Letters

To the Editor: The Guidelines for the management of acute coronary syndromes 20061 state: “Enoxaparin may be used in conjunction with fibrin-specific fibrinolytic agents in patients under the age of 75 years, provided they do not have significant renal dysfunction. An intravenous bolus dose of 30 mg followed by a 1 mg/kg subcutaneous injection every 12 hours in combination with tenecteplase is the most comprehensively studied therapy.”1 In Australia, enoxaparin is not licensed for intravenous use (Tony Hall, Team Leader, High Risk Medications and Systems, and Christine Maclean, Associate Director, Safe Medication Practice Unit, Queensland Health, personal communication) and there is no recommendation for the intravenous use of enoxaparin in the drug product information.2 Are the authors recommending “off-label” use of intravenous enoxaparin, or do they wish to modify the guidelines to reflect what the management should be if clinicians are unable to use intravenous enoxaparin?

Mark Little · Chris Johnstone

In reply: The guidelines were published to provide clinicians with the most contemporary information on the management of acute coronary syndromes based on the international literature, and may include treatments which are not currently available, officially licensed or available through the Pharmaceutical Benefits Scheme in Australia. In the context of adjuvant therapy for patients with ST-segment-elevation myocardial infarction (STEMI), the guidelines recommend that antithrombin therapy should be used with fibrin-specific fibrinolytic agents.1 Based on the best evidence available at the time, the guidelines mention two antithrombins, unfractionated heparin and enoxaparin, to be considered for use in this setting. The recommendation for enoxaparin is based on comprehensive evidence of clinical benefit with the regimen of an initial intravenous (IV) bolus dose followed by subcutaneous injections every 12 hours. It is up to individual practitioners to determine whether the IV dose should be provided “off-label” or omitted, based on the evidence and the circumstances of the individual patient and setting. The issue of superiority of enoxaparin over unfractionated heparin as adjuvant therapy for patients with STEMI is currently being evaluated in light of recent evidence,2 and will be included in a future update of the guidelines.

Constantine N Aroney · Philip Aylward

To the Editor: I read with great interest the recent updated review of amoebiasis by van Hal and colleagues1 and their previous letter2 describing three cases of locally acquired amoebiasis due to Entamoeba histolytica in Australian men who have sex with men (MSM). These articles should alert clinicians to the emergence of invasive amoebiasis and the possibility of person-to-person transmission of E. histolytica through oral–anal or oral–genital sex among MSM in developed countries. The same phenomenon has been reported in Taiwan3 and Japan.4 The prevalence or incidence of intestinal amoebiasis among people at risk may have been underestimated in the past, as microscopy of stool specimens has lower sensitivity and specificity than E. histolytica antigen detection methods for diagnosing the disease.1,5 Cases of amoebiasis may evade detection using the diagnostic algorithm proposed by van Hal and colleagues,1 which suggests using microscopy of stool specimens to detect E. histolytica complex followed by confirmation with specific antigen detection methods or molecular methods. To increase diagnostic sensitivity and specificity, I suggest revising the diagnostic algorithm for intestinal amoebiasis in developed countries to include more accurate first-line detection methods. For example, specific antigen detection methods or polymerase chain reactions, as proposed by Tanyuksel and Petri,5 could be incorporated.

