Volume 177 Issue 4

Australia does not do well in the early detection of congenital hearing impairment. Only about 25% of infants born with hearing impairment are diagnosed by the age of 12 months, and for many children deafness remains a disability leading to severe and lasting language impairment.1 The technology for newborn hearing screening has now been in regular use in many parts of the world for much of the past decade, and there is at last some persuasive evidence that very early detection helps these children achieve normal language skills.2,3 This evidence is far from perfect: 4 only one randomised controlled trial of detection rates with and without newborn screening has been reported, and no randomised controlled trial has yet examined outcomes of hearing screening. Nonetheless, universal newborn hearing screening has become not only possible but expected in the United States and Canada, the United Kingdom and many European countries. However, it has not yet been widely implemented in Australia. As a result, the excellent diagnostic and rehabilitative services available to all Australian children once the diagnosis of hearing impairment has been made contrasts strongly with our patchy and very incomplete ascertainment of hearing impairment in the first year of life. The Western Australian Newborn Hearing Screening Programme is therefore an important step, as is the recent announcement that a program will commence throughout New South Wales by the end of 2002. In a report of the WA program in this issue of the Journal, Bailey et al (page 180)5 demonstrate that a high-quality, sustainable universal newborn hearing screening program can operate in Australian birthing hospitals. It appears to be a model program, with exceptionally high coverage, high acceptability, low referral rates, and low rates of babies lost to follow-up. It exceeds most benchmarks set in 2000 by the US Joint Committee on Infant Hearing,6 and is in line with the Australian National Consensus Statement on Newborn Hearing Screening.7 Nonetheless, it raises a number of difficult issues. Bailey and colleagues report that the hearing screening program has achieved more than 96% coverage in the five participating metropolitan hospitals. However, together these screened infants represent only about half Western Australia's annual births — unfortunately, the "easy" half. The program operating throughout the US State of Colorado,8 one of the few approaching a true population coverage, has demonstrated that hospitals with fewer than 400 births annually do worse on average than large hospitals in terms of coverage (substantially lower) and referral rates (substantially higher). Australia is characterised by vast distances and a very large number of small hospitals. For instance, the State of Victoria has a similar birthrate to Colorado, but nearly twice as many birthing hospitals (about 110, compared with 60), most of which are small. Statewide or national newborn hearing screening therefore poses considerable logistic and economic obstacles in Australia, and these are not necessarily surmountable. But what are the consequences of limiting ourselves to larger hospitals? Let us assume that 50% of a State's population receives a very high quality hearing screening program which achieves 95% coverage, 90% sensitivity, 95% follow-up, and 80% compliance with early fitting of hearing aids and intervention (as some parents choose neither). This equates to less than a third of that State's hearing-impaired children benefiting from the program. If any one of these parameters is lower, then the number of children potentially benefiting falls even further. Despite individual gain, median age at diagnosis and overall outcomes for the State would improve little. If universal screening is to lead to population benefits, then universal it needs to be — despite the challenges. A poor alternative is to screen only babies with a risk factor for deafness. Asking about the presence of a risk factor becomes the universal "screen", followed by a targeted screening test of hearing itself. At face value, this may seem cheaper, but it is not easier and certainly detects fewer children. While almost all children with hearing loss detected in the Western Australian series so far have had a risk factor, in larger series this applies to only about 50% of babies.8,9 Neonatal intensive care and special care nurseries typically contain about 30%–40% of all infants found to have moderate or greater hearing loss in newborn screening programs9,10 and are relatively easily targeted, as are babies with obvious head and neck abnormalities. Other risk factors, such as family history of early hearing impairment, pose greater problems. Accurate elicitation requires skilled enquiry and mothers may not recall, or even know, that a risk factor is present until after the diagnosis is made, thus reducing sensitivity. The Victorian Infant Hearing Screening Program has recently highlighted the very low positive predictive value of family history and some other risk factors, with close to 200 babies needing to be referred to diagnose one child with hearing loss.11 Low sensitivity combined with poor positive predictive values equates to spending a lot of money to miss many children. Finally, risk-factor screening raises issues of equity, as the many children with hearing impairment, but without a discernible risk factor, would be denied access to hearing screens in such a program. A final issue is that of program sensitivity. At 0.7 per 1000, Western Australia's detection rate for children with bilateral congenital hearing impairment of more than 35 dB HL (hearing level) is lower than the usual rate of 0.9–1.0 per 1000 detected (with hearing impairment of more than 40 dB HL in the better ear).8,9 Most likely, this is a chance finding reflecting the small size of the series — it "just happened" that relatively few babies with hearing impairment were born during this time period. Alternative explanations include equipment problems or program insensitivity. The Western Australian program is unusual in that a baby is not referred until screening has shown three "fail" responses. This lowers the false positive rate and increases program specificity — both of which are desirable. But in screening programs rises in specificity are typically accompanied by falls in sensitivity. It may be that, in this case, the pendulum has swung too far towards specificity at the expense of sensitivity, and that, after years of worrying about excessive referral rates, they are — at last — too low. Currently, we are not serving well the hundreds of children born each year with moderate or greater hearing impairment in Australia. Universal newborn hearing screening seems one way of improving this situation. It is not reasonable to defer implementing a program until the evidence is stronger, since stronger evidence is unlikely to be available soon. Rather than stopping us from implementing programs, this should spur us to acquire such evidence. Because Australia has not yet widely introduced newborn hearing screening, we have an unusual capacity to study these questions prospectively. National benchmarks and a minimum dataset should be established, and we should start carefully and systematically examining outcomes for hearing-impaired babies born now against which to compare gains over the coming years. We should also keep an open mind. In 10 years' time, Australia should be able either to guarantee continuation of an effective program, or to move resources rapidly from a program that, despite best efforts, has proved ineffective.

