Letters

To the Editor: There appear to be regional differences in the prescribing of amino acid infant formula in Australia. This is possibly due to differing practices in use of this formula as a first-line treatment for cow’s milk allergy or as a strategy for preventing allergy. This has financial implications, as the cost to the Pharmaceutical Benefits Scheme (PBS) of amino acid formula is $371 per prescription, compared with $106 for hydrolysed protein formula.1 In infants at high risk of allergic disease who are unable to be completely breastfed, there is evidence that prolonged feeding with a formula based on hydrolysed cow’s milk protein rather than conventional cow’s milk formula reduces infant and childhood allergy.2,3 There is no clear evidence that amino acid formula should be substituted for extensively hydrolysed protein formula as a primary preventive strategy.3 The current PBS indication for hydrolysed protein formula is treatment of intolerance to both cow’s milk and soy protein, but not primary allergy prevention. Similarly, current PBS guidelines restrict the use of amino acid formulas to proven intolerance to cow’s milk, soy protein and protein hydrolysate. Among children who are allergic to cow’s milk, 10% or less are also sensitive to protein hydrolysate formula.4 Thus, if current guidelines were followed, one might expect nine times the use of hydrolysed protein formula compared with amino acid formula. I obtained statistics on PBS items supplied for the period January 2003 to January 2004 from the Health Insurance Commission (www.hic.gov.au/statistics/dyn_pbs/forms/pbs_tab1.shtml) for hydrolysed protein formula (item numbers 2676W and 8259Q) and synthetic amino acid formula (item numbers 3066J, 8443J, 8574G and 8575H). These showed that 8374 hydrolysed protein formula items were supplied, half the number of amino acid formula items (16 886). Numbers of amino acid formula items supplied per 1000 children aged 4 years and younger were calculated using population statistics from the Australian Bureau of Statistics census figures 2001. These are compared in the Box with numbers of paediatric physicians per 1000 children (obtained from the Royal Australasian College of Physicians 2004) and paediatric allergists (derived from the Australasian Society of Clinical Immunology and Allergy membership handbook 2003). Prescribing practice varied markedly between states and territories. The Australian Capital Territory, New South Wales and Victoria had six to seven times more amino acid formula items per 1000 children than Western Australia. This did not appear related to numbers of paediatricians or paediatric allergists, as Western Australia had a similar number of paediatricians and more paediatric allergists per 1000 children than NSW and Victoria. The differences found were unlikely to be related to variation in numbers of adult immunology/allergy specialists, who are unlikely to treat many infants aged under 2 years. Nor were they likely to be due to differing prevalence of combined milk, soy and protein hydrolysate intolerance, as the prevalence of allergic disease does not differ markedly between Australian states. For example, the prevalence of atopic eczema at age 6 years in four cities (Adelaide, Melbourne, Sydney and Perth) was very similar, ranging from 10.1% to 11.4%.5 It seems unlikely that 80% of cases of combined intolerance are being missed in Western Australia. The estimated cost to the PBS for amino acid formula for 2003–2004 of $7 107 627 was 10 times that of hydrolysed formula ($757 570). Amino acid formula prescription rates, January 2003 to January 2004, compared with numbers of paediatric physicians and allergists per 1000 children aged 4 years or younger Amino acid formula items per 1000 children Paediatric physicians per 1000 children Paediatric allergists per 1000 children Australian Capital Territory 22.3 0.79 0 New South Wales 18.8 1.02 0.033 Victoria 17.8 1.00 0.030 Tasmania 12.3 0.53 0.033 South Australia 9.3 1.01 0.067 Northern Territory 9.1 0.92 0 Queensland 5.9 0.72 0.008 Western Australia 3.3 0.99 0.049

Andrew S Kemp

To the Editor: Colonic irrigation is the introduction of a large volume of fluid into the colon via the rectum. This volume may be up to 50 litres, run in and out by means of a rectal tube, in an effort to empty the bowel. This treatment is often administered by a practitioner of complementary or alternative medicine, without medical advice. The fluid may be driven by gravitational or mechanical force.1 Recognised risks from colonic irrigation are electrolyte imbalance, bowel perforation and communicable diseases such as amoebiasis.2 Colonic irrigation is different from a standard enema given to relieve constipation or to treat a primary bowel disease. An enema involves a small amount of fluid and is usually authorised by a medical practitioner and administered by a trained nurse, attendant or is self-administered. Perforation of the rectum has rarely been reported.3 We document three cases of perforation of the rectum from colonic irrigation, treated by different surgeons at different institutions (Box). All have required surgical intervention. Each patient underwent colonic irrigation to relieve chronic constipation, to “cleanse” or “clear out stale faeces”. None had primary colonic or rectal pathology. None of the three patients were warned about the complication of perforation. Importantly, one patient initially denied the use of colonic irrigation, even with direct enquiry (Case 1), presumably because of embarrassment. This has the potential to delay the diagnosis or lead to inappropriate treatment. Perforation may occur in the rectum by direct injury from the irrigation device (Case 1), or after the irrigation has commenced (Cases 2 and 3), and may be caused by the generation of a high pressure within the lumen of the bowel. Rectal perforation from colonic irrigation may be diagnosed from the history, plain abdominal x-rays or a computed tomography scan with or without meglumine diatrizoate enema. A high degree of suspicion by the attending physician will prompt the diagnosis. Intensive medical therapy with appropriate antibiotics and surgery is necessary. Plain abdominal x-ray did not show an abnormality at 12 hours in the one case where x-ray was taken. We feel that colonic irrigation is of dubious benefit, especially when delivered to remove so-called “toxic waste” when bowel function is satisfactory. There is potential for serious harm. The apparent failure of the operators to warn patients about a risk of any serious complication, the failure to diagnose the possible perforation at the time of injury, and the failure to provide any subsequent follow-up, which might have led to an earlier diagnosis of any complication, probably indicates suboptimal practice. Cases 2 and 3 occurred at the same clinic within a few weeks of each other, suggesting a possible systems failure of the irrigation device. Primary healthcare practitioners need to be aware of the dangers of this treatment. Colonic irrigation should be urgently and formally assessed from an evidence-based, risk–benefit perspective. Case descriptions for three women who had rectal perforation after undergoing colonic irrigation Case Age (years) Timing of symptoms Clinical features Investigations Management 1 59 Pain immediately on insertion of enema tube. No irrigation. Attended emergency department 24 hours after the tube insertion. Lower abdominal and deep pelvic pain. Sepsis. Abdominal computed tomography scan showing perirectal oedema and extrarectal gas. Intravenous antibiotics and transrectal drainage of perirectal abscess. 2 51 Pain started during irrigation. Attended emergency department 4 days after irrigation. Lower abdominal pain. Sepsis. Abdominal computed tomography scan showing gas and fluid in the perirectal fat and retroperitoneum. Intravenous antibiotics and initial transrectal drainage of perirectal abscess. Recurrent abscess formation required laparotomy and rectal resection with stoma formation. 3 56 Pain started during irrigation. Attended emergency department the same day, but was discharged. Re-presented 7 days later. Lower abdominal and deep pelvic pain. Constipation and urine retention leading to urinary infection. Sepsis. Abdominal computed tomography scan showing pelvic abscess posterior to the rectum. Emergency laparotomy, sigmoid loop colostomy and drainage of abscess. Residual abscess drained transrectally 2 weeks after initial surgery.

