Letters

To the Editor: A whole issue of the Journal devoted to Death and Dying [19 November 2001 issue] and not a single obituary!

Paul B Harris MB BS FRACR

In reply: I am reminded of a line from the American poet Edwin Arlington Robinson: "I shall have more to say when I am dead." Nowadays, the opportunity to be the voice commemorating the life of a colleague through an obituary in the Journal seems to be of low priority for members of Australia's medical profession. The decade 1991–2000 saw the lowest number of obituaries published by the Journal in the five decades since 1951.1 We did not include an obituary in the "Death and Dying" issue because, fortunately or unfortunately, the obituary tray was empty.

Martin B Van Der Weyden

To the Editor: We wish to report the identification of a novel virus causing lower respiratory tract disease in Australian children. The presence of this virus was recently described in Dutch children and tentatively called human metapneumovirus (hMPV).1 Clinical symptoms of infection are reported to resemble those of human respiratory syncytial virus (hRSV) infection. We therefore investigated whether the virus was present in Australian children. Three isolates were identified from a random selection of 200 nasopharyngeal aspirate (NPA) specimens collected throughout 2001 from children presenting to the Royal Children's Hospital, Brisbane, or the Logan Hospital, a public hospital to the south of Brisbane, with clinical respiratory tract disease. All NPA specimens were initially negative for hRSV, influenza A and B, parainfluenza 1, 2 and 3 and adenovirus by direct fluorescent antigen testing and subsequent viral culture. These negative NPA specimens were then screened by polymerase chain reaction (PCR) for hMPV, based on the known sequence of the virus.2 Sequencing of the PCR product in all three positive samples was 100% homologous with the known hMPV sequence. Viral growth was subsequently detected in culture from two of these samples, and confirmed as hMPV, using the method of van den Hoogen et al.1 Co-existent infection with coronavirus, rhinovirus, Bordetella pertussis, Chlamydia pneumoniae and Mycoplasma pneumoniae was excluded by PCR screening of the three hMPV isolates using validated in-house methods based on established protocols. Clinical features of the infected children are summarised in the Box. This is the first report of the presence of hMPV infection in Australian children and describes a new viral respiratory syndrome. It also adds to the clinical spectrum and understanding of respiratory viruses causing acute bronchiolitis in children. Only 25%–33% of NPA specimens collected from our population with suspected respiratory tract disease yield a positive result for a known viral or bacterial pathogen. Clinical features in this small cohort are difficult to separate retrospectively from hRSV. Based on the findings of this limited preliminary study of children presenting to hospital with respiratory tract symptoms, we would predict that hMPV is also relatively common in the Australian community. We are currently undertaking further characterisation of the hMPV isolates, a more detailed study of the epidemiology of hMPV disease, as well as developing improved diagnostic assays to rapidly identify clinical cases and assess seroprevalence of immunity to hMPV. Clinical features of human metapneumovirus in three Australian children Case 1 (Girl, 12 months) Case 2 (Boy, 5 years 11 months) Case 3 (Boy, 20 months) Date of nasopharyngeal aspirate collection 17/2/01 21/3/01 11/5/01 Presenting symptoms Rhinorrhoea, cough, tachypnoea, wheeze, vomiting Rhinorrhoea, cough, pharyngitis, conjunctivitis Rhinorrhoea, cough, fever Symptom duration before presentation (days) 4 3 4 Clinical signs Respiratory distress with hypoxia, rhinorrhoea, pharyngitis, chest wheeze with crackles Pharyngitis, chest wheeze Rhinorrhoea, pharyngitis, chest wheeze, cervical lymphadenopathy Chest X-ray Not performed Bilateral parahilar pneumonic infiltrates Bilateral parahilar pneumonic infiltrates Clinical diagnosis Bronchiolitis Viral lower respiratory tract infection Viral lower respiratory tract infection Outcome Admitted for oxygen therapy and nasal suctioning for three days Symptomatic treatment at home Symptomatic treatment at home

Michael D Nissen · Ian M Mackay · Stephen J Withers · David J Siebert · Theo P Sloots

To the Editor: I write to offer a re-analysis of the data presented by Whitby and colleagues.1 They reported a meta-analysis of crude estimates and relative risk of death derived from nine published studies for Staphylococcus aureus bacteraemia. They concluded that bacteraemia caused by methicillin-resistant S. aureus (MRSA) is associated with a "real increase in risk of death" compared with bacteraemia caused by methicillin-sensitive S. aureus (MSSA), with a relative risk of 2.12. However, they failed to explore fully the possible confounding effect of the patients' underlying diseases and treatment in their analysis. With this in mind, I offer a re-analysis of their data using regression analysis. Mortality rates versus median length of stay in hospital before bacteraemia (LOS) are shown in the Box (next page) for the five studies for which these data were presented by Whitby et al (in Boxes 1 and 2). The four studies without LOS data were combined, using the median LOS from the other five studies in the figure and the regression model. The regression analysis was performed with and without the weights provided by Whitby et al (Box 2), and also with and without the four studies for which LOS data were not available. Regression analysis revealed a significant association between mortality rate and LOS (P < 0.005). However, the addition of group status (MRSA or MSSA) failed to achieve significance in any iteration of the regression, while LOS remained a significant predictor of mortality risk. This suggests that, with S. aureus bacteraemia, mortality rate increases with length of time in hospital before the bacteraemia. The likely explanation is that patients residing in hospital for longer periods are sicker. Moreover, they are more likely to have been exposed to antibiotics, leading to increased risk of acquiring an S. aureus strain that is methicillin-resistant. The mortality risk is no different for MRSA versus MSSA bacteraemia if LOS, a surrogate marker for severity of patient illness, is taken into account. The difference that Whitby et al observed between the groups of patients with MRSA and MSSA bacteraemia could be accounted for by the difference in LOS between these groups. Mortality rate versus hospital length of stay before bacteraemia (LOS) in patients with MRSA or MSSA bacteraemia