Melissa A Wake MD, FRACP, MB ChB

In 1997, South Australian women around the age of menopause had one of the highest reported rates of hormone replacement therapy (HRT) use in the world.1 Among women aged 55–64 years, 60% had used HRT and nearly 40% were current users, with a mean length of HRT use of 70 months. HRT is effective at relieving menopausal symptoms, and many women can stop taking HRT within a few years without recurrence of these symptoms. For the women who do experience return of menopausal symptoms after ceasing HRT, there has been the comfort of observational studies that showed that long-term HRT use, although increasing the risk of breast cancer and thromboembolic disease, reduced osteoporosis, bowel cancer, cardiovascular events, Alzheimer's dementia, and possibly stroke.2 Critics of long-term HRT use have argued that selection of relatively healthy women to receive HRT may have influenced its reported long-term effects in unrandomised observational studies.3 Two large randomised trials of postmenopausal long-term HRT use were commenced in the 1990s to determine the benefits and risks. The Women's Health Initiative (WHI) in the United States (see website <http://www.whi.org>) focuses on defining the value of different strategies (eg, low-fat diet, calcium and vitamin D supplementation) that could potentially reduce the incidence of heart disease, breast and colorectal cancer and low-impact fractures in postmenopausal women aged 50–79 years. The Women's International Study of long Duration Oestrogen after the Menopause (WISDOM) (http://www.generalpractice.adelaideuni.org/research_index.htm [No longer available]) is a UK-initiated, placebo-controlled study of women aged 50–69 years taking oestrogen, or oestrogen and progestogen, for 10 years. Endpoints of the study include fracture, cardiac events, cancer, dementia, thromboembolism, quality of life, and death. Some Australian women have been recruited to the WISDOM study. Late in the evening (Australian time) of 9 July 2002, the American Medical Assocation posted a report of a WHI trial and an accompanying editorial on its JAMA website.4,5 The report revealed that this randomised, placebo-controlled, double-blind trial to evaluate combined oestrogen and progestogen therapy in postmenopausal women had been stopped early because there was compelling evidence that health risks exceeded health benefits. Graham Colditz (Professor of Medicine at Harvard School of Public Health and one of the authors of the JAMA editorial), who was visiting Australia at the time, and the Cancer Council, New South Wales, were ready to issue press releases (embargoed until 11.30 pm that evening) highlighting the 26% increased risk of breast cancer in women taking HRT. One of these releases was headed "Women advised to stop combined hormone replacement therapy". By the next morning (10 July), the Australian media were awash with headlines and reports that fuelled considerable alarm among women taking HRT. On the same day, the Australian Therapeutic Goods Administration (TGA) requested that the Australian Drug Evaluation Committee (ADEC) establish an Expert Committee to examine the JAMA article and provide advice on the significance of the study outcomes in the Australian context, the necessary and appropriate action required of the TGA, and the information that should be provided to Australian health professionals and consumers. The rapidly convened ADEC Committee reviewed the JAMA article and editorial and gave the TGA its report, which was released on the TGA website in the late afternoon of 11 July. The report noted that the WHI trial was designed to investigate the efficacy and safety of long-term combined HRT in preventing diseases such as coronary heart disease and hip fracture in postmenopausal women. It was not designed to study the effects of HRT being used to treat menopausal symptoms or established osteoporosis. The mean age of women in the study was 63 years, with two-thirds being over 60. This, and the apparently high frequency of cardiac risk factors in the population (one-third being overweight and one-third obese, 50% being previous or current cigarette smokers, one-third having received treatment for high blood pressure, and over 10% having raised cholesterol requiring medication), may have led to a higher risk of cardiovascular events. However, this must be set against a likely underestimate of the excess risk as a result of treatment dropout and crossover. There was no difference in overall mortality between the HRT and control groups for the duration of the study (mean, 5.2 years). The absolute increase in disease risk for an individual woman shown in the study was small: among 10 000 women in the age group studied and with their characteristics taking combination HRT for a year, there would be seven more cases of coronary heart disease (37 v 30), eight more cases of invasive breast cancer (38 v 30), eight more cases of stroke (29 v 21), and eight more cases of pulmonary embolism (15 v 7), but six fewer bowel cancers (10 v 16) and five fewer hip fractures (10 v 15), than among women not using HRT. Over the five years of the trial, there would be one extra case of an adverse event per 100 women taking the combined HRT continuously. The Expert Committee noted the increase in harm reported was smaller in the first two to three years after starting HRT than it was after three or more years of combined HRT use. Conclusions of the Expert Committee of the Australian Drug Evaluation Committee Combination hormone replacement therapy (HRT) in any form should not be used for long-term disease prevention in postmenopausal women, because the benefits are not sufficient to justify the risks. This conclusion is not necessarily restricted to the particular products used in the trial, but could potentially apply to all oestrogen/progestin combination hormone products. Women can be assured that short-term use of combination HRT and other products to manage symptoms of menopause remains an appropriate treatment option, but women should discuss their particular medical circumstances with their doctors, as individual factors may affect the risks and benefits for them. This is even more so for younger women with a premature menopause, in whom the benefits of HRT would be expected to be greater, and the risks are probably smaller. The continued use of combined HRT for women with established osteoporosis is also an acceptable option for many, but women should discuss the benefits and risks with the treating doctor. In another arm of the Women's Health Initiative study, which has not been discontinued, the use of oestrogen alone for the prevention of disease in postmenopausal women who have had a hysterectomy continues under investigation. It is unsafe for women who have a uterus to use oestrogen without progestin, as use of oestrogen alone increases the risk of uterine cancer. The conclusions of the Expert Committee are presented in the Box. The Committee recommended that the TGA ensure updating of product and consumer information for all products used in combination HRT, undertake a full review of the use of combination HRT in long-term treatment and prevention of osteoporosis, and review all ongoing trials using combination HRT for chronic diseases. The WHI trial report and the abrupt cessation of the combined oestrogen plus progestogen trial have raised concerns among health practitioners, prescribers and consumers of combined HRT products. The previously anticipated health benefits from prolonged combined HRT use — reduced heart disease and strokes — were not borne out in the WHI study. However, the absolute risks associated with HRT are small. Women who are currently taking combined HRT, and their doctors, should not panic, but consider these new findings carefully in the light of their reasons for starting and continuing HRT before deciding whether to continue or stop. In women with osteoporosis, the benefit of a reduced fracture rate with long-term combined HRT must now be balanced against the increased risks of breast cancer, stroke, heart disease and thromboembolism. The relative efficacy and safety of HRT must be considered against that of other interventions, including ensuring adequate calcium intake and vitamin D status, exercise, or taking bisphosphonates or selective oestrogen-receptor modulators.

Martin H N Tattersall MD FRACP

On 8 July 2002, the National Health and Medical Research Council released a discussion paper1 and draft guidelines for xenotransplantation research, with the aim of promoting widespread community debate of the issues involved. In the discussion paper, xenotransplantation is defined as the placement of animal cells, tissues or organs into humans, and includes the exposure of human tissue or cells to animal cells. Examples include the external perfusion of blood through a "bioartificial liver" (ie, an external apparatus containing pig liver cells which are separated from the perfused human blood by a semipermeable membrane), or culture of human skin cells on mouse fibroblasts for later use in treating burns. This definition excludes implantation of inert, sterilised animal tissues, as currently used to create artificial heart valves. The concept of xenotransplantation has arisen because of an ongoing shortage of human donor organs. The discussion paper provides information on this shortfall, and measures pursued in Australia and overseas to try to improve organ donation rates. As there is general acceptance that the demand for donor organs is such that even increased human donation will not overcome the problem, the complex issues attending the shortage of human donors are not pursued further in the discussion paper. So, what are some of the matters requiring community consideration and debate? A key issue is the risk that an infectious agent could cross from an animal to humans, and produce unknown infectious risks for the general community. Cross-species transmission of most known viral and bacterial pathogens is preventable by appropriate breeding, housing and testing of source animals. However, there is serious concern that a virus, such as the endogenous retrovirus present in the pig genome (the pig is currently the preferred source of organs), could "reactivate" in human recipients and, theoretically, later infect close contacts, healthcare workers or the wider community. Although experimental work has demonstrated that isolated human cell lines can be infected with porcine endogenous retrovirus (PERV), retrospective testing of 160 patients exposed to date to pig xenotransplants, such as islet cells or neural cells, or to external perfusion using pig liver cells, has not revealed evidence of PERV infection.2 This risk of infection brings a new ethical dimension to how consent for xenotransplantation research might be given. The discussion paper emphasises that not only will any potential recipient need to be fully informed of any risks, but so too will close contacts of the recipient and members of the healthcare team. An additional ethical issue relates to how a prospective recipient might reasonably choose between risking an experimental therapy or waiting for a human organ transplant. Another issue which requires community debate is the potential use of genetically modified pigs to overcome the intense rejection reaction which, so far, has made xenotransplantation unfeasible. While experimental work to date has involved minimal genetic manipulation, more extensive modification (which could be seen to significantly alter the essential nature of the animal) may not be acceptable ethically or to our community. In all human research, a key ethical principle is that the putative benefits must outweigh the known and theoretical risks. Weighing this balance for any human xenotransplantation research proposal will not be an easy task. The draft guidelines outline multiple conditions which must be met before research can be approved. One such requirement is obtaining convincing data of the efficacy of animal-to-animal experiments (eg, pig-to-baboon xenotransplantation) before pig-to-human trials can be contemplated. A further issue relates to which group of individuals should be empowered to weigh up these benefits and risks and give approval for such human research on the community's behalf. The discussion paper recommends that this should be a task for a national committee, whose membership would include people with relevant scientific, ethical and regulatory expertise, as well as community members. Local human research ethics committees would play a role in monitoring the research, and could reject a proposal, but could not approve a proposal unless it had also received approval from the national committee. The full text of the document, entitled Draft guidelines and discussion paper on xenotransplantation, is available on the National Health and Medical Research Council (NHMRC) website,1 or can be obtained from the NHMRC at PO Box 9848, Canberra, ACT 2601. The document contains advice on how to make a submission by the closing date of 6 September 2002. Submissions will be carefully considered by the working party in making its final recommendations to the Council. The NHMRC regards xenotransplantation research as one of the more important issues for community consideration, and wishes to actively involve medical practitioners in the debate. Medical practitioners are invited to either develop and communicate their own views, or to assist in stimulating debate in the wider community.

Kerry J Breen, on behalf of the NHMRC Working Party on Xenotransplantation MD, FRACP

