Letters

To the Editor: In a valuable review of low-molecular-weight heparins (LMWH), Eikelboom and Hankey1 stray off the beaten path into the unwelcoming area of obstetric therapeutics — a notoriously hostile environment replete with traps and hazards. Their statement that "low-molecular-weight heparins are being used increasingly in pregnant women with prosthetic heart valves and for the prevention and treatment of venous thromboembolism" is contentious and requires considerable qualification. The Journal has already published a position statement concerning the use of these heparins in pregnancy.2 It clearly stated that the initial treatment for pulmonary embolism in pregnancy remains intravenous unfractionated heparin, because so far there are no trials of LMWH in pulmonary embolism in pregnancy. The guidelines of the American College of Chest Physicians do endorse the use of LMWH for this indication,3 but base that view on data in non-pregnant patients. We believe that, as yet, there is insufficient evidence to recommend LMWH for the initial management of pulmonary embolism in pregnancy, although, on theoretical grounds, the treatment seems attractive. In anticoagulation therapy for artificial heart valves in pregnancy, there are serious problems. Unfortunately, the conscientious adviser must be very circumspect in counselling women with these prostheses. Pregnancy for these women presents significant risks. None of the heparins, unfractionated or low molecular weight, has been shown to protect reliably against embolism from, or thrombosis of, these valves in pregnancy. Whether LMWH is better than unfractionated heparin has not been established and awaits appropriate trials. Warfarin, which crosses the placenta, remains a valid, but worrying, choice in pregnancy for antico-agulation in patients with prosthetic heart valves. This drug provides optimal protection from valve thrombosis, but with the potential for teratogenicity in the first trimester and fetal (and maternal) haemorrhage later in pregnancy. Many experts use heparin and warfarin sequentially in this situation.3 Thus, anticoagulation therapy for pregnant women with serious medical problems remains, as always, perplexing, difficult and dangerous. While LMWH offer considerable promise and have undoubted utility in several areas, there are very compelling caveats about their current use for pulmonary embolism and prosthetic heart valves in pregnant women. For these reasons and others, women with prosthetic heart valves planning pregnancy, as well as those already pregnant, should be counselled about these problems by a physician experienced in managing medical problems in pregnancy.

Barry NJ Walters · Dorothy Graham

To the Editor: The recent "New Drugs, Old Drugs" review of low molecular weight heparins (LMWH) and heparinoids1 provides a timely reminder of the limitations of studies that support the use of these agents in preventing venous thromboembolism (VTE), particularly in orthopaedic surgery. A new class of anticoagulants has recently been released in Australia and is being promoted as being more effective than LMWH in preventing VTE. However, while several randomised controlled trials suggest that fondaparinux reduces the risk of asymptomatic deep vein thrombosis (DVT) in patients undergoing hip and knee replacement surgery,2,3 there is currently no evidence to suggest that it reduces the risk of symptomatic VTE. Fondaparinux is a synthetic penta-saccharide that selectively binds to antithrombin III, enhancing the neutralisation of factor Xa and inhibiting generation of thrombin and subsequent clot formation.2 Unlike LMWH, fondaparinux does not appear to affect platelet function, thus potentially reducing bleeding tendencies and avoiding the risk of immune-mediated thrombocytopenia. The main problem facing researchers who study VTE prophylaxis in patients undergoing orthopaedic surgery is that, while asymptomatic DVT is common, symptomatic VTE is rare. The rate of fatal pulmonary embolism in patients undergoing hip replacement surgery is 0.1%–0.2% in those who receive no prophylaxis.4 Trials to demonstrate a reduction in symptomatic VTE are not performed because huge sample sizes are required to show a statistically significant difference in outcome (50 000 patients would need to be enrolled in a trial to show a reduction in the rate of fatal pulmonary embolism from 0.2% to 0.1% with 80% power). If such a difference could be shown, it would probably be clinically irrelevant to an orthopaedic surgeon performing 50 joint replacements a year. Although asymptomatic DVT is used as a surrogate endpoint for trials that support VTE prophylaxis, the natural history of asymptomatic DVT is poorly documented. There is some evidence to suggest that asymptomatic DVT is not associated with an increased risk of subsequent chronic venous insufficiency,5 and the association between asymptomatic DVT and subsequent clot propagation and embolisation is not well established. Further information on the natural history of asymptomatic DVT must be obtained before the clinical relevance of results from current studies of VTE prophylaxis can be determined. Until then, the clinical relevance of studies comparing the use of "new drugs" with "old drugs" in preventing VTE in orthopaedic surgery cannot be assessed.