James C Hurley MB BS, PhD, FRACP

In Reply: We thank Hurley for his comments on our meta-analysis.1 However, we strongly dispute that our analytical technique is flawed, and argue that we have been extremely cautious in drawing our conclusions. Hurley's contention is that hospital length of stay before bacteraemia (LOS) is a surrogate for severity of underlying disease and risk for colonisation with methicillin-resistant Staphylococcus aureus (MRSA), and that these factors explain the higher mortality in patients with MRSA. We agree that LOS may be a confounder. It may be an effect modifier, whereby patients in hospital for longer may be more ill, and therefore more susceptible to infection with and death from MRSA. Both are intuitive and biologically plausible conclusions. In fact, we referred to these possibilities in our Discussion, writing that "patients who ultimately become infected with MRSA are more seriously ill than those who become infected with MSSA [methicillin-sensitive S. aureus]" and "separating the effect of the bacteraemia per se from the effects of patients' underlying disease and treatment is a major problem when comparing outcomes". We also cautioned readers that available published data on mortality made it impossible for us to adjust for numerous potential confounders, including LOS, as the information given did not link these potential confounders with the outcome in individual patients. Hurley has not, as he suggests, undertaken an analysis that would allow him to control correctly for the potential confounder, LOS. He, like us, used "group-as-a-unit" data, but, although the groups are homogeneous for MRSA or MSSA, they are heterogeneous for LOS. Adequate examination of and control for potential confounders requires either individual patient data or data from homogeneous groups. Hurley has attempted to use analysis normally reserved for individual data.4 His analysis was analogous to treating the data as though from an ecological study, a design in which control of confounding is difficult,5 and thus does not permit him to draw his conclusions. Our analysis (not presented in our original article) of only those studies where the authors attributed mortality to bacteraemia6-8 found that the magnitude of effect remained (fixed-effect relative risk, 2.27; 95% CI, 1.75–2.96; P < 0.001; test for heterogeneity, χ2 = 6.14, df = 4, P = 0.19). As MRSA bacteraemia is a rare event and published studies are small, the statistical ability to control for confounding and effect modification is limited. Until sufficient suitable data for individual patients are available for analysis, we have remained restrained in our assessment. Mindful that MRSA bacteraemia is associated with increased mortality, regardless of the cause, we hold with our original conclusion that "our findings justify ongoing surveillance and proactive management of MRSA in healthcare facilities".

Michael Whitby · Mary-Louise McLaws · Geoffrey Berry

To the Editor: The article by Nelson et al1 estimates Pharmaceutical Benefits Scheme and Repatriation Pharmaceutical Benefits Scheme (PBS/RPBS) savings if hypertensive patients on monotherapy were prescribed the agents recommended in guidelines; however, the analysis contains algebraic errors and insufficient sensitivity analyses. The question of excessive costs through the use of expensive agents for which there is no evidence of increased benefit for most patients is an important one, but the estimates of extent of overuse should be methodologically sound. The three main concerns we have with the paper's estimates are as follows: The total number of patients on monotherapy in Box 3 of the article adds to 1.1 million, whereas elsewhere the authors state that 60% of all 1.2 million Australian patients treated for hypertension are on monotherapy, giving an estimate of 0.72 million. (These estimates of 60% and 1.2 million are not referenced in the article.) One reason for this discrepancy is that the authors have treated the sum of column 4 in Box 2 as patients, not patient-years of treatment (some patients are on dual or triple therapy), leading to a 40% overestimate of numbers of patients on monotherapy reported in Box 3. Utilisation of prescription drugs is recorded by PBS/RPBS only if the cost to patient is subsidised. Therefore, PBS/RPBS expenditure divided by total patient numbers (Box 2) underestimates consumer cost for diuretics and β-blockers, both of which cost less than the non-concessional co-payment. Of total PBS/RPBS scripts, 16% are for non-cardholders,2 and the cost per script to these patients is about three to four times the prevailing 1998 cardholder co-payment. As a rough estimate, total consumer cost for these agents may need to be doubled, and their omission is therefore material. Although non-concessional patients still have a saving, it is less than that estimated in the article. Sensitivity analysis should have been performed on the following critical assumptions: (1) proportion of use for hypertension for each class of drugs, (2) the number of unsubsidised users of diuretics and β-blockers, and (3) the proportion of patients on each agent who are on monotherapy. It is vital that the current scrutiny by all stakeholders of PBS/RPBS expenditure be informed by reasonable estimates of inappropriate utilisation. The contribution made by the authors in developing a technique to estimate appropriate use for this group of drugs is valuable. However, use of unreferenced estimates of key variables, insufficient application of sensitivity analyses, algebraic errors and inappropriately combining PBS with non-PBS data may cloud rather than shed light on this issue.

Ben D Ewald · Brita A Pekarsky

In reply: We thank Pekarsky and Ewald for their comments. It is difficult to estimate the percentage of patients on monotherapy from any source. We used data from IMS Health (http: //www.ims-global.com/) to determine the number of person-years of exposure to drugs prescribed with a principal indication of hypertension. Some of these drugs were prescribed as a sole agent if the script was for this single drug alone. Exposure for such agents was expressed as a percentage of the total exposure of this drug. For example, angiotensin-converting enzyme (ACE) inhibitors were sole agents in 63.9%. In the other 36.1%, the co-prescribed drugs may have been another antihypertensive drug or another type of drug altogether. Corresponding figures for calcium-channel blockers were 61.3%, for diuretics 53.6%, and for β-blockers 60.0%. As an approximation, we used the estimation that 60% of patients were likely to have been on monotherapy for hypertension. Adding the number on monotherapy for each drug gives an estimate of 1.2 million for the total population on monotherapy for hypertension. Therefore, the total number on drugs is likely to be greater than the 1.2 million as estimated in our article. However, the essential figure is that of 1.2 million for monotherapy, which we stand by. It is true that a minority of prescriptions (16%) are written for people without a concession card and that these are more likely to pay the full cost of a cheaper drug. Our economic perspective was that of the PBS/RPBS. Hence, consumer costs were only included where the government made a copayment. It is acknowledged in the Methods section that "with some drugs, the patient copayment covers the total cost; in these instances the Commonwealth makes no contribution to the cost and these prescriptions are not recorded in the PBS/RPBS data" (page 566). It is also stated in the Discussion that the PBS/RPBS captures "much more of the cost of the newer, more expensive agents than thiazide diuretics or β-blockers" (page 567). We chose to limit our sensitivity analysis to the key issue of redistribution of agents after initiation of monotherapy. The data we presented allow interested parties to conduct their own further sensitivity analyses, such as those suggested by Pekarsky and Ewald.

