Letters

Ian R Rogers,* George A Jelinek,† Ian Jacobs* * Associate Professor, † Professor, Discipline of Emergency Medicine, Queen Elizabeth II Medical Centre, Nedlands, WA 6009. Ian. RogersAThealth.wa.gov.au To the Editor: We applaud the call of Levi and his co-contributors for collegiate communication and consensus regarding the use of tissue plasminogen activator in acute ischaemic stroke.1 Emergency care providers are acutely aware of their role at the centre of the acute healthcare system. Daily, we interact with colleagues from other disciplines in the course of seeking the best clinical care for our patients. However, the views expressed by Hoffman2 are shared by many emergency physicians and prehospital care providers. We remain unconvinced of the role of thrombolysis in acute ischaemic stroke outside the setting of properly constituted clinical trials. On review of the contributors list in Levi’s article, we are unable to identify a single specialist emergency medicine or prehospital care provider. Consensus is not likely to be achieved until position statements from expert groups include a strong representation from all the specialty disciplines involved in the care of stroke patients. We look forward to developments in this direction.

Ian R Rogers · George A Jelinek · Ian Jacobs

Christopher R Levi (on behalf of the Australasian Stroke Unit Network, the New South Wales Greater Metropolitan Clinical Taskforce Stroke Initiative, and the Towards A Safer Culture Stroke Expert Working Group) Director, Acute Stroke Services, John Hunter Hospital, Locked Bag No. 1, Hunter Region Mail Centre, NSW 2310. christopher.leviAThunter.health.nsw.gov.au In reply: We thank the authors for their comments on our recent position statement.1 We fully agree and accept the view of Rogers and colleagues that emergency physicians are central to the timely and safe delivery of emergency medical care in our health system. This is especially the case for a therapy such as intravenous tPA, given the narrow therapeutic window and coordination challenges. We view the development of linkages with our colleagues in emergency medicine as crucial in implementing not only tPA but also a number of acute stroke therapies showing great promise in the advanced stages of development.2 Our position statement is a starting point for broader discussion, and we are pleased that discussions between the key groups are under way. We agree that, when considering patient suitability for intravenous tPA, a number of uncertainties remain, and we fully support the rationale for the ongoing clinical trials of thrombolysis in acute ischaemic stroke (see www.astn.org.au/epithet/index.html and www.ist3.com/). The risk–benefit ratio will be improved in the 0–90-minute window, as indicated by Fatovich. However, it is likely that some patients at much later time points will also gain benefit. We would emphasise, however, that according to Australia’s independent arbiter of therapeutic safety and efficacy, the Therapeutic Goods Administration, intravenous tPA is an approved therapy if given within a 3-hour window, under appropriate clinical circumstances and within appropriate healthcare settings. Regarding the comments by Fatovich on number needed to harm, it is important to recognise that the most serious adverse outcome of intravenous tPA — fatal intracerebral haemorrhage — is already accounted for in the calculations of number needed to treat (for patients to survive free from dependency). Intra-arterial thrombolytic therapy in the form of prourokinase has been found to be effective in reducing dependency in acute ischaemic stroke, shown angiographically to be caused by middle cerebral artery occlusion.3 Feasibility issues, however, presently limit the application of the intra-arterial approach, and the relative risk of intracranial haemorrhage, even with this more targeted approach, is similar to that seen with intravenous therapy. The importance of cross-disciplinary teamwork in the effective application of current and future acute stroke therapies cannot be underestimated. Central to this is the need to develop an effective dialogue between the leaders of these teams — stroke physicians and emergency physicians. The Australasian Stroke Unit Network, the New South Wales Greater Metropolitan Clinical Taskforce Stroke Initiative, and the Towards A Safer Culture Stroke Expert Working Group are committed to the task of helping to build better links between stroke units and emergency departments.