Owen D Williamson · Alison M. Street

In reply: Walters and Graham question the role of low-molecular-weight heparin (LMWH) as a replacement for unfractionated heparin during pregnancy, and cite the lack of randomised comparisons to support their view that the standard initial treatment for pulmonary embolism during pregnancy remains intravenous unfractionated heparin. We do not deny the lack of clinical trials of LMWH in pregnancy; we were simply referring to the increased use of LMWH.1,2 However, the lack of evidence of effectiveness does not equate with evidence of lack of effectiveness of LMWH in pregnancy. Clinical trials are needed to determine optimal anticoagulant strategies during pregnancy, particularly in patients with prosthetic heart valves. While awaiting the results of these trials, we believe that the major pharmaco-kinetic and safety advantages of LMWH over unfractionated heparin, coupled with an extensive body of evidence demonstrating their efficacy and safety in non-pregnant patients, should not be ignored in our pursuit of optimal anticoagulation therapies. Williamson and Street question the validity of asymptomatic deep vein thrombosis as a surrogate for symptomatic venous thromboembolism in patients undergoing major orthopaedic surgery. Further, they cite a 0.1%–0.2% incidence of pulmonary embolism in patients undergoing hip replacement surgery without prophylaxis3 to support the conclusion that any effect of thromboprophylaxis on reducing symptomatic events is likely to be irrelevant for individual orthopaedic surgeons. We believe that their argument is seriously flawed. Firstly, the "meta-analysis" they cite3 had major methodological limitations, as elegantly highlighted by "Sherlock Holmes" in his critical appraisal of systematic reviews of surgical thromboprophylaxis.4 Secondly, rigorously conducted randomised trials and meta-analyses of randomised trials have demonstrated the efficacy of antithrombotic therapy for the prevention of both symptomatic and fatal venous thromboembolism in high-risk surgical patients, including lower-limb orthopaedic surgery.5,6 Thirdly, the clear correlation between reduction in asymptomatic and symptomatic venous thromboembolism in patients undergoing elective joint replacement surgery7 suggests that asymptomatic thrombosis detected by screening venography is a valid surrogate for symptomatic events. Fourthly, we agree that an individual orthopaedic surgeon performing 50 joint replacements per year may remain unaware of a small reduction in fatal pulmonary emboli in his or her own practice (eg, a 0.1% absolute risk reduction would be equivalent to preventing one death in 20 years of practice). Yet, on a population basis, even a 0.1% absolute reduction (which is likely to be an underestimate — the PEP study showed a 0.3% absolute reduction in fatal pulmonary embolism with aspirin5) equates to 50 preventable deaths per year in Australia alone8 and many thousands worldwide. There is now overwhelming evidence of the efficacy of thromboprophylaxis for preventing venous thromboembolism, including symptomatic and fatal pulmonary embolism, in high-risk surgical patients. With the rapid ageing of the Australian population and the expected increase in joint replacement surgery in coming years,9 the failure to use effective thromboprophylaxis in orthopaedic patients will likely result in a growing burden of preventable morbidity and mortality from venous thromboembolism.

John W Eikelboom · Graeme J Hankey

To the Editor: Koenig's rebuttal of some of the conclusions I drew in my recent article was perhaps more vigorous than can be justified given recent changes in Australian culture and the paucity of practice-oriented research.1,2 I accept that religious patients may be healthier in many respects, and being religious may help some patients cope with illness. However, it does not follow that having doctors in Australia enquire into their patients' religious beliefs almost as a matter of routine would be a cost-effective use of their time. In hospitals, doctors are part of a team, and do not themselves have to identify religious concerns and mobilise spiritual resources. Nurses commonly ascertain whether patients are religious, identify concerns, and liaise with chaplains and pastoral workers. Chaplains themselves are highly regarded by all members of the healthcare team; they counsel and help patients cope with illness as part of their role, and are effective.3 For most Australians, religious affiliation is largely nominal. Consequently, only a minority of patients presenting to general practitioners are likely to have religious beliefs affecting their care. Rather than take a religious history routinely, it might be better if GPs were to enquire into religious beliefs when a patient or the family is known to be particularly religious or if the clinical situation warrants it. Urging doctors to take a religious history ignores those patients who are not religious but who might have a spirituality that helps them cope with illness and their particular needs.4 It also ignores changes which have occurred in Australian culture since the mid-1970s.5 Organised religion has declined, while spirituality has surged.5 Moreover, whereas Christians understand spirituality in terms of their relationship with God, in the wider community, spirituality needs no God association. It is often seen as a previously ignored aspect of being human, alongside physical, emotional and social aspects.5 It is increasingly regarded as the integrating holistic factor in life, associated with healing, therapy and well-being. The healthcare system as a whole will need to consider the relevance of these cultural shifts and how it is going to respond. Medical professionals should keep this in mind when discussing the relevance for medical practice and how they will respond. Spirituality has already assumed greater prominence in the practice and education of nurses, psychologists and social workers, and medical professionals should take account of the skills and experience of these groups.

Hedley G Peach

In reply: Despite recent changes in Australian culture, Peach underestimates the importance of religious beliefs to older Australians likely to see physicians today.1-3 As people age and experience negative life events, such as medical illness, longitudinal studies show that they become more and more religious.4 Given the potential impact that spiritual issues have on treatment decisions, the physician–patient relationship and medical outcomes, physicians cannot simply defer these issues to nurses or chaplains, nor do many physicians wish to do so.5 Deferring such issues could, in fact, be more costly than the few additional minutes necessary to take a spiritual history, particularly in patients with serious or chronic medical illness. For patients who are not religious, the doctor should enquire about secular beliefs that could influence medical decisions or that give the patient's life meaning and purpose in the context of their illness. I do agree with Peach that physicians should always phrase enquiries in terms of "spirituality", allowing patients to determine for themselves what this involves — whether it be God, church, or the random forces of nature. Keeping the spiritual history "patient-centred" in this way ensures that no one is excluded and provides many additional safeguards.