Research and practice in grief and loss have been undergoing something of a sea-change in recent years. Past research-based models of grief have attracted much criticism, not only from practitioners but also from researchers in the social sciences. There have been persistent calls for greater sensitivity to the contexts of grief and a more balanced understanding of its positive and cultural influences in our lives. Most of our understanding about grief has been drawn from psychoanalytical sources (eg, the work of Freud or Klein) and later from attachment theory (eg, the work of Bowlby).1 These sources have emphasised the role of the emotions and psychological defences. Research commonly focused on particular populations (such as children, the terminally ill, the mentally ill, or victims of disasters), while the research on community samples examining the loss of spouses, parents or children overidentified grief with bereavement. The conceptual emphasis that emerged from this research stressed issues such as "loss", "disengagement" or "resolution".2 There were debates about whether grief was a "state" or a "process", and later, when the process theories became popular, whether these processes had "phases" or "stages". Many practitioners and popular writers working in bereavement care embraced much of this important early work, which still forms the basis of our understanding of personal control and adaptation in the face of loss. But a concentration on the psychodynamics of attachment and defence inadvertently resulted in overattention to professional interventions and an underemphasis on social relationships, contexts and cross-cultural issues.3 The early work by the psychological professions also led to a concentration on the negative experiences of grief. The traumatic, obsessional and socially destructive aspects of grief were stressed and examined. The concern was to reduce the morbidity and mortality associated with grief, particularly to lessen its role in suicide, substance misuse and other psychiatric conditions, such as severe anxiety or depression. Recent research has attempted to restore greater professional and conceptual balance to these early insights and concerns. There are now increasing numbers of sociologists, anthropologists and historians entering the field, and many of these have been critical of the psychological emphasis on attachment, separation and "letting go".4,5 There has been greater attention to the different ways people grieve according to their own social norms, cultural prescriptions and personal styles.6 There is a growing awareness and theoretical interest in the relationship between bereavement and other kinds of loss, such as the dispossession felt by Indigenous people and refugees, or losses associated with adoption.7 There has been growing international acceptance of a theory of "continuing bonds" — a recognition that people do not necessarily "let go", but transform their former relationships by renewing their meanings about them and continuing the relationship in new ways.8 There has been some recognition of the limits to professional help, reflected by the growing interest, worldwide, in support and self-help groups. The growing input of the social sciences has encouraged a parallel interest in the role of social and cultural differences in the expression of grief and its diverse coping styles. There has been a renewed interest in normal and positive aspects of grieving. There is a growing realisation that the dead may be important role models for the grieving; that they may continue to be "significant others" to the bereaved. People continue to relate to their dead as "active and living memories" at times of personal crisis and success.9 Grief can also create a positive social legacy — in advocacy (influencing policy and education), in political activism (giving rise to groups such as Mothers Against Drink Drivers), in foundations (supporting research or service development) and in careers (heightening the personal achievements and ambitions of survivors).10 Grief also creates "social ghosts" in the form of influential memories, dreams, or visions.11 These can be both comforting and disturbing; motivating and hope-giving as well as upsetting. Furthermore, the general experience of grief can enhance personal empathy and social compassion. These previously under-recognised perspectives present new but complementary challenges for research and practice in the care of people suffering grief. We need to return our attention to the diverse expressions of normal and healthy grieving, while continuing to recognise that grief can cause marked health changes in some individuals. The new insights also highlight the limits to professional care and the need to create supportive environments in our communities for people living with loss. There is a major need for government policy development in this area to reflect a broader public health sensitivity towards our diverse national grief and loss needs. Policy and research priorities might address issues such as the social impact of grief on Indigenous health, on the lives of elderly people, or on the desire for suicide. These research directions will assist us to understand public expressions of creativity or personal experiences of resilience. Our referral options for people suffering grief should include community support, such as pastoral care or the National Association for Loss and Grief, as well as specialist medical and psychological services. These issues are only some of the recent practice and research challenges to emerge in the field of grief and loss, but they point to its constructive and positive revival.

Allan Kellehear

Otitis media — definitions Acute otitis media without perforation: Presence of middle-ear fluid with symptoms or signs of suppurative infection. Bulging of the tympanic membrane is the most reliable sign in Aboriginal children. Acute otitis media with perforation: Acute suppurative infection with recent discharge from the middle ear (within the last 7 days). Otitis media with effusion: Presence of middle-ear fluid without symptoms or signs of suppurative infection. Chronic suppurative otitis media: Persistent discharge from the middle ear through a tympanic membrane perforation for more than 6 weeks. Chronic suppurative otitis media (CSOM) (see Box) is very uncommon in First World countries and is best regarded as a disease of poverty. The World Health Organization has indicated that a prevalence rate of CSOM greater than 4% in a defined population of children is indicative of a massive public health problem requiring urgent attention.1 That CSOM affects up to ten times this proportion of children in many Aboriginal communities is an indictment of the poor living conditions in these communities.2 The associated hearing loss has a life-long impact, as it occurs during speech and language development and the early school years. Why is chronic suppurative otitis media so recalcitrant?Many factors contribute to poor health outcomes. In biological terms, the greatest risk factor for the early onset and persistence of otitis media is nasopharyngeal colonisation by multiple bacterial species and subtypes.3 In Aboriginal communities with overcrowded households, infants are frequently exposed to siblings whose nasopharyngeal carriage rates are almost 100% for each of the major otitis media bacterial pathogens.3 In non-Aboriginal children, the host response to a low-dose infection usually eradicates pathogens, which, in turn, down-regulates inflammation and limits tissue damage. In contrast, we believe that early exposure of very young Aboriginal infants to a large bacterial inoculum (or frequent exposures to immunologically distinct pathogens)4 provides constant stimulation of the inflammatory cascade, which damages mucosal tissue yet fails to eradicate pathogens.5 This begins a vicious cycle that may persist throughout childhood: early exposure, persistent bacterial colonisation, and chronic mucosal disease. Furthermore, such infants themselves become chronic carriers and pose a risk to other, younger infants. This cycle is facilitated by overcrowded and poor living conditions, lack of appropriate washing facilities,6 and limited access to appropriate healthcare services. Bulging of the tympanic membrane is the best diagnostic predictor of perforation.7 Other signs and symptoms of acute otitis media (such as pain, fever, irritability or redness of the tympanic membrane) are frequently absent in this population. The implications of this lack of signs or symptoms are clear — parents do not see their child as unwell and thus children remain untreated. Together, this biological model and clinical pattern help us to understand the intractable nature of otitis media in Aboriginal children. Currently, failure to apply existing knowledge is a more important problem than lack of knowledge. Aboriginal children have poorer access to therapy, hearing aids, special teachers, classroom soundfield systems and other rehabilitative programs.2 Furthermore, there is inequitable distribution of funds from the Commonwealth Hearing Health Services Program, with evidence that the hearing health needs of Aboriginal children are not being met.8 What strategies have worked?A systematic review of existing evidence and primary care guidelines for the management of otitis media in Aboriginal and Torres Strait Islander people2 identified effective primary prevention strategies: improving nutrition and the home environment, increasing breastfeeding, and reducing passive smoking. A small but important role was noted for vaccines (the polysaccharide, polyvalent pneumococcal vaccine and the new pneumococcal conjugate vaccine). Controversies remain regarding the effectiveness of antibiotics in primary prevention and the impact of maternal pneumococcal vaccination on infant disease.2 High doses and prolonged courses of antibiotics are often required for the treatment of acute otitis media and CSOM,7 but the optimal use of topical ear preparations remains uncertain.2 Where appropriate primary healthcare interventions have failed, timely referral to otolaryngologists for assessment and surgical interventions can improve hearing outcomes.2 However, access to such specialist care for children in remote Aboriginal communities is suboptimal. Audiological rehabilitation is critical, requiring the provision of ongoing education about effective communication strategies and appropriate use of devices to assist hearing. These include standard hearing aids and bone conductors, as well as classroom devices such as soundfield amplification systems (which provide a uniform soundfield throughout the classroom and increase the speech-signal : noise ratio), and FM systems (a form of personal amplification whereby an FM signal from a microphone worn by the teacher is picked up by a receiver worn by a child with hearing loss).9 What needs to happen in the future?Greater community control over improvements to education, employment opportunities, housing infrastructure and primary healthcare services is long overdue. To realise these improvements requires substantially increased resources, linked to community responsibility. In the meantime, initiatives that increase access to primary healthcare for the detection and management of ear disease and facilitate access to other services should continue. An example is the Office for Aboriginal and Torres Strait Islanders Health Hearing Health Program.10 Realistic expectations about the benefits and harms of evidence-based healthcare interventions should be incorporated into updates of currently available clinical guidelines, and the information made accessible to families. The Commonwealth needs to reform the provision of rehabilitative services and coordinate approaches to soundfield amplification in schools. The research priority is to determine the best use of preventive strategies and interventions (including educational, medical, surgical and audiological initiatives). Multidisciplinary research in the areas of diagnosis, new antibiotics, the role of biofilm and vaccines is also appropriate. Bacterial biofilm is a community of interacting bacteria attached to a surface and encased in a protective matrix of exopolysaccharide. Formation of biofilm in the middle-ear mucosa of Aboriginal children with CSOM may explain the recrudescence of bacterial otorrhoea after viral upper respiratory tract infections.11 Pneumococcal conjugate and innovative protein-based vaccines are aimed at inducing a mucosal immune response. Several Australian trials are currently examining the impact of pneumococcal conjugate vaccine on nasopharyngeal carriage rates and perforation of the tympanic membrane. Only with urgent attention to improving housing and access to running water, nutrition and quality of care, and giving communities greater control over these improvements, will this massive public health problem be solved so that Aboriginal children can take their rightful place in this, the century of communication.