Doug V Handley · Nick A Rieger · David J Rodda

To the Editor: There is no substitute for injectable thiamine in the treatment and prevention of Wernicke’s encephalopathy, for which the oral form of thiamine is considered inadequate.1 If the condition is not treated promptly with parenteral thiamine, permanent brain damage can occur. A shortage of injectable thiamine noted in a South Australian hospital led us to enquire into the extent of the problem in Australia. In the first week of July 2004, we undertook an Australia-wide survey of major teaching hospital pharmacies. Sixteen hospitals were contacted by phone, and 15 chief hospital pharmacists provided information about thiamine stock, normal thiamine usage over a 6-month period, shortages of other drugs, and reasons for shortages. Data on thiamine are shown in the Box. Most hospitals (11/15) were unable to provide injectable thiamine for periods ranging from a few weeks to 5 months. Rationing reduced the use of injectable thiamine in 13/15 hospitals. There was a total shortfall of 2000 ampoules per month for the 13 hospitals. Given an average of six ampoules used per admission, we estimate that 330 patients a month were untreated or inadequately treated. Half the hospitals surveyed obtained some ampoules either directly from suppliers or through the Special Access Scheme (SAS) protocol of the Therapeutic Goods Administration (TGA). This protocol is time-consuming and cumbersome, while the non-SAS system is expensive (10 times the usual price per ampoule). Pharmacists reported having many other drugs (40–60) on back order. The pharmacists stated that drug shortages were caused by scarcity of raw materials and TGA restrictions. However, the current shortage of thiamine in Australia was foreseeable in 2003, when the main manufacturer stopped thiamine production. The TGA did not alert pharmacists or doctors to the potential shortage in writing, nor provide comprehensive help to prevent or alleviate the shortages. The public health response to shortages of essential medicines should include surveillance and a systematic analysis of the causes. Better communication between pharmacists, clinicians and government authorities, and the formation of contingency plans and guidelines, are needed. It was only through informal networking and the quick thinking of hospital pharmacists that a crisis was averted in Australia. It is unconscionable that an inexpensive essential medicine is not available to those Australians who may need it. In this respect, our public health system has failed. Because injectable thiamine has been unavailable or rationed, an increase in the incidence of alcohol-related brain damage may have occurred. Australian health ministers should act immediately to prevent critical shortages of essential medication, which could be tragic and costly. Stocks and usage of injectable thiamine in 15 Australian hospitals, as at 3 July 2004* Number of vials Use/month Hospital Lowest Current Previous 2 months Usual 1 0 0 0 16 2 0 0 0 50 3 0 0 0 50 4 0 0 0 65 5 0 12 0 20 6 0 10 0 35 7 0 25 0 20 8 0 200 0 130 9 0 120 0 1200 10 0 25 25 70 11 0 10 10 150 12 1 35 40 120 13 5 160 17 180 14 25 86 100 100 15 30 90 30 30 * The table compares the level of stock at its lowest during the shortage with the level at July 2004, along with estimates of use at July 2004 and before the shortage.

Simon Spedding · Matt D Gaughwin

To the Editor: Pertussis (whooping cough) is a readily transmissible respiratory infection that may cause severe respiratory illness. The burden of severe pertussis affects infants, often resulting in hospitalisation (especially those aged under 6 months) and death (1 in every 200 patients aged under 6 months).1,2 In Australia, there were nine deaths from pertussis between 1993 and 1997, predominantly in young infants, and a further five young infant deaths during the 2001–2002 epidemic.3,4 Epidemics occur every 3 to 4 years.2 Pertussis cases and hospitalisations in children aged under 6 months continue to occur in south-east Queensland, with 19 notifications since January 2003. There has been a shift in the epidemiology of pertussis in Australia and the United States, from a disease of young children to a disease of adolescents and adults of child-bearing age.1,5 In Australia, there has been a preponderance of pertussis notifications in adult females.5 Pertussis vaccine is already provided free to children at ages 2, 4 and 6 months, 4 years and 15 years, as part of the National Immunisation Program.2 However, young infants remain incompletely protected by vaccination, as the third, completion dose of the primary course of pertussis vaccination is not given until 6 months of age. A national study of hospitalised infant pertussis cases in 2001 indicated that parents were the presumptive source of pertussis infection for their children in more than 50% of cases.6 This has led the National Health and Medical Research Council to recommend that both parents should receive a (once-only) adult booster dose of pertussis vaccine, either when planning pregnancy or as soon as possible after delivery of an infant.2 The cost of the vaccine is about $30. As yet there is no suggestion that funding will be made available to provide this vaccine to all new parents as part of the National Immunisation Program. However, the amount is not a high price to pay for the protection of a new baby and its parents, particularly now that new parents will receive additional financial support from the federal government. The potential exists to promote opportunistic maternity-ward-based administration of this vaccine to post-partum mothers and their partners. We encourage all medical practitioners, especially obstetricians and paediatricians, to discuss this important issue with parents.