Harold G Koenig

To the Editor: The recent articles about spirituality and health1,2 provide a welcome discussion about the very soul of medicine as well as the soul of the individual healthcare practitioner. If spirituality is "whatever is left over when the doctor, social worker, psychologist, community education officer or psychiatrist have had a go",3 then indeed spiritual questions should be left to the particular expert on that fragment of the person. However, if spirituality is the integration of every aspect of the person, the plumbing of depth, the search and discovery of meaning and purpose, the exercise of compassion and love often in relation to the divine,4 then our whole practice of medicine needs to be spiritually conceived and executed, both for our patients and for ourselves. We need to pause and reflect on the quality of our care of ourselves as well as of our patients.5 We need to rescue healthcare delivery from the reductionism of a mere science of "fixing bits" according to economic criteria. We need to deliver healthcare with humanity, compassion and wisdom. Some would include godliness. This is not an optional extra, but the core of true healthcare, in which each of us will need to freely contribute, without imperialism, from the depths of our own spiritual journey.

Alan J Gijsbers

To the Editor: I am happy to inform Whiteman and colleagues1 that, should they wish to undertake a project in Australian general practices, the Royal Australian College of General Practitioners (RACGP) has one ethics committee which covers the whole of Australia. As a researcher, I have participated in many multicentre trials under the aegis of this committee over the past 8 years. Details of the RACGP national ethics committee may be found at <http://www.racgp.org.au/document.asp?id=523>.

Christopher D Hogan

To the Editor: It was estimated in 1989 that cervical screening in Australia was preventing only 46% of squamous malignancies, against a theoretical capacity of 90%.1 This suboptimal achievement after almost 25 years of cervical screening led to a major reorganisation of the program. The 1989 analysis has been repeated, using the most recent year (1998) for which incidence rates have been published (Box). The more recent figures suggest that cervical screening in Australia is now preventing 70% of squamous carcinoma of the cervix. This remarkable improvement can probably be attributed to the improved participation by women in regular screening, improved standards within laboratories, and better follow-up of cytological abnormalities. While there is still scope for improvement, there is clear evidence of a substantially better gain from cervical screening. Continued efforts to increase the participation rate among women aged 60–69 years is appropriate given that the prevented proportion appears to be lower in this age range. Percentage of squamous carcinoma of the cervix prevented, by age group, Australia 1998 Age group Number of women (estimated number with a cervix*) in Australia2 Expected rate (per 100 000 women) of squamous carcinoma without screening† Expected number of squamous carcinomas‡ Estimated number of squamous carcinomas observed in 1998§ Percentage prevented 20–24 665 691 (665 025) 5 33.3 9.6 71.1% 25–29 733 145 (732 412) 15 109.9 34.8 68.3% 30–34 706 925 (687 838) 25 172.0 62.9 63.4% 35–39 748 913 (728 692) 45 327.9 74.7 77.2% 40–44 702 629 (608 477) 45 273.8 76.2 72.2% 45–49 649 539 (562 501) 45 253.1 81.4 67.8% 50–54 570 287 (410 607) 45 184.8 48.1 74.0% 55–59 431 183 (310 452) 45 139.7 40.7 70.9% 60–64 370 123 (251 314) 45 113.1 40.7 64.0% 65–69 348 707 (236 772) 45 106.6 44.4 58.3% Total 5 927 142 (5 194 090) 1714 514 70.0% * Calculated by multiplying the number of women in Australia by the estimated age-specific hysterectomy fractions.3 † Methodology as for the study by the International Agency for Research on Cancer,4 using incidence in Norway at a time when the rates would have been little affected by screening. ‡ Calculated by multiplying the estimated number of women in Australia with a cervix by the expected rate of squamous carcinoma of the cervix in the absence of screening.4 § Calculated by multiplying the number of cases of cervical cancer observed in 1998 by 0.74, which was the proportion of all cervical cancers that were squamous.5

Heather S Mitchell

To the Editor: The recent article by Scott and colleagues1 described a retrospective analysis by postal questionnaire of the attitudes of family members to participation (about a year earlier) in a face-to-face interview about their child's diagnosis of Ewing's sarcoma. This was accompanied by an editorial exposing the complexities of research participation, including the potential risks of interviews as well as the role of altruism.2 Although results derived from the questionnaire have only recently been published (November 2002), the questionnaire was distributed in November 1997, before introduction of the National statement on the ethical conduct of research involving humans.3 Some ethical uncertainties and questions of historical interest arise. First, what was the nature of the original consent obtained for the initial interviews? Presumably it involved written informed consent in which the risks of participation were clearly mentioned, including the possibility of distress associated with the interview. Did it mention a procedure for aborting or complaining about the interview? Second, did the patients (aged up to about 35 years) and their families give permission to be contacted again by the same research group? Third, for the follow-up on research participation, was consent implied simply by return of the questionnaire? Finally, how would the conduct of the initial interviews and the follow-up questionnaire differ in the light of recent developments in the ethics of research involving humans? Importantly, the respondents (84% of those surveyed) indicated that participation in the original study had not "upset them".1 While the attitude of non-responders is unknown, this would seem to confirm that the original process had been sensitive and appropriate. This is supported by the finding that families whose child had died after the initial interview were more likely to respond to the questionnaire. As a long-time member of a university human research ethics committee, I have often been required to evaluate research protocols that involve potentially threatening or distressing interviews. This has occurred more frequently since introduction of the National statement, as much qualitative research previously conducted under different jurisdictions (such as quality control or clinical audit) has been submitted for formal ethical review. The risk of harm to participants in qualitative research cannot be trivialised. Its impact can be minimised by wording the consent form to warn of possible adverse psychological reactions to interviews and questionnaires, using trained interviewers and providing counselling support if needed.