Harvey L Coates MS, FRACS · Peter S Morris PhD, FRACP · Amanda J Leach PhD · Sophie Couzos FRACGP, FACREM, FAFPHM

Aim: To report the preliminary findings of a pilot program to screen newborn babies for congenital bilateral permanent hearing loss.Setting: The five largest maternity hospitals in Perth, Western Australia. Screening was gradually introduced over seven months from February to August 2000.Participants: All babies born at these hospitals after the introduction of hearing screening until 30 June 2001.Methods: One or both of two automated screening devices were used: one measuring transient evoked otoacoustic emissions (TEOAE) and the other automated auditory brainstem responses (AABR). If a "pass" was not obtained in both ears, screening was repeated. All babies who did not obtain a pass in either ear at follow-up were referred for audiological assessment.Main outcome measures: Prevalence of permanent bilateral hearing loss.Results: Of 13 214 eligible babies, 12 708 (96.2%) received screening. The main reason for missing screening was early hospital discharge (309; 2.3%). Of the screened babies, 99% had a pass response in both ears at either the initial or follow-up screen. Twenty-three babies were referred for audiological assessment, and nine were diagnosed with bilateral permanent hearing loss (0.68/1000; 95% CI, 0.31–1.28).Conclusions: Despite our program meeting process quality indicators, our detection rate was low. Before extending the program to smaller hospitals, we need to validate our screening instruments and put in place a system to monitor false negative results.

Helen D Bailey BHealthSci(Nurs)Hons, MPH · Carol Bower MB BS, PhD · Jay Krishnaswamy MSc · Harvey L Coates MS, FRACS

Objectives: To investigate the circumstances that led general practitioners to refer dementia sufferers and their carers to community support services.Design: Qualitative study using semi-structured interviews, carried out between 1 September 1999 and 30 April 2000.Setting and participants: 21 live-in carers of patients with dementia referred for the first time to a Western Australian metropolitan Aged Care Assessment Team, and 19 of their referring general practitioners.Results: Most referrals occurred after the carers had been experiencing carer stress, and were precipitated by crisis situations. Carers failed to discuss their difficulties with the referring GP for a variety of reasons, including the belief that they should cope because it was their duty. The doctors found it difficult to know how the carers were coping or when to intervene, and some carers tended to resist their attempts to help. Time constraints were a significant problem for both groups.Conclusion: Attitudinal barriers in both carers of patients with dementia and GPs, combined with time constraints, often lead to inadequate assessment of carer problems. While it is important that strategies to improve communication between carers and GPs are developed, it would be sensible for GPs to assume that dementia carers are at risk of carer stress and should be encouraged to use community care services.

David G Bruce MD, FRACP · Glenys A Paley BSc, Dip Hlth Prom · Peter J Underwood MB BS, PhD · David Roberts RN, PhD · Duncan Steed MB BS

Objective: To implement and evaluate a collaborative medication management service model.Design: Participatory action research.Setting and participants: The study was conducted from March 1999 to March 2000; 1000 patients, 63 pharmacists and 129 general practitioners from six Divisions of General Practice in South Australia participated.Interventions: A collaborative service delivery model, involving a preliminary case conference, a home visit and a second case conference, was agreed through discussions with medical and pharmacy organisations and then implemented.Outcome measures: Medication-related problems; actions recommended; actions implemented; and outcomes after actions taken.Results: Overall, 2764 problems were identified. The most common medication-related problem (17.5% of all problems) was the need for additional tests. Thirty-seven per cent of problems related to medicine selection, 20% to patient knowledge, and 17% to the medication regimen. Of 2764 actions recommended to resolve medication-related problems, 42% were implemented. Of the 978 problems for which action was taken and follow-up data were available, 81% were reported to be "resolved", "well managed" or "improving".Conclusion: This implementation model was successful in engaging GPs and pharmacists and in assisting in the resolution of medication-related problems.

Andrew L Gilbert BPharm, PhD · Elizabeth E Roughead BPharm, PhD · Kathy Mott BA · John D Barratt BPharm, BAppSc (Comp Studies) · Justin Beilby MB BS, MD, FRACGP

Chronic lead poisoning may manifest clinically as abdominal pain, constipation, proteinuria, haematuria, peripheral neuropathy and muscle weakness.1 With more significant lead poisoning, encephalopathy may occur.2 Sustained blood lead levels of over 0.5 μmol/L in early childhood are likely to be associated with intellectual underperformance.3 However, congenital lead poisoning and its subsequent management has rarely been reported in preterm infants. Treatment is with chelating agents, which reduce lead concentrations in the blood and tissues by forming water-soluble complexes that are cleared by the kidneys.4 We report a case in which the neonatal blood lead level was the highest recorded for a surviving infant. Clinical recordA 24-year-old pregnant woman, who had recently emigrated from India, was found to have a haemoglobin level of 70 g/L at 24 weeks' gestation. At that time it was noted that she was a vegan and had a normal blood film and iron studies. At 30 weeks' gestation, she presented with abdominal pain and a progressive confusional state culminating in seizures. The blood film now showed basophilic stippling, a typical sign of lead poisoning (Box 1), and subsequent testing showed she had a blood lead concentration of 5.2 μmol/L (the National Health and Medical Research Council's public health goal is a level of ≤ 0.48 μmol/L).3 Chelating therapy was initiated with intramuscular dimercaprol and intravenous calcium disodium edetate (CaNa2EDTA).5 Thirty-six hours later the woman had an antepartum haemorrhage, and, after induction of labour, she gave birth to a 1.6 kg (75th percentile) female baby by vaginal delivery. Apgar scores were 4 and 6. The infant was flaccid and areflexic and did not move in response to noxious stimuli, although spontaneous ocular movements were present. As she had emerging alveolar hypoventilation and no gag reflex, she was intubated and ventilated. The clinical suspicion of bilateral diaphragmatic palsy was later confirmed by fluoroscopy. Basophilic stippling was not seen on the infant's blood films, although Heinz bodies were present. Lead concentration in the cord blood was 7.6 μmol/L (12 hours before birth, maternal blood lead concentration had been 2.3 μmol/L). The concentration of erythrocyte porphyrins was 20.3 μmol/L (normal range, 0.4–1.7 μmol/L), and radiographs of the long bones showed an increase in the bone density adjacent to the metaphyses (both signs of lead poisoning). Within 24 hours of birth, the infant was commenced on chelation therapy (intramuscular dimercaprol 4 mg/kg/dose every four hours and intravenous CaNa2EDTA 50 mg/kg/day, given after the second dose of dimercaprol). The blood lead concentration initially rose to 11.8 μmol/L within the first 48 hours of therapy, then fell rapidly over the next few days. The high urinary lead concentration of 52 μmol/L on Day 3 was an indicator that lead was being excreted. The time course of blood and urinary lead concentrations for the first 14 weeks post partum is shown in Box 2. On Day 7, it was judged appropriate to cease intravenous chelating therapy. Succimer (an oral chelating agent) 30 mg/kg/day5 was commenced three days later. At that time, the urinary lead concentration had fallen to 4.2 μmol/L. Over the three-week course of succimer, urinary lead concentrations fell further, while blood lead concentrations remained relatively constant. As the succimer appeared to be having little effect, it was discontinued on Day 31, and intravenous CaNa2EDTA was recommenced 48 hours later. A rise in urinary lead excretion was observed after this course and subsequent courses of parenteral therapy. By Day 42, facial, bulbar, proximal-limb and diaphragmatic muscle activity had improved sufficiently to allow successful extubation. By Day 53, the blood lead concentration appeared to have fallen to a satisfactory level, and an attempt at maintenance therapy using oral succimer at the higher dose of 60 mg/kg/day was commenced.6,7 However, the blood lead concentration increased during the second course of succimer, with a corresponding decrease in the urinary lead concentration. Intravenous CaNa2EDTA was recommenced. When chelation therapy was subsequently discontinued for two weeks, the blood lead concentration again rose, and a fifth course of CaNa2EDTA was initiated. Progress of infant after first 14 weeks. By three months' corrected age (ie, about 5 months after birth) the infant was able to fully feed by sucking, although there was significant gastroesophageal reflux. Her peripheral weakness had almost resolved, but bilateral wrist drop and poor head control persisted. Blood lead concentration had fallen to 1.8 μmol/L. It was decided to reintroduce oral succimer at 60 mg/kg/day. This appeared to be effective, as the lead levels not only fell in the blood but increased in the urine. A brainstem auditory response at four months' corrected age showed right sensorineural deafness. (A magnetic resonance image of the brain at three weeks of age had been normal.) Throughout the hospital stay her serum calcium, zinc, iron, renal and liver function tests were normal. The infant was discharged home, on succimer, at five months' corrected age with a blood lead concentration of 0.95 μmol/L. A neurodevelopmental examination at the time revealed a two-month delay. Her two siblings, aged two and four years, were found to have blood lead concentrations of 0.6 and 0.3 μmol/L, respectively. Lead source identification. An environmental audit of the home and the local Sikh community kitchen revealed no obvious source of lead. Interviews conducted with the mother established that she had been taking several tablets, prescribed by an Ayurvedic doctor in India for treatment of a gastrointestinal complaint, periodically over the course of the past nine years. Analytical results for the various tablets are presented in Box 3, the most notable being the high lead content of two of the tablet types (4.5%–8.9% lead). The mother's tablet use in the nine months before the child's birth represented a lead intake of at least 50 times the average weekly lead intake of Western populations.2,8 Correspondence with the Ayurvedic doctor in India, who prescribed the brown ("HSY-15") tablets in this case, has not yet provided any clues as to the origin of the lead in these tablets. DiscussionClinical considerationsThe diagnosis of intrauterine lead intoxication was made on the basis of a maternal encephalopathy with a high blood lead concentration, maternal anaemia with basophilic stippling, and a high cord-blood lead concentration. Infant blood lead levels of a third to a half the peak level reported here are usually associated with severe cerebral oedema and death.2 In this instance, the infant was encephalopathic and profoundly weak and had diaphragmatic palsy at birth. The limb weakness clinically appeared to be predominantly neuropathic. Several electrophysiological attempts to clarify the presence of either a neuropathy or a myopathy failed owing to technical and interpretive difficulties. Although lead-induced peripheral neuropathy is well described,9 diaphragmatic palsy is unreported. There was no evidence of renal involvement or proteinuria, possibly due to the infant's renal immaturity. There was no basophilic stippling in any neonatal blood film. This relative paradox — the absence of basophilic stippling despite lead intoxication — has been noted previously.10 The unilateral sensorineural deafness is likely to be due to lead toxicity.11 Previous reports of congenital lead intoxication indicate that maternal and cord blood lead levels correlate.12 The marked discrepancy in this case (2.3 μmol/L [mother] v 7.6 μmol/L [cord]) could be due to the possibility that at high maternal blood lead concentrations the lead-binding capacity of the erythrocytes becomes saturated13 and more lead is available for transfer to the fetus. Alternatively, the discrepancy could be due to in-utero mobilisation of lead from fetal tissues without adequate maternal clearance. This latter consideration indicates a potential detrimental effect on the fetus of chelation therapy in pregnancy. As chelating agents bind lead into complexes that are cleared by the kidneys, an increase in urinary lead concentration was expected after administration of each of the chelating agents. This phenomenon was consistently observed after courses of dimercaprol and CaNa2EDTA. However, variable doses of oral succimer during the preterm period did not lead to corresponding increases in urinary lead concentration, despite raising the dose to a level higher than those recommended in the literature.5-7 Only when oral succimer was recommenced at three months' corrected age did the predicted response occur. This apparent early ineffectiveness of succimer could be due to absorptive failure from the infant's immature gut. Furthermore, succimer is a prodrug that requires cysteine for activation.2 It is unclear whether or not this enzymatic activation process is mature in the premature infant. Public health considerationsWhile lead was the principal concern in this case, mercury was also detected in some of the tablets (Box 3). Weekly ingestion of one of the tablets containing 400 μg would exceed the Australian average weekly mercury intake by at least fourfold.8 Mercury poisoning was of secondary concern in the current circumstance, and chelation therapy was expected to remove the mercury along with the lead. This does, however, illustrate that herbal medicines may contain more than one potentially toxic component. In many countries, including Australia, it is legal to import herbal remedies for personal use, although some restrictions apply.14 In addition, testing programs for contaminants in herbal remedies are virtually non-existent. Acute lead poisoning has been reported from traditional and herbal medicines and cosmetics obtained from India,15-17 the Middle East,18-19 Mexico20 and Asia.20-21 This should be a matter of grave concern to patients who take such remedies, and to health professionals and health authorities in these countries and in Australia. 1: Mother's blood film just before parturition, showing basophilic stippling of red cells 2: Infant blood and urinary lead concentrations from birth to 14 weeks of age* *Horizontal lines across top of graph indicate periods of parenteral therapy with calcium disodium edetate and oral succimer. Dotted horizontal line shows National Health and Medical Research Council public health goal for maximum lead concentration in blood (0.48 μmol/L). 3: Metal analysis of tablets used by the patient* Tablet colour Lead per tablet (mg) (%) Mercury per tablet (μg) (%) Brown ("HSY-15") 45 (8.9%) 15 (0.003%) Red 23 (4.5%) NA Pink 1 (0.2%) 400 (0.08%) Green 2 (0.003%) 10 (0.002%) *Analysis by IMVS Laboratories, Adelaide. NA = not analysed.