Chien-Ching Hung

To the Editor: van Hal and colleagues deserve congratulations for their lucid, concise and timely review of the complex problem of human amoebic infection and its diagnosis.1 Not surprisingly, however, their article raises more questions than it answers. To me, the gist of their message was as follows: what was in the past diagnosed as Entamoeba histolytica infection, based on the microscopic identification of organisms from faeces, culture or histological sections, actually may have been caused by other species, viz. E. dispar (a recently described non-pathogen) or E. moshkovskii (known for a long time from sewage samples, but only recently found to infect humans). Because these species are all identical morphologically, they can be distinguished reliably only by sophisticated molecular techniques. To complicate matters further, despite E. dispar having been virtually defined as the “non-invasive form” of Entamoeba, most true E. histolytica infections are still asymptomatic.2 Not only the parasite, but also individual host factors (perhaps including genetics), determine pathogenicity. Thus, not all people infected with the same pathogenic strain will manifest symptoms or signs of invasive disease. Given their biology and evolution, it is conceivable that, eventually, invasive strains of even E. dispar will be discovered! Furthermore — and this seems not to have been investigated yet — mixed infections involving different species and strains of these parasites almost certainly occur (not to mention the “traditional” non-pathogenic amoebae, which frequently do occur in mixed infections). The authors advocate treatment of even asymptomatic E. histolytica infections, but how would these be detected outside epidemiological surveys or healthy population screening programs? Given the difficulty and expense of specifically identifying the infective organism even in symptomatic cases, and the relative cheapness of treatment, surely it would be sufficient simply to treat on the basis of clinical presentation plus the identification of E. histolytica-like parasites, with or without objective evidence of histopathology. Anything more could be justified only within the context of a well funded and carefully designed research program and/or epidemiological study.

Paul Prociv

In reply: We agree with Hung that molecular and antigen testing methods are more sensitive for Entamoeba histolytica detection than microscopy and that reliance on microscopy alone would result in under-detection. Our algorithm1 was presented the way it was for several reasons. Firstly, both molecular and antigen testing are significantly more expensive than microscopy. Secondly, as these tests can currently only detect a single pathogen, they would not replace microscopy. Most patients, especially men who have sex with men (MSM), have multiple intestinal parasites, so the more specific methods would remain an adjunct in parasite detection.2 Thirdly, the positive predictive value of any test is dependent on the prevalence of the disease. The prevalence of E. histolytica in Australia, based on current data, is less than 1% in high-risk populations, including MSM. Thus, at present, molecular and antigen tests would be more likely to give false positive than true positive results. However, we agree that our algorithm could be modified as suggested if prevalence rates were between 5% and 10%. Finally, as seen in the MSM population in Taiwan, this is not a static situation, and ongoing local surveillance is required.3 We agree with Prociv that, before the introduction of molecular techniques, E. histolytica prevalence would have been overestimated. We also agree that specific host factors and/or undefined parasitic virulence factors can lead to invasive disease. However, given the extensive molecular work that has been undertaken, we believe it unlikely that invasive strains of E. dispar will be discovered.4 Furthermore, recent studies show that mixed infections are common.2,5 In symptomatic patients, empirical amoebicidal therapy is warranted. However, to ensure that alternative diagnoses (eg, inflammatory bowel disease) that require different treatment are not overlooked, all attempts to accurately speciate Entamoeba complex should be undertaken. We acknowledge that speciation using the polymerase chain reaction is beyond the means of most laboratories, but this is not the case for enzyme immunoassay testing of stool samples, which is rapid, sensitive and relatively cheap. For asymptomatic patients who are carriers of E. histolytica cysts, the World Health Organization recommends treatment.5 However, in areas of low prevalence such as Australia, Entamoeba cysts are more likely to be non-pathogenic E. dispar or E. moshkovskii species than E. histolytica.3 Thus, in Australia, treatment would be unnecessary in a high proportion of patients. Furthermore, therapy requires a luminal agent (paramomycin), which is difficult to obtain. The most practical solution is to either give no treatment or to treat only those patients who have tested positive for E. histolytica.