Brad J McCall · Rod P Davison · Michael D Nissen · Clare B Nourse

To the Editor: A recent editorial1 and article2 continue to promulgate and link the unproven concepts that patients with chronic fatigue syndrome (CFS) are “deconditioned” and exercise is beneficial in treatment. The cited study by Fulcher and White3 is open to opposite conclusions, depending on their use of the outcome descriptor “better”. If the term is restricted to “much better” and “very much better”, then, as cited by Lloyd,1 16 of 29 people with CFS rated themselves as “better” after a graded exercise program, compared with only 8 of 30 in the control group who completed a flexibility treatment regimen. However, if the “better” descriptor combines “a little better”, “much better” and “very much better”, which is the interpretation used by Wallman et al,2 then the scores for the exercise versus flexibility groups are not different, being 27 of 29 and 26 of 30, respectively, agreeing with the conclusion of Wallman et al.2 Whichever interpretation is applied, any beneficial effect of the graded exercise program in people with CFS in these studies must be independent of any training effect or change in level of “conditioning”, as this was reported in one study,2 but not in the other.3 A fundamental flaw with most exercise studies in CFS is the use of submaximal or symptom-limited tests, which provide notoriously misleading data when compared with maximal exercise testing procedures.4,5 Wallman et al2 correctly identify maximal oxygen consumption as the “gold standard” measure of exercise capacity, yet such measurements were not made in the three articles they cited. When such procedures are applied, the exercise capacity of people with CFS is not significantly different from either measured or age-predicted values for healthy sedentary people.6 Wallman et al2 suggested that maximal testing procedures could favour the recruitment of “more robust or healthier” patients and provide misleading information. In the first place this is denied by the study of Sargent et al,6 in which the illness status reported by patients who completed the maximal tests was similar to that in previous CFS studies. In the second place, the maximal test protocol chosen for a given population should be designed to exclude any influence of fatigue on the metabolic measurements. This is confirmed by the results from the study cited,6 in which the metabolic measurements met the published criteria of a maximal test.4,5 In summary, patients with CFS are not “deconditioned”. Neither their muscle strength nor their exercise capacity is different from that of other sedentary members of the community (> 70%). We remain unaware of any incontrovertible evidence that the various “exercise training” programs suggested in previous articles improve either the physiological or clinical status of people with CFS.

Garry C Scroop · Richard B Burnet

To the Editor: The claim in Lloyd’s editorial1 that “the criteria for diagnosis are well accepted internationally” ignores the recent publication of the Canadian consensus guidelines for the diagnosis and management of myalgic encephalomyelitis/chronic fatigue syndrome,2 which were sponsored by Health Canada and written by an international group of well published researchers. The Canadian definition of chronic fatigue syndrome (CFS) requires the concurrent presence for six months of fatigue, post-exertional fatigue, sleep dysfunction, pain (including headaches) and neurological/cognitive manifestations, as well as at least one symptom from two of autonomic, neuroendocrine and immune manifestation categories (pp 12–13). These requirements add clinical specificity to the Fukuda criteria and exclude subjects who may have chronic fatigue for other reasons, such as psychiatric disorder without multiple physical symptoms. Lloyd refers to the “recent refinements to improve reliability” in the revision of the research case definition by Reeves et al.3 The SPHERE screening instrument recommended by that article was designed for psychiatric screening in primary care. It arbitrarily classifies people with multiple physical symptoms, often severe in degree and associated with major disability, as having somatisation disorder. This is akin to subclassifying people with severe multiple sclerosis as having somatoform disorder and those with fewer and less severe symptoms as the “core” multiple sclerosis group, a finding which is not supported by the evidence. Conclusions from the article by Wallman et al4 cannot be generalised to the severely ill. Recruitment was from “notices placed in medical surgeries and by advertisements in local newspapers”. Patients with severe CFS, who can barely venture outside their homes and are often too ill to read, would be unlikely to participate. Loblay, Chair of the Royal Australasian College of Physicians Working Group for CFS Clinical Practice Guidelines, urges caution about generalising from exercise studies, which never include people with severe CFS: “All these studies involve people willing and able to participate. The people who find it makes them feel lousy drop out.”5 Lloyd asserts exercise is no longer a question (“. . . graded physical exercise should become a cornerstone of the management approach for patients with CFS”). To promote such a strong, unqualified message to busy general practitioners who may be unfamiliar with the range of severity in CFS risks serious harm to patients.

Ellie Stein · Christine Hunter

In reply: Scroop and Burnet correctly identify the vagaries of the necessarily subjective measurement of outcomes in intervention studies of chronic fatigue syndrome (CFS). Given that muscle strength, endurance and recovery are essentially normal in patients with CFS,1 rather than become too focused on the best approach to measurement of exercise capacity the key issue is whether patients benefit in terms of self-reported symptom severity or functional status. The weight of evidence indicates that graded physical exercise does provide such benefits. Whether this occurs via improvements in aerobic fitness or via the well-recognised psychological and social benefits of exercise is something of a side-issue. Stein and Hunter draw attention to the recently published Canadian consensus guidelines for the diagnosis and management of myalgic encephalomyelitis/CFS. Although this document may provide a welcome recognition for Canadian patients with the disorder, unlike the Australian guidelines,2 it is devoid of an evidence base for the recommendations. Sadly, rather than “add[ing] clinical specificity”, it is also highly likely that the modified diagnostic criteria fall into the trap of preferentially identifying patients with somatisation disorder,3 as such individuals often report large numbers of unexplained symptoms, and hence the addition of 20 or more symptoms to the diagnostic criteria may well bias towards inclusion of such patients. Stein and Hunter are incorrect in the assertion that SPHERE was designed for psychiatric screening in primary care, as the instrument arose out of our studies in CFS specifically seeking to identify clinically significant fatigue states.4 I support the recommendation about caution in generalising from existing published data regarding graded exercise to patients who are severely ill, as such patients are indeed likely to be under-represented in published studies. Nevertheless, it is noteworthy that the recommendations made in the Canadian document cited by Stein and Hunter also clearly support the notion of graded physical exercise: “Patients should gently and gradually increase their level of activity.” Thus, rather than leave the severely affected to continue to “barely venture outside their homes”, I would recommend a carefully designed graded exercise program in the home, with a goal of improving functional performance sufficiently to escape those confines.

