Editorials

Australia needs a distinctive “rural health” approach that recognises the valuable role played by the “outback” in our economy and our national psyche The year 2002, the "Year of the Outback", is an opportune time to reflect on why rural health matters and why it continues to be important for Australia. It is the culmination of a decade of initiatives and activity by governments, health organisations and communities seeking to address the "problem of rural health". Rural health emerged in the 1990s as an identifiable field of activity focusing on improving the health status and meeting the specific health needs of people living "out back" of metropolitan areas. The key rural health issues are medical workforce supply, including appropriate training and education; transport and access to appropriate services; funding and costs to patients; and the health status of Aboriginal and Torres Strait Islander peoples in particular, which remains a national shame.1 Under strong pressure from the rural electorate and from advocacy bodies such as the National Rural Health Alliance, there has been a positive government response to rural health issues in recent years. This has included a policy framework that coordinates different levels of government;2 support for advocacy groups and rural professional associations; a significant investment in rural and remote academic infrastructure through the university departments of rural health and rural clinical schools;3 and increased funding for regional and Aboriginal health services. As it is too early to fully evaluate the outcomes of Commonwealth investment in rural health, a sustained effort is required. Rural health issues warrant specific and ongoing attention for a number of reasons. Firstly, outback Australia is different from metropolitan Australia. While the defining characteristic of rural health remains its geography (and related issues of access to healthcare services), rural and remote Australia is also sociologically, culturally, economically and spiritually different from metropolitan areas, as well as internally diverse. It is these characteristics that define the health behaviour of its residents, determine their health status and influence the way health and medical care is provided.4 Nowhere is this more evident than in dealing with the healthcare needs of Aboriginal and Torres Strait Islander peoples in rural and remote regions. Secondly, rural health matters because of health differentials between the city and the outback. Nationally, there is a trend towards a higher mortality rate with increasing remoteness, mostly attributable to the higher proportion of Aboriginal and Torres Strait Islander peoples in remote and very remote regions.5 Given the right of all Australians to optimal health and equitable access to health services, the significantly poorer health status of people in outback Australia remains a fundamental concern. Thirdly, improving rural health is integral to rural and regional development in Australia. Currently, outback Australia fares worst in statistical comparisons of the underlying social determinants of health — namely, housing, employment, income level, education, transport, and social security.6 Good health does not result from access to health services alone. Without a comprehensive regional development policy that focuses on a healthy rural economy, many outback communities face a bleak future — a future characterised by continued poor health status of rural dwellers. Complementary local initiatives based on community empowerment will also be required to address specific problems. Lastly, rural health matters because of the valuable lessons to be learned from the many innovative solutions that have arisen in response to the problems of rural health in Australia. The tyranny of distance, the deficit of resources and the passion of a number of dedicated practitioners to cater for the diverse geographical circumstances of non-metropolitan Australia have resulted in many innovative health sector responses, including the Royal Flying Doctor Service, multipurpose and regional health service models, and telemedicine. Nurse practitioners (a concept currently being trialled in several States) have been working effectively in Australia's remote communities for decades. Australia is a world leader in rural health education, particularly medical education.7,8 Implementation of a true primary health care approach has long characterised the way healthcare is practised and delivered in many small outback communities, particularly by Aboriginal community controlled health services.9 In summary, innovation born of both local need and community action is a hallmark of much rural and remote healthcare practice. Strong rural and regional representation in setting national policy is imperative. Moreover, improved coordination between government departments and between different levels of government on issues affecting rural areas is required. Metropolitan-based clinicians, educators, policymakers and those responsible for implementing health programs should at the very least have an awareness of the geographical, economic and cultural diversity of their constituents and patients. We in the medical profession can collectively continue to press for appropriate health infrastructure, improved access to education and economic opportunities for rural and remote communities. The issue of how the "outback" is defined (whether in terms of "rural" or "remote" areas) is likely to be an ongoing debate, if for no other reason than its significance in terms of resource allocation and monitoring of health outcomes. What should not be in dispute, however, is the need for a distinctive "rural health" approach and national recognition of the valuable role in the Australian economy and psyche played by a healthy "outback" in all its diversity.

John Wakerman MTH, FAFPHM, FACRRM · John S Humphreys BA(Hons), DipEd, PhD

Notification of abuse should trigger initiatives to prevent further abuse and ameliorate adverse consequences There has been concern recently in Australia about the sexual abuse of children by those in authority. Clearly, we expect such people to behave better. However, child sexual abuse is much more likely to involve the ordinary people comprising a child's family and their friends. In 1990 the World Health Organization Global Burden of Disease project1 identified 10 risk factors that, if averted, would reduce the burden of disease by a third (eg, malnutrition, poor sanitation, unsafe sex). For the next revision of the risk estimates, the WHO Collaborating Centre at St Vincent's Hospital, Sydney, was asked to prepare a report on the prevalence and impact of child sexual abuse on health status around the world.2 Here, we comment on the situation in Australia. Child sexual abuse can be subdivided into three levels of severity. Non-contact abuse includes sexual solicitation or exposure by an older person; contact abuse involves genital touching or fondling; and penetrative abuse includes oral, anal or vaginal intercourse by an older person. Prospective studies of the prevalence of child sexual abuse are ethically and legally difficult. Thus, all data are from retrospective reports of men and women asked about their experience of unwanted sexual activity before the age of 18 years. However, establishing the validity of retrospective reports is not easy — only a minority of children who have experienced child sexual abuse report it to their parents, and only a minority of these parents report the abuse to the authorities. Furthermore, unreliable recall represents a threat to the validity of the results. However, follow-up studies show that a false-negative rather than a false-positive bias is the rule.3 Methodological factors like the type of sample used and the number of questions asked to ascertain abuse may also compromise the validity of results. Accordingly, for the WHO study, such method factors were statistically controlled for. Seven studies of child sexual abuse have been performed in Australia.4-12 The adjusted prevalence estimate in males was 5.1% and in females 27.5%, which corresponds with rates in comparable countries. The rates for contact plus penetrative abuse were two-thirds of these (ie, 3.6% in males and 17.9% in females). The onset of abuse occurs at a mean age of 10 years, with most starting before age 12. The abuser is a family member in about 40% of cases, and is known to the child in 75% of cases. The abuser is usually male, mean age 32 years. Child sexual abuse is more frequent in families beset by other adversity, and it is difficult to determine the cause of any increased rate of mental disorders in the presence of an aggregation of risk factors. Two reports of a twin study11,12 that was able to control for the effect of family environment showed increased rates of anxiety, and depressive and substance-use disorders in the abused twin. Rates of suicide attempts were also increased in the abused twin. Child development studies in other countries, in which the family environment was measured independently of sexual abuse or mental disorder, have generated similar results.13,14 People who report contact or penetrative abuse in childhood have double the normal rates of mental disorders and suicide attempts. Attributable risk calculations suggest that 11% of depression in women and 3% of depression in men could be attributed to contact or penetrative abuse in childhood. Quite apart from increased rates of mental disorders, children who have experienced sexual abuse continue for years to show significantly more distress and disturbed behaviour.8 A minority of children are able to surmount this type of adversity and remain unaffected. For those who do not the sequelae can be serious, with great societal costs. What can be done? Teachers and doctors are required to report sexual abuse that comes to their notice. However, this system has the potential to encourage a "don't ask, don't know" attitude. At the same time, it does serve notice to abusers that they are at risk of discovery. In some States, criminal record checks required of anyone who works with children have removed any suggestion that child sexual abuse will be tolerated or excused. Conviction of offenders is not simple, even in the minority of cases in which there is clear medical evidence, as, apart from the child, there are usually no witnesses. Nevertheless, the change in the judicial attitude to child sexual abuse is expected to result in a reduction in incidence. Notification of abuse should trigger other initiatives to prevent further abuse and ameliorate any adverse consequences. Firstly, help for the mother/carer to keep the child safe from further abuse, whether achieved by health visitor support, family counselling, or physical relocation of the family; and secondly, treatment for the child to ensure that disturbed and dysfunctional behaviours and the increased risk of mental disorders do not occur. A recent review of controlled studies of treatment for sexually abused children has provided preliminary evidence that the sequelae can be minimised in the short term.15 It is clear, however, that not all abused children benefit and more research is needed. The management of such children should be driven by science and not simply by compassion.

Gavin Andrews · Bronwyn Gould · Justine Corry

Communication overload may well lead to errors, but this is yet to be firmly established Although stories of misunderstandings, ambiguity, amnesia and lack of cooperation abound, there have been few studies of communication between healthcare professionals. Recently, the topic has been given new impetus as communication problems have been identified as a major contributory factor to the occurrence of errors and adverse events.1 In this issue of the Journal, Coiera and colleagues (page 415) report a study of communication in two Australian emergency departments,2 extending earlier work carried out in the United Kingdom.3 The "communication load" was high, occupying about 80% of clinicians' time. As in other studies,4 almost a third of communications were interruptions, and about 10% of the time two or more conversations were occurring simultaneously (multitasking). Synchronous communication (face-to-face or telephone conversations) accounted for almost 90% of communications traffic. The authors argue that the combination of interruptions, multitasking, and sheer volume of information (much of it unwanted or irrelevant) may produce clinical errors by disrupting memory processes. Communication problems may take a number of different forms and it is important to distinguish between them, as both the contribution to error or adverse outcome and the appropriate remedy vary considerably. Communications may simply be omitted, as when a surgeon fails to inform the anaesthetist of a drug being administered, thus not preparing him or her for a fall in blood pressure. A common cause of omitted communication is an excessively deferential and hierarchical workplace social structure. The classic examples derive from copilots being reluctant to inform senior pilots of potentially dangerous situations.5,6 There is evidence that medical hierarchies and attitudes are even more entrenched than those in aviation.7 Communications may be ambiguous in a variety of ways. Semantic ambiguity occurs when the same phrase is correctly sent and received, but assigned different meanings by the parties. For example, in a child with a right forearm fracture of both the ulna and radius and a dislocation of the right elbow, a plan to reduce "both injuries" might refer to the two fractures, or to the forearm injury (taken as a whole) and the dislocation. Phonetic or lexical ambiguity (eg, aortic stenosis confused with atherosclerosis8) underlies the problem of sound-alike or look-alike drugs. And finally, message ambiguity can occur because the channel is noisy and the message received does not match the one transmitted. Emergency departments, in particular, are literally noisy channels, with high levels of ambient noise from patients, staff, telephones, alarms, pagers and equipment. Ironically, the natural response to noise interfering with communication is to speak more loudly, creating a positive-feedback loop and an ever-increasing din. Communication may also become problematic because the sheer volume of information overwhelms short-term memory, causing some of the information to be lost before processing is completed.9 In addition, the incoming information may be distracting, interrupting and disrupting complex procedures and decision-making. When levels of interruption are high, clinicians may react by ignoring pagers and messages, or waiting until they are paged twice before responding, to separate the trivial from the truly urgent, which, paradoxically, increases the volume of communications still further. A particularly interesting insight arising from previous studies by Coiera and colleagues is that, despite their own disinclination to be interrupted, clinicians often initiate communication or request information without any thought of the impact of their request on the other person.3,10 This is a form of suboptimisation, in which trying to increase one's own performance results in a net decrement in performance over the entire organisation. Solutions to communication difficulties are often couched in terms of training — "we must learn to communicate better". In a sense this will always be true, in that, ultimately, most improvements in communication will require a change in human behaviour. However, depending on the nature of the problem, the key intervention may be individual training, or involve technical aids, or be team oriented. Training of individuals might focus on giving precise information according to a standard format and considering the impact of the information on the other person. More thought might also be given to how clinicians could be trained to maintain focus and concentration in the face of multiple demands and a constantly changing environment; Technical aids might be simply the introduction of a white board in the emergency department, cutting down the need for multiple face-to-face interactions; and Team-based interventions might include restrictions on interruptions and face-to-face interactions (when information might be easily available in written form), or restrictions on communication and interruption at certain critical phases of procedures, analogous to the "sterile cockpit" rules prohibiting extraneous conversation during takeoff and landing. Human beings are immersed in a sea of communications for much of their waking life, and are well equipped for interpreting ambiguous messages when using information-rich channels such as face-to-face conversation. While communication overload may well lead to errors, this is yet to be firmly established and further studies of the nature of communication between clinicians may be needed first. It is important to realise that safety in high-risk environments relies heavily on continuous communication and rapid updating of information. The task for researchers is to begin to separate out the irrelevant and ambiguous communication from the necessary, if sometimes burdensome, flow of important information.11 Until this issue is clearer, any interventions to reduce communication overload should be implemented with caution. There is a risk that attempts to reduce the communication burden in healthcare by shifting it to progressively terser, more impoverished channels might inadvertently increase miscommunication, or result in even greater demand for synchronous communication. Coiera rightly points out in another article that the benefits of technical solutions may be limited unless they are well understood and carefully targeted.12 Observational studies of the many factors which affect human performance in complex environments have a long history, going back at least to World War II.7 However, in medicine, with a few notable exceptions,13 such studies have been infrequent. The approach taken by Coiera and colleagues2 to the understanding of error and adverse events is important in that it involves direct observation and study of work and workers "in the wild".14 While many valuable studies of error and adverse events have been conducted from records or other documents, it is clear that the full range of factors involved in the genesis of adverse events15 can never be captured completely by such methods. The fluidity and complexity of the clinical environment16 and the need to appreciate clinicians' decision making and cognitive load require studies in which interviews and verbal protocols are combined with observation or video recordings. These methods are not familiar to medicine, and will require collaboration with psychology and engineering.17 Future studies will also have to tackle the difficult topic of linking the details of communication to the occurrence of error or some more general aspect of clinical performance or outcome.