Simon C Gandevia

To the Editor: The article by Mant et al1 and the letters following its publication focus attention on a long-standing problem that, despite concerted efforts by governments, healthcare providers and other stakeholders to address it, remains a major obstacle to effective and appropriate continuity of pharmacotherapy following discharge from hospital. There is little doubt that many of the difficulties arise as a result of poor communication between hospitals and general practitioners. This is further exacerbated by a lack of standard protocols for the preparation and dissemination of discharge summaries. Nowhere is this more evident than in the case of residents of aged-care facilities returning from hospital with radically changed medication regimens. To establish appropriate communication channels, Mant et al mention hospital GP liaison officers.1 New canvasses the potential problems and suggests sensible solutions, including the involvement of community pharmacists.2 However, every hospital has a readymade resource that requires only a set of formal protocols and procedures to make it function — clinical pharmacists. Clinical pharmacists view every patient's chart at least once every day. The chart not only provides information for dispensing, but also gives pharmacists an opportunity to monitor Quality Use of Medicines and communicate with hospital doctors regarding existing or potential problems. By the time the "prescription" is processed and the medication dispensed, quality issues have been addressed and a detailed record created. From the dispensing record, a "medication profile" could be generated. This can provide the patient with consumer information regarding each drug, its dose, frequency of administration and mode of action, and can act as an accurate and up-to-date discharge summary. In addition, a clear, legible copy can be faxed, mailed or electronically transmitted to the patient's GP, pharmacist, specialist, allied healthcare professional, rehabilitation hospital or aged-care facility. Our organisation provides medication management services to a large number of aged-care facilities as well as to public and private hospitals, and correctional facilities. Quality Use of Medicines monitoring constitutes a vital part of our clinical pharmacists' duties. It provides an effective, accurate and timely method of communicating detailed discharge summaries (which have undergone thorough Quality Use of Medicines screening) to GPs and other interested parties. By including hospital clinical pharmacists in the Quality Use of Medicines monitoring and evaluation process, meaningful information can be obtained, appropriate judgements made, effective communication conducted and optimum pharmacotherapy outcomes achieved.

Joseph J Gelb

In reply: Gelb points out that clinical pharmacists can, and in some cases do, provide useful communication to general practitioners following hospitalisation, as well as for their patients in aged care facilities. Regrettably, clinical pharmacists are in short supply, even in teaching hospitals; thus, in practice, their expertise often cannot be fully utilised.1 Attention to this shortage is clearly warranted to safeguard patient care. We agree that clinical pharmacists (hospital and community based) should be included in the Quality Use of Medicines monitoring and evaluation process. In addition, we urge all healthcare providers to take responsibility for careful and timely communication to ensure continuity of patient care.

Karen I Kaye · Andrea Mant · Linda Kehoe · Wendy C Rotem

To the Editor: We would like to comment on a recent article by Chan et al on clinical practice guidelines for depression in young people.1 We disagree with their proposal to amend National Health and Medical Research Council (NHMRC) guidelines2 to include a statement that "SSRIs [selective serotonin reuptake inhibitors], particularly fluoxetine and paroxetine, should also be considered as a first-line treatment" for major depression in young people. We believe that there is insufficient evidence to assign a grade of "E1"2 to this statement. Chan et al1 quote three randomised controlled trials (RCTs) and one systematic review in support of their argument, but as yet the results of only two of the three RCTs have been published.3,4 Unfortunately, Chan et al do not include a critical appraisal of the significant methodological and analytical problems with each of the studies. Nor is any comment made about risk–benefit ratios, or the fact that even if the results were sound the clinical relevance of such small differences between active drug and placebo is questionable.5 The following brief commentary on the two studies highlights the dangers of carrying out sophisticated procedures such as meta-analysis without sufficient attention to the quality of the trials included in the analysis. The very high dropout rates (46% of 48 for placebo; 29% of 48 for fluoxetine) in the study by Emslie et al3 raise questions about the reliability of the results. Other interpretations of the findings are plausible. For example, in their study, significant advantage to fluoxetine over placebo on the Clinical Global Impressions improvement rating (a primary outcome measure) was lost when only patients completing the trial were counted (P = 0.2). More worrying is that Chan and colleagues do not seem to have noticed the dangerously distorted reporting in the study by Keller et al.4 On neither of the two designated primary outcome measures (change from baseline in Hamilton Rating Scale for Depression [HAM-D], and response, set as "fall in HAM-D to ≤ 8 or by ≥ 50%") did paroxetine differ significantly from placebo. But Keller and colleagues never report this negative finding. Instead, the criteria for response are covertly altered (to "fall in HAM-D to ≤ 8", which does achieve significance). The authors then erroneously claim significance on this (altered) primary outcome measure, ignoring the lack of significant change. Thus, a study that showed no significant improvement on either of two primary outcome measures is reported as demonstrating unqualified efficacy. Similar problems can be found in a more recent article by Emslie and colleagues6 (published after the review by Chan et al1), in which the authors openly acknowledge that the difference between fluoxetine and placebo on their prospectively defined primary outcome measure did not reach statistical significance, yet claim to have demonstrated the drug's efficacy. Another worry is that Chan and colleagues, in their list of proposed changes to NHMRC recommendations,1 suggest that the availability of SSRIs obviates the need for more expert and thoughtful assessment and management of depression. We are uncomfortable that the prescribing and management of psychotropic medication is portrayed as requiring relatively few skills and resources, to be carried out by those general practitioners who lack training in mental health and/or access to expert mental health services. We urge the NHMRC to maintain a conservative approach to the use of psychotropic drugs in children with depression unless more convincing evidence is forthcoming.