Paul A Tait BPharm · Amish Vora MB BS · Simon James FRACP · D James Fitzgerald PhD · Beverly A Pester BA MA

Chemical, biological and radiological (CBR) incidents have the potential to shut down emergency departments that do not have an adequate CBR response. Secondary contamination also poses a threat to the safety and wellbeing of staff and other patients. On activation of a CBR response, "clean" and "contaminated" areas should be clearly marked, and all patients decontaminated before being allowed into the emergency department or outpatients department. Personal protective equipment (PPE) is needed for all staff. Staff using PPE must be monitored for signs of heat illness. Stocks of coveralls, bags for contaminated clothes, plastic sheeting for radiological incidents, barriers for crowd control, and selected drugs should be obtained. Staff required include medical, nursing, security, clerical, orderlies, patient care assistants and other staff, depending on the type of threat. An on-call roster that allows regular rotation of staff is needed. All hospital personnel should understand the response plan, and recognise that the emergency department and hospital is a community asset that requires protection.

Gim A Tan DRANZCOG, FACEM · Mark C B Fitzgerald FACEM, MRACMA

The rates of bronchiectasis for Indigenous children from remote Australian communities are unacceptably high, with one study showing 14.7/1000 Aboriginal children. Children with bronchiectasis need to be identified early for optimisation of medical treatment. Under-reporting of cough is common. Bronchiectasis should be suspected in children with recurrent bronchitis or pneumonia, and when, despite appropriate therapy, pulmonary infiltrates or atelectasis persist 12 weeks beyond the index illness. During acute infective episodes, oral antibiotics and chest physiotherapy to clear the airways should produce prompt resolution; otherwise, hospitalisation is necessary. Management follows the cystic fibrosis model of regular review, encouragement of physical activity, optimising nutrition, maintenance of immunisation and avoidance of environmental toxicants, including passive smoke exposure. Successful management and prevention of bronchiectasis will require improvements in housing, nutrition, and education, as well as access to comprehensive healthcare services, with coordination between primary and hospital-based healthcare providers.