Andrew R Lloyd

To the Editor: While the article by Henry and colleagues provides food for thought and possible action,1 do they exhibit the fairness they exhort to solve the problem they perceive? There appears to be a distinct lack of logic in some of their deductions in the Box on page 517. “Body part funding” is not confined to Aboriginal health. For the 43 years I was associated with NSW Health, it was an integral part of the system and, together with its variations, increased as the years passed. The authors claim that as only $80 per head being spent on medical and pharmaceutical benefits in a remote Aboriginal community compared with the $900 spent in Double Bay is an example of racism. Surely, it is only a reflection of the lack of both a pharmacy and doctor in the remote community compared with the easy access to both in the inner-Sydney suburb. Comparison between the remote Aboriginal community and an all-white community of similar characteristics would have more validity.

Raymond S Hyslop

To the Editor: In their challenging article, Henry and coauthors assert that the poor health of Australian Aboriginals is the result of the “divided, divisive, racist, socially unjust society” of “this Australia”.1 I cannot agree. The health standards enjoyed by “white Australia” are not an isolated phenomenon, but rather a part of the fabric of an advanced technological society. Efforts to bring Australian Aboriginal health to the same standard without the Indigenous Australians being fully part of this 21st-century society will never be successful, even with limitless resources and endless goodwill. It is possible to maintain cultural identity and remain cognizant of past hurts while playing a full, if not leading, role in this technological society. If the Aboriginal elders were to lead their people into mainstream society they would find, I’m sure, an inclusive, tolerant, exciting and advancing society where they could play a full role, enjoy the same health as the rest of Australia, while still maintaining their unique identity.

Christopher R Strakosch

To the Editor: We write in response to the article by Faunce and Bolsin on the lessons to be drawn from three Australian whistleblowing sagas.1 Their summary of events at King Edward Memorial Hospital, Perth, deserves comment. Michael Moodie, the Chief Executive Officer (CEO) of King Edward Memorial Hospital, was also CEO of Princess Margaret Hospital for Children (PMH). He was stood down from PMH because of the concerns of workers in response to events at PMH unrelated to those at King Edward Memorial Hospital, as Faunce and Bolsin implied. Moodie was the senior administrator charged by the government with ensuring that appropriate standards were in place and were being met. Staff at PMH believed he was unable to fulfil his brief, culminating in votes of no confidence from the PMH Clinical Staff Association, the PMH Medical Advisory Committee, and a petition signed by 80 PMH doctors.

Francis Lannigan · Geoff Knight · Gary C Geelhoed · Alan Duncan · Peter Chauvel · Ian Hewitt · Peter Le Souëf

In reply: Our reference to Michael Moodie as a “whistleblower” merely reiterates his description as such in the report of the Inquiry into Obstetrics and Gynaecological Services at King Edward Memorial Hospital by the Australian Council for Safety and Quality in Health Care.1 That report states: “Both the Bristol and King Edward case arose from ‘whistle-blowers’ reporting serious problems rather than from established safety and quality monitoring systems. In Bristol’s case, the whistle-blower was an anaesthetist and, in King Edward’s case, it was the recently appointed Chief Executive. In both cases, either directly or indirectly, the department of health received information about management and clinical performance problems that had not been addressed over a significant period of time.” The report then lists nine examples of problems established at both institutions, ranging from a “closed culture and environment unsupportive of openly disclosing errors and adverse events” to “poor clinical and emotional outcomes for patients and families”. The report continues: “However, there were differences in the Hospitals’ response to the inquiries. Bristol welcomed an inquiry and actively supported the process. In contrast, King Edward tolerated the process and the Western Australian branch of the Australian Medical Association actively and publicly fought it.”

Thomas A Faunce · Stephen N C Bolsin

To the Editor: The complementary and alternative medicine (CAM) series raised awareness and provided balanced and thoughtful debate. The article by Kerridge and McPhee in that series1 is no exception, but we would like to question their conclusion that “not only is it unclear whether a true integration of conventional and unconventional medicines is possible, but, more importantly, whether it is even desirable”. For a variety of reasons we believe that it is both possible and desirable. There are increasing examples of situations in which medical practitioners can integrate ethical, evidence-based CAM into practice. Apart from the well-known and validated examples, such as Hypericum perforatum (St John’s wort) for depression, ginger for nausea in pregnancy, and Gingko biloba for intermittent claudication, there are other, less well known, but increasingly investigated, examples of CAM for common conditions. With quality information and a little training, these can be readily incorporated into medical practice. To illustrate, Hippocrates was known to use the herb Vitex agnus-castus (chasteberry) for treating symptoms of premenstrual syndrome. Today we have a randomised controlled trial (RCT) to support its use.2 There are RCTs to support the use of Serenoa repens (saw palmetto) for symptomatic relief of benign prostatic hypertrophy,3 and good evidence is accumulating for the use of glucosamine for osteoarthritis4 and mindfulness meditation for preventing relapse in recurrent depression.5 With systematic reviews on these CAMs doctors should be informed about them. However, the resources for promoting them are minimal compared with those used to promote pharmaceuticals. Considering side-effect profiles and patient autonomy, why shouldn’t trained medical practitioners offer effective CAM remedies as first-line therapy instead of a pharmaceutical? To say these therapies should only belong to the realm of CAM practitioners would be to deprive the medical practitioner and patient of a wider choice of treatments. Communication, holism, balance and individualised care are the hallmarks of quality general practice and do not just belong to CAM therapists. If orthodox medical practice is to remain current, evidence-based and relevant, general practitioners have no option but to integrate safe, validated and ethical forms of CAM into their practice. If they are not adequately trained in the relevant discipline they may wish to refer to an appropriately qualified CAM practitioner, although statistics indicate that GPs prefer to refer to GPs already trained in CAM.6

Vicki Kotsirilos · John R McPhee

To the Editor: Although Kerridge and McPhee stress the need to find an evidence base (if there is any) for CAM, they nevertheless claim “medical practitioners and students no longer have any choice but to gain some knowledge about CAM and the interface between conventional and complementary medicine.”1 I suppose that archaeologists, geologists, palaeontologists and biologists now need to gain some knowledge about the interface between Darwinism and Creation Science. And our astronomers need some knowledge about the interface between astronomy and astrology. Science, including effective medical care, is not advanced by pandering to unscientific consumerism about unproven theories, especially if it manages to get the law on its side. Galileo was persecuted for “his heretical view” that the earth revolved around the sun. Have we learnt nothing from his experience?