Sebastiaan J van Hal · Damien J Stark · Debbie Marriott · Jock L Harkness

To the Editor: Two recent articles in the Journal touch on the current plight of medical academics. Hays emphasises the need to reassert the role of teaching in academic medicine — otherwise, “our aim to produce safer, more efficient doctors will be under threat”.1 Joyce and colleagues outline the projected increase in the number of graduates from Australian medical schools, although their concern is more for the post-graduate careers of these young doctors than for their initial clinical training.2 In 2006, Van Der Weyden warned that not only do new ways of teaching medical students need to be rapidly explored but also that more skilled teachers must be found and trained.3 Medical students themselves believe that more clinical teachers are required to ensure that the increasing numbers of students are taught effectively.4 From personal experience we know that, while many full-time clinicians are both willing and inspiring teachers at undergraduate level, a core of permanent academics is needed to direct teaching during these clinical years. But why would anyone choose to be a medical academic today? Certainly not for the money — a recently qualified obstetrician/gynaecologist, starting at senior lecturer level after about 15 years of training, is looking at an income of less than half that of a staff specialist at the same level, and a quarter of that possible in private practice. One day of private practice per week does not help — obstetrics is a full-time commitment, and even in gynaecology the need to pay practice and indemnity costs outweighs any financial benefits. Is it the kudos? Adjunct academic titles are easily gained by non-academics: hospitals are awash with adjunct associate professors and lecturers. The adjunct appointment system often lacks regular and critical appraisal, and in some cases titles are used to the professional or financial gain of the recipient, with little reciprocal input into teaching at the institution concerned. (However, there are indications of attempts to crack down on such practices.)5 The lifestyle then? Academics may have a less frenetic clinical schedule, but the continuing pressure to produce quality research and to jump increasingly higher hurdles to obtain grants can mean that the limits of the working week are much less defined than for our staff specialist colleagues. We have seen many colleagues depart academia in the past few years for the more verdant pastures of full-time clinical practice. While we are in agreement with Hays about the need for more research into how best to design medical education, we believe that, unless there are urgent improvements in the remuneration, career structure and professional regard for clinical academics, the core workforce of skilled teachers so clearly needed for incoming students will just not be there to deliver that education.

Ajay Rane · Caroline de Costa

To the Editor: Like Haley’s father,1 I too lament the fact that Latin terms have fallen out of use in medical terminology. I also think it retrograde that Latin is being taught to fewer and fewer of our secondary students, as they are missing out on an opportunity to learn so much more about our own language, let alone terms that they might use later in their clinical practice. However, I do not think that it was Latin that helped the young teacher out of a difficult predicament in the 1950s. I can assure Haley that “pseudocyesis” is all Greek to me.

Peter Piazza

To the Editor: Thank you for the charming letter about “non-pseudocyesis” published in the 19 March issue.1 It reminded me of the Brander Matthews quote: “A gentleman need not know Latin, but at least he should have forgotten it.” This is particularly apt, as the term “pseudocyesis” is from Greek.

James Mitchell

To the Editor: The tale told by Katherine Haley’s father about his clever advice on how to protect the privacy of a young pregnant woman makes a good story.1 However, while “non” is a Latin word, “pseudocyesis” is very good Ancient Greek (ψευδοκύησις). Queen Mary I (“Bloody Mary”), who was believed for many months to be with child but ultimately returned to court childless, may have suffered from pseudocyesis. I agree with Dr Haley’s opinion about the lamentable decline in the use of both Latin and Greek terms in medical practice. I take the time to teach my students, residents and registrars enough Latin and Greek to render classical plurals correctly (eg, fistulae, diverticula, carcinomata). Whether they take any notice of this classical teaching is another matter.