Mark R Nelson MFM, FRACGP · John J McNeil PhD, FRACP · Anna Peeters BSc(Hons), PhD · Henry Krum PhD, FRACP · Christopher M Reid MSc, PhD

To the Editor: In his recent Commentary on hastening death in terminally ill patients,1 Hunt may not have fully appreciated a very cogent point made in the research by Douglas and colleagues.2 The surgeons surveyed clearly reported the intent of their prescribing. This is contrary to Hunt's assertion that "Intention is inherently subjective . . . complex [and] ambiguous". Some surgeons gave a dose appropriate to the symptoms, others deliberately increased the dose beyond direct symptomatic control, and a few deliberately ended life, at times with no explicit request. As Douglas points out, the dose of a medication given will be an important clue in this. Good clinical practice is about minimum effective dose (MED), not maximum administrable dose (MAD). This is the case for all patients, whether they are near the end of life or not. Hunt also states that "The duty of doctors is to strive to satisfy the wishes and interests of their patients and their patients' loved ones".1 This is a disturbing comment if left unqualified. There is a broader accountability for doctors to the community through the registration process, quality assurance and continuing education, and the criminal code. If the article by Douglas et al highlights nothing else, it should be clear that there are certain members of the medical profession who believe that they are above the law and have control over the life and death of their patients, with no external review.2 It is frightening that such paternalism still exists. Unfortunately, the Dutch experience of tolerating euthanasia does not appear to have decreased unilateral decision-making on the part of some doctors.3,4 If the premise that the interests of the patients' loved ones is a consideration in the duty of care,1 then we are risking the loss of patient autonomy in an unprecedented way. As a practising clinician, the majority of requests that I receive to hasten death are from relatives, not patients. These relatives ask that they be put out of their own misery by ending the patient's life prematurely. To do something to a patient for a third party, however concerned or distressed, is an unacceptable action for clinicians. For the profession to credibly engage in the debate about end-of-life care, we must accept that we are part of the community and hence governed by its laws. There are reference points external to the profession by which we will be judged.

David C Currow

In reply: The survey by Douglas et al1 indicated that, under the current criminal code, about one in three Australian general surgeons are at risk of prosecution for murder because of the way they treat their dying patients. It is likely that many other Australian doctors are similarly at risk of prosecution. This is a serious problem that raises important questions: Why are so many doctors breaking the law? Should these practices be kept covert or brought out into the open for audit and discussion? Is the law serving the needs and interests of dying patients, those who care for them, and the wider community? Rather than argue that doctors are above the law, I have argued that the practice of medicine should be congruent with the law.2 Laws have been established and refined over time so doctors can help their patients (eg, with procedures and the administration of drugs) in ways that are illegal for others. An integral part of the medical role involves the negotiation of life–death decisions. I believe murder laws should be refined to reflect the reality that some terminally ill patients want death as a release from suffering and seek the help of their doctor to provide this. Just as there are differences between rape and making love, I see obvious differences between common murder and the hastening of death that doctors provide for terminally ill patients out of compassion, mercy, and respect for their wishes. Unfortunately, the ethics of current practices are difficult to elucidate because the existing law makes investigations problematic. The current crude law does not reflect community values — Morgan Gallup polls indicate about 80% of Australians are in favour of allowing voluntary euthanasia in certain circumstances.3 As Currow observes, these widely held values are sometimes expressed by the relatives of dying patients. In my experience, however, these relatives are usually advocating for the patient's wishes and interests, rather than undermining patient autonomy. I support the established hospice tenet that "the family is the unit of care" and there is a duty to address the concerns not only of patients but also of their loved ones. I think it is only a matter of time before politicians introduce the reforms that render the legal framework for terminal care more congruent with community values, the wishes of patients and their families, and current medical practices. These reforms should enable research, audit and the better regulation of end-of-life care.

Roger W Hunt BM BS, GDPH, FAChPM

To the Editor: Australia has been successful so far in maintaining a low prevalence of HIV infection among injecting drug users (IDUs). This has been achieved by adopting a harm-reduction approach to the prevention of bloodborne virus transmission, including needle and syringe programs, methadone maintenance and peer-education. Sharing of needles and syringes has declined markedly: cross-sectional surveys among users of needle and syringe programs across Australia have shown a decrease in the prevalence of reported sharing from 31% in 1995 to 15% in 1997.1 However, there is evidence that among some subpopulations, especially those of Indo-Chinese origin, unsafe injecting practices remain common. In a survey of Indo-Chinese IDUs in Sydney and Melbourne, Maher et al reported that 22% of those surveyed had shared needles and syringes in the preceding month.1 Although the Indo-Chinese community is becoming increasingly aware of issues related to drug use, IDUs are under-represented in drug treatment programs.3 There is also evidence that parents send their children back to their country of origin to escape the Australian heroin scene. In a Melbourne survey of Vietnamese IDUs, Kelsall et al reported that 19% of their sample (38 of 200) had returned to Vietnam during the previous five years for drug-related reasons. Of these, 24 reported using heroin in Vietnam, a disturbing finding given that HIV prevalence among IDUs in parts of Vietnam is greater than 50%.4 We analysed HIV surveillance data in Victoria to investigate whether there was an over-representation of Indo-Chinese-born IDUs. Country of birth has been collected as part of HIV notification in Victoria since January 1996. Since then, there have been 38 notifications of HIV infection in individuals reporting intravenous drug use as a risk factor. Of these 38, 11 (29%; 95% CI, 15%–46%) reported an Indo-Chinese country of birth — a higher proportion than expected given the 1996 census finding that 1.5% of Victoria's population was born in an Indo-Chinese country.5 These 11, all men, were significantly younger than other IDUs notified in this time (mean, 23.3 years v 31.3 years, respectively; P < 0.05). Although these numbers are small, they highlight a group at increased risk of HIV who are not currently being effectively reached by prevention services. These data also suggest a hidden route for spread of HIV from Asia into the Australian community. There is an urgent need to provide culturally relevant education and harm-reduction programs to prevent transmission of HIV within this group. The Victorian Department of Human Services is allocating additional resources to working with culturally and linguistically diverse communities on prevention activities to address this issue.