Charles A Vincent PhD · Robert L Wears MD, MS, FACEP

Neurosurgery is now an effective treatment option for some patients with epilepsy When a seizure disorder persists despite optimum drug therapy and significantly affects quality of life, surgical treatment should be considered. Many patients with severe refractory epilepsy can benefit from appropriate surgery and should be given this option by timely referral and investigation. Extrapolating US studies,1 there are probably several thousand eligible people in Australia. In the past, operations were confined to removal of obvious structural causes of seizure, such as tumours or post-traumatic scars. Over the past 50 years, it has become increasingly apparent that there are many patients with persisting epilepsy who could benefit from surgical resection of foci previously difficult to define. The development of increasingly precise methods of anatomical and functional seizure localisation has expanded this group. The evidence for effectiveness of surgery for epilepsy can be seen by outcome studies comparing patients who have had surgery with patients who have had long-term medical therapy. An important recent Canadian study2 of 80 patients refractory to at least two anticonvulsants who were randomly assigned to either undergo temporal lobe surgery or receive further drug treatment showed clear statistical evidence of the success of surgery. At one year, 58% of patients in the surgical group and 8% in the medical group were free of seizures. It should be noted that four patients had adverse effects of surgery, including one small thalamic infarct, one wound infection, and reduced verbal memory in two cases. One patient in the medical group died. Not all patients with refractory epilepsy can be treated surgically. A prerequisite for successful surgery for epilepsy is the precise definition of a discrete seizure focus involving an area of cortex amenable to safe excision. Psychiatric and social factors must also be taken into account. The sequence of events leading to surgery will usually include a period of video electroencephalography (EEG) to define and localise the seizure syndrome, magnetic resonance imaging (MRI), and localisation of eloquent cortex (ie, functional [speech or motor] cortex) by neuropsychological or functional testing. Intraictal single-photon emission computed tomography (SPECT) scanning of regional blood-flow changes is an extremely useful tool for confirmation of a seizure focus. Where available, positron emission tomography is helpful to correlate abnormal glucose metabolism with areas of anatomical abnormality. Anterior temporal lobectomy with hippocampectomy is the most commonly performed surgical procedure for treating epilepsy (see Box). This is because the procedure has a high rate of cure or significant reduction of seizures in patients with complex partial seizures due to hippocampal sclerosis, the largest group of suitable patients. The long-term result of this operation, performed on appropriately selected patients, is that about 70% of patients will become seizure-free.3 Resection of areas of cortical dysplasia has been performed more frequently in recent years, as this condition can now usually be defined with MRI. Where cortical dysplasia occurs close to motor or language areas of the cortex, surgery is often performed under local anaesthesia so that motor function or speech can be monitored by cortical stimulation, reducing the risks of postoperative paresis or dysphasia. In addition, electrocorticography (EEG recorded directly from the cortex), performed either acutely, during surgery, or electively, after placement of subdural electrodes, can further define the boundary between functional and non-functional cortex. Image-guided surgery linked to MRI has enhanced the accuracy and safety of cortical excision. Hemispherectomy is the most successful form of excisional surgery. This major procedure is occasionally indicated for young patients with developmental or acquired affections of one hemisphere leading to catastrophic and continued seizure patterns, although it constitutes a high-risk procedure. Many of these patients make a good recovery once their seizures are eliminated. Corpus callostomy or vagotomy are palliative procedures that may benefit some patients with severe generalised seizure patterns. The former may also be helpful (although rarely curative) in some patients with atonic seizures or drop attacks. Chronic stimulation of the left vagal nerve via a subcutaneous stimulator linked to electrodes placed in the cervical region is a low-risk, albeit expensive, procedure that reduces seizure frequency in about 50% of patients with otherwise untreatable severe epilepsy. A small group of patients with hypothalamic hamartomas leading to the syndrome of gelastic ("laughing") epilepsy may now be treated successfully surgically using an image-guided technique via the third ventricle.4 Postoperatively, adequate support systems are extremely important. Most patients will require ongoing anticonvulsant treatment for two or more years. Mortality and major morbidity after surgery for epilepsy are nowadays low: mortality is less than 0.5% and hemiparesis and hemianopia occur in less than 2% of cases.5 Devastating memory disorders following temporal lobectomy can be avoided by appropriate patient selection and preoperative neuropsychological testing. For example, verbal memory deficits suggesting a left or dominant hippocampal lesion would contraindicate a right hippocampal resection. Considering the poor long-term prognosis for patients with refractory seizures, appropriate surgery has unequivocal advantages. In addition to the social and psychological benefits to the individual, cost–benefit analysis has demonstrated the advantages of surgical treatment compared with life-long medical management.6 The requirements for input from various specialists and the need for particular investigative techniques means that such patients should be assessed in Comprehensive Epilepsy Centres. Some notable contributions to the development of surgery for epilepsy have come from Australia and New Zealand.7-9 There are many more Australians who could benefit from surgical treatment, and this option should be considered by those caring for patients whose seizures continue to be disabling despite best medical treatment.

Gavin C A Fabinyi FRACS

To avoid confusion, the term "autistic spectrum disorders" should only be used as the collective term for a group of defined disorders Autism is a severe neurodevelopmental disorder associated with considerable personal suffering, parental burden and community cost. In recent reports, the prevalence of autism has varied widely from five to 67 cases per 10 000 children, an increase compared with the 3.5–4.5 cases per 10 000 children reported in the 1970s.1,2 This apparent prevalence increase has raised considerable public concern, particularly as it has been temporally linked to the introduction of the measles–mumps–rubella (MMR) vaccine. However, recent epidemiological investigations found no causal link between autism and the MMR vaccine.3,4 The increase in prevalence might indicate a true increase in incidence, but most of the increase can be accounted for by changes in case-finding methods and diagnostic criteria, and by differences in sample sizes, and the age range and intellectual ability of the populations studied.3 The increase in numbers identified has led to a corresponding increase in demand for services. The predominant international approach to diagnosis used by the ICD-10 classification of mental and behavioural disorders5 and the Diagnostic and statistical manual of mental disorders, 4th edition [DSM-IV],6 groups autistic conditions in the category pervasive developmental disorder (PDD) and specifies criteria for the subtypes autistic disorder, Asperger's disorder and atypical autism (PDD – not otherwise specified [PDD-NOS]) (Box). Recently, some confusion has been introduced, as there is a general move away from the term PDD towards the term autistic spectrum disorder (ASD), which has been used in at least four different ways. 1. To refer to a broader group of conditions sharing a "triad of impairments" in social interaction, verbal and non-verbal communication and imagination. Wing7 introduced the term ASD for this purpose. These conditions include the PDDs, but also disorders of empathy and deficits in attention, motor control and perception.8 The term ASD implies a continuum of disturbance in each of these three domains and has led to empirical studies of the continuum of social reciprocity which has implications for testing the clinical validity of categorical diagnostic subtypes of ASD.9,10 Contemporary genetic studies of autism provide evidence of a broad phenotype of social disability, anxiety, depression and unusual personality traits, and a complex interaction of several genes.11 It is not known whether specific patterns of genetic abnormality or the interaction of other risk factors with a common genetic predisposition operate to produce different developmental outcomes, such as severe language disability. Ultimately, genetic studies will determine the validity of categorical diagnoses. In the meantime, for this broad phenotype construct of ASD to have better research and clinical utility each subtype requires international consensus on the discriminating diagnostic criteria, and reliable methods to measure the continuum of each domain. 2. To describe a continuum of intellectual ability among children with PDD — from normal IQ levels (functioning at a high level) through to severe levels of intellectual disability. Some argue that autism is a single-spectrum condition, with the observed differences resulting from different levels of intellectual ability, and that subtypes (eg, Asperger's disorder) are not empirically justified.12 Other studies have used the criterion of significant delay in language development to differentiate children with autism who function at a high level from those with Asperger's disorder. They have found higher levels of psychopathology in children with Asperger's disorder,13 and significant differences in executive function and motor planning between these two groups.14 3. As a description of symptom severity. For example, the Department of Education and Training in Victoria uses the Childhood Autism Rating Scale15 completed by clinicians to provide a cumulative score on the severity of some autistic symptoms to assist in determining funding for education aides. Applying the concept of severity to a disorder that has multiple diagnostic criteria is problematic. For example, a child with autism might have relatively better developed language skills and only a few untroublesome rituals, but may have severe social withdrawal. Can a concept of overall severity be meaningfully applied to such a child and might it overshadow the recognition of a potentially treatable comorbid condition such as anxiety, depression, or attention deficit hyperactivity symptoms? Children with autism who function at a high level are referred to by some as having mild symptoms,12 even though there is evidence that they are often handicapped by high levels of psychopathology.13 4. As a developmental concept. Autistic spectrum is used to describe how skills, such as language, might improve relatively over time so that some children with autism might move from being less able to being more able.16 Use of the term ASD is likely to persist, but to avoid confusion it should be confined to the collective term for a group of defined disorders. Wing used it to promote access to services otherwise denied to young people with autism functioning at a high level.7 This problem still exists, for example in Victoria. Such children do not meet the criteria for funding for an education aide, even though they have a range of severe social, emotional and behavioural problems. Should the inclusion criteria for services be broadened to include the full range of social, emotional and behavioural needs, or, to contain costs, should they be confined to intellectual ability? Behavioural and educational approaches to treatment have received the best empirical support.17 Therefore, allocation of increased funding to support a flexible range of behavioural, educational and family support programs, based on a comprehensive assessment of the diagnostic and cognitive profile and the emotional and behavioural needs of all young people with a PDD, is likely to prove the most economical use of resources in the long term. Pervasive developmental disorders: broad diagnostic criteria Autistic disorder (DSM-IV) Childhood autism (ICD-10) Asperger's disorder (DSM-IV) Asperger's syndrome (ICD-10) Social interaction disability Social interaction disability (as for autistic disorder) Language delay and communication disability No delay in language Restricted, stereotyped behaviour Restricted stereotyped behaviour (as for autistic disorder) Onset before age 3 No delay in cognitive development (DSM-IV only) Other subtypes: Rett's disorder, childhood disintegrative disorder, atypical autism (PDD-NOS). DSM-IV = Diagnostic and statistical manual of mental disorders, 4th edition.6 ICD-10 = ICD-10 Classification of mental and behavioural disorders.5

Bruce J Tonge MD, FRANZCP

The latest triennial review of maternal deaths showed a rise in the maternal death ratio. Whether this represents a new trend or just a statistical fluctuation remains to be seen. The Report on maternal deaths in Australia, 1994–961 was released in September 2001. It is the eleventh in a series of triennial reports that detail maternal deaths in a case summary format. The principal aim of the Report is to improve the quality and safety of healthcare during pregnancy and the puerperium through the education of obstetric practitioners. The Report defines a "maternal death" as the death of a woman while pregnant or within 42 days of the pregnancy being delivered or terminated, and classifies maternal deaths occurring in Australia into three categories: Direct deaths, resulting from obstetric complications of the pregnant state; Indirect deaths, resulting from pre-existing disease or disease that developed during pregnancy and was not due to obstetric causes, but which may have been aggravated by the physiological effects of pregnancy; and Incidental deaths, due to condition(s) occurring in pregnancy, in cases where the pregnancy is unlikely to have contributed significantly to the death. The current Report documents the first rise in the maternal death ratio in Australia since the 1988–1990 triennium — a rise from 10.9 deaths per 100 000 confinements in 1991–1993 (total number of deaths, 84) to 13.0 deaths per 100 000 confinements in 1994–1996 (total number of deaths, 100). Of particular concern is the finding that the rise in the number of deaths was almost exclusively in the "direct deaths" category (see Box). However, as the rise was non-significant in a statistical sense, we will not know, until the next two triennial maternal death reviews are completed, whether this represents the beginning of a new trend or just a statistical fluctuation in very rare events. Although a high proportion of the direct deaths (22/46 [48%]) involved the presence of avoidable or preventable factors, the lack of uniform assessment of avoidable factors across all States and Territories, and the absence of any single factor that could account for the rise in deaths, suggests the apparent increase in avoidable factors should be interpreted with caution. The disparity between Indigenous and non-Indigenous maternal mortality rates has previously been observed2 and remains an issue of concern. The Indigenous maternal mortality rate did decline, from 41.4 to 34.8 deaths per 100 000 confinements, between the 1991–1993 and 1994–1996 reviews. However, changes in ascertainment of Indigenous status over the past nine triennia make it difficult to determine whether there has been a consistent decline, particularly among direct Indigenous maternal deaths. A number of factors may have contributed to the increase in deaths in the most recent triennium. In other countries,3 improved ascertainment of maternal deaths through the use of multiple data sources, including vital statistics and hospital morbidity collections, has resulted in the identification of more deaths. However, in the latest Australian Report, only three of the 12 deaths identified using additional data sources were direct deaths. The changing risk profile of women becoming pregnant may account for some of the increase in deaths. Many women are delaying child-bearing,4 leading to an older cohort of women being pregnant and at increased risk of maternal death.5 Furthermore, with advances in technology an increasing number of women who previously were unable to have children because of infertility or complex medical problems are now having children. Also to be considered is the largely unevaluated impact on maternal death rates of the implementation of multiple models of delivery of obstetric care as well as the larger structural changes in healthcare delivery. Both require further investigation. Despite recent publicity to the contrary, the rise in maternal deaths does not appear to be attributable to the increasing caesarean section rate. The proportion of maternal deaths associated with caesarean section has remained higher than the proportion of all caesarean births over the past four triennia. However, despite rising caesarean section rates (18.4% of all births in 1991–1993 and 19.4% in 1994–1996), maternal deaths associated with caesarean section, excluding those on recently dead or moribund women, fell from 29.8% of deaths in 1991–1993 to 24.0% in 1994–1996. There are no data causally relating the rising caesearan section rate with the increase in the number of maternal deaths. With a small number of deaths from a range of very different causes, it is difficult to draw meaningful conclusions about the impact of the many factors purported to relate to maternal death in Australia. Furthermore, without the availability of the 1997–1999 and probably the 2000–2002 results, it cannot be determined whether the increase in deaths represents a new trend or merely an aberration. Overall, the risk of maternal death during pregnancy and the puerperium remains small. Although differences in definition and collection procedures make international comparisons difficult, Australia appears to compare well with other developed countries, having a similar adjusted maternal mortality ratio to Canada, and a lower ratio than New Zealand, the United States and the United Kingdom.6 With improved general health status and family planning and increased access to general and specialised healthcare, maternal mortality declined considerably in the 20th century. Nevertheless, life-threatening complications still occur, often unpredictably and relatively more often among Indigenous women. It is therefore important that we closely monitor and review all maternal deaths and develop a surveillance system for severe maternal morbidity to ensure the health and safety of all women during pregnancy and the puerperium. The inclusion of pregnancy tick-boxes on Australian death certificates and the use of a standardised national maternal death reporting form should facilitate more accurate reporting of maternal deaths in the future. Summary of key findings from the Report on maternal deaths in Australia, 1994–961 The 1994–1996 Australian maternal mortality ratio was 13.0 per 100 000 confinements, compared with the 1991–1993 ratio of 10.9 per 100 000 confinements. In the 1994–1996 triennium, there were 100 maternal deaths, of which 46 (46%) were direct deaths, 20 (20%) were indirect deaths and 34 (34%) were incidental in nature. This represented an increase of 19% in the number of deaths compared with the 1991–1993 triennium. The increase in deaths occurred almost exclusively in the direct deaths category: 27 (32%) direct deaths were reported in the 1991–1993 triennium, compared with 46 (46%) direct deaths in 1994–1996. There was an increase in the proportion of direct maternal deaths in which avoidable factors were considered to be possibly or certainly present from 7 (26%) of 27 deaths in 1991–1993 to 22 (48%) of 46 deaths in 1994–1996. The principal causes of direct maternal deaths remained pulmonary embolism (8 deaths [17%]), amniotic fluid embolism (8 deaths [17%]) and pre-eclampsia (6 deaths [13%]). Cardiorespiratory disease was the most common cause of indirect maternal death, with 10 (50%) indirect deaths falling into this category, while the leading causes of incidental death were injuries (16 deaths [47%]), neoplasms (5 deaths [15%]) and cerebrovascular disease (4 deaths [12%]). The Indigenous maternal mortality ratio (34.8 deaths per 100 000 confinements) remains about three times that of the non-Indigenous maternal mortality ratio (10.1 deaths per 100 000 confinements).