Jon N Jureidini · Anne L Tonkin

In reply: We thank Jureidini and Tonkin for their comments. In relation to their criticism of the study by Emslie et al,1 intention-to-treat analysis is the accepted standard. In relation to the study by Keller et al,2 their criticism about the criteria for response has already been answered elsewhere. (Criteria were defined in the report as a final Hamilton Rating Scale for Depression [HAM-D] score that was ≤ 8 or a reduction from baseline of ≥ 50%. Dual criteria were selected because the scores at entry could range from a minimum of 12 [set by protocol] to a maximum of 53 [highest scores for the 17-item HAM-D]. Limiting response to either a 50% reduction or a specified cut-off point would impede patients at the lower end of the ranges from meeting the criterion.3) The concern about the absence of differences in change scores on the HAM-D cannot be resolved, as mean change in scores and standard errors of the means were not reported. However, 63.3% (57/90) of subjects taking paroxetine (P = 0.02 versus placebo) achieved a HAM-D total score of ≤ 8 at endpoint. With respect to the size of difference in response rate to active treatment versus placebo, the results of trials involving selective serotonin reuptake inhibitors (SSRIs) in children and adolescents are similar to those reported in adults (ie, SSRIs achieve a response in about 20% more participants than placebo,4 which is similar to the 26% difference between cognitive behavioural therapy and various control conditions5). Consistent with these results, the US Food and Drug Administration has recently approved fluoxetine to treat children and adolescents aged seven to 17 years for major depression. We believe that there are sufficient new treatment data (including a study,6 published since the submission of our article, showing fluoxetine's superiority over placebo in symptom improvement and in remission rates) to warrant revision of the 1997 guidelines. Depression affects one in 20 Australian teenagers, few of whom will access specialist mental health services.7 Contrary to the view of Jureidini and Tonkin, we believe general practitioners must provide treatment for young people suffering depression. A strength of the National Health and Medical Research Council guidelines is that they offer comprehensive advice to promote thoughtful assessment and management of depression in young people.

Raphael TW Chan · Joseph M Rey · Philip L Hazell

To the Editor: I do not believe that Dinnen's comments1 should be so easily dismissed as suggested by the academics proposing that general practitioners should do questionnaires,2,3 at least in New South Wales. I write this as barely a month has passed since a most damning report was released by a NSW Parliamentary Inquiry into Mental Health Delivery. A prime example of arrogance and loss of contact with the reality of clinical services by academia and administration is that, during the demise of mental health services in NSW, the services have been forced to complete a new 30-page admission process for every admission. Just what was needed by registrars spending hours trying to find beds for seriously mentally ill patients! The gulf between academia and administration on the one hand and real clinical services on the other is now huge in NSW, at least in mental health services. No one outside real clinical services has any credibility or right to demand doctors, let alone hard-pressed GPs, engage in dubious and very likely useless research projects without very special funding to support the project. I found the K10 questionnaire extraordinarily simplistic compared with a Mental State Examination (MSE). Surely, if there is concern, doctors should be encouraged to revise how the MSE is carried out, and not encouraged to adopt "cookbook" medicine.

Brian M Boettcher

To the Editor: As a general practitioner I was gratified to see Dinnen's letter1 in which he questioned the "urgent need" for GPs to use more questionnaires for depression management. Reading the professorial reply,2 I despair. As more and more specific health promotions are introduced (eg, Asthma 3-Step Plans, Diabetic Care protocols, Health Assessments, Care Plans) we have to consider not just our patient's problems, but which forms to fill out or numbers to put down to fulfil Health Insurance Commission requirements or be correctly remunerated. By the time a depressed patient is sitting in my room, he or she wants to be correctly diagnosed and treated, not to be given a form to fill out. In my opinion, to hand a form to a depressed patient who has tearfully told me his or her problems is an insult. We do not (yet) expect patients to fill out a checklist for heart failure. As to the suggestion that the form be filled out in the waiting room, how is this to be done? Should the patient be sent out again with form in hand? Privacy concerns do not allow reception staff to hand out such forms, and the waiting room is not the best place to fill them out if they are needed. In reality, the GP is likely to give the patient a form and then go have a coffee or make a telephone call. No psychiatrist will ever receive a referral from me based on a K10 score. I may, however, mention that my patient still has suicidal impulses, cries a lot, has trouble sleeping and cannot concentrate at work. That should be easy enough for anyone to understand.