Jane S Hocking · Peter G Higgs · Cathy M Keenan · Nick Crofts

To the Editor: On reviewing the results of the Wimmera clinical risk management program,1 we are prompted to ask whether the model can be generalised to a tertiary hospital. The program outlined by Wolff and colleagues is a good model for local quality improvement and provides a foundation for developing a model for tertiary hospitals. However, in considering its applicability to tertiary hospitals, a number of issues must be addressed. The number of separations and emergency department presentations at tertiary hospitals does not lend itself to review of all medical records. Such review is time- and resource-intensive and probably unrealistic in a tertiary setting. A sampling strategy might be more suitable, but would introduce the possibility of sampling error and missing adverse events. The availability of medical staff to review records is also limited, with clinicians often having public, private and teaching commitments. It would also not be feasible for a medical director to be involved regularly in the day-to-day tasks of the process. Nevertheless, these issues could be addressed by allocating the review process to a dedicated, trained team. Development of a review pathway would ensure participation of senior medical or management staff when necessary. The interface between tertiary hospitals and local general practitioners is broader and less defined than in rural areas, making the involvement of GPs difficult. The clinical mix and complexity of patients requiring tertiary care differ significantly from those at a rural base hospital, and restricting screening criteria for adverse events to eight items, as in the Wimmera program, would likely result in adverse events being missed. In addition, the clinical structure of tertiary hospitals is not uniform, and specific criteria may need to be developed to address the clinical specialties of the hospital. Lastly, in this era of cost containment in healthcare, Wolff et al did not address the cost of its clinical risk management program. While this is not a fault in the study, cost would be an essential consideration in generalising the program to a tertiary hospital. The model used in the Wimmera program has limitations when considering adaptability to tertiary hospitals, because of issues of scale and day-to-day practicalities. Further examination of the costs involved in ongoing operation of the program and a cost–benefit analysis are required. In addition, investigation is needed into feasible options that deliver useful results in a tertiary setting before a quality improvement model can be developed that is relevant, appropriate and cost-effective for tertiary hospitals.

Kathy M Brown · Humsha Naidoo · Arona E Offenberger

In reply: The model developed in the Wimmera hospital for clinical quality improvement has formed the basis for quality improvement systems in several regional and tertiary hospitals in Australia. The resources required to implement the model have been costed, and the Victorian Department of Human Services has allocated $4.8 million to establish clinical risk management programs based on the Wimmera model in every Victorian public hospital in 2001–2002.1 Whichever programs are implemented, some adverse events will be missed. However, not all medical records need to be reviewed, nor all adverse events found. Regular identification of some events provides significant opportunities to improve care. As clinician time is limited, some hospitals that have implemented the Wimmera model have paid clinicians with existing appointments for extra hours to participate in risk-management programs. Although feedback to general practitioners is logistically more difficult in a tertiary centre, it can still provide valuable information if limited to only a sample of inpatients. We agree that some departments in tertiary hospitals, because of their specialised nature, would need to develop additional screening criteria. The actual cost of running a clinical risk-management program based on the Wimmera model depends on how many components of the model are implemented, but in our experience should not exceed 0.5% of a hospital's total budget. Cost–benefit analyses are difficult to undertake, as some adverse events arise through underuse of available evidence, and additional resources would be needed for full implementation of the evidence (eg, giving prophylactic antibiotics immediately before surgery to prevent postoperative infection,2 or low molecular weight heparin postoperatively to prevent thromboembolism3). We believe that in any institution, whatever its size, the initiation of effective programs for clinical quality improvement needs both enthusiastic support from the highest level of management and champions at the "coalface" of patient care. If these two elements are present, adequate resources will often be found. However, providing resources without appropriate clinical and administrative support is unlikely to improve patient care.

Alan M Wolff · Jo Bourke · lan A Campbell · David W Leembruggen

To the Editor: The recent supplement by Hickie et al looking at the mental health of Australians attending general practice1 would have us believe that we are quite a mentally unwell nation indeed! The authors propose a broad concept of "mental disorder" which they found in 49% of general practice attenders based on 12 questionnaire items (the SPHERE-12). These 12 items include six relating to psychiatric symptoms (PSYCH-6) and six relating to somatic symptoms (SOMA-6).2 The SOMA-6 items are muscle pain after activity, needing to sleep longer, prolonged tiredness after activity, poor sleep, poor concentration, and tired muscles after activity. Patients with a total score of two or more in PSYCH-6 and/or three or more on SOMA-6 were classified as having a "mental disorder". Firstly, the SPHERE-12 is grossly oversensitive, as the six somatic items detect many medical conditions, glandular fever being just one example. Other validity issues include the two-week cut-off for symptoms (further adding to the overinclusiveness because of temporary distress and minor illnesses), and the lack of discussion regarding transcultural and inter-rater reliability, particularly with so many general practitioners involved. Secondly, the authors' interchangeable use of neurasthenia and chronic fatigue syndrome and somatisation needs discussion. Ten years ago, Hickie and several New South Wales physicians were dismissive of an article linking chronic fatigue syndrome and neurasthenia: "We have demonstrated immunological abnormalities in patients with chronic fatigue syndrome as compared with both normal controls and patients with major depression. Further, the demonstration of abnormal cytokine production in patients with chronic fatigue syndrome may underpin 'acquired neurasthenia'."3 All the SOMA-6 items are key symptoms of chronic fatigue syndrome. With the overwhelming amount of biological data now available, purely psychological theories about chronic fatigue syndrome (as opposed to chronic fatigue) are totally untenable, as is the use of the term neurasthenia, introduced into medicine in 1869 and discarded by the American Psychiatric Association's Diagnostic and statistical manual of mental disorders4 as invalid.5 A recent study from the Fatigue Clinic, King's College Hospital, UK,6 found that an astonishing 68% of patients had been inappropriately misdiagnosed with a psychiatric illness. This is surely a warning for overzealous psychiatrists. Thirdly, treatment implications are a concern. The authors comment that "only 27% of patients with Level 1 disorders received pharmacological interventions" (Level 1 implying positivity for PSYCH and SOMA items). They say that general practitioners mostly used "relatively ineffective non-pharmacological strategies", and that they had responded to missing all this "unmet need" by "criticising the oversensitivity of the screening instrument and inappropriateness of diagnostic systems used", implying an underprescribing of antidepressants. The recent National Survey of Mental Health and Well-being7 showed that somewhere between two-thirds and a half of the 23% of the population diagnosed with psychiatric disorders did not visit their general practitioner. How does this fit in with the 49% found by Hickie et al? In summary, the authors' broad and idiosyncratic conceptualisation of "mental disorder" and their use of a screening tool which labels many physically ill people with or without concurrent distress as cases of "mental disorder" implies that general practitioners need to prescribe more antidepressants — at what cost and for whose benefit?