Ron Borland,* Catherine J Segan† * Nigel Gray Distinguished Fellow, † Behavioural Scientist, The Cancer Council Victoria, 1 Rathdowne Street, Carlton, VIC 3053 ron.borlandATcancervic.org.au To the Editor: The editorial on web and telephone counselling in Australia1 has the capacity to seriously mislead readers. It asserts: Despite this extensive use, the review confirmed that no randomised controlled trials (RCTs) have been conducted of the efficacy of web or telecounselling either in Australia or internationally.1 The assertion was based on a review commissioned by the Commonwealth Department of Health and Ageing and from a review in the United Kingdom, but is simply not true. It may be true for services designed to deal with mental health problems, narrowly defined, but it is patently false if it is taken to include services to facilitate smoking cessation. We note that nicotine dependence is a recognised mental disorder,2 and thus, strictly speaking, even if the review asserted that it was restricted to mental health, it would still be wrong. We do not know about the accuracy of the statements in relation to other drug use problems, but for smoking cessation there are a number of randomised trials of telephone-based systems,3 and at least two web-based resources are translations to the Internet of tailored computer advice services shown to be effective in RCTs.4,5 Both include Australian examples of RCTs. Our group demonstrated that the Quitline callback service as operated by Quit Victoria (phone 131 848) enhances cessation outcomes.6 Another study showed that an interactive personalised computer advice program called the QuitCoach (www.theQuitCoach.org.au) is effective in facilitating cessation, particularly by reducing relapse.4 It is currently available through the Department of Health and Ageing’s website at www.quitnow.info.au. We wonder why this omission has happened. What makes a health issue as important as smoking so invisible? Are other drug and alcohol issues similarly invisible? Tobacco kills about 19 000 Australians each year, and disables many more. There is increasing evidence suggesting it plays an important aetiological role in the development of some mental disorders. Smoking rates among people with schizophrenia and depression are extraordinarily high.7-9 The Victorian Quitline has pioneered the integration of support for psychiatric conditions with smoking-cessation counselling,10 and, although this service has not yet been subject to outcome evaluation, it is apparent that it meets the proximal needs of both smokers with concurrent mental disorders and their carers. Telephone and web-based services hold tremendous potential both as stand-alone services and as integrable components of comprehensive, coordinated care. High quality evaluations are required, and they need to be seen as an integral part of service delivery. People in other healthcare areas could learn a lot from what has been achieved in smoking cessation.

Ron Borland · Catherine J Segan

Helen Christensen,* Barbara Hocking,† Dawn Smith‡ * Deputy Director, Centre for Mental Health Research, Australian National University, Canberra, ACT 0200; † Executive Director, SANE Australia, Melbourne, VIC; ‡ Chief Executive Officer, Lifeline Australia, Canberra, ACT. helen.christensenATanu.edu.au In reply: Borland and Segan are correct in assuming that we did not include substance disorder randomised controlled trials (RCTs) in the assessment of the efficacy of web and telecounselling services in our editorial.1 Our definition of web and telecounselling was also strict in that we included only contact that involved a person (a counsellor) online or by telephone. We specifically excluded interactive personalised web programs such as www.theQuitCoach.org.au or others specifically in mental health (narrowly defined), which have been found effective when delivered by the Internet. (Such programs include Panic Online,2 MoodGYM and BluePages.3) The use of RCTs in evaluating the areas of substance use, anxiety, depression and other mental health problems is to be applauded. Borland and Segan’s letter is also instructive in reminding us of the importance of coexistent substance-use disorders and mental health problems. Organisations such as SANE are committed to reducing the health costs of smoking in people with mental health problems and have developed specific programs for this purpose. Importantly, we are in agreement with Borland and Segan that telephone and web-based services “hold tremendous potential both as stand-alone services and as integrable components of comprehensive, coordinated care”. However, our editorial reported that web and telecounselling (not integrated web-based management systems) have yet to be evaluated through RCTs. One point we contest is the view that smoking is invisible. Our systematic review of funding allocations to mental health research has found that the category of substance-use disorders, of which smoking was the third-largest component (below alcohol and opioids), received the most Australian research funding in 2000.4 The level of funding for substance use exceeded that for childhood disorders and dementia. Compared with substance-use research, depression research received less than half, and psychosis and anxiety less than a third, of funding. Affective disorders contribute the highest disease burden, and dementia has the highest health system costs. Although all our projects in these important areas require proportionately more funding, it is not helpful to claim that the omission of smoking outcome research is due to failure to recognise its importance.