for the Working Group on Indigenous Paediatric Respiratory Health

For most doctors, it would be inconceivable to manage common long term disorders (such as diabetes or asthma) or serious risk factors (like hypertension or hypercholesterolaemia) without using standard clinical, pathology or other investigative parameters. The data from standard clinical measures have underpinned the drive towards outcomes-based healthcare and have long been recognised as the optimal response to "uninformed patients, skeptical payers, frustrated physicians and besieged health care executives".1 Recent Commonwealth Department of Health and Ageing measures provide incentives for general practitioners to improve the management of patients with complex, chronic or relapsing disorders, including asthma, diabetes and mental disorders.2 Doctors do not need to be convinced of the need to monitor peak flow in asthma or blood glucose (or other metabolic parameters) in diabetes. These simple measures do not try to describe the aetiology of the disease, the breadth of clinical manifestations or the patient's experience of illness. However, as proxy measures of clinical status, they can be used reliably over time and be gauged by different care providers operating in different care settings. Furthermore, the significance of the results can be easily communicated to the patient. Such measures are also used to monitor the response to treatment over time or responses to different types of interventions. Hence, such outcome data, in combination with other clinical and patient factors, are a crucial part of high-quality clinical practice. By contrast, few patients treated for depressive or anxiety disorders by GPs or psychiatrists will have any systematic measure of their ongoing clinical status or outcome documented.3 This deficit is confined largely to doctors, as clinical psychologists consider repeated systematic measurement an essential clinical tool.4 This deficiency in clinical record keeping by medical professionals persists despite the availability of valid and reliable outcome measures. Depression and anxiety are relapsing or chronic conditions5 and are often comorbid with other medical conditions in primary care. Patients will be managed mainly by primary care providers6 and the time frame for such care is years (not weeks or months). Consequently, we propose that all medical providers need to incorporate standard outcome measures for depression or anxiety into the management plans of patients with depression or anxiety. The other, clinical reasons why such a practice should be pursued are detailed in Box 1. Although not the prime concern for the treating clinician, health services planning and other research benefits rely on the collation of clinical data in combination with other practitioner and organisational information. The evidence base for high-quality mental health practice in primary care is limited and urgently needs relevant longitudinal data.9 These non-clinical outcomes (Box 2) should also be of concern to the wider medical profession. What measures should be used in day-to-day practice?Although there are no specific laboratory-based diagnostic tests for depression or anxiety, clinical diagnoses can be made reliable by determining whether a sufficient number and type of clinical symptoms are present. The number of diagnostic categories that are relevant to primary care is limited and easily incorporated within standard checklist formats.9 There are specialised neuroimaging and neuropsychology strategies that may emerge as useful clinical markers of risk factors for illness, severity of illness, or predictors of course or response to treatment; however, none are yet suitable for application in everyday clinical practice. Consequently, our current focus is more on the use of appropriate outcome measures rather than diagnostic measures. We now have a wide range of instruments that rate relevant psychological symptoms or resultant disability. For people with depression or anxiety, it is necessary to recommend the measurement of symptoms and disability, because some people minimise their symptoms simply by avoiding stressful situations. For example, a housebound person with agoraphobia, or a socially withdrawn person with chronic depression, may show only mild elevations on current symptom measures but reveal severe disability on other measures. Similarly, while people with comorbid physical and mental disorders can show elevated symptom scores, inspection of the mental and physical scores on disability measures can be helpful in prioritising treatment. Importantly, the common general disability measures (eg, Short Form Health Survey [SF-12]14 and Brief Disability Questionnaire15) can be used across the broad spectrum of general medical practice. To encourage widespread application in general medical settings, measures need to have a number of key characteristics. These include brevity, low cost (preferably being in the public domain), self-report rather than clinician-administered format, results that are readily communicated to the patient, and demonstrated responsiveness to change in clinical status. Further, symptom-based instruments should be focused on the common symptoms of depression, anxiety or related somatic constructs.9 Such instruments also lend themselves to automation and electronic record keeping. While illness-specific measures are commonly used in specialist practice (eg, for major depression, panic disorder, social anxiety or obsessive compulsive disorder only), they are far less attractive in general medical settings. Given these considerations, we recommend a small series of instruments for use in general medical settings. For the assessment of common symptoms of depression and anxiety, we recommend the Kessler Psychological Distress Scale (K10),16 the Somatic and Psychological HEalth REport (SPHERE),8 or the Hospital Anxiety and Depression Scale (HADS).17 The K10 is a 10-item instrument that was developed internationally and has been used in the Australian National Survey of Mental Health and Wellbeing. Scores range from 10 to 50, with scores above 30 being highly predictive of a depressive or anxiety disorder. The sensitivity and specificity of the K10 (ie, its ability to predict diagnosis) is superior to that of the 30-item General Health Questionnaire (GHQ).18 In the national mental health survey, it correlated 0.5 with the GHQ, –0.6 with the SF-12 disability measure, and 0.3 with the number of consultations for a mental health problem in the previous year.19 It measures the relevant constructs, is simple to use and requires little expertise to score and interpret the results. The SPHERE has a 34-item version that was developed to rate the psychological and somatic symptoms reported by people with common mental disorders in primary and other medical care settings. The utility of the shorter 12-item version for use in primary care was demonstrated as part of SPHERE: a national depression project and was based on more than 46 000 consultations in Australian general practice.8 The instrument is best used to differentiate two levels (and three types) of common mental disorders (patients reporting both characteristic psychological and somatic symptoms [Level 1, Type 1], and patients reporting either psychological symptoms [Level 2, Type 2] or somatic symptoms [Level 2, Type 3]). These levels predict not only formal psychiatric diagnoses, but also disability and doctor- and patient-perceived need for mental healthcare.8 The HADS is a 14-item instrument that was developed to rate the severity of specific depressive and anxiety symptoms in patients with comorbid medical disorders. Hence, it avoids rating those common somatic symptoms that accompany many mental disorders. While this narrower focus is advantageous for assessing changes in depressive and anxiety symptoms, it may mean that it is less useful in patients with the more mixed psychological states that are commonly seen in primary care. For rating disability, we recommend the SF-12.14 The 36-item Medical Outcomes Study Short Form Health Survey (SF-36) was developed as a measure of disability or functioning and is applicable to people with any illness, physical or mental. It is now available as a 12-item version (SF-12) that correlates 0.95 with the results of the parent SF-36 instrument. It has three sections: a preliminary question about self-perceived health status; eight questions about the extent to which current health status limits activities; and three questions about feelings. Two scores are generated: a mental and a physical component score. The scoring method is complex and is arranged so that scores on the physical and mental components are independent. The SF-12 has excellent psychometric characteristics, is sensitive to change, and is probably the de facto world standard for measuring outcome of treatment for both physical and mental disorders. ConclusionsFor physicians who work predominantly in academic, specialist or administrative settings, the arguments for routine outcome measurement are obvious.3,20 In association with the move to manage the common psychological disorders like depression and anxiety more effectively in primary care, there is now an urgent need to promote the clinical utility of standard outcome measures to GPs. The historical and professional resistance to the use of such measures has hampered the delivery of standardised and effective treatment in primary care settings. As new treatments are developed and as governments move to support major service innovations in primary mental healthcare, we need to measure routinely whether "improved" treatments and services are actually changing the lives of the individual patients who present for treatment. 1: Clinical reasons for using standard outcome measures in individual patients with depression or anxiety A. The instruction of patients in the collection of standardised illness measures maximises their involvement in a long term partnership. The provision of accurate information and recruitment to take an active role are empowering and serve to reduce both stigma and a sense of helplessness. These approaches improve compliance with standard clinical treatments.7 B. Standard measures can be used to document a range of clinical outcomes, including: psychological and somatic symptom severity, key illness-related behaviours (eg, extent of avoidance behaviour or substance misuse), cognitive and interpersonal distortions, comorbid medical difficulties, and health-related disability.8 C. Patients with depression or anxiety who monitor their own symptom or disability state can recognise signs of early relapse and seek earlier intervention for subsequent episodes. D. Patients with more severe or more complex disorders are likely to be exposed to an ever-increasing number of pharmacological or psychological treatments. Standardised outcome measurement permits comparison of responses (within each individual) to different treatment approaches. E. Patients with depression or anxiety will often require assessment by specialist providers. Standardised measures permit the determination of the short and long term benefits achieved by such specialised interventions. F. Clinical record keeping is enhanced and can be linked (electronically or through disease management systems) with appropriate triggers to consider changes in management planning. For example, if a patient treated for depression fails to achieve a significant reduction in standard symptom severity or disability measures, then a change in treatment approach or referral to a specialist service would need to be considered. 2: Health services planning and other research outcomes A. Evaluation of clinical effectiveness of new pharmacological or psychological treatments in relevant primary care settings. Given the range of new treatments and the differing views of clinicians, such studies are an important aspect of the evidence base for mental health.10 B. Cost-effectiveness research focused on the long term benefits of new pharmacological or psychological treatments. C. Investigation of the patient, practitioner and organisational factors that predict variations in the quality of clinical practice11 or access to various types of mental health assessments and treatments.12 D. Evaluation of the impact of major health service innovations on a range of clinical outcomes (eg, Primary Mental Health Care Teams in Victoria, 2001). E. Evaluation of the impact of specific incentives (eg, Better Outcomes in Mental Health Care, 2001) or innovative education or disease management support processes on clinical practice (eg, mental health training and clinical audits).13

Ian B Hickie MD, FRANZCP · Tracey A Davenport BA(Hons) · Gavin Andrews MD, FRANZCP

Physicians' dual roles — as healer and professional — are linked by codes of ethics governing behaviour and are empowered by science. Being part of a profession entails a societal contract. The profession is granted a monopoly over the use of a body of knowledge and the privilege of self-regulation and, in return, guarantees society professional competence, integrity and the provision of altruistic service. Societal attitudes to professionalism have changed from supportive to increasingly critical — with physicians being criticised for pursuing their own financial interests, and failing to self-regulate in a way that guarantees competence. Professional values are also threatened by many other factors. The most important are the changes in healthcare delivery in the developed world, with control shifting from the profession to the State and/or the corporate sector. For the ideal of professionalism to survive, physicians must understand it and its role in the social contract. They must meet the obligations necessary to sustain professionalism and ensure that healthcare systems support, rather than subvert, behaviour that is compatible with professionalism's values.

Sylvia R Cruess MD · Sharon Johnston LLM · Richard L Cruess MD

The usual presentation of a returned traveller is with a particular syndrome — fever, respiratory infection, diarrhoea, eosinophilia, or skin or soft tissue infection — or for screening for asymptomatic infection. Fever in a returned traveller requires prompt investigation to prevent deaths from malaria; diagnosis of malaria may require up to three blood films over 36–48 hours. Diarrhoea is the most common health problem in travellers and is caused predominantly by bacteria; persistent diarrhoea is less likely to have an infectious cause, but its prognosis is usually good. While most travel-related infections present within six months of return, some important chronic infections may present months or years later (eg, strongyloidiasis, schistosomiasis). Travellers who have been bitten by an animal require evaluation for rabies prophylaxis.