William AW Walters FRCOG FRANZCOG PhD · Jane B Ford BA (Hons) PhD · Elizabeth A Sullivan MPH FAFPHM · James F King

For most of the 20th century, Australia's Medical Colleges have played an important role in our healthcare system. The Colleges were founded to maintain and enhance professional standards in medicine's various disciplines. This was achieved through providing opportunities for the continuing medical education of College Fellows, by certifying that aspiring specialists could practise independently, and by encouraging research. The training role of Colleges was progressively developed, with evolution of training curricula, and through involvement in selection of trainees, appointment of supervisors and accreditation of hospitals and other healthcare providers as suitable sites for specialist training. Over the years, the Colleges have attained considerable professional and community respect. This respect has underpinned the freedom that Colleges enjoy and allowed for their participation in the medical profession's regime of self-regulation. However, this respect and standing could rapidly diminish if the Colleges do not jealously guard their independence, while acknowledging their accountability to society. In this, they should be concerned primarily with the knowledge, competence and performance of their Fellows and with ways to assist in the maintenance of these attributes. More recently, Colleges have sought to have the expertise of their Fellows contribute to community debates on the safety and quality of healthcare and broader health policy issues. This has been facilitated, in a number of instances, by the establishment of health policy units such as that of the Royal Australasian College of Physicians, which provides an evidence base for College views. For this expertise to be widely accepted, the Colleges must not be subject to external influences, nor have a major role in protecting their Fellows' financial and narrow professional interests. Our Colleges increasingly recognise that they must be actively involved with the community and other key organisations in the healthcare and educational systems and that their activities should be open to external scrutiny. The acceptance of this move to external scrutiny is demonstrated by the strong support of the Colleges for the Australian Medical Council (AMC) to become the accrediting body for specialist education and professional development programs. Already, trial accreditation of two Colleges (the Royal Australian and New Zealand College of Radiologists and the Royal Australasian College of Surgeons) has demonstrated the rigour and value of the process.1,2 Areas requiring improvement have been identified and the Colleges taking part have to report to the AMC on a regular basis on how these shortcomings are being addressed. Accreditation is helping the Colleges to ensure that they are meeting the expectations of their Fellows, trainees, providers of healthcare and consumers, and that they are publicly accountable. Hopefully, it will ensure that College trainees are not only skilled clinicians but also appreciate the issues associated with the delivery of safe, high-quality care in the Australian healthcare system. AMC accreditation is also providing a transparent pathway for other organisations to seek accreditation for training and professional development programs in competition with those of existing Colleges. No other country has developed such a robust external system of accreditation of specialist education and training, and the process is attracting considerable international interest. Our Colleges are also working closely with the AMC and Medical Boards to establish specialist medical registers in all States and Territories. Among other benefits, these registers will allow the community to more readily identify medical practitioners as recognised specialists. As part of this process, Colleges are contributing to the development of the criteria for regular re-registration and examining how these can reflect the maintenance of professional standards. Rightly, the community expects that all medical practitioners will maintain their competence and behave in a professionally appropriate way. While it may seem appropriate for Colleges to consider complaints that one of their Fellows has failed to meet these standards, Colleges in Australia do not have this role. Medical Boards, but not Colleges, have the statutory authority to investigate complaints against doctors and can give protection to the complainant. The legal position of Colleges in undertaking such investigations is far from certain. The appropriate role of the Colleges in such difficult matters should be to provide independent advice on standards to Medical Boards and other statutory bodies, and to provide assistance to the Board in the re-education and retraining of underperforming Fellows. The traditional discipline base of the Colleges may impede innovative developments in healthcare delivery. Increasingly, there is overlap and close collaboration in clinical activities (such as in radiation oncology and medical oncology) and there is a trend to bring together, in one service unit, physicians and surgeons dealing with the same body system. Strengthening the intercollegiate body (the Committee of Presidents of Medical Colleges), while maintaining individual College autonomy, may well assist this process by promoting multiple College training and professional development programs. This would seem preferable to formation of new Colleges, although the AMC now has a more robust and transparent process for these to be recognised. If Colleges are to continue to command the respect and confidence of the medical profession and society, they must not become financially or otherwise dependent on government or other organisations with a vested interest in their opinions and contributions to public debate. While it is understandable that Colleges, because of their unique expertise, may undertake some contractual work for governments or other organisations to assist in improvements to healthcare, this must be done with great caution. Colleges should ensure they are not influenced by the provider of the funds; furthermore, it would be extremely unwise to build up a significant College bureaucracy or facilities that are dependent on such external funding. Equally, Colleges should be extremely reluctant to become fundholders for government-sponsored training programs or to build up organisations dependent on such funding. Political decisions, as has recently happened with the training program for general practitioners, can place a College in a very difficult position. The threat of removal of such funding and the resulting impact on the financial viability of a College could temper criticism of the policies of government or other organisations. These issues have received considerable attention in North America and Europe. Pellegrino and Relman3 recently argued strongly that a professional organisation such as a Medical College can not become involved in protecting its members' financial welfare or other narrow professional interests: "It would be far better . . . for physicians to promote patients' interests on ethical and medical grounds as members of medical associations than to seek confrontation as union members. In our view, unions and truly professional associations are simply incompatible." These sentiments obviously have parallels in Australia. As the eminent ethicist Sullivan4 points out, true professionalism depends on the moral contract between the professional and society. It is only when the responsibility to patients and to the public interest is held to be paramount that members of the medical profession can expect society to accept self-regulation of the profession and to listen carefully to proffered opinions and advice. Colleges must continue to promote these principles to their Fellows and trainees, and Colleges and their Fellows must demonstrate to society their commitment to them.

Peter D Phelan MD FRACP

We are making progress in our understanding of the hepatitis C virus, but there is still a long way to go The identification of the hepatitis C virus (HCV) in 19891 delineated a disease previously masquerading under the title of "non-A, non-B hepatitis". In the ensuing years, hepatitis C has become a national epidemic, with more than 150 000 Australians known to be infected. It is estimated that an additional 11 000 new infections occurred each year during the 1990s.2 Escalating rates of HCV infection will have enormous consequences, as 10%–15% of people infected have the potential to progress to end-stage liver disease, with all the implications that has for healthcare services in the years ahead.3 Australia has taken many unique steps in its handling of the hepatitis C epidemic. In 1994 and 1997, the National Health and Medical Research Council published two major reports from working parties comprised of specialists, general practitioners and community representatives.4,5 These were seminal in directing approaches to the diagnosis, treatment and management of HCV-infected people and, to a lesser extent, prevention of further spread. Indeed, Australia was the first country to develop a National Strategy for HCV.6,7 NSW Health has held successful Hepatitis C Awareness Weeks in 2000 and, more recently, in 2002, which have increased public awareness of many issues relating to HCV. NSW Health has recently released a Treatment and Care Plan for HCV, which, among other things, emphasises the importance of GPs in the evaluation and management of HCV-infected people.8 The possibility of accrediting appropriately trained GPs to prescribe anti-viral therapy for HCV is also discussed. So, where are we going? The recent report by the Anti-Discrimination Board of NSW on hepatitis-C-related discrimination presents compelling evidence that there is still much to be done if we as a society are to be seen to be dealing caringly and rationally with this disease.9 The report highlights the disturbing reality that most discriminatory actions against people infected with HCV are perpetrated in healthcare settings. The HCV Projections Working Group of the Australian National Council on AIDS, Hepatitis C and Related Diseases, which advises the federal Minister for Health on these diseases, will report later this year on the increasing rate of HCV acquisition, highlighting the imperative of improving our prevention strategies. The rate of infection is increasing, in large part, because an increasing number of young people are choosing to commence injecting drug use. While public messages on safe injecting practices are promoted widely, many young people ignore these messages in their early phase of drug use. The HCV antibody prevalence rate in those injecting for less than three years fell from 22% in 1995 to 13% in 1997,10 but, despite enormous efforts to increase the availability of clean needles to users, the rate has not dropped any further. Treatment availability and efficacy also remain problematic. Australia offers, through the "highly specialised drugs" program, combination therapy with alpha interferon and ribavirin, providing a sustained viral response rate of 40% overall (ie, in 40% of treated patients, HCV RNA remains undetectable by polymerase chain reaction) (patients with HCV genotype 2 or 3 can expect a 60%–70% sustained response rate).11 By limiting treatment to patients with fibrosis on liver biopsy, the Pharmaceutical Benefits Advisory Committee led, rather than followed, a trend to downplay the need for treatment of all patients. This has highlighted the need for management strategies for those not eligible for, or choosing not to have, treatment. Many major centres now offer support services and education programs, allowing individuals to defer treatment, awaiting better options in the future. Progress is being made in providing better services for prison inmates, among whom there is a high prevalence of HCV infection. In the past, access to therapy has been limited, but the appointment of specialists to Corrections Health services and the funding of a health study of the Tasmanian corrections system is changing that. Prevention strategies are harder to implement. Bleach is made available in most prisons, and methadone programs are expanding, but needle/syringe programs are not available. HCV-infected people from non-English-speaking backgrounds have the added problem of a language barrier. Treatment facilities have become increasingly aware of the need to provide special support for these patients. This is particularly needed if antiviral therapy is to be commenced. What needs to be done better? Greater attention must be directed to reducing spread within the most at-risk community, namely our population of injecting drug users. This group remains marginalised for reasons that are easy to explicate but difficult to overcome. Debate must continue on optimal ways to reduce the risk of young people contracting HCV infection. Needle/syringe programs, while unpopular with many people in our society, have the potential to reduce the risk and must be supported by those who are in a position to influence policy. We need to increase public awareness of the improved efficacy of treatments. We also need to direct more effort towards improving the evaluation and assessment of patients by GPs before referral to busy liver clinics, so that only those who are eligible for and wanting treatment are referred. The HCV research effort requires further support from major funding bodies, and relevant groups are pursuing this actively. A greater understanding of the virus, the mechanisms of viral clearance and the immunopathogenesis of the disease is required urgently. Research is under way to develop a vaccine. In summary, we are some of the way there, and making progress, but there is still a long way to go!

Robert G Batey MD FRACP FRCP

Stress is a normal part of everyday life, but it can lead to psychological strain and difficulty coping with life's demands. Although a variety of non-specific symptoms such as headaches, disturbed sleep, depression, anxiety, irritability or substance misuse may result when individuals are stressed, there is generally little evidence that such symptoms are a direct result of particular stressful events. Rather, they are non-specific and can be precipitated by a variety of other causes, including other stressors to which the individual may be exposed. The issue becomes more complex when stress occurs in the occupational arena because of issues of confidentiality and the sometimes competing interests of patients, insurers and employers. In addition, organisational problems related to work stress, such as high absenteeism, high staff turnover, industrial disputes and poor quality control (leading to inferior products and reduced competitiveness for the organisation) may further complicate matters. In this issue of the Journal, the cross-sectional survey of Western Australian general practitioners by Russell and Roach (page 367) attempts to start gathering information on the variety of approaches taken by GPs when faced with symptoms of anxiety which are apparently caused predominantly by occupational stress.1 Obviously, the article has been written in the context of a political agenda in Western Australia, with a desire by some to consider accreditation for general practitioners in managing work-related stress claims. This was clearly opposed by about 70% of respondents to the survey. The findings of Russell and Roach suggest that GPs with experience in the practice of occupational medicine are less likely to recommend time off work. Additionally, those who had knowledge of the specific requirements for lodging a work-related stress claim (which is likely to include those with experience in occupational medicine) were more likely to recommend initiating a claim. Many of the GPs surveyed were concerned about practising medicine in a workers compensation environment, and the implications this has for patient confidentiality. Many also reported reluctance to get involved in the workers compensation system. Some of the reasons for this include a lack of confidence in their knowledge of legislative requirements for opening workers compensation claims and concerns that such an approach has the potential to further compromise their patients' health. In Australia, whether a claim is eligible for compensation is determined by the relevant insuring authority. While some jurisdictions have the option of allowing payment of medical and rehabilitation expenses and reimbursement of salary while claims are being determined, until a claim is accepted no benefits are technically payable, and, if reimbursements have been paid, these may have to be repaid if the claim is subsequently rejected. Thus, incurring treatment expenses while the claim is being determined can have substantial financial complications for an already stressed worker. This is further compounded by the sometimes significant time delays in the determination of some stress claims. For example, in South Australia (which is the only jurisdiction from which I was able to obtain data), 500 claims with stress as the primary cause of injury were lodged in the 1998–99 financial year. It took an average of 77 days to determine whether a claim was compensable or not; 223 claims were initially rejected, but 88 of these were eventually accepted after litigation (H Woznitza, Program Manager – Education, WorkCover Corporation SA, personal communication). There is no reason to expect that this sobering picture is substantially different in other jurisdictions. Obviously, this uncertainty and tardiness cannot assist the mental health of someone who already has a stress-related illness. As Russell and Roach note, guidelines support a therapeutic benefit from early return to work,2 although the evidence for this is scanty. There is some support for the benefits of early return to work in the South Australian data. For claims lodged between July 1996 and 30 June 1998 (see Box ), in cases of occupational stress where there was an early return to work the likelihood of patients requiring long term ongoing support was reduced. However, these data need to be treated with caution because they are not controlled for severity of illness. In contrast, there is good evidence to suggest that people who are injured and claim compensation for the injury have poorer health outcomes than those not involved in the compensation process.3-5 A recent report produced by the Australasian Faculty of Occupational Medicine of the Royal Australasian College of Physicians highlighted the deficiencies in knowledge in this area.5 In particular, research into causes of poor health outcomes for individuals in the compensation system is limited and inconclusive, and not enough is known of the effects of different types of schemes or methods of case management. Not so long ago in the Journal, Cameron outlined some of the technical and ethical problems doctors face when working within the workers compensation system framework.6 Issues of role confusion (gatekeeper versus patient advocate), objectivity in the face of coercion, and patient and insurer mistrust all contribute to many practitioners shying away from workers compensation cases. These concerns were reflected in the issues perceived by the GPs in the survey by Russell and Roach as barriers to effective management of patients with work-related stress.1 So, what messages can be drawn? Given the recognised adverse health outcomes that commonly occur after lodging a compensation claim, and the obvious stress involved in the process, it is not surprising that many general practitioners elected to temporise rather than immediately commence a compensation claim. However, patients have rights under workers compensation legislation to receive benefits for work-related illness and injury. These benefits are more generous than those available under the Medicare system (eg, the payment of treatment from a psychologist is able to be reimbursed through workers compensation). Indeed, claiming benefits from Medicare for a workers compensation injury is specifically precluded. There is also a need for systems that enable treatment to occur with certainty of reimbursement of costs while claims are being determined and disputed. Obviously, practitioners would benefit from increased education and skills, and the proposed Western Australian accreditation system may be one way to assist this process. Increased education and skill sharing of all participants (including consumers and the legal profession) in the compensation system may address some of the concerns about the adversarial system. Another approach may be to change the system itself, particularly by reducing its adversarial nature so that more time and effort is available for patient care. Exploring solutions that recognise "work stress" as a multifactorial problem, often with some of its origins outside the workplace, may be a worthwhile approach. This would necessitate a collaborative approach to managing work-related stress, with all stakeholders contributing their particular skills and perspectives. Finally, confidentiality issues in workers compensation stress claims remain significant barriers in the minds of medical practitioners and their patients. Clearly, there is a need for appropriate research strategies to examine and address these issues systematically to optimise health outcomes in a cost-effective way. Stress claims for which salary reimbursements were received from the South Australian WorkCover Corporation between 1 July 1996 and 30 June 1998* Claims still receiving reimbursement of all or part of salary Time from date of injury to return to work Number of claims 12–15 months from date of injury 24–27 months from date of injury Up to 4 weeks 81 16 (20%) 11 (14%) 4 weeks to 3 months 87 23 (26%) 14 (16%) 3–15 months 90 36 (40%) 24 (27%) * H Woznitza, Program Manager – Education, WorkCover Corporation SA, personal communication.