In reply: We agree with Kotsirilos and Hassed that there are many examples of successful integration of “proven” CAM into conventional medical practice. Our question, however, is whether it is possible to integrate CAM where its theoretical maxims and practices are incommensurate with allopathic medicine (eg, homoeopathy) and whether “integrative medicine” will ulti-mately fragment and diminish CAM, further isolate “non-evidence-based” CAM practi-tioners and make less visible those views of health and disease that are not consistent with modern medicine.1 It is misleading for Arnold to imply that there may be no evidence base for complementary and alternative medicines (CAMs). We suggest that medical practitioners should ask themselves not whether an “evidence base” exists, but what the existing evidence shows. The picture that emerges from a review of the literature is one of variable clinical efficacy. Thus, there is no evidence to support the use of chiropractic for childhood asthma,2 but there is good evidence that phytomedicines may reduce crises in sickle-cell disease,3 that cranberry juice may reduce the frequency of symptomatic urinary tract infections in women,4 and that horse chestnut seed extract is an efficacious treatment for chronic venous insufficiency.5 There is also clinically important evidence about harmful interactions, for example that St John’s Wort, garlic and ginseng may lower blood levels of warfarin.6 Medical practitioners should be critical and sceptical of all untested claims of therapeutic benefit. We suggest they acquaint themselves with evidence about risks and benefits of CAMs, particularly in their own area of practice. This is not pandering to anything. It is evidence-based practice. By the same token, use of CAM may reflect evidence-based decision-making by doctors and patients. It is simply divisive to dismiss it as “unscientific consumerism about unproven theories”, and it is foolish in any case to dismiss the latter. Medicine and science must compete with non-scientific perspectives in the public sphere, for the contest of ideas is never over in human history. Ideological positions are black and white. Science prefers shades of grey. We have indeed learnt much from Galileo’s experience.

To the Editor: I read with interest the article by Byles and colleagues that shows the minimal impact of health assessments in a section of the older Australian community.1 While these assessments may not be identical to the assessments covered by Enhanced Primary Care (EPC) items on the Medicare Benefits Schedule, my experience performing the latter in older people leads me to believe that they also have limited impact. I am now in part-time clinical practice, with a reasonably well-defined practice population, comprising mostly older patients with complex problems. My practice philosophy is closer to the (perhaps old-fashioned) notion of continuing, comprehensive care, which means I have not been afraid to spend the time needed to understand those patients and to document their health information. So far, I am not sure I have learned anything new in any of the EPC health assessments in which I have participated, although they have been useful for initial assessments of newer patients, as at least they remunerate practices better for the time-consuming task of doing this well. However, EPC assessments may be performed every 12 months. Is this really necessary, unless patient circumstances change? In my practice the answer is probably no, although they may be more useful in practices with less stable doctor–patient relationships. Would it not be a more effective use of resources to instead allow for better-funded initial assessments and assessments when a patient’s condition changes, irrespective of the timing?

Richard B Hays

To the Editor: Telemedicine in eye care (teleophthalmology) is one of the established technologies in medicine, providing the means for undertaking sophisticated eye care and for maintaining contact with patients in rural and remote areas.1 Telemedicine in Australia has been primarily facilitated by government, against a background of complex funding arrangements and interwoven healthcare responsibilities (it is funded mostly by project grants and state government telehealth initiatives).2 This funding mechanism impedes the efficient use and integration of telemedicine services.2 The current healthcare environment demands a detailed economic evaluation to justify continuous funding for teleophthalmology. However, some of the economic benefits of teleophthalmology may not be directly visible in the healthcare system itself. Significant benefit may be obtained by, for example, savings in time and travel expenses, thereby contributing to society indirectly. Furthermore, the cost-effectiveness of a telemedicine service improves considerably when it is integrated with existing routine healthcare services.3 But organisational and attitudinal barriers and lack of funding have delayed such integration.4 These barriers relate to human resource allocation issues in an already overstressed healthcare system and the mindset of some critics who view telemedicine as a peripheral activity and a “novelty” area for technological enthusiasts. The cost-effectiveness of telemedicine will not be improved unless the perception that it is an “add on” is changed.4 The question of whether teleophthalmology should be integrated into routine services, with Medicare reimbursement, can be judged by four criteria:5 Is the technology sound? (ie, does it fulfil its purpose?) Is the program effective compared with existing care? Is the program cost-effective? Is the program practical? (ie, are there any significant problems associated with it?). On the basis of our own comprehensive evaluation of teleophthalmology in Western Australia,6 we believe that all four questions can be answered affirmatively, and that teleophthalmology would be most efficiently provided if integrated into existing healthcare services. Its inclusion in the Medicare Benefits Schedule would benefit many patients in remote and rural areas in Australia.

Sajeesh K R Kumar · Yogesan Kanagasingam · Ian J Constable

To the Editor: The Postcard from Heller, Weller and Jamrozik1 may reflect a nostalgic and unrealistic view of how good things are back home. They suggest that, in New South Wales, the health chances of both advantaged and disadvantaged populations are improving, and, in relative terms, social inequalities in health may also be showing “some improvement”. In fact, despite impressive overall declines in mortality, there remain important differences in health status between NSW populations. Figures for the mid-1990s show that life expectancy at birth for both Aboriginal males and females is markedly less (by 20 years and 18 years, respectively). Similarly, socioeconomic disadvantage shortens life expectancy for both rural men and women (by 14 and 10 years, respectively) and urban men and women (by 10 and 7 years, respectively).2 The relative gap is also widening for some important health indices. For example, from 1980 to 2000, the percentage difference in premature death rates (< 70 years of age) between high and low socioeconomic groups has increased from 30% to 52% for men and from 24% to 32% for women, and for potentially avoidable mortality from 34% to 63% for men and from 27% to 40% for women.3 How should one respond to such inequalities? Heller et al suggest universal rather than targeted programs, as they are based on sound population health principles. To construct this as a simple choice is not helpful. Unless we recognise and address the barriers facing people in adverse social circumstances, universal programs may unintentionally widen health inequalities. For example, universal access to healthcare in the UK and Australia has not equally benefited those from the most disadvantaged circumstances compared with wealthier and better-educated populations.4 The Postcard authors suggest that Australia is saved from class divisions by the established “fair go” tradition, where shared values overcome structural inequalities in “socioeconomic status”. In fact, social class continues to be a powerful but complex and changing influence in Australia.5 It is important to acknowledge the evidence that structural inequalities are significant and worsening in Australia,6 and that the most disadvantaged experience continued social exclusion.7 We need to shift from a “trickle down” perspective that sees the greatest health gains accruing to the most advantaged — with a hope that these benefits will eventually be achieved by everyone — to a more explicit social justice perspective that ensures that resources for health are allocated in ways that produce fair outcomes. This may help address “socially entrenched self-denial of the chance for better health”.