Helen Christensen · Barbara Hocking · Dawn Smith

Ailsa Goulding,* Andrea M Grant,† Peter L Davidson‡ * Professorial Research Fellow, † Assistant Research Fellow, Department of Medical and Surgical Sciences, ‡ Research Fellow, Injury Prevention Research Unit, University of Otago, Dunedin, New Zealand. Ailsa. GouldingATstonebow.otago.ac.nz To the Editor: The interesting article on playground safety and arm fractures by Sherker and Ozanne-Smith1 documents a steady increase in hospitalisation rates for arm fractures among Victorian children between 1987 and 2002. It would appear that the increase over this 15-year period was about 45%. These figures may represent the tip of the iceberg, as few children with arm fractures are admitted to hospital and most are treated on an outpatient basis. Increases of similar magnitude in forearm fractures in adolescence have also been reported recently in the United States.2 It would seem that children are becoming more vulnerable to such fractures. This is a concern, as fractures of the distal forearm are extremely common during growth. Indeed, about a quarter of all fractures during childhood and adolescence occur at this site. One factor that might be contributing to this rising incidence of arm fractures during growth is increasing childhood adiposity. Childhood obesity has increased sharply in Australian children over recent years.3 Obese children fall with more force, and, although they may have more bone for chronological age than children of healthy bodyweight, adaptive increases in bone mass are not enough to accommodate their high bodyweight gain, placing them at a biomechanical disadvantage during falls on the outstretched arm.4 Our studies of consecutive series of girls and boys with distal forearm fractures indicate that a high proportion of these children are overweight. Moreover, in a 4-year prospective study of 170 girls, we found that high bodyweight at baseline increased the risk of new fractures.5 In their study, Sherker and Ozanne-Smith measured the heights and weights of 402 children under 13 years of age who had broken their arm falling from playground equipment between 2000 and 2002. We wonder how many of these children were overweight or obese for their age. Examination of the body mass index values would provide this information, and we ask that the authors report these data for both girls and boys using international cut-off points. We would like to know whether or not overweight is contributing to rising rates of arm fracture in Australian playgrounds.

Ailsa Goulding · Andrea M Grant · Peter L Davidson

Shauna Sherker,* Joan Ozanne-Smith† * Postdoctoral Research Fellow, NSW Injury Risk Management Research Centre, University of New South Wales, Sydney, NSW; † Chair of Injury Prevention, Accident Research Centre, Monash University, Melbourne, VIC. Shauna. SherkerATunsw.edu.au In reply: The prevalence of obesity has increased dramatically among Australian children, particularly over the past 2 decades.1 However, the role of obesity as a risk factor for fall-related arm fracture remains unclear. Using standard definitions for child overweight and obesity,2 our study population3 (Box) did not demonstrate quite as high a prevalence of obesity as had been previously reported for Victorian schoolchildren.1 This case series was part of a larger, yet to be published case–control study, the results of which indicate no significant difference in body mass index between children who fell from playground equipment and fractured their arm (cases) and those who fell and landed on their arm with no significant injury (controls). The negative public health effects of increasing prevalence of obesity among Australian children highlight the need to promote safe and enjoyable physical activity. Playground equipment provides a very popular means of physical activity for children. Improving playground safety standards to minimise the risk of arm fracture — a traumatic, costly and preventable childhood injury — has never been more urgent. Children with arm fracture caused by falls from playground equipment, showing proportion of children who were normal weight, overweight or obese.* * Based on unpublished data from Sherker and Ozanne-Smith.3