Ian D Steven MB BS, MD, MPH, FRACGP, FAFPHM · E Michael Shanahan BM BS, MPH, FAFOM, FRACP

To fill this important gap in our knowledge would require collaboration between researchers from the manipulation disciplines and neurologists Manipulation of the spine is a popular treatment which is used frequently by chiropractors. In the past 25 years, its use has been evaluated by increasingly sophisticated randomised trials. In a recent review of the emergence of the chiropractic profession from "alternative" to more "mainstream",1 the results of 20 randomised controlled trials of cervical manipulation (for migraine and tension headache, cervicogenic headache or neck pain) were described: 11 were positive, and nine equivocal. Given this supporting evidence, as well as the frequency of use of manipulation2 and the health and social impact of the conditions treated, it is important to consider any suggestions that manipulation may do more harm than good with some care. In this issue of the Journal, Ernst (page 376)3 reviews case reports of serious adverse events associated with cervical spine manipulation. Although Ernst acknowledges the considerable doubt about a causal relationship between the manipulation and the adverse event, he is inconsistent in suggesting that the anecdotal and uncontrolled evidence of the case reports favours the adverse events, often strokes, being an effect of manipulation. Elucidating a causal relationship calls for greater clarity, less ambivalence and generally better science in the present evidence-based climate. Thus, the important question to be answered in the light of Ernst's article is whether the association between neck manipulation and stroke is actually causal and, if so, in what direction? The incidence of cerebrovascular accidents after neck manipulation has been estimated by various authors to range from 1 in 400 000 to between 3 and 6 per 10 million manipulations.1 Ernst's article suggests that the mechanism of the strokes associated with neck manipulation tends to be dissection of the vertebral or carotid arteries, an observation also made by others.4 However, dissection is not the only mechanism proposed in Ernst's review. Of the 42 cases tabulated, 20 were not attributed to dissection (although only two such cases appear to have been confirmed by angiography). Of these 20, nine seem to be either intracranial events or lesions such as cervical canal stenosis, intradural mass or cervical disc hernias, which are more likely to have been pre-existing conditions. Strokes following manipulation could also be linked to other pre-existing conditions, such as vasospasm, or kinking of the vertebral arteries and thrombus without dissection.5 Smith and Estridge, reporting two cases of stroke after manipulation, suggested that smaller forces than those used in neck manipulation may be all that is required to precipitate stroke in the presence of such pre-existing lesions.5 They proposed that some premanipulation testing of the neck in rotation and extension might warn of the presence of such lesions. However, a recent review of the literature6 and a study of patients with positive premanipulation tests7 failed to demonstrate such a link. In favour of neck manipulation causing stroke is the fact that it is a mechanical intervention. Particularly if a dissection were already in progress, a mechanical intervention might accelerate it. However, an argument can also be made that the dissection, before manifesting itself as a stroke, causes head or neck symptoms requiring treatment from a chiropractor, osteopath or other manipulation practitioner. The ensuing stroke could be the natural progression of the condition regardless of the manipulation. This hypothesis is further supported by recent evidence that the strain to the vertebral artery conferred by a high-velocity neck manipulation is almost an order of magnitude lower than that required to mechanically disrupt it.8 Both hypotheses are reasonable, but bring us no closer to answering the question of whether or not it is more likely that a stroke will follow neck manipulation than occur without manipulation, and, if it is more likely to occur after manipulation, which subgroups of patients are susceptible. If practitioners of manipulation are precipitating certain types of strokes then they must be made aware of how to recognise these. If, on the other hand, they are mere bystanders in an ongoing process, this also needs to be established. Either way, they may have an important role to play in detection. There are no high-quality data available to provide the denominator to enable us to calculate either the risk or the odds ratios of stroke following manipulation and to thereby assess causation. To fill this important gap in our knowledge would require collaboration between researchers from the manipulation disciplines and neurologists. Community-based studies could examine exposed and unexposed groups who have or have not been affected by strokes or transient ischaemic attacks. A stroke registry employing rigorous case-ascertainment methods could support this. Considerable care would be needed in selecting controls, matching for stroke risk as well as age and sex. Exposure data would need to be detailed for both cases and controls, including an account of the intervention itself. Careful consideration would need to be given to whether to examine the relationship between manipulation and all strokes, or limit studies to vertebral and carotid artery dissections in younger patients only. The latter subgroup approach would help to provide the statistical power needed to draw conclusions, but the case for dispensing with a more global approach would need to be made carefully. The increased use of spinal manipulation for its demonstrated benefits in healthcare means that, in the future, even without any causal link to stroke, more of the strokes that do occur will follow manipulation, just as they follow other common events. Given the expectation that has been generated, this is likely to increase public alarm unless this logical fallacy is appreciated and manipulation professionals come to be regarded as responsible partners instead of pariahs.

Alan Breen DC, PhD

The impact of stroke remains considerable, despite a modest decline in case fatality1 and an encouraging reduction in incidence on the west coast of Australia during the past decade.2 To the optimists among us, it appears that some efforts, particularly in public health and primary care, are paying off. However, population risk-factor surveys indicate that, although the prevalence of smoking has declined, the prevalences of hypertension and hypercholesterolaemia have changed minimally and the prevalences of obesity and diabetes have increased dramatically over the past decade.1,3 The role of the general practitioner is pivotal in identifying and managing these risk factors. The Avoid Stroke as Soon as Possible (ASAP) general practice stroke audit, published in this issue of the Journal (page 312),4 provides further evidence that modifiable risk factors for stroke and vascular disease are highly prevalent in the Australian community. Importantly, the ASAP audit has measured the prevalence of atrial fibrillation and transient ischaemic attack (TIA). These factors are unique to stroke pathophysiology and are associated with high absolute risk, but have received limited attention in previous risk-factor surveys. Sturm et al reviewed 16 148 general practice consultations surveyed from a random sample of 321 GPs across five States. Seventy per cent of patients aged 30 years or more had at least one major risk factor; 34% had two or more. Not surprisingly, hypertension (44%) and hypercholesterolaemia (43%) were the most prevalent modifiable factors. Importantly, the proportion of older patients at high absolute risk was considerable. For example, among the men, 14% aged 70–79 years and 16% aged over 80 years had atrial fibrillation. Reliable measurement of the occurrence of TIA is more difficult given the variability in presentation and clinical assessments. However, the figure of 4% for any history of TIA is valuable information and provides a baseline for further assessments. The high prevalence of vascular risk factors identified in the ASAP survey highlights the potential value of screening during all routine general practice consultations to identify individuals with high absolute risk of stroke. The use of absolute-risk estimates in guiding therapeutic decision making is a well-established paradigm and is being adopted increasingly often in national and international vascular disease management guidelines.5 The value of risk stratification is highlighted by the exercise of choosing the most appropriate antithrombotic agent for primary stroke prevention in atrial fibrillation. Although the risk of first stroke in atrial fibrillation averages 5% per year, risk varies from 1% or less per year up to 12%, depending on additional clinical characteristics.6 At 1% risk, any benefit from anticoagulation therapy would be nullified by the approximately 1% risk of major bleeding events. Antiplatelet therapy would be the more appropriate option in this setting. In contrast, at 12%, the reduction in risk of thromboembolic events achieved with anticoagulation far outweighs the risk of adverse bleeding events. In this setting, warfarin shows a clear net benefit and would be more appropriate. Absolute risk translates readily into clinically useful statistics, such as "number needed to treat" at the bedside, and, at the population level, the recently proposed "population impact number".7 At a practical level, however, owing to the complexity of interacting risk factors, risk stratification typically requires decision-assistance charts or computer programs (generally based on Framingham risk estimates).8,9 At present, such systems are still under evaluation or just beginning to be adopted in general practice. From the cost–benefit perspective, in the absence of a framework for risk stratification, identifying relatively low-risk populations with isolated risk factors increases the possibility that expensive drug therapies will be used as first-line options when low-cost, non-pharmacological interventions would be more appropriate. An example is a 58-year-old woman with moderate hypertension (repeated blood pressure readings 160/95 mmHg) and no other risk factors. Her absolute risk of stroke is 1.5% over five years.10 Although she is a potential candidate for antihypertensive drug therapy, the low absolute risk may suggest to the patient there is questionable value in complying with prolonged drug therapy with its attendant side-effects. It indicates to the clinician that the number needed to treat over five years in this type of patient exceeds 120 to prevent one stroke.11 Accepting the various difficulties and risks associated with screening in general practice, combining a "high risk" approach and an appropriately organised "mass" approach is likely to have a much greater impact on the overall burden of vascular disease. This combination helps minimise the problem of focusing efforts on very cost-effective treatment of small populations at high risk while ignoring the larger subgroup of the population at moderate risk, from where most vascular events emerge. Low-risk groups would also benefit from further surveillance for progression into higher-risk categories. The ASAP stroke audit provides further evidence that considerable opportunity exists to reduce the burden of stroke and other vascular diseases. Quite rightly, the authors emphasise the importance of making the most of this opportunity. However, a prerequisite for success is a framework to facilitate rational use of interventions, balancing absolute risk and potential benefit at both the individual and population levels. Although debate continues about the best decision-assistance tool to be used, any system will need to be simple and practical to use within the time and resource constraints of an already overburdened primary healthcare sector.

Christopher R Levi FRACP · Parker J Magin FRACGP · Balakrishnan R Nair FRCP, FRACP

The ascendancy of evidence-based medicine over the last decade has fostered an unprecedented growth in practice guidelines.1-3 Departments of health and associated agencies, specialty societies and other medical organisations have all embraced the development of guidelines in the belief that adherence to their recommendations translates into benefits for patients (improved outcomes), practitioners (improved quality of care), and providers (improved cost-effectiveness).4 As the practice guideline movement has matured, the interest and debate surrounding guideline developments has shifted from the what to the how.5 In fact, the National Health and Medical Research Council's Guidelines for the development and implementation of clinical practice guidelines, published in 1995,6 was a pacesetter in the how of guidelines, and at its core are the three criteria that underpin the quality of guidelines: a balance of healthcare disciplines in the guideline development group, together with consumer representation; a systematic review of relevant literature and its stratification of the data according to a hierarchy of levels of evidence; and the generation of evidence-graded recommendations that also take into account the generalisability of the evidence, its practice relevance and resource implications. Despite the availability of guidelines for developing guidelines,6,7 recent reviews of practice guidelines have shown that most fail to meet quality standards.1-3 This is hardly surprising, as guideline development is an intensive, laborious and at times uncertain task.8 In essence, it is a human affair with all its attendant nuances, complexities and biases. These human elements are illustrated in this issue of the Journal by Edmonds and colleagues (page 332)9 in their account of the workings of the Australian COX-2-Specific Inhibitor Prescribing Group. The outcome of its deliberations is also published in this issue of the Journal (page 328).10 The process pursued by the Prescribing Group followed the essentials outlined in the guidelines for guidelines.6,7 The working party was multidisciplinary, but with a difference! It had a high proportion of academics and clinicians with connections with the pharmaceutical industry, together with an undeniable first — representatives from the pharmaceutical companies involved in marketing COX-2 inhibitors. Initially, the group was embroiled in a debate on conflict of interest and its impact on the credibility of the outcomes, but this was only the beginning. A clash of minds in the interpretation of evidence led to resignations from the group, as did irreconcilable differences with its ultimate recommendations. This story suggests that the debate in guideline development should now shift even further from the how to the who . The major issues arising from the Australian COX-2-Specific Inhibitor Prescribing Group's deliberations involve aspects of conflicts of interest and the management of differing interpretations of evidence. The definition of conflict of interest is complex, but a pragmatic description is "conflicts of interests comprise those which may not be fully apparent and which may influence judgment of authors reviewers or editors. They have been described as those which, revealed later, would make a reasonable reader feel misled or deceived".11 In contrast to the recent emphasis in disclosure of conflict of interest in scientific and medical publishing, it appears that this dsclosure has a low profile in practice guidelines. In two extensive surveys on quality in more than 700 practice guidelines, a statement of conflict of interest was not among the standards surveyed.1,2 Further, in a recent survey exploring the relationships between authors of clinical practice guidelines and the pharmaceutical industry,3 financial support for authors by pharmaceutical companies was declared in only two of the 44 guidelines surveyed, and industry financial support for the creation of the guideline was reported in only 20. Relationships with the pharmaceutical industry are widely accepted as being a potent catalyst for the potentiality of conflict of interest.12 But the time has come to explore conflicts in relationships with health departments, other government agencies, various healthcare providers and specialty organisations. Full and candid disclosure of conflict, as pursued by Edmonds and colleagues and as advocated by others (Box), is the only solution. One inherent assumption of evidence-based medicine is that differences and controversies stemming from interpretation of data are inversely related to the quality of evidence. However, if the experience of the Australian COX-2-Specific Inhibitor Prescribing Group is anything to go by, this assumption would appear to be optimistic, as at the end of the exercise eight members of the group had resigned, essentially because of differing mindsets. The Journal has long encouraged authors of practice guidelines to cite the level of evidence underpinning recommendations. What remains intriguingly unknown is the range of levels of agreement on the evidence. The account by Edmonds and colleagues is a refreshing and welcome exposition of the "real world" of guidelines development. Its central message is that practice guideline development is not a black-and-white affair, and that the time has come for open disclosure of conflicts of interest and the degrees of consensus or dissent. As guidelines have a powerful influence on clinical practice, doctors and their patients deserve nothing less than complete openness and transparency. Recommendations for managing conflict of interests in practice guidelines development3 A formal process should exist to disclose potential conflict of interest before the guideline development begins. All members of the guideline group should be involved in a discussion of conflicts of interest and how significant relationships will be managed. Participants who have relationships with industry, government agencies , healthcare organisations or specialty societies need not necessarily be excluded, but the group has to decide among itself a threshold for exclusion. There must be complete disclosure to readers of the practice guidelines of financial and/or other relationships with industry, government agencies, healthcare organisations and specialty societies.

