: 2701-2705. Wilcox AJ, Baird DD, Weinberg CR, et al. Fertility in men exposed prenatally to diethylstilbestrol. N Engl J Med 1995; 332: 1411-1416. Make a comment

Editorial Herbal medicines for menopause: do they work and are they safe? Evidence about efficacy and safety of herbal medicines is accumulating MJA 2001; 174: 63-64 Menopause is a natural event, and some women are understandably reticent to take a drug therapy such as hormone replacement therapy (HRT) for a "natural event". Women are also discouraged by the side effects of HRT, particularly the small increased risk of breast cancer associated with long term use.1 Thus, many women use herbal medicines, supplements or dietary changes to try to manage the symptoms of menopause, and some of the "natural alternatives" used include extracts of red clover, soy, black cohosh, dong quai, vitamin supplements (vitamin E in particular), and evening primrose oil. From a medical perspective, the menopause presents two potential problems. First, about a third of women will have significant symptoms, such as severe flushes often associated with insomnia, muscle aches and pains, formication, fatigue, palpitations and mood swings. Second are the long term issues, in particular the prevention and treatment of osteoporosis. Unfortunately, the first symptom of osteoporosis is fracture, and over the past decade medical research has taught us that clinical trials focusing on surrogate endpoints such as bone density are not good enough. The gold standard clinical bone trial measures fractures as the primary endpoint. However, these studies are very expensive (typically around US$500 million), and are well beyond the budget of most herbal or supplement companies. Thus, herbal medicines may have a short term role in managing the symptoms of menopause, rather than treating the long term aspects. For most women the acute symptoms of menopause last 1-3 years and then disappear, although around 10% of women have persistent flushes. Around half will have symptomatic vaginal atrophy requiring topical oestrogens, vaginal moisturisers or lubricants. What is the evidence that these herbal medicines are efficacious and safe? The findings by Davis and colleagues in this issue of the Journal add to the body of knowledge on herbal medicines and menopause.2 Their carefully constructed double-blind randomised placebo-controlled trial, which took great care in designing a placebo, found no evidence of efficacy. Over 12 weeks there was a large placebo effect (of approximately one third) and no significant difference between the placebo and the herbal preparation. The safety of Chinese herbal medicines has come under recent scrutiny. Aristolochia fangchi is a Chinese herb that can cause a progressive form of renal fibrosis and renal failure, and recently it has been reported that 46% of those affected by aristolochia nephropathy also had uroepithelial carcinoma.3 This herb has no therapeutic value, but is sometimes inadvertently replaced for other herbs such as stephania or magnolia. The Therapeutic Goods Administration recently banned aristolochia, but importers of Chinese herbal medicines may not be aware that their product has been contaminated by aristolochia. Clearly, some form of testing needs to be instituted. It is also apparent that some herbal therapies have undesirable hormonal effects. A popular, commercially available combination of eight herbal medicines used to treat prostate disease in the United States was found to have potent oestrogenic activity.4 Finally, some herbals may interact with medical treatments, the best known example being St John's wort, which inhibits monoamine oxidase activity,5 and so can potentiate the effect of pharmacological antidepressants. The efficacy and safety of phytoestrogens was recently reviewed by the North American Menopause Society and the data published as a consensus opinion.6 In essence, it seems that phytoestrogens are largely safe, although safety has not yet been established among particular subgroups of patients (eg, women who have had breast cancer). Basic science studies have shown that these compounds have some effect on the cardiovascular system, improving elasticity and compliance of large vessels and perhaps some effect on the lipoprotein profile; however, the body of evidence at the moment suggests that phytoestrogens have little, if any, beneficial effect on bone metabolism, and, if there is an effect on menopausal symptoms, it is mild and not much greater than that of placebo. In a double-blind randomised controlled trial using dong quai for treating menopausal symptoms,7 no therapeutic effect was found and no oestrogenic