John Furler · Elizabeth Harris · Don Nutbeam · Mark Harris

To the Editor: Pseudoephedrine is no longer a banned substance in sport.1 It was originally banned to protect athletes from overuse and its dangers. Has it become harmless or are athletes more intelligent? This highlights much of the confusion in drug testing. Athletes with diabetes are permitted to use insulin for therapy, but those with hypertension are not allowed to take β-blockers. Both drugs are popularly believed in athletic circles to improve performance. What is to stop an athlete with diabetes from taking extra insulin for performance enhancement? Why do we discriminate against those with hypertension? There is a ban on oxygen-transport drugs and on physical environment enhancers such as hypobaric chambers. Both are alleged to produce the same result, but only use of the drug can be tested. The penalty for the drug user is disqualification, but for the hypobaric enthusiast a rousing cheer for a drug-free effort. The crime is the same, so why vary the penalty? There is never likely to be a level playing field under the present system, in which one reads of positive test results being swept under the table. How will drug testing eliminate the genetic inequalities between athletes? How will testing improve the availability of top-level coaches and training facilities to all? How can it eliminate the inequality in financial incentives, allowing some athletes to train for 6 hours daily while others have to work to enable them to train for even 2 hours daily? We have swimming costumes that decrease drag in the water,1 resulting in faster times. These are not universally available, giving their owners an advantage. A level playing field will never exist in our present system. It is incongruous that in all this mess, only drugs are available to all. The current frenzy to test blood has ethical problems which have not been addressed.2 What is to happen to an athlete who develops an infection from a dirty needle? Who is responsible for the tester who has a needlestick injury from an HIV-positive athlete? It is worth remembering that this diagnosis will only be made 3 months after the Games, when everyone has dispersed. The whole area needs to be reviewed by an outside body with no vested interest in the outcome.

Anthony P Millar

Janine M Smith,* Edwin P E Kirk† * Senior Fellow in Clinical Genetics, Department of Clinical Genetics, The Children’s Hospital at Westmead, Westmead, NSW; † Clinical Geneticist, Department of Medical Genetics, Sydney Children’s Hospital, Randwick, NSW. kirkedATsesahs.nsw.gov.au To the Editor: The original understanding of cystic fibrosis (CF) as a well-defined, severe disorder has changed dramatically with the recent description of a wide range of clinical presentations. Correlations between genotype and phenotype have been reported, although the genotype–phenotype relationship is not a simple one.1 We report on a patient, now a 39-year-old woman, who had a single episode of distal intestinal obstruction (meconium ileus equivalent) at the age of 5 years, leading to a diagnosis of CF. She had a lower respiratory tract infection (caused by Klebsiella species) at the age of 10 years, but has otherwise been well, and is now asymptomatic, despite not being treated for CF since her teenage years. Her two pregnancies have been uncomplicated. She presented wishing to clarify the previous diagnosis of CF and to determine the health implications for her, if any. Her sweat chloride level was 93 mmol/L. Levels above 70 mmol/L are abnormal in adults, and this cutoff value reliably distinguishes people with CF from controls.2 Lung function testing and a chest x-ray were normal. Genetic testing revealed a genotype consistent with a diagnosis of CF. CF is caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene on chromosome 7. The most common mutation is ΔF508, which produces misfolding of the CFTR protein. The polythymidine tract is a region in the CFTR gene that varies in size depending on the number of thymidine bases present — most commonly 5, 7 or 9. The 5T variant causes a reduction in functional CFTR protein, but is not of itself associated with classic CF. In this case, testing for 30 CFTR mutations showed heterozygosity for ΔF508. Testing for the poly-T polymorphism showed the presence of 9T and 5T alleles. As ΔF508 is essentially always found in cis (on the same chromosome) with 9T,3 we conclude that the patient’s genotype is ΔF508(9T)/5T. The symptoms a patient develops and their severity are thought to be related to the amount of functional CFTR protein produced. If this is above 10% of normal, an abnormal phenotype is unlikely. Levels < 10% are associated with congenital bilateral absence of the vas deferens (CBAVD), levels < 4.5% with progressive pulmonary disease, and levels < 1% with pancreatic exocrine deficiency.4 Homozygosity for ΔF508 is associated with a severe phenotype, whereas the genotype ΔF508(9T)/5T has been associated with a range of clinical phenotypes, including CBAVD, atypical CF, or no clinical features.5 Currently, our patient has no symptoms attributable to CF. She is presumably at increased risk of chronic lung disease, and has been advised to have her lung function monitored. Giving a long-term prognosis for individuals with mild variants of CF is challenging, and a normal outcome should be considered. In future, it may be possible to predict which patients with ΔF508(9T)/5T are likely to develop symptoms. CF and its variants need to be considered in an increasingly wide range of clinical presentations. Testing for CF mutations is available from a number of Australian laboratories (listed on the Human Genetics Society of Australasia website, www.hgsa.com.au) and should be conducted in the setting of appropriate genetic counselling.