Martin B Van Der Weyden MD, FRACP, FRCPA

The widespread application of public iodine supplementation programs, which cover about 3–4 billion people worldwide,1,2 is a response to the paucity of iodine in the natural diet in many regions of the world and the severe public health consequences of iodine deficiency.3 However, in some countries, the tendency to low iodine intake has mostly been corrected by haphazard increases in the iodine content of certain parts of the diet.4 In the United Kingdom, dairy products may contain extra iodine as a result of adding iodine to cow feed to increase the animals' reproductive performance or of using iodine-containing cleansing agents in the dairy industry. As reviewed by Phillips,5 this unplanned increase in iodine intake has eliminated endemic goitre in Britain during the last 30–40 years. In the United States, London and colleagues encountered cases of unexplained very high iodine intakes (1100–1300 µg per day) in 1964. Subsequently, they discovered that bakers used iodine-containing conditioners in bread and that this caused high levels of iodine intake.6 Obviously, such unplanned variation in dietary iodine is a hazardous way of providing a population with an adequate intake of iodine, as mechanisms unrelated to disease prevention can profoundly alter iodine intake. To some extent, Australia may be a country where factors other than disease prevention have modulated the intake of iodine, and iodine intake may now be in an unplanned phase of decrease.7 A report by McElduff et al8 (page 317) in this issue of the Journal seems to support this proposition. McElduff and colleagues looked at the frequency distribution of whole-blood thyroid-stimulating hormone (TSH) concentrations in newborns in the northern Sydney area. TSH is measured as part of screening for congenital hypothyroidism. In 5%–10% of infants around 72 hours after birth, TSH values were above 5 mIU/L. The World Health Organization (WHO) recommends assessment of TSH concentrations in newborns to detect population iodine deficiency, and specifies that less than 3% of newborns should have a whole-blood TSH concentration over 5 mIU/L. In a subsample of neonates, McElduff et al found that, during pregnancy, their mothers had a median urinary iodine concentration of 109 µg/L, indicating borderline mild iodine deficiency. WHO specifies that the median urinary iodine concentration in adults should be over 100 µg/L, and an extra iodine intake of 50 µg/day in pregnant and lactating women.1 Thus, the corresponding median urinary iodine concentration of pregnant women would be around 130 µg/L. McElduff et al warn that Sydney may be an area of iodine deficiency, and suggest that iodine intake and risk of disease should be investigated in more detail. Their concern is well founded. Even if there is no documentation that these borderline iodine values are harmful to a mother and child, the margin of safety is small. Furthermore, in Australia, there is apparently no regular surveillance of population iodine status, or of the variable iodine content of dairy products and other foods. The iodine intake may well be even lower in other sections of the Australian population. Severe iodine deficiency may cause brain damage and other developmental disorders,3 and goitre and its complications may affect a significant proportion of the population at all levels of iodine deficiency.9 Any public healthcare system should evaluate iodine intake and prevent disorders caused by iodine deficiency. Several factors need to be taken into account in such an evaluation and prevention program: The relationship between iodine intake and the risk of thyroid disease is not a simple one. Even if iodine supplementation may decrease the risk of some thyroid disorders, the risk of other disturbances at a younger age, such as hypothyroidism and Graves' disease, may increase.4 Severe iodine deficiency, with a median urinary iodine excretion of less than 25 µg/24 h, is an instance where giving any type of iodine supplementation is better than doing nothing. However, at higher levels of intake, careful planning and surveillance are needed. The methods often used for evaluating iodine intake and the risk of disease are not perfect. Neonatal screening showing more than 3% of TSH values over 5 mIU/L is not, by itself, enough to indicate insufficient maternal iodine intake. Detection of neonatal hypothyroidism requires identification of relatively high TSH levels (20–25 mIU/L), and many TSH assays and screening programs are not designed to identify TSH values around 5 mIU/L with reasonable confidence. Technical aberrations can easily give an increased frequency of elevated blood TSH concentrations. One such aberration occurs with sampling of blood before TSH has fully returned to baseline levels after the early postnatal surge. As discussed by McElduff et al,8 early sampling may have contributed to their findings. Iodine deficiency is not the only pathogenetic mechanism leading to an increase in blood TSH levels in neonates. Iodine has an autoregulatory inhibitory effect on the thyroid gland, with a fall in both thyroid hormone synthesis and secretion. Possibly, this mechanism has been developed to protect against hyperthyroidism induced by a sudden iodine load. In a variety of abnormal states the thyroid gland overreacts, producing hypothyroidism. The thyroid of the fetus and infant is considerably more sensitive to iodine inhibition than the maternal thyroid. Excess iodine intake, rather than iodine deficiency, in mother or infant has been a more common cause of transient neonatal hypothyroidism in countries with a relatively low iodine intake, such as Germany, Italy and Belgium.4 In severe iodine deficiency, iodine supplementation to the mother decreases the abnormally high serum TSH in both the mother and the newborn.10 On the other hand, in pregnant women with urinary iodine concentrations around 50 µg/L, iodine supplementation decreases TSH levels in mothers, but not in cord blood. TSH levels in the newborn may even be higher after iodine supplementation.11 The finding of McElduff et al of a positive correlation between maternal urinary iodine concentrations during pregnancy and whole-blood TSH levels in neonates needs further elaboration,8 but it may be an example of iodine autoregulation of the fetal thyroid. Should pregnant women living in mild and moderately iodine-deficient areas receive iodine supplements, and does supplementation involve any risk? An increase in iodine intake will improve thyroid function in pregnant women, which is important for early brain development in their infants.12 There are still things to be learned about the influence of small amounts of iodine on neonatal thyroid function in mild iodine deficiency, and about pituitary/thyroid feedback regulation in the fetus and small infant. A tendency to a slight increase in neonatal TSH level after iodine supplementation may be of little importance, as, in these infants, the serum concentration of T4 (which may be the major thyroid hormone influencing brain development12) does not show a concomitant reduction.11 Finally, iodine supplementation imposes no risk of worsening of postpartum thyroid dysfunction in the mother.13 In conclusion, pregnant women should not be iodine deficient. To strictly follow WHO guidelines on iodine intake, pregnant women with similar urinary iodine levels to those found by McElduff et al could alter their diet towards more iodine-rich foods, or they could take a small iodine supplement as part of the vitamin and mineral supplements recommended for pregnant women in most countries. However, there is at present no evidence that a supplement will have beneficial effects. Ideally, iodine intake should be evaluated and kept optimal in the entire population, taking into account that unnecessary high iodine intakes may be associated with more hypothyroidism.4 The studies by McElduff et al8 and other researchers7 demonstrate the need for national monitoring and adjustment of iodine intake as part of a program of prevention of thyroid disorders and their complications. Such initiatives normally involve government nutrition or public health agencies in collaboration with experts in thyroid diseases, nutrition and epidemiology and prevention.1,2 It would be an added bonus if the program elucidated some of the unresolved issues in the field of population iodine supplementation in developed countries. This would continue the considerable contribution of Australian scientists to the understanding and correction of iodine-deficiency disorders.3,14

Peter Laurberg MD, DMedSci · Susanne B Nøhr

Screening by high-quality programs successfully detects cancers at an earlier stage In 2002, the 10th anniversary of Australia's national program of mammographic screening for breast cancer, it is perhaps timely to reflect and review. The need for reassessment is highlighted by the recent furore in the breast-screening world1-4 precipitated by a Cochrane review by Olsen and Gøtzsche.1 In this issue of the Journal, the article by Barratt et al5 (page 266) also encourages us to review breast-screening policies — in this case for women 70 years and over who are no longer in the target group for free mammographic screening (50–69 years). Barratt et al5 estimated the benefit of screening women 70–79 years to be about one-third to three-quarters that achieved in women aged 50–69 years. As women age, the benefit of screening — reduced risk of death from breast cancer — is increasingly offset by the other causes of death. Furthermore, while the benefit is delayed, the hazards of screening — tests for false-positive films, discomfort and anxiety — are immediate. Thus, with increasing age, the data show a further decline in benefit, which is exaggerated when adjustment is made for qualit-of-life factors.5 Barrett et al also provide a rough estimate of the cost-effectiveness of screening older women. The wide range of cost estimates (per quality-adjusted life-year saved) underlines their imprecise nature, but suggests that mammographic screening of women aged 70–79 years is as cost-effective as screening the other outlier group — women 40–49 years. However, Barratt et al remind us that the estimation of benefits, harms and costs would be improved with data from randomised trials in the appropriate age group — which unfortunately are still lacking. In 1999, 63.7% of women in the target age group for mammographic screening in Victoria (50–69 years) were screened.6 In view of Barratt and colleagues' estimates of benefits and costs per quality-adjusted life-year saved, it could be argued that money for screening older — or younger — women could be better spent on recruiting more women in the target group to achieve the desired 70% participation. Trials of mammographic screening commenced in the 1960s and seven have been completed and reported. On the basis of these trials, which showed a reduction in mortality from breast cancer in screened women, mammographic screening recommendations have been drawn up (eg, in the United States), and in several countries political decisions were made to institute national programs (eg, in the United Kingdom, Australia and New Zealand). In 2000, Gøtzsche and Olsen, publishing a "Cochrane review" of the seven trials in the Lancet,7 reported that they found no reliable evidence that screening for breast cancer reduced mortality. However, this report did not fulfil the Cochrane Group protocol for such a review. Since then Gøtzsche and Olsen have worked with the Cochrane Breast Cancer Editorial Group, and in October 2001 part of their review was accepted and included in the Cochrane Library.1 Almost simultaneously, the Lancet published Gøtzsche and Olsen's review in full on its website, and a research letter in its printed journal2 with an editorial commentary3 criticising the Cochrane Breast Cancer Editorial Group for interference. The whole episode has drawn a flurry of criticism and countercriticism.4. After all this, what should women believe, especially as the systematic review of Barratt et al5 suggests that screening for women over 70 years may be of some benefit (and as cost-effective as it is for those under 50 years), on the basis that screening is beneficial in women aged 50–69 years? Although clinical-trial methodology has improved in four decades, population-health intervention studies remain notoriously difficult to perform because of problems associated with large cohort numbers, the randomisation process and guaranteeing reliable stratification. It is not surprising that the seven, now old, trials can be criticised. However, not all would suggest ditching them and their conclusions on these grounds. The Cochrane Breast Cancer Editorial Group has not accepted the other conclusion of Olsen and Gøtzsche — that screening leads to more aggressive treatments8 — and has not included that section of their review in the Cochrane Library. Others4 reject Olsen and Gøtzsche's conclusions because they are based on all-cause mortality, which may be inappropriate in population studies. Do we have other surrogate measures to guide us? Cancer registry data from Victoria9 suggest a "slight downward trend since 1994" in breast cancer mortality, but it cannot be assumed that any of this trend is due to screening. However, from 1982 to 1996, there was no change in breast cancer mortality in Australia.10 The impact of breast screening may be seen more readily in the stages at which breast cancer is detected. In 1997, when the national program was six years old and well established, 30% of new breast cancers were detected through screening. Data suggest that screen-detected invasive cancers were smaller, less likely to involve nodes, and, if node positive, more likely to involve fewer nodes (Box).11 Tumour size, nodal involvement and number of nodes involved — the basis of the tumour–node–metastases (TNM) staging system — are all known to be of prognostic significance. Hence, it is likely that the cohort of women with screen-detected invasive cancer will have a better prognosis and live longer, provided lead-time bias does not negate the prognostic effect of lower staging by detecting cancer earlier while not influencing the natural history of the disease. The prognostic significance of non-invasive cancer (ductal carcinoma in situ), its treatment and the appropriateness of various local and systemic treatments for any breast cancer can be debated and argued. However, the histopathological prognostic (TNM) data would suggest that mammographic screening by high-quality programs successfully detects cancers at an earlier stage, giving a better prognosis and probably improved survival. Women should be made aware of these facts, along with any doubts raised by reviewers of somewhat out-of-date trials. Impact of breast screening on stage at which cancer is detected11 Tumour size/node involvement Screen detected All cancers < 15 mm 60.3% 42.7% Node positive 22.5% 30.0% 1–3 nodes positive 18.7% 23.4% > 3 nodes positive 8.4% 14.2%

Alan Rodger

A study design that was simple, relevant and that avoided particular sensitivities in the study population might have helped, as might considerably more guidance from the national funding body The combination of hazardous consumption of alcohol, Aboriginal people, primary care and a randomised controlled trial (RCT) of interventions sets a daunting challenge as a research project. In this issue of the Journal, Sibthorpe et al (page 273) describe, with disarming candour, how they took on this challenge and failed.1 After two false starts, and having recruited only one participant per fortnight (when they had originally aimed to enrol two per working day), the research team felt they had no option but to abandon the project and return the funds to the National Health and Medical Research Council (NHMRC). There is little that is new for clinical practice here, but there are important lessons about the design, execution and funding of research studies. The project was motivated by concerns about the limited external validity of existing evidence about the impact of simple interventions on hazardous drinking in an Indigenous primary care setting. The attempt to conduct a new RCT in such a setting was laudable, but the NHMRC process of reviewing grant applications apparently did not detect that failure was predictable. The inability of the team to conduct the study as conceived should not compound any negative perceptions about Aboriginal Medical Services and Aboriginal patients. Rather, the NHMRC might have served them better by advising the researchers about simplifying recruitment, need for consent and statistical power, as well as taking a more critical view of the underlying rationale for the project. It is not clear whether the original application to the NHMRC was supported by a feasibility study, but, given the challenge faced by the investigators, funding should not have been granted without one. As the project was initially designed, the complexity of the screening and recruitment processes flew in the face of well established principles.2 Simple requirements for enrolment make participation in RCTs easy for both patients and providers of healthcare services. By contrast, the combination of a detailed interview about a taboo subject, extensive paperwork and the need for blood all act as disincentives to participation by members of a community whose standard of education and reading ability are often poor, that sees paperwork as the hallmark of an officialdom that too often has been oppressive, and that attaches special significance to body fluids. All of these should have been identified by the NHMRC's assessors as likely to be prejudicial to success. A requirement to seek informed consent to participation runs contrary to the stated aim of the study to assess "effectiveness" (as opposed to "efficacy"3) of brief advice about drinking in a primary care setting. Alerting potential participants to the existence of a trial of this kind is likely to have a Hawthorne effect, thereby eroding statistical power. It is not clear from the account whether gaining consent was originally proposed by the investigators or imposed by an ethics committee — both would be conscious of the special nature of the target population — but it is another neat example of ethics getting in the way of good science.4 Trials of effectiveness do need ethical oversight, but clear thinking about ethical requirements is required when the control group is to receive "usual care". The counterargument that consent was needed because the study required additional blood tests that did not form part of routine care would not have any bearing when screening and recruitment were simplified. The investigators may have wanted to use γ-glutamyltransferase as an endpoint, but this is "medicalising" a social problem long before it becomes a biochemical one, and, in any case, represents a further departure from a study of "effectiveness". Part of the challenge of working in primary care and Aboriginal health is to devise and apply measures of impact and outcome that are relevant and robust, but also simple and credible. The trial as conceived was almost certainly underpowered statistically through overestimating the likely net effect of a brief intervention. In the study on general practitioner intervention in excessive alcohol consumption by Wallace et al,5 the initial prevalence of imprudent drinking was 35%, and the trial was designed on the assumption that 30% of men drinking excessively would respond to the intervention compared with 20% in the control group, the corresponding figures for women being 40% and 20%. Sibthorpe et al were aiming for an absolute difference in response between intervention and control groups of 20%, a bigger average change. They calculated correctly that 200 participants per group would be required to have a 90% chance of detecting such a difference and declaring it significant at P < 0.01. However, it is easy to overestimate the likely impacts of treatments, and changing personal and social behaviour can be even more difficult. Rather than anticipating that anywhere between 5% and 50% of members of the control group might stop drinking hazardously during the course of the study, a pilot study would have been particularly useful for clarifying the likely absolute prevalences and between-group difference in heavy drinking at follow-up. Finally, the whole concept of this study again throws into sharp focus the tension between high-risk and population-wide approaches to prevention, intervention and control of common health problems so eloquently described by Geoffrey Rose.6 Notwithstanding the fact that the prevalence of drinking alcohol is actually lower in the Aboriginal than in the mainstream population, the damage done by hazardous drinking affects a very great proportion of many Aboriginal communities and social factors play a significant role in the behaviour. Rose has clearly identified the futility of trying to get individuals to change their own health-threatening behaviour in such unsupportive circumstances. In Sibthorpe's project, the principles enunciated by Rose would have dictated that, from the outset, one should simply have attempted to ascertain which of the patients drank alcohol at all; given all of these a simple and unambiguous message about the NHMRC's recommendations about patterns of drinking consistent with best health; told them all about the Aboriginal Sobriety Group; and offered to provide extra help, probably at a separate consultation, to those who then felt that they needed it to achieve change. Eventually, Sibthorpe and colleagues began to stumble down something like this path, but the lesson is a salutary one. Too often, clinicians identify the screening/high-risk/selective medical intervention sequence as a first response to problems that are actually present on a mass scale. There is also an important lesson about both investigators and the NHMRC having available good epidemiological, biostatistical and public health advice at all phases of development and assessment of applications for research funding.