effect on the endometrial thickness or on vaginal epithelium was demonstrated. Similarly negative trials are available for evening primrose oil8 and wild yam cream.9 At present, the most promising candidate for an effective herbal medicine for treating menopausal symptoms is an extract of black cohosh, Remifemin (Scinat, Australia), which has been subjected to two clinical trials.10,11 Both trials showed a significant effect on menopausal symptoms compared with a placebo (typically, a 60% to 70% improvement over 12 weeks), with no oestrogenic effect on vaginal epithelium, endocrine hormone levels, or endometrial thickness. Interestingly, in Germany, extract of black cohosh is commonly combined with St John's wort for the treatment of menopausal symptoms. Thus, currently available evidence indicates that most of the herbal products that our patients take for menopausal symptoms are ineffective, and some have serious questions concerning safety. Davis and colleagues are to be congratulated for conducting a quality double-blind randomised trial that adds to our knowledge on herbal medicines and menopause. Doctors should make use of this knowledge base, and be proactive in providing accurate information about both HRT and herbal medicines (Box) to women seeking relief for their menopausal symptoms. John A Eden Associate Professor, Reproductive Endocrinology School of Obstetrics and Gynaecology, Faculty of Medicine University of New South Wales, Sydney, NSW Collaborative group on hormone factors in breast cancer. Breast cancer and hormone replacement therapy: collaborative re-analysis of data from 51 epidemiological studies of 5,705 women with breast cancer and 108,411 women without breast cancer. Lancet 1997; 350: 1047-1059. Davis SR, Briganti EM, Chen RQ, et al. The effects of Chinese medicinal herbs on postmenopausal vasomotor symptoms of Australian women. A randomised controlled trial. Med J Aust 2001; 174: 68-71. Nortier JL, Martinez MCM, Schmeiser HH, et al. Urothelial carcinoma associated with the use of a Chinese herb (Aristolochia fangchi). N Engl J Med 2000; 342: 1686-1692. Di Paola RS, Shang H, Lambert GH, et al. Clinical and biological activity of an estrogenic herbal combination (PC-SPES) in prostate cancer. N Engl J Med 1998; 339: 785-791. Cott JM. In vitro receptor binding and enzyme inhibition by Hypericum perforatum extract. Pharmacopsychiatry 1997; 30 Suppl 2: 108-112. The role of isoflavones in menopausal health: Consensus opinion of the North American Menopause Society. Menopause 2000; 7: 215-229. Hirata JD, Swiersz LM, Zell B, et al. Does Dong Quai have estrogenic effects in postmenopausal women? A double blind placebo controlled trial. Fertil Steril 1997; 68: 981-986. Chenoy R, Hussain S, Tayob Y, et al. Effective oral gamolenic acid from evening primrose oil on menopausal flushing. BMJ 1994; 308: 501-503. Komesaroff PA, Black CVS, Cable V. Effects of wild yam extract on menopausal symptoms and hormonal and biochemical parameters [abstract]. Australasian Menopause Congress, Auckland, October 1998. Eden JA, Mackey R, McFarland K, et al. A pilot study of Remifemin for menopausal symptoms [abstract]. Australasian Menopause Society Congress, October 1997, abstract book: 97. Stoll W. Phytopharmacon influences atrophic vaginal epithelium: double blind study -- cimifuga vs estrogenic substances. Therapeuticon 1987: 1; 23-31. Make a comment Recommendations for advising women about relief of menopausal symptoms Herbal medicines can not be recommended for the prevention or treatment of osteoporosis. Women should be told that commencing HRT for the relief of menopausal symptoms does not necessarily mean that they have to take the treatment for life - many women take HRT for a year or two and can then be safely and easily weaned off the treatment without recurrence of menopausal symptoms. However, some women will need continued HRT to relieve persistent symptoms. Menopausal women who do not take long term HRT should be encouraged to have serial bone mineral density (BMD) assessments. If their BMD becomes low, then HRT, or an alternative therapy (such as alendronate or raloxifene), can be commenced. Women who choose to treat menopausal symptoms with herbal medicines should be encouraged to maintain a good calcium intake (1000-1500mg per day), either in the diet or by supplementation, and to consider having a BMD scan every two years. Some women will require topical oestrogens for vaginal symptoms. Back to text

John A Eden

Editorial "Should we treat leuchæmia in children?" Fifty years ago the first controlled clinical trial of cancer chemotherapy was published MJA 2000; 173: 568-569

Peter J Smith