William E M Renton-Power

To the Editor: I was both delighted and a little perturbed to read the recent letter by Katherine Haley about her general practitioner father who outsmarted the Department of Education by a medical sleight of hand, stating that his patient had “non-pseudocyesis”.1 However, it was not Latin, but Greek, that did the trick. Despite Dr Haley’s background in Latin, he, like all physicians, had unwittingly used Greek during his medical course. I was fortunate to do a year of Ancient Greek during my undergraduate medical course and, like my late GP father, also did Latin for matriculation. It is unfortunate that Greek is no longer taught in Queensland schools, and Latin only in a few. I believe that we are the poorer for this, and it shows in all sorts of ways, including a general decline in literacy even at the tertiary level. A classical grounding demands scholarship and precision. I have found that knowledge of both Greek and Latin has enriched my knowledge of English literature and Western philosophy, as well as French. Such a grounding also trains the mind in analytical and ordered thought and provides greater insight into the workings of syntax and grammar and a greater facility with words — the building blocks of our language, many of which are derived from Greek and Latin. At the risk of stating the obvious, I will remind readers that anatomical words in medicine are predominately Latin or Greek and that the names of nearly all symptoms and diseases are Greek (with some exceptions, such as “angina pectoris”). In Dr Haley’s time, it was common for potential doctors to receive an arguably more “polished” education that embraced one or two languages, including Latin and, in some private schools, Greek. Alas, the current system of medical student selection favours those “idiots savants” who excel in mathematics and science and not the arts. With respect, I would like to point out that in the term “non-pseudocyesis”, the only Latin component is “non”, the rest being Greek (ψευδής, false; κύησις, pregnancy). For both the enthusiast and the non-classicist, may I recommend my father’s 5th edition of Gould’s medical dictionary (1943), which contains the etymology of every medical word.

Roger K A Allen

To the Editor: The recent article by Venn et al reported that childhood overweight carries through into adult overweight and obesity, but that most obese young adults in their study were “healthy” weight as children in 1985.1 As demonstrated by National Health Surveys, age is one of the strongest predictors of overweight,2 with body mass index (BMI) increasing as we grow older. However, there are two additional time-related components influencing obesity. Since 1985 (when Venn et al reported the prevalence of overweight and obesity in children was less than 10%), the environment appears to have become more obesogenic — a 2004 survey in New South Wales showed that 26% of children were overweight or obese.3 It is not only children who are vulnerable — the percentage of overweight adult Australians increased for almost all age groups from 1990 through 2001, and the mean BMI at which Australians enter adulthood has increased with each subsequent survey. For example, for women aged 20–24 years, mean BMI increased from 22.1 kg/m2 (1990) to 22.5 kg/m2 (1995) to 23.2 kg/m2 (2001) to 23.3 kg/m2 (2004). As the heights and weights were self-reported in these surveys, true BMI values may be even higher. We recently reported that year of birth (birth cohort) also predicts prevalence of overweight and obesity, independent of age and survey period; the prevalence of overweight and obesity in adults increased progressively with birth cohorts born since 1960.4 This birth span includes the cohort in the study by Venn et al.1 While obesity begins in childhood for only a small proportion of adults, the so-called healthy weight children now have a higher mean BMI, giving little margin for the seemingly inevitable increases in weight with ageing, before the population mean BMI reaches the cutpoint for overweight and later obesity. The 2004–2005 National Health Survey showed that men reached the overweight cutpoint at 25–29 years and women reached it at 30–34 years.5 Given increasing child and adult obesity, the need for allocation of public health resources to improve dietary and physical activity habits is undisputed. However, these data1,4 indicate that efforts should be directed to the hard-to-reach group, young adults, to prevent weight gain at this point. This will pose considerable challenges, because this group has minimal contact with health services, and perceives the threat of chronic illness as irrelevant. However, swift intervention is required, not only for their own health and that of their children as they become parents, but also because they will become overconsumers of health care for chronic diseases within a generation.

Margaret A Allman-Farinelli · Lesley King · Adrian E Bauman

In reply: Allman-Farinelli et al make an important point about the influence of age, survey period and cohort effects on the prevalence of overweight and obesity. While age and cohort effects could not be clearly separated in the 1985 Australian Schools Health and Fitness Survey, the prevalence of overweight and obesity increased with age in 7–15-year-olds.1 Our data collected from 4571 of the individuals in that survey at follow-up about 20 years later also showed an increase in the prevalence of overweight and obesity with age, although these findings were not presented in our report.2 In the Box, we show the distribution of body mass index (BMI) values for men and women in three age groups (24–27 years, 28–30 years and 31–34 years). Mean BMI values across the age groups were 25.2 kg/m2, 25.6 kg/m2, and 26.5 kg/m2 in men and 23.5 kg/m2, 24.2 kg/m2, and 24.6 kg/m2 in women. The prevalence of obesity (BMI ≥ 30 kg/m2) increased with increasing age as follows: age 24–27 years — men 12.2%, women 9.9%; age 28–30 years — men 12.3%, women 12.0%; and age 31–34 years — men 15.6%, women 14.6%. Distribution of body mass index values for men and women in three different age groups* * 24–27 years, 757 men and 854 women; 28–30 years, 767 men and 807 women; and 31–34 years, 673 men and 691 women in the 20-year follow-up of the 1985 Australian Schools Health and Fitness Survey.