Konrad Jamrozik MB BS, DPhil

Comprehensive management of pregnancy loss is enhanced by psychological support and follow-up counselling It is generally accepted that 12%–15% of confirmed pregnancies do not progress to term, with the risk of pregnancy loss increasing with maternal age. In particular, early pregnancy loss (< 20 weeks' gestation) is experienced by one in four women. In about half these women, a medical explanation can be found,1 although, in clinical practice, investigations to identify the cause are rarely pursued. Most women go on to have successful subsequent pregnancies, although there is a slightly increased risk of a second miscarriage that increases incrementally with each subsequent loss.1 Although early-pregnancy loss is relatively straightforward medically, the psychological outcome is more problematic and the grieving process is complicated.2 First, there is no tangible life or memory to grieve. Instead, the woman has to come to terms with grieving for a potential life with all its hopes and aspirations. Second, the grieving is often complicated by feelings of self-blame, particularly when there is no medical explanation for the loss or the woman has engaged in potentially hazardous behaviour (eg, alcohol consumption or smoking). Her partner may also harbour feelings of responsibility for the loss. Other factors which may influence the grieving process and the emotional outcome include miscarrying later in gestation (especially if the woman has felt the fetus move and formed an emotional attachment to it);2,3 the importance and meaning of the pregnancy (eg, a first, wanted pregnancy lost near the end of the reproductive lifespan); and the difficulty experienced in conceiving the pregnancy (eg, an assisted conception). Finally, psychosocial factors, such as a woman's support network (especially her intimate relationship) and her personality style and culture, will affect how she appraises her loss and her level of distress. The psychological sequelae after a late pregnancy loss and stillbirth are well described;3 those after an early pregnancy loss are similar but may not be as severe. There can be high levels of psychological distress characterised by anxiety, depression and somatisation, which can persist for at least six months4 and are only partly accounted for by grieving for the loss of a potential child. There is an increased risk of developing a depressive or anxiety disorder in the six months after a pregnancy loss, and any pre-existing psychotic disorders can be precipitated. The risk of developing depression is high, with studies reporting rates between 10%5 and 48%,6 depending on the study methods.7 One of the more rigorous controlled studies5 reported that 10.9% of women developed major depression after a miscarriage, compared with 4.3% of women (controls) from the same community who had not been pregnant in the previous year. Depression is more likely in women with a history of depression or past psychopathology, and in women who have had a previous pregnancy loss or have no other children. Other factors precipitating depression, such as poor social support or having a vulnerable personality style, are well recognised. The rates of anxiety disorder are lower than those for depression. Recently, exacerbation of obsessive–compulsive disorder after miscarriage has been reported.8 Finally, if the pregnancy loss has been traumatic (eg, an ectopic pregnancy or the woman's life was at risk), post-traumatic stress disorder can arise.9 The comprehensive management of pregnancy loss will be enhanced by psychological support and follow-up counselling.7,10 This can be provided by the woman's obstetrician, general practitioner or another health professional involved in her care, who can address medical as well as psychological issues.11 The purpose is to allow open discussion about the loss, monitor progress and counsel the woman about future pregnancies. In the initial stages, she will benefit from the opportunity to talk about her loss and have her grieving acknowledged. Providing information about the normal grief process may help a woman who is masking her grief or does not believe it is legitimate. The grief process will be facilitated by the opportunity to talk about feelings of guilt and self-blame, particularly when there is no medical explanation.12,13 In our opinion, there should also be an opportunity to discuss dissatisfaction with medical care, as the woman may feel angry and blame her medical practitioner for the loss. An open discussion about this will help her, and may reduce the possibility of litigation. Medical practitioners, particularly when the issue is pregnancy loss or stillbirth, are often reluctant to use the phrase "I'm sorry" because of fears that this equates with an acknowledgement of guilt and may have legal implications. Bereaved parents are often highly aware of this omission, angered by it, and may actually retaliate through litigation. Both obstetricians and insurance companies need to seriously look at the distinction between empathic expression of "sorrow" for the distress experienced as opposed to an apology for negligent action. Regular follow-up is recommended for the first six months. Distinguishing between feelings of grief (which may require grief counselling) and the onset of a depressive illness (which may require specific treatment) can be difficult. Depression is suggested by persistence of depressed mood, lack of enjoyment in pleasurable activities, low self-esteem or excessive guilt, and sleep or appetite disturbance or fatigue.14,15 A pathological grief reaction, characterised by excessive distress, guilt feelings or a preoccupation with the loss, may require more specific counselling. Sometimes a woman may have her depressed feelings dismissed as "grieving" and miss out on appropriate and effective treatment for a depressive disorder. Other family members may also need psychological support. The woman's partner may experience similar feelings of loss.16 In such situations, the father is often neglected ("men aren't expected to talk about their feelings"). He will also benefit from an opportunity to talk about his feelings of loss, as will other children in the family, especially as they may feel responsible if they had feelings of jealousy about the new sibling. The sense of loss may dissipate when the woman becomes pregnant again, and some studies suggest that the shorter the time between a pregnancy loss and a subsequent pregnancy the better the outcome for the woman.13 Such women usually feel anxious during the stage of pregnancy at which the previous loss occurred. Finally, women may benefit from the opportunity to talk to other women who have experienced a pregnancy loss through support groups such as SANDS <http://www.sands.org.au/>.

Philip M Boyce MD, FRANZCP · John T Condon MD, FRANZCP · David A Ellwood DPhil(Oxon), FRANZCOG

How real is the threat, and how prepared are we? The world changed on September 11, 2001, and again on October 4, when the first case of inhalational anthrax in the United States raised worldwide fears of bioterrorism. Although the threat of bioterrorism in Australia has been assessed as low,1 defence and civil authorities had upgraded preparations before the 2000 Olympics.2 Those plans, coordinated by Emergency Management Australia, provided a basis for responses by state emergency services, health services and postal services to the numerous false alarms, "white powder" incidents and hoaxes that followed the US events. No anthrax spores or human anthrax cases associated with these incidents have been detected in Australia, but understandably they have caused considerable public anxiety. In retrospect, it now appears that the anthrax-containing letters in the US were probably of domestic origin, with no targets outside that country.3 After the US incidents, health departments were swamped with calls from the public asking what had been done to protect them. They wanted to know how to protect themselves, and whether they needed antibiotics, vaccines for anthrax or smallpox, or gas masks. Health authorities emphasised communication to reassure those who were worried, as well as to provide authoritative information and planning advice about anthrax and other conceivable threats. Should a biological incident ever occur in Australia, communication would be even more important, not only in managing the emergency, but also in minimising community alarm, which could cause more damage than the biological agent itself. In any incident, healthcare agencies would play a key role in recognising resulting illnesses and managing the health consequences. The anthrax threat has highlighted the importance of multidisciplinary approaches to biological emergencies. Security intelligence must be wedded to health intelligence, and the lessons learned from past disaster management appropriately applied. As an editorial in the Lancet recently said, "Appropriate reaction to such deliberate attacks, but also to any other emerging epidemic, by a well-organised and well-functioning public health system requires preparedness at all times on all levels".4 Australia's federal system requires close collaboration between the Commonwealth, States and Territories. Emergency service responses are coordinated by Emergency Management Australia. Public health agencies work with emergency services in the States and collaborate through the Communicable Diseases Network Australia and the Public Health Laboratory Network to coordinate national reporting, surveillance, laboratory diagnosis and public health responses for communicable disease outbreaks. Biosecurity planning in Australia has built on these existing disease and disaster surveillance systems.2 Recently, these networks have collaborated to revise training schedules and case definitions to support the earliest possible recognition of any event resulting from deliberate release of a biological agent. Health authorities, through the Communicable Diseases and Public Health Laboratory networks and the network of Chief Health Officers of the States, have also strengthened their linkages with Emergency Management Australia, the federal department of Defence and other government agencies. Anthrax: The review of Australia's policies has adapted advice from the US Centers for Disease Control and Prevention (CDC), World Health Organization (WHO) and United Kingdom Public Health Laboratory Service for local needs. Guidelines for anthrax treatment and post-exposure prophylaxis have been developed by public health physicians, microbiologists and infectious disease specialists, and endorsed by Australia's Chief Health Officers and directors of public health services. It has been agreed that primary care providers should not prescribe chemoprophylaxis in the event of suspected anthrax. Instead, they should immediately contact their local public health unit for advice about referral for diagnosis and further management (contact details for State and Territory health authorities are available on Fact sheet — anthrax <http://www.health.gov.au/pubhlth/strateg/communic/factsheets/anthrax_fact.htm>). To minimise inappropriate antibiotic use, general practitioners should not provide individuals with a contingency supply of antibiotics for prophylaxis. State and Territory health authorities are ensuring that there are adequate supplies of appropriate antibiotics in case of an emergency, and the Commonwealth Government is working with pharmaceutical companies to ensure continuity of supply. Anthrax vaccine is not currently registered for use in Australia and is not recommended as a first-line response to an anthrax incident. Smallpox: The US government's intention to procure 250–300 million doses of smallpox vaccine for mass vaccination appears to have been modified after expert advice. Existing vaccine is effective but has significant adverse effects. The calf-lymph-derived live smallpox vaccine used in the WHO smallpox eradication program is associated with a post-vaccinal encephalitis rate of 3–4 per million primary vaccine doses.5 Forty per cent of encephalitis cases are fatal, and some survivors have permanent neurological deficits. Progressive vaccinia occurs among those who are immunocompromised. WHO guidance is that, given the substantial risk of adverse events after vaccination, mass vaccination of populations is not recommended when there is little or no real risk of exposure. Despite the stated intention of the US to develop a new vaccine supply against a possible bioterrorism incident, no country is planning to give smallpox vaccine routinely to its citizens. Smallpox is not transmissible until the onset of rash, when the individual becomes ill and is likely to be confined to bed. This provides the rationale for measures to contain any outbreak: after the first cases are identified and isolated, contacts are vaccinated; vaccination prevents or ameliorates disease, even when it is undertaken after exposure to the virus.5 Thus, both WHO and CDC recommend an approach which involves early case detection and post-exposure vaccination with a view to "ring fencing" any outbreak.5-7 Australia has no smallpox vaccine available at present. As a precautionary measure, the Commonwealth Government has arranged with international agencies to secure access to vaccine in the unlikely event of a smallpox incident; arrangements have also been made to secure supplies of vaccine to be held in Australia. If smallpox were introduced into Australia, we would then be in a position to implement a strategy of surveillance, quarantine and vaccination. WHO has pledged support to any country in which an incident occurs, as this would constitute an international emergency. WHO will help countries pool resources to contain any outbreak as rapidly as possible. Conclusions: Although the risk to Australia is regarded as low, we need to be prepared for a bioterrorism incident. Australia's strong public health infrastructure forms the basis for an effective response to any such incident. While much of the initial planning has focused on anthrax and smallpox, progress has been made on public health and clinical protocols for other potential bioterrorism agents. No public health or security system can guarantee complete safety from bioterrorism attack, but Australia's public health expertise will ensure that harm to the community is minimised. For the assistance of doctors, a comprehensive guide for dealing with patient inquiries is available on the website of the Commonwealth Department of Health and Ageing (<http://www.health.gov.au/pubhlth/strateg/bio/index.htm>). This also contains a list of contacts for public health authorities around Australia. Relevant information can also be accessed through the WHO and CDC sites (<http://www.who.int/emc/deliberate_epi.html> and <http://www.cdc.gov>, respectively).

Richard A Smallwood · Angela Merianos · John D Mathews

Current practices should be re-examined in light of current evidence Antenatal care includes screening asymptomatic pregnant women, with the aim of detecting, and thereby preventing, both maternal and neonatal adverse events. The introduction of antenatal care in 1913 has been widely attributed to the efforts of Ballantyne at the University of Edinburgh. He suggested that the high maternal and perinatal mortality rates observed at the beginning of the 20th century reflected inadequate maternity care during pregnancy and lack of supervision of the progress of labour. Ballantyne's flow diagram, an antecedent of guidelines, defined interactions of many disciplines in antenatal care. During the 1930s, there was increased emphasis on educating healthcare professionals who provided maternity care. Women were encouraged to present during pregnancy, and were advised to give birth in hospital. The subsequent fall in perinatal mortality rates was attributed to antenatal care, without consideration of the contribution from social and other medical improvements.1 The falling mortality rates corresponded with a gradual increase in the number of antenatal visits recommended. By the 1950s, a schedule of monthly visits to 28 weeks, fortnightly visits to 36 weeks, and then weekly visits until birth had become standard.1 Although programs with fewer visits have been proposed, this schedule is widely accepted in clinical practice. This has remained largely unchallenged, as noted by Archie Cochrane, who stated "by some curious chance, antenatal care has escaped the critical assessment to which most screening procedures have been subjected".2 Traditional antenatal care was critically appraised in a retrospective review of 1907 pregnant women who gave birth at the Aberdeen Maternity Hospital in 1975.1 Antenatal and birth records were reviewed to determine the rates at which complications were diagnosed, misdiagnosed and overdiagnosed, in addition to the rate at which complications occurred despite routine antenatal care. Breech presentation and pre-eclampsia were the only complications reliably detected in the antenatal period, and the benefit in the detection of pre-eclampsia was confined to primigravid women beyond 34 weeks' gestation. Most antenatal admissions, apart from admissions for labour and birth, were for conditions that had arisen despite routine antenatal care — conditions that had not been prevented or detected by it. More recently, randomised controlled trials have assessed the optimal frequency of antenatal visits in preventing maternal and fetal complications. The main hypothesis tested in these trials is that models of care with fewer antenatal visits are as effective as the traditional model in terms of clinical outcomes and maternal satisfaction.3 A systematic review of seven randomised controlled trials involving 57 418 women found no differences in the detection of pre-eclampsia (odds ratio [OR], 0.91; 95% CI, 0.66–1.26), urinary tract infection (OR, 0.93; 95% CI, 0.79–1.10), low birthweight (OR, 1.04; 95% CI, 0.93–1.17) or maternal mortality (OR, 0.91; 95% CI, 0.55–1.51) when a schedule of reduced antenatal visits was compared with more traditional regimens of antenatal visits.4 However, women were more dissatisfied with fewer visits. Whether increased maternal satisfaction is of measurable benefit in terms of pregnancy and birth outcomes remains less certain. Clinical practice guidelines should define best practice, limit variations in the provision of care, recommend care that is cost-effective, and provide care in a way that meets the needs of all patients. In this issue of the Journal (page 255), Hunt and Lumley have reviewed guidelines used in Australian maternity units.5 They found that recommendations for the content of antenatal visits and screening procedures vary considerably across Australia. The value of certain tests or interventions can be readily appreciated in terms of a low cost treatment capable of disease modification (eg, provision of anti-D to rhesus-negative women); however, evidence of benefit is lacking in other circumstances (eg, routine screening for carbohydrate intolerance), although current clinical trials will address some of these issues. Routine antenatal screening for syphilis, although low cost and with effective therapy available for patients testing positive, could be questioned given the low prevalence of the disease among pregnant white Australians. However, selective testing and treatment has not been supported.6 Hunt and Lumley also demonstrate the other end of the clinical spectrum, where good-quality evidence exists to support a treatment or policy but institutions have no relevant guidelines. Good-quality evidence exists to support the cessation of smoking during pregnancy,7 and yet remarkably few institutions had a guideline providing practical information for caregivers to support women in smoking cessation. This also highlights the difficulty of implementing changes in policy, despite evidence of an important clinical effect, and reflects the wider challenges of translating research findings into clinical practice. The article by Hunt and Lumley describes the broad range of accepted antenatal care in Australia. Where to from here? The purpose of antenatal care needs to be redefined. The aims may differ for consumers and caregivers, and both should be incorporated into the "ideal" model of care. In addition, current practices (including timing and frequency of visits, and "routine" screening investigations) should be questioned in light of predetermined outcome measures and best available evidence. The principles of antenatal care were adopted over half a century ago; their maintenance can only be supported when rigorously tested against the best currently available evidence, which can then be incorporated into national guidelines for best practice.