Heidi Andersen-Dalheim

To the Editor: I read with great interest about your search in dictionaries for the word "pathography".1 Pathography2 originates from reflections on genius and its possible association with insanity, a question that has occupied experts in many fields since Socrates, Plato and Aristotle. The first psychiatric scientific treatise concerning this question was contributed by Moreau de Tours in 1859.3 Inspired by him, Cesare Lombroso, in 1863, coined the famous expression genio et follia, and contributed many, albeit somewhat uncritical, pathographies. The term pathography was first used about 1899 by the German psychiatrist Paul Julius Möbius, who contributed with several seminal pathographies, including Rousseau, Goethe, Schopenhauer and Nietzsche. Among other famous pathographers should be mentioned Freud, W Lange, Jaspers, Birnbaum and Kretschmer. Pathography can be defined4 as . . . historical biography from a medical, psychological and psychiatric viewpoint. It analyses a single individual's biological heredity, development, personality, life history, and mental and physical pathology, within the socio-cultural context of his/her time, in order to evaluate the impact of these factors upon his/her decision-making, performance and achievements. No preconceived format can be assumed as the method depends on the nature of the various available materials and on the specific inquiry. A prerequisite for plausible pathographical results is a thorough knowledge and understanding of psychopathology, and of the borderland between normal and abnormal mental life, combined with a capacity for [sober] historical judgement. . . . The pathographical method is applicable to any personality, sick or sound, provided that sufficient biographical sources are available. The pathographical result is a facet but often an indispensable one. Subjects of pathography have traditionally been famous people in all areas of human achievement. Pathography is also indispensable in assisting historians, political scientists and other groups in their quest for a better understanding of events where leaders or other "very important persons" have played a significant role, and where personality or illness, physical or mental, has been decisive, at times with far-reaching consequences for nations.5,6 History is replete with such examples.

Johan A Schioldann

To the Editor: In the abstract of his article on asthma prevention with dietary manipulation,1 Mellis states that "we know" that the major modifiable dietary environmental risk factors for childhood asthma are not having been breastfed and low intake of omega-3 fatty acids. In his discussion of the evidence, Mellis suggests that breastfeeding may be protective and, importantly, acknowledges the controversy. He further states (in the abstract) that observational studies have shown a reduction in childhood asthma in children who eat fish regularly (that is, have a high intake of omega-3 fatty acids), similar to those who were exclusively breastfed for three months. However, he provides no references for these observational studies, and nor does he discuss any specific evidence in support of including omega-3 fatty acids for reducing childhood asthma. While there are some suggestions of such an association, the evidence is extremely limited compared with the extensive literature on the potential for the protective effect of breastfeeding. Further, there are substantial methodological issues associated with the few studies that do exist, not the least of which is the measurement of the relevant dietary parameters. Australian studies have suggested a protective influence of at least two fish meals per week on bronchial hyperresponsiveness in 7–11-year olds2 and of eating oily fish3 on the prevalence of childhood asthma. However, neither of these studies had the capacity to measure omega-3 fatty acid nor fish intake in a valid way. These limitations were acknowledged by the authors of the studies, and have been noted by others;4 they need to be included in any discussion of a putative protective effect. It should also be noted that the biological plausibility of such an association has been challenged.4 There are many valid reasons for promoting the consumption of omega-3 fatty acids, but shouldn't we wait for the outcome of the randomised clinical trial currently under way before accepting the statement that "we know" that a low intake of these fatty acids increases the risk of childhood asthma?

Jill L Sherriff

In reply: Sherriff is correct in pointing out that the studies showing protection from bronchial asthma (and bronchial hyperresponsiveness) are based on consumption of fish meals rather than a direct measure of omega-3 fatty acid intake. This protection has been observed consistently in cross-sectional studies of New South Wales primary school children. Thus, the level of evidence is at best Level III, albeit using a proxy for omega-3 fatty acid intake. Results of a randomised-controlled trial of omega-3 fatty acid supplementation currently under way in western Sydney are now in the public arena at 18-month follow-up.1,2 At this early stage, it is uncertain who has genuine asthma rather than other wheezing syndromes. Nevertheless, the group who received omega-3 fatty acid supplementation have differences in rates of wheeze compared with those not supplemented.1,2 For example, the rate of "ever" having had wheeze was 52.6% in the controls versus 42.8% in the supplemented group (absolute risk reduction, 9.8%; number need to treat, about 10). In the table of recommendations in my article,3 I carefully pointed out that supplementing infants with omega-3 fatty acid is something to "consider" rather than strongly recommending it. It should also be noted the level of evidence is low (Level III). Stronger recommendations will depend on the long-term results of randomised trials, such as the western Sydney trial.1,2 In summary, at this stage the only strong dietary recommendations which can be made are: not to use strict elimination diets during pregnancy (Level I evidence); and to consider using lactobacillus probiotic supplements. The evidence for lactobacillus is Level II (from a single randomised controlled trial), although the protection shown is for atopy rather than asthma. Clearly, the children in the lactobacillus study will need further follow-up, and the trial will need to be repeated in other populations. All of this highlights the need for better-quality studies in the area of primary prevention of asthma, based on dietary factors during pregnancy or early infancy.

Craig M Mellis

To the Editor: The publication of the main results of the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT), and the accompanying editorial, triumph the role of thiazide diuretics as first-line management for hypertension.1,2 It brought to mind the lines from the nursery rhyme Old Mother Hubbard — "And when she went there, the cupboard was bare." Simple frequency analysis of diuretic antihypertensive medications listed in the Australian Medicines Handbook (1998 and 2003) revealed that the total number of thiazide diuretics available as monotherapy in 1998 was six (bendrofluazide chlorothiazide, chlorthalidone, hydrochlorothiazide, methyclothiazide and indapamide), and in 2003 three (bendrofluazide, chlorthalidone and indapamide).3,4