Alison J Venn · Russell J Thomson · Michael D Schmidt · Verity J Cleland · Beverley A Curry · Hanni C Gennat · Terence Dwyer

To the Editor: O’Leary and colleagues1 rightly point to the need for better evidence on whether low to moderate maternal alcohol intake affects the fetus. Evidence to date is weak and inconsistent, largely because alcohol consumption in pregnancy is generally poorly documented,2 and few studies have recorded data on factors that could potentially modify fetal exposure. Evidence could come from large pregnancy cohort studies, usually designed to address other issues, but there are no published guidelines on how to collect information relevant to fetal alcohol exposure during gestation. There is, therefore, a great need to define a core dataset for research studies, as well as one that is sufficiently simple to use in routine pregnancy care settings. We have identified a number of issues that need to be addressed. To stimulate discussion, the Box shows our suggested core dataset. Maternal alcohol intake: Alcohol questionnaires have largely been designed to identify women who are heavy drinkers, misuse alcohol or are alcohol-dependent.3 Questionnaires are needed that capture information on alcohol intake across the range, from minimal to heavy drinking, as well as information on drinking patterns and alcohol intake at different periods of gestation. Factors that may modify the relationship between maternal intake and fetal alcohol exposure: For a given maternal intake over a given period, maternal blood alcohol level and hence fetal alcohol exposure may vary according to maternal size and body composition. Other factors can affect maternal alcohol absorption and elimination, such as whether alcohol is taken with food,4 and possibly maternal genotype.5 This information is rarely reported in pregnancy studies. Factors that may modify effects of alcohol on the fetus: There is animal evidence that maternal micronutrient supplementation may protect the fetus against some of the adverse effects of gestational alcohol exposure.6 We need to consider recording supplement use and measures of maternal nutritional intake or status. In well resourced studies, fetal genotype could also be considered.6 Researchers with expertise in the field need to reach consensus and provide guidelines on the best way to assess fetal alcohol exposure, so that pregnancy researchers and clinicians with little experience of alcohol research do not need to create their own. Better data should provide better evidence on which to base advice to women who are (or may be) pregnant. Good studies may also provide explanations for the apparently variable link between maternal alcohol consumption and adverse sequelae in the offspring. Suggested core dataset for studies of maternal alcohol intake during gestation and outcome of offspring As a basis for discussion, we suggest the folllowing dataset: Baseline Weeks of gestation at pregnancy recognition, or expected date of delivery and date that pregnancy was recognised (to allow calculation) Height For specific periods of gestation (eg, from date of start of last menstrual period until pregnancy recognition; from pregnancy recognition to 12 weeks’ gestation; from 13 to 28 weeks; and from 28 weeks to term) Body weight (eg, at 12 and 28 weeks) Alcohol intake — we suggest: Average number of standard alcoholic drinks per week; Average number of days per week on which alcoholic drinks are taken; and Maximum number of drinks on one occasion. Whether alcohol is taken with or soon after food (never, sometimes, usually or always) Dietary intake of fruit and vegetables Use of nutritional supplements