Shauna Sherker · Joan Ozanne-Smith

Erica L Mann Managing Director, Wyeth Australia and New Zealand, 17-19 Solent Circuit, Norwest Business Park, Baulkham Hills, NSW 2153. To the Editor: Wyeth Australia welcomes the opportunity to comment on Lu and colleagues’ discussion of whether rheumatoid factor status is a predictor of tumour necrosis factor-α (TNFα)-inhibitor response in rheumatoid arthritis (RA).1 Wyeth provided the data used by the Pharmaceutical Benefits Advisory Committee (PBAC) to originally exclude patients who test negative for rheumatoid factor from access to TNF-α inhibitors. Although Wyeth agreed with the PBAC’s interpretation that only patients with positive rheumatoid factor status may benefit from etanercept, efficacy in those testing negative for rheumatoid factor was not clearly established because of the small number of patients in these subgroups. Importantly, the subgroup analysis divided all study participants into two groups depending on their rheumatoid factor status and only included ACR 20 response (a standard from the American College of Rheumatology which requires at least 20% reduction in swollen joint count, tender joint count, and in three out of five of patient’s assessment of pain, patient’s assessment of disease activity, investigator’s assessment of disease activity, acute phase reactant levels and patient’s assessment of disability). This analysis may not represent the likely response of patients who test negative for rheumatoid factor, but who develop severe, progressive rheumatoid arthritis and otherwise meet the stringent eligibility criteria associated with Pharmaceutical Benefits Schedule listing (excluding positive rheumatoid factor status). It is possible that the small number of unique rheumatoid-factor-negative patients who have severe disease will not have a different response to etanercept from similar patients who are rheumatoid-factor positive. More recent data are available from a large multicentre study that compared treatment with etanercept in combination with methotrexate to either monotherapy alone for control of RA disease activity.2 Subgroup analysis for the effect of rheumatoid factor on treatment responses showed that the presence of rheumatoid factor in the circulation of study patients did not significantly affect the responses to therapy among treatment groups. Although these new data have yet to be presented to the PBAC for reconsideration, a submission on this matter is under way.

Erica L Mann

To the Editor: We report an unusual case of Ross River virus (RRV) disease in a 7-year-old child. The patient presented to her general practitioner with fever, rash and pain in the lower limbs. Swelling of the joints of the hands and left knee was found, with a widespread rash that covered the trunk, limbs and face. The rash comprised lesions of varying types, including maculopapular, vesicular and petechial lesions (Box). Rash in a child with Ross River virus disease The general practitioner transferred the patient to the state tertiary paediatric service. No antibiotics were given before transfer. On arrival at Princess Margaret Hospital for Children, Perth, the patient was unwell, with a fever of 38°C. A provisional diagnosis was made of septicaemia (probably meningococcal), and treatment was begun with intravenous ceftriaxone. Extensive investigations were performed, but results of all initial serological, polymerase chain reaction and culture investigations were negative. Rheumatology review was requested because of the prominent arthritic component of the illness. This revealed widespread polyarthritis, and the illness was felt to be a reactive or post-infectious process. The child’s family raised the possibility of RRV disease, as her grandmother had had this disease several years previously, and the child had stayed overnight at her grandmother’s home in a coastal lake area 2 weeks before disease onset. The area had abundant mosquitoes, as well as kangaroos, which are vertebrate amplifiers for RRV.1 Serological tests for RRV were performed 3 days after admission, and were negative for IgG and positive for IgM. Repeat serological testing during convalescence showed a fourfold rise in IgG titre (from 80 to 320), confirming the diagnosis of RRV disease. The patient’s rash decreased over several days. She had persistent synovitis in the left knee at review 3 weeks after admission. At review at 8 weeks all symptoms and signs had resolved, and she had full function. This case highlights the fact that, while RRV disease with severe symptoms and arthritic manifestations is uncommon in children, it nevertheless should still be considered in the differential diagnosis of children with a febrile and arthritic disease.1,2 This child’s illness appears to have been a reactive vasculitis and polyarthritis, which, while well recognised with other infections, is not well described in association with RRV disease in children. RRV arthritis is caused by joint infection, and treatment is currently based on empirical anti-inflammatory regimens. During the recent RRV disease epidemic in Western Australia, 1174 notifications for RRV disease were received between 1 October 2003 and 31 March 2004. Of these, 21 patients were aged 15 years or younger. Thus, while RRV disease is an infrequent illness in children, it does occur, and should be considered in the differential diagnosis of a child who presents with a febrile illness, rash and joint symptoms from an area with known autochthonous transmission of RRV.