Series Editors:

To the Editor: The practice of radiology and pathology has changed dramatically in the past two decades. Increased use of multidisciplinary assessments and interventional techniques has meant greater exposure of patients to radiologists and pathologists. When patients undergo investigations, they are invariably anxious, usually expect the worst, and want the result as soon as possible. Therefore, there is pressure to provide an immediate answer to the problem at hand. In most instances, it would be possible to offer a diagnosis. However, many radiologists and pathologists are reluctant to discuss investigations with patients in detail.1 During interventional procedures, radiologists and pathologists see patients only briefly; they often don't know all the facts about them, and are not ultimately responsible for their clinical management.1 As the patient is only temporarily in the care of the radiologist or the pathologist, it is not appropriate to discuss complex issues or offer opinions and advice. Such advice may put the patient's doctor in an awkward position, forcing the referring practitioner to follow a course of action which may not be in the best interests of the patient. At a patient's insistence, radiologists and pathologists can sometimes indicate to someone who has a clearly benign condition that the problem under investigation is unlikely to be serious.2-4 This may be the case with screening mammography, as, in most cases, the results are either normal or indicate a non-malignant condition. However, in diagnostic radiology and pathology, such an opinion is usually based on a preliminary impression, which may change when all the facts are considered. The cost of providing on-the-spot written reports to the patient has to be factored into the equation. It has been estimated that the additional cost of immediate reporting of results of screening mammography is about US$28.22. When additional equipment and space were not required, the cost would increase by US$4.38. Although most patients in the study preferred immediate reporting, they were unwilling to pay the additional fees.5 With respect to pathology, a formal fine-needle aspiration result can be delivered within an hour, but, for the reasons outlined above, this would not be advisable. Further, the pathologist's contract is with the referring doctor and the report is written in scientific language, which may not be easily understood by the patient, leading to unnecessary anxiety. Giving bad news to a patient is not an easy task even for trained professionals. It is even harder for radiologists and pathologists who are not generally equipped to provide counselling and support, and who may not be indemnified by their insurers to carry out such tasks. Further, neither radiology departments nor pathology laboratories are suitable settings for giving bad news,1 as very few support avenues are usually available to patients there. Predicting the impact that bad news will have on a patient is extremely difficult, and radiologists and pathologists should, for compassionate and for medicolegal reasons, refrain from providing immediate answers to patients.

Ibrahim M Zardawi

To the Editor: Jamrozik's editorial1 about our report of a failed randomised controlled trial (RCT)2 in an Aboriginal medical service helps to explain why researchers might be reluctant to submit articles describing unsuccessful trials, thus limiting potential for the scientific community to learn from such experiences. The main point of our article was to describe the manifest difficulties of implementing an RCT — the evidence "gold standard" — in this type of setting. Interestingly, Jamrozik largely attributes these difficulties to incompetence or naivety (or both) on the part of the researchers and funders, rather than to complexities inherent in the study design, the setting and the intervention. A separately funded pilot study is, in principle, a good idea, but extremely difficult to get funding for in today's environment. Of course, we did conduct a pilot — that, in fact, was what we reported on — but it is unclear how this would have helped us better estimate absolute prevalences and effect sizes for intervention and control groups, as a substantial number of participants, followed up for six months, would have been needed to do this. Nor is it clear how taking a population approach and distributing guidelines to all drinkers rather than offering personalised advice to hazardous drinkers would have helped — firstly, because we were specifically trialling the internationally validated brief intervention, and secondly, because the effect size of the alternative approach would have been so small that we would have needed very much larger numbers to test its effectiveness. We had no intention of "stumbling down something like this path". Nor do we agree that the blood tests were "medicalising a social problem". They were intended not only to provide robust outcome measures (a mark of a good trial), but also tangible evidence to clients of the health effects of alcohol, shown from previous research to be well received by Aboriginal people.3,4 They were not a requirement for participation. Further, that we should have got around the potentially off-putting business of seeking informed consent by bypassing this step almost defies comment. While trials of some therapeutic interventions can be undertaken blind with patient consent by using placebos, this does not mean that where blinding is not possible patient consent should be done away with in order to avoid a Hawthorne effect! However, we do agree with Jamrozik on one point — nothing about this study or our report could reasonably "compound any negative perceptions about Aboriginal Medical Services and Aboriginal patients".1

Beverly M Sibthorpe · Ross S Bailie · Maggie A Brady · Sandra A Ball · Polly Sumner-Dodd · Wayne D Hall · Alan Pettigrew · Tom Gavranic

To the Editor: I am responding to a recent editorial by Jamrozik1 commenting on a study proposed by Sibthorpe and colleagues to assess a brief intervention for hazardous use of alcohol by Indigenous people in an urban setting.2 After two unsuccessful attempts to recruit participants, the study was discontinued and funds returned to the National Health and Medical Research Council (NHMRC) in 1998. Sibthorpe et al identified their difficulties as primarily the result of having overestimated the number of suitable participants, for a number of complex reasons. Jamrozik's criticisms rest disproportionately with the NHMRC and are based on procedures and processes in effect in 1996 and 1997, yet they are informed by contemporary knowledge and wisdom. This seems somewhat anomalous. In 2000, the NHMRC revised its system for assessing research applications. This involved several developments which would have had a direct impact on the assessment of this application had they been instituted in 1996. Some of these include: the introduction of panels comprising 11 experts in the domain of the application; the introduction of the Indigenous Health Research Panel (IHRP), which provides advice on cultural appropriateness, community consultation and methods in applications with an Indigenous component (most members are Indigenous people); and the opportunity for IHRP to make stipulations upon which funding is contingent. Also of significance was the establishment of the Research Agenda Working Group (RAWG), which oversaw the formulation of intervention-based criteria. Colloquially known as the "Darwin criteria", these principles ensure that all Indigenous research design has: sufficient Indigenous community consultation and participation; transferability (of the methods to other settings); and sustainability (of resulting changes). The NHMRC was disappointed that the study by Sibthorpe et al did not proceed and did not result in usable data to inform a significant problem. However, it is also important to recognise that unanticipated outcomes, which can often lead to other, very positive results, are an integral part of the learning process. The NHMRC has supported Australian health and medical research since 1936. It has a strong commitment to ensuring the continuing evolution of its procedures and practices. The new systems implemented in 2000 were designed to ensure the continuing tradition of funding high quality, relevant and applicable research.

Beverly M Sibthorpe BA(Hons), PhD · Ross S Bailie MD, FAFPHM · Maggie A Brady MA, PhD · Sandra A Ball BCom, GradDip Public Administration · Polly Sumner-Dodd DipManagement · Wayne D Hall BSc, PhD · Alan Pettigrew BSc, PhD · Tom Gavranic MB BS, DPH, FRACGP

To the Editor: The recent article by Sibthorpe et al1 and the accompanying editorial2 on the issue of the failure of an alcohol intervention trial in an Aboriginal Health Service deal with problems facing all primary care practitioners in the field of "alcohol misuse" and should not be seen as a peculiarly Aboriginal problem. Firstly, despite what the academics may tell us, administering an Alcohol Use Disorders Identification Test (AUDIT) questionnaire in general practice as a screening measure meets with huge resistance, no matter where you practice. Denial of the disease-inducing potential of alcohol is certainly not peculiar to Aboriginal society. Secondly, I find that the bulk of the medical profession reinforces this community denial by diagnosing conditions such as diabetes, hypertension, obesity, anxiety, depression and schizophrenia instead of seeing these problems as being a manifestation of alcoholism or other "alcohol misuse" until proven otherwise. Indeed, the denial is so extreme that they tend to avoid the term "alcoholism" altogether. Specialists are in even greater denial and are more often a hindrance than a help to general practitioners in this regard. As a consequence, community leaders and affected families are unable to develop effective strategies for dealing with their problems. What they get instead is increasing healthcare costs, hospital bed shortages, increasing domestic violence, more "drug problems" and more prisons. So "GP reluctance or inability to follow through . . ."2 is not surprising. Indeed, denial of alcohol is so strong in the medical profession that it is harder, in my experience, to get doctors and even medical students (let alone healthcare workers) to attend open meetings of Alcholics Anonymous and Al-Anon than it is to persuade affected people to do so. Thirdly, general practice throughout Australia has been organised for episodic, fast-throughput care. People have become so accustomed to this that they see any attempt at a comprehensive preventive approach to illness as odd, out of place, time-consuming and even intrusive, especially so where alcohol and family histories are concerned. That Aboriginal people are no different from the rest of us in this regard should cause no surprise.