Ruth Morley · Jane L Halliday · Susan M Donath

To the Editor: I would like to put forward a consumer’s perspective in response to the recent article by O’Leary and colleagues.1 I am puzzled that they concluded that the National Health and Medical Research Council (NHMRC) guideline is in step with policies of the United Kingdom and Canada. My research of Canadian policy suggests that it is in direct contrast to current NHMRC guidelines. Health Canada states very clearly, “Whether you are trying to get pregnant or are pregnant already, stop drinking alcohol”,2 and “No amount or type of alcohol during pregnancy is considered safe”.3,4 The potential harm to the birth mother that results from an abstinence-based message was also raised by O’Leary and colleagues. Elizabeth Russell, the birth mother of two sons affected by prenatal exposure to alcohol, offers an alternative viewpoint: By not discussing alcohol and pregnancy through misplaced compassion, we are hurting one person for the sake of another. Very few mothers would want that but that is exactly what is happening — children are being sacrificed to ensure that the anxiety level of a mother is kept within acceptable limits — neither mother nor child will benefit from this methodology.5 Many pregnant women give up eating shellfish and processed meats and drinking coffee but still continue to consume alcohol, thinking it is safe because they have not been told otherwise. I would like to pose the following questions. What is the potential harm of not having an abstinence message? Might this prevent women who are alcohol-dependent from seeking help to alter their drinking behaviour when pregnant because they are not aware of the risks? Should further research to “elucidate the true association between low to moderate alcohol consumption and fetal harm” really be a priority? What are the benefits to the unborn child of trying to ascertain a safe level of consumption of a teratogen and neurotoxin that is known to disrupt fetal development, particularly the fetal brain, throughout the three trimesters of pregnancy?6 While I acknowledge the importance of scientifically sound research on the risks of prenatal exposure to alcohol, I am concerned that this argument is diverting attention and dollars away from the urgent need for diagnosis and management of fetal alcohol spectrum disorder (FASD) in Australia. The reality is that children, adolescents and adults with FASD are seldom recognised, seldom treated effectively, and seldom connected to service dollars. Addressing this situation needs to be the priority.

Sue Miers

In reply: Morley and colleagues and Miers raise a number of interesting discussion points. As we reported in our policy review, the Canadian, United Kingdom and Australian guidelines have similar intent but differ in emphasis.1 Health Canada’s policy position is that, although abstinence is the prudent choice, fetal risk is relative to the amount of alcohol consumed and is minimal with low levels of maternal alcohol intake. Australian policy addresses the same issues, with less emphasis on abstinence and more on avoiding intoxication and ensuring low-level alcohol consumption. Since our review was published, UK guidelines have been reframed to emphasise abstinence, but their message has not changed — they now place more weight on avoiding alcohol during pregnancy.2 We strongly agree with Morley and colleagues that screening for alcohol should be routine in all pregnant women, and that standardised items should be included in a core dataset.3 If this were implemented, Australia would be in a unique position to make a valuable contribution to alcohol and pregnancy research. Miers comments that research into the impact of low to moderate alcohol exposure during pregnancy should not be a priority, because it may direct “attention and dollars away from the urgent need for diagnosis and management of fetal alcohol spectrum disorder”. Although we agree that specialised clinical services are important — and lacking — in Australia, it is short-sighted to suggest that there is no need for further research to establish the true risks from low to moderate alcohol consumption. Rates of alcohol consumption in Australia are high: about 80% of women report alcohol consumption in the 3 months before pregnancy, 14% report binge drinking, while 47% report that pregnancy was unplanned.4 Many fetuses may thus be exposed to alcohol before women are aware they are pregnant. Unfortunately, many women are unable to stop drinking and may expose their babies to high alcohol levels. Health professionals need to have a true estimate of risk to the fetus and know what additional factors (eg, genetics and nutrition) may alter risk, and women deserve to be well informed. The need for research is well articulated by Morley et al. Research evidence in humans does not clearly indicate a risk to the fetus from low levels of alcohol consumption, and this has led to inconsistent policy.5,6 As we point out, the potential for harm from an abstinence message should be considered when Australian alcohol guidelines are reframed. Whatever the policy, it needs to be widely disseminated, in a “digestible” format, to health professionals and the community. Research being conducted at the Telethon Institute for Child Health Research is evaluating educational materials for health professionals about alcohol and pregnancy.