Nicole Phillips MB ChB, FRANZCP · Michael J Oldmeadow MB BS, FRACP · Natalie Krapivensky MB BS, FRANZCP

In reply: It is with great pleasure that we resume our ongoing correspondence with Phillips concerning the medical and psychological status of patients who present with non-specific somatic complaints such as chronic fatigue.1 As we have reported previously,2 we have been strong advocates of both the need to develop appropriate instruments for measuring neuropsychiatric states characterised by non-specific somatic symptoms and to promote effective medical and psychological management of patients with these disabling conditions.3 In their letter, Phillips and colleagues fail to grasp the essential issue. To describe a condition as a neuropsychiatric state (or mental disorder) does not necessarily lead to simplistic and entirely unhelpful assumptions about "medical" versus "psychological" causes or treatments. Phillips et al attempt to promote once again the notion of "biological" (ie, acceptable) versus "psychological" (ie, unacceptable) theories of the causation of chronic fatigue syndrome. Such an approach is not only intellectually sterile and inconsistent with the past decade of intensive research by a wide range of medical and psychological research teams,4 but also profoundly unhelpful to people affected by these disabling disorders.3 In recent years, the very significant health burden of common mental disorders such as depression, anxiety, alcohol or other substance misuse, and neurasthenia (prolonged fatigue states lasting longer than three months) has been well documented in the Australian community5 and in the primary care setting.6 Phillips and colleagues appear to have no knowledge of the basic epidemiological fact that mental disorders are two to three times more common in primary and other medical care settings than in community studies (hence the total rate of disorder in our study is about twice that detected in the Australian National Survey of Mental Health and Well-being). Contrary to their implications, the total rates reported in our general practice study are entirely consistent with the largest multinational study of primary care ever conducted.7 That study indicated that a third of all primary care patients have mental disorders and another third have mental health difficulties (with or without concurrent medical disorders) requiring specific psychological assessment. The significance of our study is that it has brought the extent of common mental health needs (including depression, anxiety, alcohol or other substance-misuse and somatoform disorders) to the attention of the Australian medical profession. What is now required is a concerted and integrated response — not a return to dualistic notions of illness that have for so long hampered the provision of effective pharmacological and non-pharmacological treatments to patients with mental disorders who present for medical care.

Ian B Hickie MD, FRANZCP · Tracey A Davenport BA(Hons) · Elizabeth M Scott FRANZCP · Sharon L Naismith BA(Hons)

To the Editor: The EBM in Action article on laser treatment by Del Mar et al1 raises my anxiety about the reliability of evidence-based medicine (EBM) in general and, at the very least, the authors' assessment of the question they set out to answer. One is seldom, if ever, in a position to understand the breadth and depth of an issue unless it is the subject of particular study. Most of us can not challenge statements made in such articles without an intimate knowledge of the literature. As laser therapy is the topic of my PhD thesis, I am in a unique position to have much of the literature on the subject at my fingertips. The authors state in their conclusions that "low power laser therapy appears to be no more efficacious than placebo in relieving musculoskeletal pain". Several aspects of the analysis on which they base this conclusion cause me great concern. Firstly, they state that "The search report highlighted the high quality of evidence supporting the refined question". Quite the contrary. One of the two systematic reviews they cite2 has been criticised in the literature for its many inadequacies, not the least being that laser acupuncture and laser therapy are included in that review as if they were the same, which they are certainly not.3 In addition, the review by Beckerman et al concludes, with regard to musculoskeletal pain, that "the efficacy of laser therapy for musculoskeletal disorders seems, on average, to be larger than the efficacy of placebo treatment. More specifically, for rheumatoid arthritis, post-traumatic joint disorders and myofascial pain, laser therapy seems to have a substantial specific therapeutic effect".4 How can this fit with the conclusion of Del Mar et al? Furthermore, Gross et al state in their review, which consisted of three trials of laser therapy, that "In general, all therapies have not been studied in enough detail to adequately assess either efficacy or effectiveness".5 The choice of other articles by Del Mar et al is also somewhat mystifying in that, out of the nine references cited, one is in Russian and two in Danish. There are many other relevant articles in English that they have not cited.6,7 There is no doubt, as I myself have found, that it is difficult to search for this topic in the literature, as there are many terms used for laser therapy and the information comes from a broad range of sources. However, this is no excuse for a group that holds itself out to be "expert" in a field. It is very disappointing to see such an incomplete review with such an inappropriate conclusion based on such a poor sample of the literature. If this is an example of EBM in action, then I think we should be very concerned.

Roberta Chow MB BS (Hons), FRACGP, FAMAC, MApplSci(MedAcu)

In reply: Chow criticises us for not identifying all relevant trials. But is she willing to help others in the process of reviewing? We could not identify a systematic review of the area with her involvement, nor does she appear to have registered an appropriate protocol with the Cochrane Collaboration (instructions for which are available at <http://www.cochrane.de>). Systematic reviews are important to help clinicians make sense of a diversity of trials. If experts such as she, devoting years to the area, do not help us, who should? We were not attempting such a systematic review (which would probably take several months of work). Rather, we were trying to provide clinicians with the best obtainable answer in a 24–48-hour turnaround time.2 Given that clinicians might have one question per patient,1 attempting a systematic review with each question would give us a lifetime of work after only a fortnight of clinical work! We needed to balance the timely requirements of clinicians with the quality of the evidence obtained. As Chow points out, tracking down every last trial is difficult. Therefore, we first aimed to identify systematic reviews rather than attempting to find all trials ourselves. These reviews missed some relevant material — as indeed did Chow, who did not cite several recent studies,3,4 which makes us wonder if she has a strong prior belief that may bias her views. Would these missed trials have made any difference to the conclusions we reached previously? A systematic review published since our original literature report (January 2000) suggests not, although there may be some specific subgroups of patients and conditions for which laser therapy is effective.5 All of this highlights the need for a collective effort to sort out the mess of medical information. In seven years the Cochrane Collaboration has systematically reviewed less than 5% of more than 300 000 trials on the clinical trials registry. They are difficult to perform and maintain. Millions of dollars continue to pour into primary research that still remains inaccessible to us at the clinical frontline, the "great criticism" with which Archie Cochrane pricked the profession into action.6 Please, Dr Chow, abandon throwing bricks from the sidelines, and join us in trying to help clinicians access research evidence in the timely fashion needed for day-to-day practice!

Chris B Del Mar MD, FRACGP · Paul P Glasziou MB BS, PhD, FAFPHM

To the Editor: With respect to the article by Ferson in the Christmas issue of the Journal, a personal experience of an unwanted side effect which occurred in 1927 may be of interest. I was a boarder at school, and four weeks before sitting for the Leaving Certificate examination I contracted a violent sore throat associated with a bodywide erythema similar to sunburn, but without any associated burning sensation. The doctor had no hesitation in diagnosing scarlet fever, and I was transferred to the Coast (now Prince Henry) Hospital, which was the infectious diseases hospital for leprosy, scarlet fever, diphtheria and the like. I had asked if I could take my textbooks to the hospital, but was told that if I did they would be destroyed when I was discharged. I left the books at school, spent four weeks in isolation and returned to school with one weekend to prepare for the examinations — the results were quite disappointing!