Jodie M Dodd · Caroline A Crowther · Jeffrey S Robinson

Few areas of medicine have undergone greater change during the past 50 years than infectious diseases. The optimism and clinical confidence associated with the development of antimicrobial agents from the 1940s onwards has been tempered by the emergence of new diseases, such as AIDS and infections associated with transplantation and cancer therapy, and by the widespread development of antibiotic resistance. Despite many advances, infectious diseases continue to account for about a quarter of all deaths worldwide1 (Box 1). Furthermore, a security dimension has emerged. A recent report on The global infectious disease threat and its implications for the United States from the US Central Intelligence Agency (CIA) analysed this "non-traditional threat": The dramatic increase in drug-resistant microbes, combined with the lag in development of new antibiotics, the rise of megacities with severe health care deficiencies, environmental degradation, and the growing ease and frequency of cross-border movements of people and produce have greatly facilitated the spread of infectious diseases.2 Clinicians today require more knowledge of infectious diseases than ever before. In this issue of the Journal (page 229), we begin MJA Practice Essentials — Infectious Diseases. This series cannot hope to cover all new aspects of infectious disease. Instead, we aim to discuss clinically important areas where recent advances have occurred in diagnosis or treatment, new diseases have been identified, or healthcare changes have necessitated new clinical approaches to "old" diseases (eg, endocarditis and cellulitis) (Box 2). Some important topics, such as HIV infection and bioterrorism, are beyond the scope of this series. Wherever possible, recommendations are evidence-based, with the evidence graded according to the system of the National Health and Medical Research Council3 (Box 3). As with much of medicine, management of infectious diseases is affected by the competing needs for prompt empirical treatment and for a definite diagnosis to allow focused therapy. Advances in diagnostic technology have enhanced the possibilities for rapid, accurate diagnosis of conditions such as sexually transmitted diseases, deep-seated infections such as endocarditis and osteomyelitis, and common viral infections.4 However, identification of bacterial pathogens and their antibiotic susceptibilities still requires careful specimen collection and slow, generally labour-intensive, microbiological culture methods. Furthermore, many rapid diagnostic tests are sufficiently expensive that initial empirical "shot-gun" therapy without investigation can seem attractive. As effective antiviral agents become ever more readily available, many of the issues faced with antibiotics, such as rapid diagnosis, susceptibility testing and dosage monitoring, must also be considered. Current administrative pressure for shorter hospital stays and fewer outpatient or general practitioner consultations appears to encourage use of broad-spectrum empirical antibiotic and antiviral therapy, rather than careful investigation, review and directed therapy. Combined with the community's apparent ready acceptance or expectation of antibiotic therapy, this may explain Australia's ranking as the world's second-largest per-capita consumer of antibiotics (after France).5-7 Similarly, in the US and Canada, it is estimated that about 50% of all outpatient prescriptions for antibiotics are unnecessary.7,8 Antibiotic resistance is now emerging as a key challenge to many healthcare programs. Indeed, developments such as multidrug-resistant tuberculosis and resistance among common pathogens in developing countries (eg, Salmonella and Shigella spp. and malaria) threaten to totally undermine many current healthcare gains.7 It is therefore essential that all Australian clinicians accept the responsibility that goes with the privilege of prescribing antimicrobial agents. In both developed and developing regions, hospital-acquired infections are increasingly recognised as a major contributor to healthcare morbidity and costs.7 For this reason, good hospital infection control practices are no longer simply a concern for microbiologists and infection control committees, but must be understood by all staff, including hospital administrators — even if the latter consider them merely as "risk management". Few health issues attract more media attention than nosocomial infection. Current training about infectious diseases appears relatively limited among some medical personnel. A recent review of the general training curricula of the 12 Australian medical colleges found that five (Anaesthetists, Ophthalmologists, Medical Administrators, Radiologists and Psychiatrists) did not mention antibiotics at all.6 Similarly, among the 19 subspecialty groups in the Royal Australasian College of Physicians, only two specify the need for training in antibiotics (Thoracic Medicine and Infectious Diseases).6 The challenge for Australian clinicians in the current era of "information overload" is to improve the appropriateness of investigations and treatment of infectious diseases to avoid unnecessary antimicrobial therapy.6,7,9,10 Thus, MJA Practice Essentials — Infectious Diseases focuses on practical clinical problems that are either common or are sufficiently acute or severe that early recognition is important to limit morbidity or restrict disease spread. Whenever possible, recommendations are evidence-based. 1: Causes of death worldwide in 1998 (% of all deaths)* * Adapted from World Health Organization leading causes of death for 1998 (total of 53.9 million deaths from all causes worldwide).1 † Cancers, cardiovascular, respiratory and digestive deaths can also be caused by infections, further raising the percentage of deaths caused by infectious diseases. 2: Infectious diseases series contents Infections in pregnancy Hospital-acquired infections Community-acquired pneumonia Acute community-acquired meningitis and encephalitis Hospital-in-the-home Emerging viral infections in Australia Sexually transmitted infections Soft tissue, bone and joint infections Infections in the returned traveller Herpes simplex and varicella Antibiotic resistance 3: Levels of evidence Throughout the series, evidence is graded using the system of the National Health and Medical Research Council:3 E1 Level I: Evidence obtained from a systematic review of all relevant randomised controlled trials. E2 Level II: Evidence obtained from at least one properly designed randomised controlled trial. E31 Level III-1: Evidence obtained from well-designed pseudo-randomised controlled trials (alternate allocation or some other method). E32 Level III-2: Evidence obtained from comparative studies (including systematic reviews of such studies), with concurrent controls and allocation not randomised, cohort studies, case–control studies, or interrupted time series with a control group. E33 Level III-3: Evidence obtained from comparative studies with historical control, two or more single-arm studies, or interrupted time series without a parallel control group. E4 Level IV: Evidence obtained from case series, either post-test or pre-test/post-test.

M Lindsay Grayson MD, FRACP, FAFPHM · Steven Wesselingh PhD, FRACP

In a rejoinder to Benjamin Franklin's observation that nothing is certain in life bar death and taxes, people's fondest wishes seem to be to live forever and pay no tax. The timely and provocative study of Weston et al in this issue of the Journal (page 208),1 reporting high acceptability of a hormonal male contraceptive among new fathers, prompts a reflection on wishful thinking, as such a new contraceptive remains unavailable. In some respects, contraception is closer to a consumer lifestyle choice than a conventional medical treatment, as illustrated by the impact of media-inspired contraceptive "scares" that have led to panic-driven abandonment of contraception and subsequent unwanted pregnancies.2 Creating a need for novel products is the raison d'être of advertising, and in the world of public relations presentation is the whole game. Responses to unfamiliar products or services are sensitive to how they are described, and almost any outcome may arise depending on how the access, convenience, safety and efficacy of hypothetical or existing contraceptive methods are described. At face value, however, the observations of Weston et al are consistent with recent findings from other cultures3,4 and earlier World Health Organization (WHO) studies,5,6 all of which similarly rely on forcing choices between hypothetical options. Even if the responses accurately reflect attitude, there is a vast gulf between human attitude and behaviour. This is the starting point for much of behavioural medicine, as illustrated by the failure of even low expectations of interventions that rely upon behavioural change (eg, interventions to deal with anger, smoking, drug addiction, obesity). Nevertheless, the strikingly positive attitudes reported by Weston et al herald major progress and the imminent availability of practical hormonal male contraceptives. Arguably, the epitome of successful applied science in the 20th century was the development of reliable and reversible contraception. The universal availability of numerous highly effective female contraceptives fostered unprecedented social change extending well beyond medicine and science. At the start of the 21st century, it is a sad reflection that the previous century passed without the addition of a single new contraceptive method that men could use to share more equitably the burden of reliable family planning.7 Historically, all deliberate family planning methods (apart from abortion) were shared responsibilities requiring active male involvement. The phenomenal success of female-oriented contraceptive development in recent decades has shifted the burden of responsibility for family planning disproportionately onto women. Worldwide, however, male involvement in family planning remains remarkably high, considering the inadequate means available.8 The central dilemma for men in stable relationships seeking to share more responsibility for family planning is that the reversible methods are not reliable and the reliable method (vasectomy) is not reversible. What is needed is a reversible male method as reliable as modern female methods. The biologically unique processes of sperm development offer ever-increasing numbers of new ways for clever biotechnology to interrupt male fertility temporarily, notably by modification of sperm and male reproductive tract ion channels. However, these require full development as new drugs, whereas hormonal methods are close to practical realisation. Although hormonal contraceptive methods were always equally feasible for men and women, during the decades when female contraceptive development flourished the development of analogous male methods languished, as it depended solely upon the limited resources available to academic researchers without pharmaceutical company product development. A decade ago, proof-of-concept for a hormonal male contraceptive was achieved jointly by the US Contraceptive Research and Development Agency and WHO's Male Task Force, which conducted the first efficacy studies for any chemical male contraceptive.9,10 These studies showed high reliability of a reversible prototype hormonal regimen, a crucial empirical finding about which the biggest surprise is that this finding lagged three decades behind the wide availability of analogous female hormonal methods. Continued impressive progress towards a practical product has been achieved. There is consensus that a combination progestin-plus-androgen approach is optimal, with several combinations approaching the ideal of universal azoospermia.7 Finally, some large pharmaceutical companies have recently upgraded their involvement from being spectators to participating in some active development of the well-advanced research produced by the academic community within the public sector. New hormonal male contraceptives are needed for couples in stable relationships rather than for those with changing partners, among whom condom use prevents sexually transmitted disease as well as pregnancy. The survey of Weston et al highlights a likely niche for the use of a hormonal male contraceptive — the postpartum period. This period is ideal, because it focuses on a stable couple with a predictable timing of contraceptive need and a situation in which reliable female contraceptives are not well suited, particularly during lactation. Other niche purposes for a hormonal male contraceptive include delaying vasectomy, offering an alternative to conventional female methods when they are not well tolerated, and replacing less reliable male methods. The finding that a hormonal male contraceptive is acceptable to an appropriate Australian target population is consistent with Australasian men having the highest rate of vasectomy in the world.11,12 These observations highlight the substantial need and market for a hormonal male contraceptive. Hopefully, this decade will see the long-overdue development of an eminently feasible and widely desirable product. The desultory response from multinational pharmaceutical companies, even after completion of much early-phase clinical research by the public sector, suggests implementation may be driven by populous countries such as China, Indonesia and India, whose family planning priorities value such developments more highly. In Western countries, development may require a more enterprising start-up company to capitalise on this opportunity, which eludes the imagination, or lurks beneath the commercial horizon, of the pharmaceutical industry behemoths.

David J Handelsman MB BS, PhD, FRACP

The Australian Council for Safety and Quality in Health Care (ACSQHC) plans to publish data about the performance of the Australian healthcare system. It is probably inevitable that this kind of information, which is actively disseminated and reported in such a way as to encourage readers to draw comparisons, will be used in the near future by the media, the public and politicians to make public judgements about the relative performance of individual hospitals or even individual doctors or groups of doctors. Initiatives such as these will therefore be perceived as a threat by some health professionals and some organisations. Would this negative response be justified? What might be gained from public disclosure and how can the policy be implemented successfully? We believe that a negative response to public disclosure in Australia would be counterproductive. Greater openness in healthcare is inevitable. Information is freely available about most areas of modern life and many believe that healthcare is one of the last bastions of protectionism. When millions of dollars are spent on healthcare, those who pay have a right to know that the money is being spent effectively, and the publication of comparative data sends a strong message about the willingness of health professionals and organisations to be accountable. In addition, public disclosure appears to be an effective way of improving quality.1 There is a growing body of evidence that the current level of quality of care is unacceptable2,3 and that quality-improvement initiatives using confidential data have been largely ineffective at changing the behaviour of health professionals.4 When comparative data are released to the public, it appears to remind providers of the issues and refocuses them towards taking action.5 Arguments in support of the status quo — that the data are inadequate, the public won't understand them and the media will misuse them — are not sustainable if public disclosure is introduced properly. There are lessons that can be learnt from other countries to guide the process of disclosure in Australia. The United States has nearly 15 years' experience of publishing data in the form of "report cards", or "provider profiles". The initiative was launched by the federal government and the momentum has been maintained by a variety of public, private, commercial and not-for-profit organisations. Consumers and purchasers of healthcare were expected to play a key role by selecting high-performing providers, but recent evidence suggests that the providers themselves make greater use of the data than the service users.6 There are some notable examples of improvements in both the processes and outcomes of care associated with the publication of performance data.1 Public reporting in Europe is less well established than in the United States, but hospital "league tables" have been published in the Netherlands for several years, and the UK government plans to introduce incentives linked to a range of publicly reported performance criteria.7 What can we learn from the initiatives that have already been introduced? First, a backlash from some doctors, professional groups and institutions (particularly those seen to be performing badly) is predictable. Some criticisms were justified in the early days of report cards but lessons are being learnt. For example, we know that forcing new initiatives on reluctant professionals is not the most effective way of changing attitudes, and the introduction of report cards is more likely to be successful if doctors are encouraged to take a lead, particularly in selecting the performance measures. Bringing the media on board at an early stage to ensure fair and balanced coverage also helps. In addition, delaying publication for a short period to allow providers time to look at and act upon the data is a useful strategy. Second, it is important that those who publish the data show a commitment to investing in the process and progressively improving the quality of the data and the validity of comparisons arising from the data. However, it makes little sense to "wait for better data" — data will always be imperfect and, as one commentator stated, it is important not to let "perfect be the enemy of good".8 Experience suggests that the process of publication can in itself act as a catalyst for data improvement. Third, the utility of comparative data comes less from making absolute judgements about performance than from the discussion arising from using the data to benchmark performance. There is therefore a strong educational component to the effective use of comparative data, and resources are required to facilitate this process.6 Finally, it is important to be cognisant of the risks of publishing comparative data.9 The danger of institutions refusing to treat certain disadvantaged groups in order to improve their apparent performance is well recognised, although probably overstated,10 and can be reduced by careful adjustment of risk and casemix. A tendency to focus on what is being measured at the expense of other areas of practice can be minimised by publishing a wide range of quality indicators. The risk of "short-termism" — an inappropriate focus on annual reporting cycles — can be reduced by ensuring a balance between short-term targets and long-term strategic aims. A greater degree of public reporting of information about healthcare quality is an inevitable and desirable way forward. Practitioners and policymakers in Australia have an opportunity to ensure that the policy is implemented in a manner that is most likely to produce positive change.