Colleen M O’Leary · Louise M Heuzenroeder · Elizabeth J Elliott · Carol I Bower

To the Editor: Kawasaki disease (KD) is an acute vasculitis of unknown aetiology occurring mostly in infants and young children. KD is characterised by fever of more than 4 days’ duration; conjunctivitis; rash; cervical lymphadenopathy; erythema of the lips, oral mucosa, palms and soles; and oedema of the hands and feet.1 Coronary artery aneurysms develop in 15%–25% of untreated children,2 with attendant risk of ischaemic heart disease, myocardial infarction and sudden death.3,4 Treatment with intravenous immunoglobulin (IVIG) within the first 10 days reduces the incidence of aneurysm to less than 5%.4 A KD diagnosis is clinical, based on the recognition of a characteristic set of signs and symptoms.4 The 10%–45% of children who meet only some of the classical criteria are said to have “atypical” or “incomplete” KD. These children have a higher risk of coronary artery aneurysm than children with typical KD.4 Abdominal symptoms, including acute appendicitis and appendicular vasculitis, can occur before the development of classical features of KD.4,5 A 50% coronary artery aneurysm rate has been reported in children with KD and acute abdomen. It is still unclear whether this reflects a delay in diagnosis and treatment or is a marker of a more severe vasculitis involving the intestinal tract. A 3-year-old boy presented with a 2-week history of remittent, high-spiking fever (37.5–39.0° C; 2–3 spikes/day), right lower quadrant abdominal pain, and McBurney’s sign with rebound tenderness. Abdominal ultrasonography suggested a diagnosis of acute appendicitis with peritonitis. The postoperative diagnosis was appendicular vasculitis with peritoneal inflammation and serous secretion. Fever persisted despite treatment with intravenous cephalosporin. Several days later, the boy developed conjunctivitis, cracked lips, a raised erythrocyte sedimentation rate and C-reactive protein level, and thrombocytosis (715 × 109 platelets/L). KD was suspected, and an echocardiogram revealed two sacciform coronary artery aneurysms (diameters, 3.1 mm and 2.9 mm) in the proximal part of the common trunk. The child was given IVIG (2 g/kg) and oral acetylsalicylic acid (100 mg/kg per day in four divided doses). As the fever failed to resolve, the patient was given a second dose of IVIG,4 this time leading to a dramatic clinical improvement. Five days later, he developed oedema of the hands and periungual peeling of the fingers. His aspirin dose was reduced to 5 mg/kg/day. Follow-up echocardiograms at 3 months and 6 months demonstrated persistent coronary artery dilatation. Persistent fever with conjunctivitis and cracked lips should alert clinicians to the possibility of KD. At our patient’s age, acute appendicitis is rare, and other causes of abdominal pain must be excluded. In this case, the unusual postoperative course, with persistent fever even after antibiotic treatment, was another clue to establishing the correct diagnosis.