Beverly M Sibthorpe · Ross S Bailie · Maggie A Brady · Sandra A Ball · Polly Sumner-Dodd · Wayne D Hall

To the Editor: I read with interest the recent correspondence in the Journal from Del Mar and Glasziou.1 Their appeal to one of their critics was to "abandon throwing bricks from the sidelines and join us in trying to help clinicians assess research evidence in [a] timely fashion". More recently, their defence in relying on generalists, rather than experts, to assess the evidence was, somewhat curiously, that "a cat may look at a king".2 In response to these comments, I believe that one of their recent presentations relating to natural remedies for osteoporosis in postmenopausal women3 falls short of current evidence-based medicine requirements. I suspect that this may be because they have no expert in the area they are reviewing to assist them in assessing the data. An expert would have been able to tell them that their statement "Although no trials specifically compared 'just walking' with 'exercise in the gym', there was reasonable evidence supporting the beneficial role of walking in this patient group"3 was incorrect.4 Furthermore, an expert would have known that the fundamental biological basis of the effect of exercise on the skeleton relates to the induction of significant strains within the skeleton.5 Because these effects are site-specific and load-dependent, the physiological mechanisms differ from those involved in cardiovascular health. Secondly, an expert in the area may have pointed out that the principal constituent of codliver oil that affects the skeleton is vitamin D. To claim that there were no benefits on bone mineral density or fracture from vitamin D would not be supported by current data.6 Keeping up-to-date in medical practice has become more difficult as the information base expands. Performing an Internet search may be adequate for answering some patient-based specific questions, but, in general, reading an up-to-date review is probably better. Presenting the results of a rapidly performed, deficient analysis in an internationally renowned journal is another thing entirely.

Richard L Prince · Christopher B Del Mar · Paul P Glasziou

In reply: We agree with Prince that expertise is needed. The only question is, expertise in what? If we rely on experts in the content area, we are subject to error from ignoring studies that do not fit the expert's view or from an overemphasis on studies familiar to the expert.1 On the other hand, if we rely on experts in systematic reviews, we are likely make other errors, especially errors of omission, because we do not know the content area so well. Perhaps what we need is a marrying of the two. First, experts should learn the business of evidence-based medicine (EBM). It should be part of the training of specialists and general practitioners, as well as medical students. In addition, the Australasian Cochrane Centre runs Australia-wide courses in preparing and interpreting systematic reviews.2 Second, we should find a content expert to assist any review being undertaken (and, indeed, we try to do this when writing systematic Cochrane reviews). But when we need to respond rapidly to clinicians' and our own questions, there is not time to consult experts for each one. (The doctor in question3 asked five rather separate questions, of which Prince addresses only two.) Instead, we try to do exactly what Prince has suggested: we first look for an up-to-date review (a systematic review, to avoid bias),1 and, in the absence of one of those, proceed with weaker levels of evidence progressively down a cascade. And that is exactly what we did in this case.3 The purpose of our rapid search service is to provide, as quickly as possible, the best available evidence to assist a doctor help a patient — "EBM in action". The five meta-analyses we identified3 did not include your references. We do not, and do not claim to, offer the last word in a very complicated area of clinical practice.

Richard L Prince MB BS FRACP MD · Christopher B Del Mar MD FRACGP FAFPHM · Paul P Glasziou MB BS PhD

Buzz off! With summer fast approaching and the spectre of evening barbecues dogged by mosquitoes, it is interesting to note that a recent US study confirms that personal repellents containing N,N-diethyl-3-methylbenzamide (DEET) are still the best available in that country. Fifteen volunteers tested 16 products three times each (a total of 720 tests) using the “arm-in-cage” technique. DEET-based products provided complete protection for 88.4 to 301.5 minutes, depending on their concentration. Citronella-based products protected for 2.8 minutes (0.5%) to 18.9 minutes (10%, combined with other botanical oils) and a 2% soybean oil product (marketed for children) protected for 94.6 minutes. Wrist bands impregnated with either DEET or citronella were completely ineffective. For those of you who swear by a popular bath oil, this failed the test after 9.6 minutes. Interestingly, a product containing eucalyptus oil came onto the US market just as the study finished. Testing on six subjects ended in a skin reaction in one and a mean complete protection time of 120 minutes in the other five. N Engl J Med 2002; 347: 13-18 ... A thousand words Recent articles in the MJA highlighting a lack of psychosocial outcome data for cosmetic surgery did not include children, but a report from a US plastic surgeon suggests that we can learn much about children’s response to such surgery from their art. The surgeon collected 200 drawings from children, before and after they underwent surgery for a variety of congenital, aesthetic and traumatic deformities. A child psychiatrist and an art therapist evaluated the drawings, finding recurring themes of low self-esteem, isolation, unhappiness and fear in the “before” drawings, with improvements in all these parameters in the “after” drawings. Twelve examples are reproduced in the printed article, which is well worth a look. Plast Reconstr Surg 2002; 109: 1777-1786 Making the news In Other Journals image At the MJA we often wonder why some of our articles capture the imagination of the popular press, while others are met with a deafening silence. A study of press releases by medical journals and medical reporting in two British newspapers suggests that bias operates at both levels. Of 1193 original research articles published in the Lancet and BMJ in 1999 and 2000, 517 received a press release and 81 were reported in either the Times or the Sun newspapers. No studies without press releases made it into the papers, but newspapers were more likely to follow-up press releases reporting “bad” than “good” news, and preferred observational studies to randomised controlled trials. The hot topics were women’s health, reproduction and cancer. BMJ 2002; 325: 81-84 Don’t worry, be happy! Expectant mothers have yet another thing to worry about, as new research reveals that anxiety in pregnancy is associated with behavioural and emotional problems in their offspring. The Avon Longitudinal Study of Parents and Children followed 7448 women in Avon, UK, from early pregnancy until their children were four years old. Maternal anxiety and depression were measured via validated self-report instruments at 18 and 32 weeks’ gestation, and four times in the three years following birth. The children’s behavioural adjustment at age four was estimated by a validated parental report measure. High antenatal maternal anxiety scores in late pregnancy were associated with behavioural and emotional problems in both boys and girls (ORs 1.56 and 1.51, respectively, after controlling for antenatal, obstetric and psychosocial factors, and postnatal depression and anxiety). Br J Psychiatry 2002; 180: 502-508 A burning issue With the annual incidence of melanoma currently in excess of 45/100 000 for men and 35/100 000 for women, Australia remains the melanoma mecca of the world. Public health messages about sun exposure are starting to show benefit, however, with a recent slight fall in incidence in younger women. The same is not true for Scotland, a country better known for its bleak weather than its opportunities for sunbathing. The Scottish Melanoma Group collated data on the 8830 patients diagnosed with invasive melanoma in Scotland between 1979 and 1998. The incidence increased steadily during the study period (from 3.5 to 10.6/100 000 in men, and 7.0 to 13.1/100 000 in women). Five-year survival rates improved, however, due to a higher proportion of thinner detected tumours in later years, suggesting that the Scots are at least responding to secondary prevention messages. Lancet Volume 360 Issue 9328 Page 23 Published online June 25 2002-07-19

To the Editor: Thalidomide (N-α-phthalimidoglutarimide) was first marketed as a sedative-hypnotic in 1957. It was withdrawn from the market in 1961 as it was found to cause congenital malformations.1 Infant mortality statistics in Germany for the years 1959 to 1963 show that about 40% of thalidomide-affected babies died in the neonatal period.2 The main causes of death were atresia of the bowel, renal dysgenesis and heart malformations. As a result of extensive studies on the pathogenesis of the malformations, it was found that thalidomide is an immunosuppressant.3 The use of two different 14C-labelled thalidomide preparations showed that a portion or the whole of the glutarimide molecule binds to the DNA of rabbit embryos.4 In Britain and Ireland, 480 thalidomide-affected infants survived. Of these, 25 died before reaching the age of 40 years. The causes of death were cancer (4), heart disease (4), diabetes (3), hypertension and renal failure (3), motor accidents (3), and substance misuse or suicide (8) (M Johnson, Director, the Thalidomide Trust [United Kingdom], personal communication). Four deaths from cancer before the age of 40 years in a cohort of 480 is an incidence of 0.83%. The death rate from cancer in England and Wales before the age of 40 is 9.4 per 100 000 population, or 0.0084%.5 Thus, the thalidomide-affected individuals had a 99-fold increase in the age-related cancer death rate. Another of the cohort died aged 41 years of round-cell sarcoma. The high incidence of malignancy, together with the knowledge that a portion of the thalidomide molecule binds with the DNA of laboratory animals, suggest a possible mutational change in some of the cells of thalidomide-affected people. Thalidomide is currently being used to treat a variety of diseases, some because of its immunosuppressant properties. These diseases include graft-versus-host disease, leprosy, AIDS, Behçet's syndrome, tuberculosis, multiple myeloma and many dermatoses. It is also being used for treating some cancers. Its chemotherapeutic value probably results from the ability of the glutarimide component of the thalidomide molecule to bind with the DNA of rapidly dividing cells. However, if the genetic injury is not accurately repaired, it may result in mutations or even cell death. Although thalidomide is now proving to be a useful therapeutic agent, its ability to bind with DNA makes it dangerous, not only when taken by pregnant women, but also potentially when taken by men, whose sperm might be affected.6

William McBride