Sir Keith Jones

To the Editor: In their recent article on the use of modelling in pharmacoeconomics to estimate the potential benefits, risks and costs of preventive drugs, Liew and colleagues highlighted important strengths and limitations of this technique.1 One limitation is that modelling is discretionary: different analysts elect different models and get different answers. We argue that modelling is the first step. The next step is testing the predictive validity of the model by systematically collecting cost and effectiveness data over a period of time. Then the predictions of the original analysis could be compared to what actually transpired. The goal of pharmacoeconomics is the most accurate estimation of costs and benefits. The more these variables are truly study outcomes (that is, experimental and not constrained by assumptions of the economic model), the more valid the process. This will help reduce model discretion, improve data quality and increase the likelihood that the experiment could be replicated independently, the acid test of validity. In reducing the discretion inherent in pharmacoeconomics, we can allay the concerns of those who have questioned its underlying theory2 and validity.3 If one does not know the benefit of a drug, one conducts a study. Equally, if one does not know the cost of a drug, one needs a study. This has been the impetus for randomisation in design of pharmacoeconomic studies, thereby decreasing reliance on economic modelling.4 Furthermore, there are well-tested methods for quantifying the uncertainty of estimates obtained with randomised studies. In contrast, economic modelling assesses the robustness of the model assumptions, as reflected in the estimate, using sensitivity analysis. However, this analysis cannot separate uncertainties attributable to the model assumptions, uncertainty inherent in the data put into the model, and uncertainty of outcome estimates. One is left with nostalgia for the simplicity of the null hypothesis. How can we move forward? To reduce reliance on modelling and to collect better data, we propose that Australia, with its "culture of evaluation",5 again take the lead by creating a new "conditional listing" category on the Pharmaceutical Benefits Scheme for all drugs, not just preventive therapy. This would be available for selected products with strong biological rationale but inadequate current evidence on cost-effectiveness. By necessity, these would include only high-volume/low-cost and low-volume/high-cost products, as high-volume/high-cost products are rarely developed, and low-volume/low-cost products are not problematic. The sellers would then collect prospective data to substantiate cost-effectiveness of the products or would have them delisted. This would be truly innovative and, like the Pharmaceutical Benefits Advisory Committee itself, a first for the Commonwealth. Certainly, no other jurisdiction is even considering this, let alone proposing systematic study. With better data, we would learn which models and model assumptions yield accurate predictions. Of course, many challenges and difficulties will need to be addressed regarding this proposal, but in our opinion none are insurmountable, and the benefits of a program of this type clearly exceed the risks.

Kent R Johnson · Marissa N Lassere

To the Editor: Carotid stenting is a new application of endovascular therapy. Its efficacy in preventing strokes is yet to be established, by contrast with the proven Level 1 evidence of benefit from carotid endarterectomy. The risks of implanting carotid stents at present appear greater than the risks of carotid endarterectomy. An overview of carotid endarterectomies in Australia is maintained by vascular surgeons, through audits such as the ongoing Melbourne Vascular Surgeons Association Audit and the New South Wales Carotid Endarterectomy Audit. The technique of carotid stenting, the stents themselves and the brain-protective devices used during the implanting of stents are expensive and still evolving. The long-term durability of stents is unknown. Australian vascular surgeons, neuroradiologists and neurologists are awaiting the outcome of two major international randomised trials of carotid stenting versus endarterectomy (the US Carotid Revascularization Endarterectomy versus Stent Trial and the European International Carotid Stenting Study). These seek Level 1 evidence of the comparative risks and success of the new stenting procedures in stroke prevention and aim to document the late outcome of stenting, particularly the incidence of restenosis, which is a significant problem in other arteries after stenting. While these definitive trials are in progress, vascular surgeons of the Royal Australasian College of Surgeons wish to add their note of caution to the reservations expressed in the NHMRC guidelines on stroke prevention1 and the recommendations of the Australian Association of Neurologists.2 A recent commentary by Spence and Eliasziw3 illustrates the disparate nature and the limitations of existing studies of carotid stenting. We consider carotid stenting is not yet appropriate for widespread use in Australia. Experienced endovascular and neurology teams should continue to evaluate the new procedure. Stenting of symptomatic carotid atheroma should only be conducted with the consent of patients who are fully informed about stenting's known hazards and unproven status and who understand that the established treatment is carotid endarterectomy.4 Clinicians should audit closely the immediate outcome and long-term complications of any carotid stenting they perform.

Peter L Field

To the Editor: Preparations containing isoflavone phytoestrogens are widely used as an alternative therapy for treating symptoms of the menopause. Although Australian government regulations strictly control the components of alternative therapies, adherence to the stated amounts of the components in alternative therapies is not routinely assessed. Isoflavones exist in two forms — aglycone (the free form) and glycosylated or glycone (the conjugated form) — the relative proportions of which vary between preparations. As glycosylation contributes considerably to the mass of isoflavone molecules, it is relevant to consider the total amount of potentially available isoflavone in alternative therapy preparations. Isoflavone-containing preparations which had a recommended daily dose on their labels were purchased at random from pharmacies around Sydney during September 1999. Where possible, products from more than one manufacturing batch were purchased and all products were well within their stated shelf life. The tablets, capsules or powder were removed from their packaging to conceal their identity and randomly allocated to numbered plastic bags by the hospital pharmacy department. The samples were then sent to PhytoChem Technologies Inc (Chelmsford, Mass, USA), an independent reference laboratory for the assay of isoflavones. There, isoflavones were extracted within four months of purchase (and before their stated use-by date) from 500 mg of each specimen after dissolution in 70% methanol. Glycosylated and free isoflavones were assayed in duplicate by gradient high-pressure liquid chromatography, with detection of isoflavones at 254 nm using a Waters 996 series photodiode detector with a limit of detection of 0.2 µg/mL. The identity of chromatogram peaks was confirmed by UV–V spectral analysis, and by comparison with standards. The mobile phase was acetonitrile, and adequate peak separation, linearity, accuracy and reproducibility were demonstrated. The total amount of available aglycone isoflavones in each sample was estimated (see Table). Only two products (Phytolife and Promensil) had total isoflavone contents close to the stated amount, and the content of the Phytolife product was variable. Estimated aglycone contents of preparations demonstrated that glycosylated isoflavones contributed substantially to the stated content of the product. A previous study of isoflavone-containing preparations marketed in the United States produced similar results to ours.1 Consumers may wish to consider not only whether an alternative therapy is of use, but also whether the product they purchase contains what they expect. Actual and stated isoflavone content of commercially available preparations Manufacturer Product No. of batches assayed Stated isoflavone content (mg) in recommended daily maximum dose of product Actual total isoflavone content per daily dose (mg) Estimated aglycone isoflavone content per daily dose (mg) Blackmores Phytolife one a day 5 40 41.02 ± 6.12 25.75 ± 6.04 Bioglan Soy powder plus 4 68 48.75 ± 1.42 30.44 ± 0.86 Earths Own Soy + calcium 1 68 42.52 25.67 Health Direction Femme phase 1 235 mg soy protein* 0.29 0.20 Herron Phyto source 1 22.5 16.27 9.93 Natural Nutrition Menopause 1 60 0.56 0.51 Natural Nutrition Phytobalance 3 90 58.12 ± 6.26 34.96 ± 3.79 Novogen Promensil 4 40 40.12 ± 1.98 38.38 ± 1.20 Pretorius Maxi soy plus red clover wild yam and calcium 4 68 50.36 ± 1.64 31.24 ± 1.13 Wagner Probiotics Femme soy plus with red clover 2 27 30.76 ± 0.12 19.65 ± 0.05 * Soy protein has a high isoflavone content. Values are the mean ± standard deviation. Total isoflavones = glycone plus aglycone. Estimated available aglycone isoflavones = weight of aglycone isoflavones plus weight of glycone isoflavones corrected for glycone content.