Kynan T Feeney · Kevin J Murray · Amanda J Whittle · Gary K Dowse

To the Editor: Previous articles in the Journal have stressed the importance of making obesity prevention a public health research priority.1,2 Participation in physical activity is one important factor in counteracting increase in body weight.3 While recent studies have focused on environmental factors that influence walking (eg, presence of paths and trails, accessibility of destinations)4 and the possibility of environmental innovations to increase rates of participation, few studies have investigated participants’ perception and understanding of variation in physical activity in relation to environmental factors across the seasons. Our study aimed to examine how people perceive the impact of changes in ambient temperature and hours of daylight across the seasons on their rates of physical activity. We compared residents of the southern and northern hemispheres: a group of women from Sydney, Australia (n = 121; mean age, 19 years [SD, 2 years]), and a group of women from Trier, Germany (n = 109; mean age, 21 years [SD, 3 years]). Participants completed a brief written survey specifically designed for our study. The survey, using an “open question” format, asked participants to describe and explain any perceived changes in their physical activity during winter and summer. The majority of Australians and Germans perceived seasonal changes in physical activity (73.6% and 71.6%, respectively), with no significant difference between the two groups. These changes typically entailed a decrease in physical activity levels during winter (noted by 55.2% and 66.2% of Australians and Germans, respectively). A significantly higher number of Australians than Germans perceived a change from outdoor activities (eg, swimming) to indoor activities (eg, squash) between summer and winter (χ1 = 9.21; P = 0.002). Significantly more Germans than Australians perceived themselves to be affected by environmental factors (χ1 = 9.37; P = 0.002). These results support the contention that environmental changes are linked to changes in activity levels,5 and that more extreme climatic changes (such as those experienced by Germans compared with Australians) are associated with a greater perceived impact on levels of physical activity. Programs aiming to encourage greater participation in physical activity in winter need to challenge people’s perception of the impact of environmental factors by offering indoor opportunities for exercise, particularly to people from Germany. It appears that Australians are more aware of indoor opportunities for physical activity. Research into environmental factors that encourage or discourage walking4 needs to be taken into account when designing programs to enhance physical activity across the seasons. For example, constructing walking or cycling paths in the neighbourhood may encourage people to continue with indoor activities during the colder seasons by making the indoor venues more easily accessible.

Tanja Hechler · Josephine Y Chau · Sarah Giesecke · Silja Vocks

To the Editor: The articles in the General Practice issue are most interesting. Sadly, the articles on how general practitioners are paid1-6 have largely missed the point. It is not only how GPs are paid, but also how much that matters. No matter how ideal the incentive incorporated in the payment method may be, if the quantum is too little even the most idealistic GP will find it impossible to work in a professional manner. Payment here includes both direct personal income and the associated practice conditions. In most countries, changes in GP financing focus more on how to keep costs down than on rewarding quality. Green was the only author to address this issue, making the point that US family medicine organisations have recently changed from showing how good GPs can be to ensuring they are paid well enough to do that good work, and to provide incentives to encourage the next generation of family physicians.6 Since the introduction of the National Health Service (NHS) in 1949, the United Kingdom has gone through several cycles of declining incomes and conditions for GPs, followed by declining interest and recruitment, in turn followed by higher pay and conditions that attracted new recruits. Overall, UK GPs have been paid relatively well compared with their hospital specialist colleagues. It is no accident that the UK has developed the highest levels in the world of academic general practice, as well as research in practice, while the British taxpayers obtain the highest value from their overall health service.7 Currently, in Australia, the Journal classifieds confirm that there are vast discrepancies between expected salaries for specialist and GP services; perhaps there is a lesson for funding. Until salaries for GPs are similar to those for specialists, bright young medical graduates will prefer to work in higher-paying, hospital-based specialties. Merely altering the payment system will make little difference. The value potentially obtained from good primary care will remain out of reach unless the total resources put into this sector are increased.

James A Dickinson

To the Editor: Proposals to manage the shortage of general practitioners by recruiting and training overseas-trained doctors and funding new medical schools will take years to take effect and be enormously expensive. The crisis is with us now. Support for properly trained practice nurses by Medicare, either as a rebate or a salary, could rapidly ameliorate the shortage of GPs, and would deliver improved patient care. I do not refer here to nurse practitioners — that is a different issue. Practice nurses in many developed countries undertake routine GP tasks. Increasing specialisation requires GPs to have more time to evaluate patients. Nurses can complete an initial case summary: these are time consuming and are often missing. Nurses can measure blood pressure; perform Pap smears, breast examination, and vaccinations; counsel people (who will often reveal important information to a nurse); sterilise instruments; explain asthma plans and puffers; give simple dietary advice; and supervise diabetes protocols. This is not a second-class option — it will improve care: doctors who have worked with the system find it improves the quality of their practice and saves them a great deal of time to do other tasks. New and bridging courses for these nurses, a few of which exist, would rapidly produce a workforce happy to work from 9 am to 3 pm, or job share. They need Medicare support. The Minister for Health and the shadow minister may wish to consider this.