Janine M Smith · Edwin P E Kirk

Emma J Glasson,* John Wray† * Research Fellow, University of Western Australia, Telethon Institute for Child Health Research, West Perth, WA, and WA Register for Autism Spectrum Disorders; † Paediatrician, State Child Development Centre, West Perth, WA, and WA Register for Autism Spectrum Disorders Emma. GlassonAThealth.wa.gov.au To the Editor: There is growing international awareness about the realities and difficulties of obtaining written informed consent from patients to compile and use data recorded in population-based registries. In some cases, such data could be of substantial benefit to the community, while posing relatively low risk of infringing patients’ privacy.1-3 The Canadian Stroke Registry achieved only a 39% participation rate from 4285 eligible patients when applying a policy of written informed consent to their data collection, resulting in significant representation bias.1 The issues and consequences are mirrored in our own endeavour, since 1999, to maintain a prospective register of people diagnosed with autism spectrum disorders in Western Australia.4 As protocol, diagnosing clinicians in Western Australia ask parents for written consent to allow their autistic child’s name, date of birth and postcode to be forwarded to the register. However, for many reasons, parents are not always asked and diagnostic information is not always forwarded. Missed cases are collected annually from the major diagnostic and service provision centres, but only the sex and year of birth are recorded for the child. Between January 1999 and December 2002, 757 new cases of autism were registered in WA, but only 35% of parents gave written consent to include identifying details. Forty-three per cent of the 757 cases were identified by cross-referencing to diagnostic centres. When clinicians remember to notify new cases to the register, 56% of parents give consent, either at the time of diagnosis, or by sending the forms directly to the register, indicating that clinicians are instrumental in encouraging patient participation. Sometimes clinicians send anonymous diagnostic information without giving parents information about the register, and sometimes parents forget to send permission forms to the register. Various characteristics of the child or the child’s family have a bearing on whether consent is given. For example, consent is received for only 31% of children living in rural areas, 25% of children with no intellectual disability, 23% of children not Australian-born, and 16% of children from families whose primary language is not English. Without consent for every case, the register cannot accurately reflect the age or geographic distribution of children with autism. If the register only collected information on consenting cases, there would be severe under-ascertainment and the output would be notably biased. Perhaps more importantly, unidentifiable records cannot be linked to other datasets. Other WA population databases include information on hospitalisations, genetic testing, genealogical links, midwife notifications, birth defects, pharmaceutical history, and people with cerebral palsy. Linkage to these datasets would enormously facilitate population-based autism research to investigate the aetiology, associations and natural progression of autism disorders. The WA autism register is an internationally unique population-based resource, but its application is limited without the inclusion of identifying information. This remains the reality at a time when the research community and affected families desperately seek information about the condition and solutions for their children.

Emma J Glasson · John Wray

Patrick G P Charles,* Michelle Ananda-Rajah,† Paul D R Johnson,‡ M Lindsay Grayson§ Infectious Diseases Physician, † Infectious Diseases Registrar, ‡ Deputy Director, § Director, Infectious Diseases, Austin Health, PO Box 5555, Heidelberg, VIC 3084. Patrick. CharlesATaustin.org.au To the Editor: We agree with Buising and colleagues1 that, in terms of predicting clinical outcomes, the Pneumonia Severity Index (PSI) developed by Fine and colleagues2 is heavily weighted towards age and pre-existing comorbidities. However, we disagree with both their proposed “solution” and the concept on which it appears to be based. Although the current Australian antibiotic guidelines suggest that admission to the intensive care unit should be considered mainly for patients with class V community-acquired pneumonia (CAP),3 a review of the data of Fine and colleagues suggests that patients in both class IV and class V are most likely to need this type of care. In the PSI’s validation cohort of 38 039 patients, 73% of those requiring intensive care fitted these classes.2 Thus, by simply modifying the current antibiotic guidelines to include patients with CAP in either class IV or V as being at greatest risk of needing intensive-care admission, the recommendations would be accurate. By comparison, Buising and colleagues advocate using the modified British Thoracic Society (BTS) rule, which was validated in only 244 patients.4 While this approach may have some future merit, we believe there are insufficient data to advocate its use at present. A comparison of the PSI and original BTS criteria found that PSI classes IV and V were more sensitive at predicting need for intensive-care admission.5 Secondly, we are concerned about the suggestion by Buising and colleagues that young patients with severe CAP who are not in PSI class V could have worse outcomes if they do not receive broad-spectrum antibiotics.1 This implies that severe CAP is more likely to be due to unusual or resistant pathogens. This is not supported by available evidence. Instead, early clinical consideration of the likely pathogens and the potential use of new diagnostic “point of care” tests (eg, pneumococcal and Legionella urinary antigen assays and analysis of throat swabs by polymerase chain reaction for respiratory viruses and “atypical” pathogens) are likely to be of greatest benefit in empirical antibiotic prescribing. Although CAP is a common admission diagnosis, there are very few published Australian studies defining its aetiology, optimal treatment and clinical outcomes. We are currently undertaking a large prospective study (the Australian Community-Acquired Pneumonia Study) at six major hospitals in three states to address these issues. Results should be available in late 2005.

Patrick G P Charles · Michelle Ananda-Rajah · Paul D R Johnson · M Lindsay Grayson

Kirsty L Buising,* Karin A Thursky,† James F Black,‡ Graham V Brown§ * Clinical Research Fellow, † Physician, ‡ Head of Epidemiology, § Head, Victorian Infectious Diseases Service, Royal Melbourne Hospital, Grattan Street, Parkville, Melbourne, VIC 3050. Kirsty.buisingATmh.org.au In reply: We thank Charles and colleagues for their comments. The modified British Thoracic Society (mBTS) severity score for patients with community-acquired pneumonia (CAP) has been validated in more than one study (the largest involving 1068 patients from three countries1) and is recommended by the British and American thoracic societies. It predicts requirement for intensive care with comparable sensitivity to the Pneumonia Severity Index (PSI) score (using classes IV and V)2 (unpublished data), and is easy to use, requiring four variables rather than 21. The study cited by Charles and colleagues showing that the BTS severity score was less sensitive used an older version of the tool. We believe the mBTS score represents a reasonable, simple alternative tool to identify severe pneumonia, although neither score should replace clinical judgement. Caution is needed when relying on a scoring system that may give false reassurance about patients not recognised to be at risk. Early recognition of severe illness enables early intensive-care intervention, which is associated with better outcome.3 The major guidelines for management of CAP recognise the entity of severe pneumonia and recommend broader-spectrum antibiotic therapy.4-6 Whether the spectrum of pathogens in severe pneumonia differs from that in mild pneumonia is not yet clear, as data are conflicting.7,8 However, a percentage of patients with severe pneumonia will have more resistant or unusual pathogens. Inadequate antibiotic therapy for patients with severe pneumonia is associated with higher mortality. For intensive-care patients, where there is less perceived “room for error”, a strategy of broad empirical antibiotic therapy and early narrowing to directed therapy is usually promoted.