Jan B Howes · Laurence G Howes

To the Editor: The 50 g glucose challenge test (GCT) is widely recommended as a screening test for gestational diabetes (GD).1 The test consists of a 50 g oral glucose load given at any time of the day, followed one hour later by the measurement of the plasma glucose concentration.2 This test is recognised as imperfect for screening, as sensitivity and specificity are not 100%.2,3 It is known that glucose tolerance deteriorates in the afternoon,4 which raises the question of whether time of day influences the response to the 50 g GCT. At Royal North Shore Hospital, screening for GD is performed at the 26–28-week visit by means of the 50 g GCT. In 2000, screening for GD was introduced into a morning midwives antenatal clinic, whereas previously it had only been performed in the afternoon. The population attending the clinic at the 26–28-week visit includes many women receiving shared care, and is regarded as being at low obstetric risk. The Table shows the results of screening at the morning clinic compared with screening in the afternoon over the same time period. The two groups were identical in terms of age, weight, ethnicity, and family history of diabetes or past history of GD. The percentage of women with a positive screening test result during the morning clinic (17.0%) was significantly lower than that during the afternoon clinic (31.1%). Positive screening results were followed up with a diagnostic 75 g glucose tolerance test, and GD was diagnosed according to the Australian Diabetes in Pregnancy Society criteria.5 Women with a positive screening test result confirmed with a 75 g glucose tolerance test in the afternoon were less likely to have GD than those with a positive test in the morning (31.5% v 40.0%). Despite the fact that a smaller percentage of women who screened positive in the afternoon had GD, a greater percentage of the total number screened in the afternoon had GD than in the morning group. In this cohort, the difference (9.8% v 6.8%) was not significant (Table; P = 0.15). These results are consistent with the hypothesis that a 50 g GCT test performed in the afternoon results in a greater number of positive results, a greater number of women undergoing diagnostic testing and a greater number of women identified with GD. The morning GCT appears to increase specificity, with an associated decrease in sensitivity. These results need to be taken into consideration when designing or implementing a screening program. Screening for gestational diabetes (GD): the effect of screening time Time Morning (0930–1200) Afternoon (1205–1710) Number screened 176 470 Age in years (mean ± SD) 31.2 ± 4.7 31.7 ± 5.0 Weight (mean ± SD) 59.4 kg ± 10.5 kg 60.8 kg ± 12.9 kg Family history of diabetes 27 24 Past history of gestational diabetes 1 3 % White/Asian/Middle Eastern 62.6/28.0/9.0 67.5/25.9/5.8 Positive result, 50 g glucose challenge test 30 (17.0%) 146* (31.1%) Abnormal result, 75 g glucose tolerance test 12 (6.8%)† 46‡ (9.8%)† *P < 0.001, χ2. † % Of number screened. ‡ P = 0.15, χ2.

Aidan McElduff · Rosemary Hitchman

To the Editor: We have recently noticed changes in the incidence of invasive cervical carcinoma in the Gippsland Health Region and would like to know whether other regions have noticed similar demographic changes. During 24 months in 1999–2000, 19 women (median age, 59 years; range, 33–88 years) with squamous carcinoma were registered in our pathology practice. Based on information from the Victorian Cervical Cytology Register, almost half (10 women) had no previous cervical smear history whatsoever, while three had had smears, but at irregular intervals up to 14 years apart. The remaining six women had had regular Pap smears, with 1–3 negative smears preceding the diagnosis of cancer. Sixteen of the women had consulted their general practitioner for some other ailment before the cervical cancer was discovered (median interval, 14 months), but no cervical smear had been obtained. Of particular interest is the fact that six of the 19 patients are in their seventh decade or older, with a median age of 80 years (range, 79–88 years). The Victorian Department of Human Services reports that the cervical-smear participation rate for eligible women in the Gippsland region is 68%, a rate not much different from the other regions.1 The two-yearly participation rate for the 60–69-years age group is 56%, and, although no official figure is available for women in their seventh or eighth decades, it is likely to be considerably lower. The Cancer Epidemiology Centre has recorded that, over a 16-year period, the incidence of cervical carcinoma in Victorian women aged over 70 years fell by 50%, and simultaneously there has been a shift in the peak incidence from the 70–74-years age group to one a decade older (Vicky Thursfield, Information Manager, personal communication). Accordingly, we suspect that women over 70 years of age still have a significant incidence of invasive cervical carcinoma, but are not being offered cervical smears, even when the National Health and Medical Research Council guidelines indicate the necessity.