Martin N Marshall MSc, MD, FRCGP · Robert H Brook MD, ScD

Should Australia follow the US decision to base prophylaxis on results of maternal screening? Ever since group B streptococcus (GBS) emerged as the commonest cause of perinatal sepsis in the late 1970s, there has been controversy about prevention strategies. A few hospitals in Australia were among the first in the world to introduce routine antenatal screening for GBS carriage and intrapartum antibiotic prophylaxis for carriers.1 This approach was later vindicated by randomised controlled trials in selected carriers2 and the demonstration of lower rates of sepsis after intrapartum prophylaxis compared with historical rates.3 However, problems remain. Group B streptococcus is a normal vaginal commensal in healthy women, but colonisation is often intermittent, and rates of colonisation can vary from 18% to 27%, depending on the detection method.4 Moreover, vaginal carriage is a very crude predictor of perinatal sepsis, with fewer than 1% of the infants of carriers affected (1–2/1000 overall) without intervention.1,5 In 1996, the Centers for Disease Control and Prevention (CDC) in the United States published consensus guidelines for selecting women for intrapartum antibiotic prophylaxis using either of two alternative strategies. One strategy was based on maternal GBS carriage, and the other on clinical risk factors — preterm labour (< 37 weeks' gestation), prolonged rupture of membranes (> 18 hours) or intrapartum fever (> 38oC).6 The rationale for the latter strategy was that, before widespread use of intrapartum antibiotics, one or more of these risk factors was found in up to 80% of mothers of infants with GBS sepsis.1,7 Gradual implementation of these consensus guidelines in the US was associated with a fall in the incidence of perinatal GBS sepsis from 1.7/1000 in 1992 to 0.5/1000 in 1999.8 In Australia, there was also a decrease in the incidence of perinatal GBS sepsis, from 1.2/1000 in 1991–1993, when three of nine neonatal units surveyed had prevention strategies in place, to 0.5/1000 in 1995–1997, when all 11 units surveyed had prevention strategies.5 A recent review concluded that there is evidence, albeit from relatively poor-quality trials, that intrapartum prophylaxis reduces the incidence of neonatal sepsis, but not deaths.9 Despite this evidence, concern continues about excessive use of intrapartum antibiotics. There have been several reports that their increasing use is associated with an increased proportion of cases of neonatal sepsis caused by penicillin-resistant bacteria.10,11 Although it is sometimes difficult to prove, there is considerable empirical evidence that increased antibiotic use generally leads to increasing bacterial resistance. It is plausible that exposure to antibiotics in utero might delay colonisation of the infant gut with penicillin-sensitive anaerobes and allow penicillin-resistant facultative bacteria — many of which are potential pathogens — to become established. Recently, the CDC published revised guidelines, recommending a single strategy for prevention based on universal prenatal screening for vaginal or rectal GBS colonisation.12 The recommendation was based on a retrospective cohort study, which showed that perinatal GBS sepsis was significantly less frequent in infants of women given intrapartum antibiotics on the basis of documented GBS screening results (0.33/1000 births) than in infants of women managed on the basis of risk factors (0.59/1000 births; relative risk, 0.48; 95% CI, 0.37–0.63).13 This result is not surprising. A risk factor-based protocol cannot, by definition, prevent sepsis in infants whose mothers have no risk factors. On the other hand, the proportion of cases prevented by a protocol based on GBS colonisation depends on the sensitivity of the screening method, effectiveness of prophylaxis and compliance with the protocol.4,14 What was surprising in the CDC study was that the anticipated overall rate of intrapartum antibiotic use was similar for both prevention strategies (31% and 29%).13 In contrast, we showed that in Australia a strategy based on risk factors would lead to significantly less use of intrapartum antibiotics (18%–20% of women) than a strategy based on antenatal screening at 35–37 weeks' gestation (35%).4 This difference is apparently due to a higher incidence of risk factors in the US compared with Australia, and failure to account for women given intrapartum antibiotics during preterm labour before results of screening are available. They suggest that obstetricians in Australia should not immediately discard the option of a risk-based strategy. Neither strategy is ideal, but either, if properly implemented, can reduce the incidence of perinatal GBS sepsis. The GBS screening strategy results in at least a third of healthy young women (and their infants) being given intravenous antibiotics during labour, at significant cost and with some risks, but can achieve a lower rate of perinatal GBS sepsis.13 In Australia, with a risk-based strategy, significantly fewer women and infants would receive intravenous antibiotics. Whichever strategy is chosen, the most important determinant of its effectiveness will be compliance.

Gwendolyn L Gilbert MD, FRACP, FRCPA

The biology of colorectal cancer provides an important opportunity for cancer prevention, as most cancers in the lower bowel evolve from polyps (adenomas). Removal of adenomas markedly reduces the subsequent risk of disease. Consequently, the rational aim of any prevention program should be not only to detect early cancer but also the precursor adenoma. The strategies to reduce mortality include: investigation of high-risk symptoms such as rectal bleeding — often by colonoscopy; colonoscopic surveillance for those with a personal or family history of colorectal cancer or polyps; and screening, beginning at age 50 years, of individuals of average risk, who account for 85% of sporadic cancers. The practice of colorectal cancer prevention in Australia has been largely influenced by recent National Health and Medical Research Council (NHMRC) guidelines.1 An attempt to finalise these guidelines began in 1997 and their slow gestation may have rendered them insensitive to more recent data and not typical of practice worldwide. Three of the major NHMRC recommendations remain controversial. Patients with a single first-degree relative with colorectal cancer diagnosed over the age of 55 do not have a sufficiently increased risk to warrant colonoscopic surveillance. The NHMRC guidelines quote a twofold increase in risk in this group. A recent analysis of 27 case–control and cohort studies indicates that the relative risk is 2.25 and that this risk doubles with more than one relative affected.2 We believe that a doubling of lifetime expected risk of colorectal cancer in men from 1 in 18 to 1 in 9 (only slightly lower in women) is sufficient to advocate colonoscopic surveillance on a five-yearly basis starting at the age of 40, irrespective of the age of the relative. Patients with a single adenoma < 1 cm in size not showing any villous component need colonoscopic follow-up only at 4–6-yearly intervals. This recommendation is mainly based on the US National Polyp Study.3 It is difficult to reconcile these data with other reports. For example, Rex et al3 showed "miss-rates" of 5% for colorectal cancer, and polyp "miss-rates" ranging from 6% to 15%, even in experienced hands. Therefore, there needs to be considerable flexibility in planning postpolypectomy surveillance. Two articles in this issue of the Journal, by

Terry Bolin MD, FRCP · Alistair E Cowen MD, FRACP · Melvyn G Korman PhD, FRACP

Sedation is a difficult concept to define, as it includes a continuum from anxiolysis to anaesthesia. The point at which sedation becomes anaesthesia is generally accepted as occurring when the patient becomes unresponsive to verbal commands.1-3 Sedation is a depression of, rather than a loss of, consciousness, and may be combined with analgesia and amnesia to facilitate otherwise unpleasant and painful procedures. There is a large demand for sedation with endoscopy in Australia, although this is not universal practice.4 For instance, most colonoscopies in Germany are performed without sedation. There has been serious concern as to the safety of sedation for endoscopy following a prospective audit of gastroscopy and sedation in the United Kingdom in 1994. This audit found a 0.05% (1 in 2000) 30-day mortality.5 Although arguable, a third of these deaths were attributed to complications of sedation. There have been no comparable large-scale audits reported since, but anecdotal reports of mortality persist. The concern becomes more apparent when the comparison is made to the Australian anaesthesia-related death rate of less than 1 in 63 000.6 There are no reliable Australian data on deaths related to sedation. Consequently, professional documents have been formulated in the UK, the United States, Australia and New Zealand based on first principles and consensus, rather than on substantial evidence. In this issue of the Journal (page 158), the audit by Clarke et al on sedation for endoscopy7 primarily demonstrates how effective these professional guidelines have been. With the universal use of dedicated trained sedationists, supplemental oxygen, monitoring of pulse oximetry, blood pressure and respiration, patient selection and an accredited facility, there was no mortality reported in 28 472 endoscopies. The only caveat to this mortality rate is that postdischarge follow-up was limited to one telephone call. Notwithstanding this good news, most of the interest generated in this report will be because it describes general practitioner sedationists using propofol. The GPs in this audit had selection criteria, training and a maintenance-of-standards program that was entirely consistent with the current guidelines.1 Furthermore, complex or high-risk patients were transferred to hospitals (numbers unknown) or to the care of an anaesthetist (21.4%), which again is in keeping with the guidelines.1 The departure from the guidelines occurs with the use of propofol — the guidelines do not allow medical practitioners other than anaesthetists to use this agent. This applies to all intravenous anaesthetic agents (eg, methohexitane and ketamine), largely because of the rapidity with which sedation becomes anaesthesia. Sedation is achieved with propofol at about a third of the anaesthetic blood concentration or dose. Problems arise with propofol because of the individual variation of the anaesthetic concentration or dose, which in itself can vary by a factor of three, and the synergistic effects of narcotics and benzodiazepines, which may reduce the anaesthetic concentration or dose by as much as 50%. Propofol is further complicated by having its peak effect at about four minutes, making titration difficult. However, propofol is redeemed by the short redistribution half-life of 2–8 minutes and the failure of blood concentrations to achieve significant levels during its long elimination half-life (3–8 hours), owing to its extremely high clearance rate. Propofol is approved in Australia for conscious sedation. The real issue is what is the intent of the propofol administration. If the intent is loss of consciousness, then it is anaesthesia, and the drug should be administered by an anaesthetist in an institution equipped and licensed for anaesthesia. In New South Wales, institutions have been prosecuted after adverse patient outcomes for administering anaesthesia with such agents while not licensed. It is difficult in this audit, because of the failure to differentiate the propofol doses used by the GPs (78.6% of cases) and the anaesthetists (21.4% of cases), to determine the doses used by the GPs. However, the doses appear consistent with planned sedation. Nevertheless, GPs had a higher incidence of adverse events (not reaching statistical significance) and, significantly, a higher intervention rate for respiratory adverse events than the anaesthetists, even though complex patients and procedures were allocated to anaesthetists. In summary, the audit by Clarke et al supports the effectiveness of the current guidelines for sedation. The use of propofol in circumstances defined by current guidelines may be sufficiently safe when the agent is administered by such appropriately trained medical practitioners. Propofol and other intravenous anaesthetic agents should not otherwise be used by medical practitioners, except those who are trained in anaesthesia.

Greg E Knoblanche

Few events are harder to deal with than sudden death in young people. Each year in the United States, about one in 200 000 high school or college athletes will die suddenly, the vast majority without any prior symptoms,1 and these devastating events are often the first clinical manifestation of an underlying cardiovascular disorder. Indeed, about 90% of sudden deaths, defined as death occurring within one hour of the onset of symptoms, are found to be caused by cardiac structural pathology in autopsy-based series. The remaining 10% relate to other cardiac electrical disorders, such as long-QT syndrome and Wolf–Parkinson–White syndrome, or commotio cordis (the result of sudden sharp chest blows), as well as complications of asthma, substance misuse, and sudden infant death syndrome (SIDS).2 The single most common disorder causing sudden cardiac death in people aged less than 35 years, including competitive athletes, is the genetically inherited cardiac disorder hypertrophic cardiomyopathy (HCM).1 HCM is characterised by cardiac hypertrophy, usually of the left ventricle, in the absence of other loading conditions such as hypertension or hyperthyroidism. This disease occurs in approximately one in 500 people. It is clinically heterogeneous, with most affected individuals having few or no symptoms, while others develop serious complications, including heart failure, arrhythmias, and sudden death.3 In a series of 158 sudden deaths in young competitive athletes (median age, 17 years), 36% were found to have HCM and an additional 10% had evidence of increased cardiac mass suggestive of HCM.1 In Australia, 34 sudden deaths in people with HCM were reported to the HCM clinic at Sydney's Royal Prince Alfred Hospital over a five-year study period.4 A substantial proportion of patients with HCM die during or immediately after vigorous physical activity, but sudden death during rest or sleep is also common. The mechanism of death relates to ventricular arrhythmias in over 90% of known cases. Over the past decade, major advances have been made in understanding the genetic basis of many of the disorders which cause sudden death. DNA defects in disease-causing genes have been identified in HCM, as well as the long-QT syndrome, Marfan syndrome, dilated cardiomyopathy and arrhythmogenic right ventricular dysplasia. Over 200 mutations in at least 10 genes, all encoding proteins of the sarcomere (the basic contractile element of the heart), have been identified.5 Not only have such discoveries thrown light on the molecular pathogenesis of this disorder, but they have also enabled us to predict an apparently favourable or unfavourable clinical course.6,7 For example, many people in families with the Arg403Gln mutation in the beta-myosin heavy chain gene develop severe symptoms and even die by age 45 years. In contrast, individuals with the Val606Met mutation in the same gene usually appear to experience minimal symptoms and have a normal life expectancy.7 Clearly, understanding the molecular mechanisms by which gene defects lead to the clinical phenotype is important. To this end, the recent sequencing of the human genome8 offers the potential to identify more causative genes in HCM and other medical disorders. It also provides the possibility of understanding the mechanisms and signalling processes with which these genes regulate and modify gene expression (either by second disease-causing or modifying genes or environmental factors), leading to recognition of therapeutic targets important in the pathogenesis of sudden death (eg, ion-channel genes and genes regulating cardiac collagen formation). Pharmacological agents ranging from β-blockers to amiodarone, while frequently used, have not been shown to be effective in preventing sudden death in HCM. However, the implantable cardioverter-defibrillator has emerged as a proven therapy.9 Patients should be selected for implantable cardioverter-defibrillator implantation based on risk-stratification parameters. Proven predictors of sudden death which should identify patients who would most benefit from an implantable cardioverter-defibrillator are shown in the Box. Further, providing automatic external defibrillators in public places where crowds are present and where people may be at higher risk (eg, sporting venues) might be of significant benefit in reducing sudden cardiac death in this setting. In HCM, sudden death has been the most visible and devastating consequence of the disease since the original report by Teare over 40 years ago.10 Accurately identifying individuals at highest risk and initiating the most effective therapy to prevent this complication are clearly the ultimate goals. Understanding the genetic basis and molecular mechanisms underlying the cardiovascular disorders that cause sudden death, using this knowledge to identify potential new therapeutic targets, coupled with the use of established therapies such as implantable defibrillators, will go a long way to achieving these goals. Risk stratification and screening in sudden cardiac death Risk factors for sudden cardiac death Family history of premature sudden death Individuals with a family history of an inherited disorder associated with sudden death (eg, hypertrophic cardiomyopathy, long-QT syndrome) Previous cardiac arrest Previous episodes of documented ventricular tachycardia Recurrent syncope A known "malignant" gene mutation Specific risk factors for a disease (eg, left ventricular wall thickness greater than 30 mm in hypertrophic cardiomyopathy) Screening tests for family members at risk of sudden cardiac death History Physical examination 12-lead electrocardiogram Echocardiogram Other tests, such as Holter monitoring and exercise testing

Christopher Semsarian MB BS, PhD · Barry J Maron MD