Mark R Nelson

To the Editor: It has been known for a long time that washing soda (crystalline sodium carbonate) is effective for removing fluid from joint effusions. The crystals are simply wrapped in a tea towel, crushed with a rolling pin and wrapped around the joint overnight. In the morning the sodium carbonate is rock solid and the joint effusion has markedly improved. I was discussing with one my patients her problem of gross upper-limb lymphoedema after surgery and radiotherapy for breast cancer to the axilla. She went home and made an appropriate pack of sodium carbonate, which she wears overnight. She can now use her arm throughout the day. Obviously, the lymph fluid reaccumulates because her lymphatic system is well and truly obstructed. This patient spoke to several other patients in the Day Centre at the Monash Medical Centre, who tried this in addition to other exercises for lymphoedema, and they have found it to be extraordinarily effective. One woman had gross oedema of her hand, which rendered it useless: she simply immersed her hand in a solution of sodium carbonate and thus dialysed the fluid from her hand. Thereafter she could use her hand for 12 hours before significant amounts of fluid reaccumulated. While this is obviously not the perfect solution to lymphoedema in patients with breast cancer, anything that may help them is worth noting. Perhaps a suitable linen device could be made which would cover the whole arm at night. Evidence for the use of this simple dialysis treatment is currently anecdotal. It might be appropriate to design a clinical trial to determine whether this method has potential in treating this extremely troublesome form of lymphoedema.

Graeme N Brodie

To the Editor: Although liver flukes (genus, Fasciola) are parasites of livestock, human infection is a significant global health problem,1 albeit seldom seen in Australia.2 Infected livestock contaminate waterways with parasite eggs, leading to infection of snails that shed metacercariae on to vegetation, such as watercress.1,3,4 Adult parasites reside in and damage the bile ducts.1,3 Liver flukes could cause disease if introduced into the food chain.1 We report the first case in Australia of liver fluke infection (fasciolosis) in a patient with no history of farm or livestock contact. She probably acquired the disease from eating watercress purchased at a Melbourne market four to five months before symptom onset. Computed tomography of the liver in a woman with fasciolosis Low density lesions (arrowed) following intrahepatic ductal branches in the right lobe of the liver were consistent with Fasciola parasites causing biliary obstruction. A 35-year-old woman presented in August 1998 with fever and right upper quadrant abdominal pain. Blood examination showed eosinophilia (2.5 x 109/L; reference range [RR], < 0.6 x 109/L]). Liver function tests gave normal results apart from elevated serum aspartate aminotransferase levels of 48 U/L (RR < 41 U/L). Abdominal computed tomography showed multiple low density lesions in the right lobe of the liver, with diameter up to 3 cm (Box). A fine needle aspirate showed no evidence of malignancy. Blood tests four weeks later revealed increasing eosinophilia (3.5 x 109/L) and worsening liver function (serum levels: alanine aminotransferase, 163 U/L [RR, 7–56 U/L]; alkaline phosphatase, 126 U/L [RR, 30–120 U/L]; γ-glutamyl transferase, 98 U/L [RR, 5–45 U/L]). A parasitic infection was suspected, but four faecal samples and serological tests for hydatids, Schistosoma, Strongyloides and Entamoeba spp. were negative. Coprological diagnosis of fasciolosis can be problematic, as eggs may be released intermittently and in small numbers, especially in low-intensity infection.1 Enzyme-linked immunosorbent assay (ELISA) using Fasciola hepatica antigen, performed at Westmead Hospital, Sydney, was borderline positive. However, ELISA for IgG4 antibodies against recombinant F. hepatica cathepsin L5 antigen, performed at Monash University, Melbourne, was strongly positive. The patient was treated with two doses of triclabendazole (12 mg/kg body weight per dose) on successive days in October 1998. Abdominal pain subsided within two weeks, her appetite was restored, and eosinophil count and liver function normalised within four weeks. Computed tomography two months after treatment showed a reduction in size of the liver lesions. The patient remained well six months later. This case demonstrates that fasciolosis may present to urban medical practitioners in Australia. Ingestion of watercress is an important clue to the aetiology.2 Serological diagnosis is possible before eggs appear in faeces using a new specific ELISA test that detects the IgG4 response to cathepsin L antigen.5

Andrew J Hughes · Terry W Spithill · Rebecca E Smith · Craig S Boutlis · Paul DR Johnson

To the Editor: Collins and colleagues1 reported a case of bacteraemic community-acquired MRSA (CAMRSA) infection that they believed to be the first reported in Australia. One of us (G N) published a reference to a case of septicaemia and osteomyelitis in Brisbane caused by CAMRSA in 2000.2 This severe case occurred in a previously healthy 16-year-old boy with no risk factors for MRSA infection who, after prolonged ventilatory and inotropic support and vancomycin therapy, required a long period of rehabilitation. A further two cases of septicaemia occurred in Ipswich and will soon be published as part of a study of CAMRSA conducted in 2000–2001.3 We recently encountered another case involving a previously well 23-year-old man who presented to the emergency department with a large abscess on his upper lip and extensive cellulitis of the surrounding face and neck, and with left-sided pleuritic chest pain and associated fevers and rigors. The patient denied previous antibiotic use or contact with healthcare facilities at any time in the past. There was no history of injecting drug use or trauma. Staphylococcus aureus was isolated from blood cultures, and resistance to oxacillin and susceptibility to erythromycin, clindamycin, tetracycline, gentamicin, ciprofloxacin, fusidic acid, rifampicin, and vancomycin was shown. Specimens from operative debridement of the facial abscess yielded S. aureus with the same susceptibility pattern. Chest x-rays showed extensive consolidation of the left lower lobe and an associated loculated pleural effusion. Clinical, radiological, and echocardiographic evaluations did not reveal another focus of infection. The patient was treated with intravenous vancomycin for three weeks followed by oral clindamycin, with complete clinical resolution. It is now clear that CAMRSA infection may result in severe, life-threatening sepsis. The possibility of pneumonia associated with CAMRSA is of particular concern. A 1999 report from Minnesota and North Dakota documented four deaths in children from CAMRSA, including two with necrotising pneumonia.4 A further two fatal cases of necrotising pneumonia caused by CAMRSA were recently reported from France.5 The strains involved in all of these cases carry the gene for Panton-Valentine (P-V) leukocidin, a staphylococcal toxin that has been shown to be strongly associated with cases of severe superficial abscesses and necrotising pneumonia.6 As the strain of CAMRSA most commonly encountered in Eastern Australia also carries the P-V leukocidin gene (Professor J Etienne, Faculty of Medicine, Claude Bernard Lyon 1 University, personal communication), doctors should be aware of the possibility of severe community-acquired pneumonia caused by this organism.