Sandy L A Reid

To the Editor: Poor adherence to therapy with asthma preventer medications is common among teenagers with asthma. This is often simple forgetfulness rather than active non-compliance. One of our adherent patients shared his secret with us — the alarm mode on his mobile phone. He set this to be activated twice daily to remind him to take his medicine. A recent survey by Newspoll showed that about 90% of teenagers aged between 13 and 19 years in Melbourne and Sydney have a mobile phone, most of them on a prepaid plan.1 We have subsequently recommended this reminder system to other patients, who have expressed interest in adopting the practice. This could be useful for all patients required to take regular medications. In the absence of a mobile phone, many household appliances (such as microwave ovens) have electronic timers that could be programmed to sound an alarm on a regular basis.

Gaudenz M Hafen · John Massie

To the Editor: Recent media reports have claimed numerous health benefits for A2 milk1,2 (eg, “new wave milk”, “wonder milk”). It is becoming more widely available, particularly in health food shops, and is advertised on Queensland television. We believe it is important to offer clear information about this product and cows’ milk allergy. A2 milk is produced by cows homozygous for the A2 polymorphic variant (his→pro) at amino acid 67 of the b-casein gene. A difference in degradation patterns of the A1 and A2 variants is purported to lead to differences in immunological or pharmacological effects,3-5 which we will not comment on here. Regarding cow’s milk allergy, β-casein is one of at least seven proteins in cows’ milk with allergenic significance (α-, β- and κ-casein, α- and β-lactoglobulin, lactoferrin and transferrin). One would not expect a single amino-acid difference in one protein to have a significant effect on milk allergenicity. We have found in discussion with parents of milk-allergic children, as well as from inquiries from the community to AllergySA, that there is a perception that A2 milk may be less allergenic than “normal” milk (which contains A1 and A2 b-casein). Although most proponents of A2 milk have made no explicit claims about allergenicity — and indeed some have cautioned against the use of A2 in milk-allergic individuals — there have been media reports that may have led to this perception.6 However, these reports are misleading. For example, it is quite likely that children with a previous history of cow’s milk allergy who have been found to tolerate A2 milk have in fact “grown out” of the allergy, which is the usual natural history. Others may never have had true milk allergy. We obtained a sample of pure A2 milk from A2 Dairy Marketers (Acacia Ridge, QLD) and used it for skin-prick testing of 11 consecutive milk-allergic children (Box). The tests compared A2 milk with “normal” (A1/A2) milk and cow’s milk protein extract. The mean diameter of the wheal raised by normal milk was not significantly different to that raised by A2 milk (8.2 mm for normal milk v 10.7 mm for A2 milk; P = 0.09, paired t test). No patient had a negative reaction to A2 milk when the reaction to normal milk was positive. We did not perform an oral challenge with A2 milk in these children, as many had experienced severe allergic reactions, and the predictive value of a positive skin-prick test in the presence of a clear recent history of clinical allergy is high. We therefore caution that A2 milk should not be used by those with IgE-mediated cow’s milk allergy, particularly those who have had recent severe reactions to milk. Mean wheal diameter* (mm) on skin-prick testing Patient Normal milk† A2 milk† Cow’s milk extract‡ Histamine positive control 1 12 10 8 4.5 2 11.5 12 11 5.5 3 4 8 6 15 4 8 11 10.5 3 5 12 8 6 9 6 3 5 2 9 7 7 15 7 10 8 7 7.5 5 7.5 9 6 7.5 4 3.5 10 13 25 4.5 3 11 7 9 3 5 Mean 8.2 10.7 6.1 6.8 * As wheals produced are not necessarily circular, it is standard to report diameter as the mean of two measurements taken perpendicular to each other. Results for all negative controls were 0 mm. † Normal and A2 milk were stored frozen, and aliquots thawed for testing. They do not produce wheal reactions in non-allergic individuals. ‡ Cows’ milk extract is manufactured for skin-prick allergy testing by Hollister-Stier, Wash, USA, and purchased from Richard Thomson, Sydney, NSW.

William B Smith · Deryn Thompson · Margaret Kummerow · Patrick Quinn · Michael S Gold

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