Nicholas J Mulvany · Norman R Sonenberg

To the Editor: In response to Leeder and Rychetnik's article,1 evidence-based medicine (EBM) also has significant potential to reduce the quality of patient care, with obvious ethical implications. I refer to two specific issues of concern. The first relates to the increased expectation that clinicians, and especially trainees, not only understand the role of EBM in clinical practice, but actively contribute to its underlying database. Indeed, some of the professional colleges (eg, the Faculty of the Australian and New Zealand College of Anaesthetists) now include formal projects (which are often, but not necessarily, clinical trials) in their final assessment of trainees.2 This is leading to increasing numbers of poorly designed trials that are unlikely to make useful contributions to the clinical database. These commonly take two forms: studies which lack sufficient power to confirm the absence of a true difference between groups,3,4 or studies which use a placebo when effective therapeutic alternatives exist.5 Yet such studies are frequently published in reputable, peer-reviewed journals.6 Both of these types of studies are unethical, and both impact adversely on patient care. Increasing the evidence base of clinical medicine is important, but our primary responsibility remains the maintenance of quality of care of all patients, especially those involved in clinical trials. Therefore, education of clinicians, and especially trainees, must emphasise the role and importance of statistics, epidemiology and study design in all areas of medicine to prevent unnecessary reductions in the quality of care of this subset of patients. The second concern relates to the increase in "quality improvement" projects that are rarely submitted to ethics committees for approval. These activities also contribute to the evidence base, primarily at a local level, but patients are usually unaware that they are involved in these projects, and that these activities may have significant quality-of-care implications for them. It is therefore important that internal hospital quality assurance activities undergo a similar level of scrutiny by ethics committees to that of clinical trials. Patients involved in any audit or project that has the potential to influence their care should be required to give informed consent. Only then can we reassure a patient that, while we are continually striving to improve the care we provide by developing the evidence base for clinical medicine, the care of each individual remains our primary concern.

Simon R Tomlinson · Kerry J Breen · Malcolm H Parker · Chris B Del Mar · Paul P Glasziou · Lucie Rychetnik and · Stephen R Leeder

Comment: Tomlinson raises two important ethical issues in clinical research. While there are several ethical issues which may arise in acquiring and applying evidence to clinical practice and health administration, as outlined previously by Kerridge et al1 and picked up well by Leeder and Rychetnik,2 it is misleading if Tomlinson wishes to imply that the two issues he has raised can be attributed to the evidence-based medicine (EBM) movement. His first issue could be summarised as "badly designed clinical research should be seen as unethical", for reasons which may include wasting scarce resources or placing participants at discomfort or risk when the likelihood of benefit is slight. He alleges that poorly designed studies are "frequently published in reputable peer-reviewed journals", a statement which would surprise most editors. Peer review prior to publication, and the earlier independent prospective scrutiny of research proposals by human research ethics committees (HRECs) (according to updated national guidelines published by the National Health and Medical Research Council [NHMRC] in 19993), are two processes designed to prevent this. Assessment of the quality of design and execution of clinical research protocols is to some extent subjective, so these processes will never be perfect. His second issue relates to the definition of quality improvement/assurance and clinical audit, and whether such studies should be regarded as clinical research, and thus subject to prospective ethical review by an HREC. His own conclusion "that internal hospital quality assurance activities should undergo a similar level of scrutiny by ethics committees" is not consistent with the NHMRC guidelines,3 which, in the context of outlining the difficulties in defining research, state (on page 6) "such lists risk including activity that would not normally be included, like quality assurance activities or audits". Nevertheless, there are definitional uncertainties. The Australian Health Ethics Committee (AHEC) of the NHMRC has recognised that clinicians, HRECs and their hospitals need clear advice on how quality assurance and audit activities, which may not need ethical review, are to be separated from clinical research, which does need review. We are not the only country considering this matter.4 AHEC has established a working party to prepare such advice. The working party includes members drawn from AHEC, HRECs, consumer groups, medical colleges and health administrators. Draft advice will be subject to wide stakeholder consultation. The working party commenced its task in November 2001 and its final report is expected by mid-2002.

Simon R Tomlinson · Kerry J Breen · Malcolm H Parker MB BS, MLitt · Chris B Del Mar MD, FRACGP, FAFPHM · Paul P Glasziou MB BS, PhD · Lucie Rychetnik MPH, PhD · Stephen R Leeder FRACP, FFPHM, FAFPHM

To the Editor: We consider that Leeder and Rychetnik make several mistakes in their exploration of the relationships between ethics and evidence-based medicine (EBM).1 We share some of their ethical concerns about the determinants of the research agenda — lack of consumer input, emphasis on the benefits of interventions rather than harms, and funding structures favouring commercially promising interventions or biased by the status of the methodology to be used. However, these are criticisms that relate to producing new research, not using available research. The definition of EBM used by Leeder and Rychetnik2 values evidence that is non-quantitative, and explicitly demands the inclusion of patient preferences in clinical decision-making. Evidence about effects comes from research, while evidence about concerns and values comes from individual patients. To incorporate a patient's pre-ferences in the consultation is crucial to ethical practice, but quite independent of any particular hierarchy of evidence. Similarly, in claiming that treatment may be denied those of low social utility if patient autonomy is not valued, they mistakenly confuse preference or value with the quality of the evidence. The sin of old-fashioned paternalism is falsely attributed to EBM. The suggestion that EBM can exclude the importance of patient narrative is also at odds with the authors' chosen definition, which emphasises the "identification and compassionate use of patients' predicaments, rights, and preferences". Next, they worry that EBM might be misused in public health policy by neglecting areas where evidence is difficult to obtain, offering mental illness as an example. In fact, mental health attracts considerable attention3 and funding as one of the Commonwealth's current priority health areas.4 It has also been an area of considerable activity in EBM, with the Cochrane Mental Health groups and the BMJ's evidence-based summary journal Evidence-Based Mental Health. It may be that EBM has done the opposite of their prediction by highlighting an area of "evidence need". We agree that patients require support when they confront ambiguity and uncertainty. Nevertheless, doctors are ethically and legally obliged5 to provide full disclosure. Patients should be given correct information — warts, uncertainty and all — as often as possible. To suggest that the time spent seeking evidence threatens other elements of clinical practice is misleading. Clinical practice requires judgement to balance all its competing demands. We suggest that, by increasing the efficiency of continuing education, EBM should actually release more time for other requirements. Leeder and Rychetnik also misinterpret the relation between EBM and the law. They suggest that some practitioners who consult evidence, but practise against published guidelines, may be compromised. The point of EBM is to find the best available evidence. If that is clinical experience, consensus or narrative, rather than quantitative data, then so be it. Similarly, it is wrong to imply that those who practise EBM may be sued because they fail "to try everything". EBM, which is simply the getting of the best available information, changes nothing in the formal relationship between clinical evidence and the legal standard of care. Moreover, we believe that, by fostering patient involvement in decision-making, EBM should help protect clinicians from medicolegal dispute. We are always at risk of using new tools overzealously. But the champions of EBM temper its promotion with words like "judgement", "incorporating patient preference" and "conscientiousness". EBM involves a sensible and systematic search for the best information to include in the decision-making process. Great care should be exercised in issuing warnings about how it might be misused, in case EBM becomes unfairly caricatured, which may reduce the motivation of health professionals to find and apply the best treatment.

Simon R Tomlinson