Graeme R Nimmo · E Geoffrey Playford

To the Editor: Kuchar et al1 describe a patient who received an implantable defibrillator discharge after a single ingestion of loratadine. We are concerned that their conclusion — that this patient "probably" had drug-induced torsade de pointes — is incorrect. Review of the intracardiac electrograms from this patient (shown in Box 2 of their article) with known monomorphic ventricular tachycardia (VT; shown in their Box 1) shows a relatively fixed rate of the VT without the large variations in cycle length consistent with torsade de pointes. While there are no established guidelines for determining torsade de pointes based on intracardiac electrograms, it is clear that during monomorphic VT electrocardiograms can show variability in amplitude and orientation. Consistent with the early stages of monomorphic VT,2 the first three electrograms have a different orientation compared with the remaining electrograms, which are largely similar. Unfortunately, as the transition from supraventricular rhythm to tachycardia was not shown, it cannot be ascertained whether the tachycardia began with a pause-dependent mechanism, an important criterion to help diagnose torsade de pointes.3 Given that this patient's implantable defibrillator intracardiac electrograms do not show a continually changing electrogram pattern, that the cycle length is relatively constant, and that there is a lack of documented QT prolongation, there is no evidence of the patient's arrhythmia being torsade de pointes. Incidentally, it is unclear whether these electrograms were recorded before (as specified in the discussion) or after defibrillator discharge (title of Box 2). It is well documented that a defibrillator discharge can have significant effects on the recording of intraventricular electrograms. Most likely, this patient, with documented pre-existing monomorphic VT (their Box 1[b]), had an episode of VT (not torsade de pointes) appropriately treated by the implanted defibrillator, probably having no direct relationship with loratadine. Notably, their Box 3 shows torsade de pointes in another patient, not receiving loratadine. In summary, Kuchar et al1 correctly state that there have been no documented episodes of torsade de pointes after ingestion of loratadine. Similarly, their report does not appear to document an episode of torsade de pointes.

Philip T Sager · Enrico P Veltri

In reply: We agree that there are no guidelines defining torsade de pointes based on intracardiac electrograms, but there are several reasons why the likelihood of torsade de pointes (as opposed to any other arrhythmia) in our patient is high. The electrogram shows the arrhythmia just before delivery of direct current shock, this being about 30 minutes after the patient took her first ever dose of loratadine. There are marked variations in electrogram morphology, despite minimal variation in RR interval, in a short strip of recording in this patient with documented QT prolongation. Further, she had no history of monomorphic ventricular tachycardia, no inducible monomorphic ventricular tachycardia at electrophysiologic examination, and no evidence of structural heart disease. Neither was a mechanism for supraventricular arrhythmia identified. The absence of initiating beats showing pause-dependence is unfortunate, but this is not provided by the generation of device implanted in this patient. Hence, we believe the word "probable" is an apt description for the observation made.

Dennis L Kuchar · Bruce D Walker · Charles W Thorburn

To the Editor: We welcome Ring and Brown's editorial comment1 on the Public Report Card 2002 No More Excuses,2 produced by the Australian Medical Association's Task Force on Indigenous Health. We hope that drawing attention to the poor outcomes of Indigenous Australians will catalyse Federal and State governments to take action, particularly as international comparisons demonstrate the likelihood of success. Australia's poor performance in relation to its Indigenous people is a complex phenomenon, involving political, sociocultural and historical factors, as well as health factors. Levels of ill health among Indigenous communities in post-colonial Australia, Canada and New Zealand are particularly disturbing from a global health perspective, as they persist despite the relative affluence and excellent health status enjoyed by the general population in these nations. One of the difficulties in assessing progress is the lack of high-quality data for comparative purposes. The types of indicators of Indigenous health in common use in Australia, Canada and New Zealand range from central indicators (such as the age-standardised rate ratios for Aboriginal people) to secondary indicators (such as change in the prevalence and incidence of chronic diseases, like diabetes, in Aboriginal communities). It would be useful to develop additional indicators that more closely reflect Aboriginal community knowledge models and values.3 Existing indicators emphasise outcomes rather than opportunities for early intervention, such as early childhood development and youth resilience. Finally, there need to be greater attempts to explore how to use and compare international experiences to help Indigenous people most effectively. The Memorandum of Understanding between the Canadian Institutes of Health Research, the Medical Research Council of Australia, and the Health Research Council of New Zealand may provide a framework for international collaboration.4

Paul Bauert · Elizabeth McMaugh · Carmel M Martin · Janet K Smylie