Kirsty L Buising · Karin A Thursky · James F Black · Graham V Brown

Kevin L Forbes Head, Years 3 and 4 MB BS Program, University of Queensland, Mayne Medical School, Herston, QLD 4006. k.forbesATuq.edu.au To the Editor: In response to the recent column on medical education,1 I would like to point out that many of the medical schools in Australia have broadened the content of their curricula to reflect the expected demands of professional practice and to satisfy the objectives of the accrediting body.2 Medical schools involved in curriculum change have tended to favour a broad education that emphasised learning across four domains (basic and clinical sciences, clinical skills, population health and ethics, and professional development). Another principle influencing changes to curricula was the need to ensure that the students were competent to enter supervised practice as an intern and be equipped with the desire to pursue life-long learning. Remarkably, medical schools have tended to deliver similar curricula in response to these and other issues (eg, emphasis on communication skills, critique and clinical application of evidence, exposure to rural health issues). Medical educators see a need to prepare medical students to cope with continuing changes in healthcare. Some of us would argue that many of the principles of such ongoing learning are fundamental to problem-based learning programs, and expect that graduates of such programs will be able to adapt to new continuing professional development programs. However, there is as yet no hard evidence that incorporating self-directed and problem-based learning techniques into medical curricula has any beneficial effect. Although it is not yet possible to measure the long-term effects of the changes in medical curricula, in the short term objective measures are encouraging. Today’s Australian medical school graduates function well as interns and residents.3 However, many in the profession are concerned about the level of knowledge of current graduates, particularly (but not exclusively) about anatomy. Although knowledge of anatomy needed by doctors varies considerably between disciplines, the basic sciences, including anatomy, do need to be included in college training programs. Clearly, the profession needs to measure the outcome of changes to medical school curricula.4 Ideally, as you say in your column, the outcome measures would be generally agreed by the profession.1 A debate in the Journal about the most appropriate outcome measures for medical schools would ensure that the concerns of many medical practitioners could be considered. Meanwhile, those involved in medical education need to develop and publish the outcomes that are measured in the medical schools.

Kevin L Forbes

Paul G McMenamin Associate Dean (Teaching and Learning), Faculty of Medicine and Dentistry, University of Western Australia, 35 Stirling Highway, Crawley, WA 6009. mcmenaminATanhb.uwa.edu.au To the Editor: In the lead-up to the description of events at a recent Royal Australasian College of Surgeons (RACS) conference,1 it appears that you do not fully agree with the changes in medical education in Australia and overseas in recent years. Firstly, it should be pointed out that problem-based learning has not “all but displaced didactic teaching”1 in Australian medical schools. Many schools have hybrid courses and a wide variety of teaching methods are used. Secondly, including outcomes such as “communication skills and compassion!”1 in the curricula can hardly be less than desirable. The desired outcomes of medical schools are driven by Australian Medical Council guidelines on the requirements for the safe and competent practice of clinical medicine by a generalised doctor in the intern setting before specialist training. Individual surgeons, the RACS, and their United Kingdom counterparts2 have lamented the decline in medical students’ anatomical knowledge for generations, even when students were taught 500–700 hours or more of anatomy.3 There is nothing new in this call-cry. A generalised doctor prepared for internship does not require much of the knowledge that some are lamenting has been lost from medical curricula. The “old” curricula were crowded with excessive amounts of topographical anatomy that was of questionable relevance and seldom taught within a clinical or medical context. The optimal time and context for students to learn detailed topographical anatomy is surely when the knowledge is most relevant and valuable. This is surely during basic and advanced surgical training programs, both administered through the RACS. There is good evidence that detailed teaching of topographical anatomy in targeted postgraduate surgical training courses is of measurable benefit and greatly appreciated.4,5 Indeed, is it really very suprising that, for example, urological and gynaecological surgeons have a greater interest in the nine branches of the anterior division of the internal iliac artery and the detailed relations of the ureter in the pelvis than 18-year-old first-year or second-year medical students? It is now the responsibility of surgeons and anatomists to deliver postgraduate programs that address the desired outcomes for RACS training (and the UK equivalent2). We at the University of Western Australia have launched a Graduate Diploma in Surgical Anatomy. A similar course has been in place in Melbourne for some years. Other states can only be encouraged to follow.

Paul G McMenamin

Martin B Van Der Weyden Editor, The Medical Journal of Australia, Locked Bag 3030, Strawberry Hills, NSW 2012. medjaustATampco.com.au In reply: McMenamin reiterates the importance of the educational components of current medical curricula: problem-based and self-directed learning, along with the enhancement of students’ capacities for communication and compassion. Forbes agrees and advances that these changes are to prepare future doctors for life-long learning. There are two issues at the centre of this discourse — what do medical students think of the curricular changes, and are these changes informed by scientific evidence? Anecdotal reports suggest that some medical students in the United Kingdom1 and Australia2 have concerns “that basic science does not get the priority that it once did”. Similar concerns have been raised in the popular press.3 Furthermore, UK academics fear that the dilution of basic sciences in current curricula may, in the long term, adversely affect medical graduates entering into research.1 Forbes concedes that the evidence underpinning these changes to medical education is wanting. And herein lies the rub. Despite continued calls for educational research that matters4,5 (and perhaps in keeping with opinions as to how difficult performing such research might be),6,7 the medical education community has yet to report solid evidence to support the intentions of these resource-intensive changes.8 The profession, hardened by the evidence-based movement, expects no less. This, I believe, was an undercurrent of the audience disquiet at the plenary session of the meeting of the Royal Australasian College of Surgeons in May this year. As to McMenamin’s robust defence of the pruning of anatomy in medical curricula, this debate is more than 2 centuries old. An 18th-century guide to the training of apothecaries (the forerunners of general practitioners) stated that “he” should be “tolerably well acquainted” with Latin, be competent in “his” own language and “acquainted with botany chemistry, and pharmacy; and have studied anatomy and physiology”. But “the minutiae of anatomy are not necessary”9 [my italics].

Martin B Van Der Weyden