Maria Cristina Maggio · Andrea Liotta · Salvino M Vitaliti · Giovanni Corsello

To the Editor: Gerber’s article1 about the case Royal Women’s Hospital v Medical Practitioners Board of Victoria raises important issues but contains significant errors. The Medical Practice Act 1994 (Vic) states that the main purposes of the Act are “to protect the public by providing for . . . investigations into the professional conduct . . . of registered medical practitioners” — Section 1(a). Section 22(1) makes it clear that any person may notify the Board if they believe a person may have engaged in unprofessional conduct. Section 25(1) states that the Board must investigate notifications unless they meet certain criteria, which the Board did not believe were met in this case. Gerber is not correct in stating that the Board made no attempt to question the medical practitioners involved. In the absence of the patient’s consent, all but one of the doctors refused to provide any information in response to the complaint. Gerber’s statement that the subcommittee of the Board that conducted the preliminary investigation concluded that the complaint was “frivolous and vexatious” is wrong. The subcommittee recommended that the matter be closed. Later, the full Board chose not to accept this recommendation, as the investigation had been hampered by lack of information, including access to the original hospital records. While formal hearing panels have the power to subpoena documents or persons, this power does not extend to the Board’s preliminary investigations. The Board does have the power to apply to a magistrate for the issue of a search warrant. Gerber refers to the powers of the Board under Section 48 and Section 49 of the Act. These powers only come into play if the Board has determined that it will conduct a formal hearing. He is also incorrect when he states that the Board can compel medical practitioners to appear before the Board. This power is not available during preliminary investigations. The considerable delay in the matter being finalised was due to the legal appeals mounted by the Royal Women’s Hospital against the decision of the Magistrate to allow the Board access to the hospital records. Another issue raised by Gerber requires clarification: the Board does not currently have the power to conciliate disputes or conduct mediations. The Board did not ultimately dismiss the matter as frivolous and vexatious. When the subcommittee, having been provided with the records, reported to the Board that it did not find evidence of unprofessional conduct, the Board closed the investigation. I trust that this information will correct the public record on this important matter.

Joanna M Flynn

In reply: Flynn points to some minor technical differences in my historical recount of the handling, by the Medical Practitioners Board of Victoria, of the complaint against the medical specialists involved in a late-term abortion.1 None requires a reply, save for Flynn’s assertion that “the Board does not currently have the power to conciliate disputes or conduct mediations”. The Board does not require statutory power to approach a hospital in a conciliatory manner so as to explore whether an impasse, involving confidentiality, can be resolved without recourse to litigation. Was the Board’s only remedy to raid the hospital, trawling for evidence to decide whether there were grounds for the possible suspension or cancellation of registration of the doctors involved in the complaint? We both agree that the relevant legislation mandated the Board, on the material before it, to investigate the charge of serious professional misconduct. Where we disagree is that, having overruled its own subcommittee’s recommendation that the matter be closed, the Board failed (I maintain) in its statutory duty to promptly institute a formal hearing. Had the various specialists been subpoenaed, this would have cleared them of professional misconduct, thereby preventing the considerable and unnecessary stress to these witnesses over a period of 5 years.

Paul Gerber

To the Editor: Breen’s timely call for a reality check on medical professionalism noted major global changes that affect contemporary doctor–patient relationships: new technology, changing market forces, evidence-based treatment protocols, and resource-driven health services and policies.1 The call by our colleagues in the United States and United Kingdom to restore “trust that the public used to have in the profession” was urgent. Breen’s thesis posits that lost trust is due to an “altered balance” of ethical issues faced by doctors because of a generational shift from the ethical principle of “beneficence” to “autonomy” to “justice” and “distributive justice”. This view contrasts with Green and Bloch’s analysis of the mental health care system’s ethical concerns arising from an adherence to “efficiency-driven” policies that started in many countries during the 1980s.2 They suggest the system itself is flawed. Green and Bloch suggested that the legacy of efficiency-driven policies created two current moral compromises for our profession: first, a threat to the “ethic of agency”; second, the constraints those policies imposed on ethical principles precisely because they were not based on justice, instead being created to meet wider socioeconomic and political considerations. Their views point to the heart of the matter, beyond Breen’s suggested remedy to be found in “stronger leadership”, which may be necessary, but is not sufficient without an urgent update on personal medical ethics. At the individual doctor’s experience, Green and Bloch locate conflict arising from competing interest when doctors’ “principle of fidelity is juxtaposing their financial interests alongside patients’ needs”. In the US, a study found 28% of physicians receive direct payment for consulting, lectures or enrolling patients in trials, and 94% report “some type of relationship with the pharmaceutical industry”.3 To avoid the conundrum posed by the ethics of conflict of interests we face when confronted by these physician–industry relationships, or by efficiency-driven policies, risks perpetuating the very loss of trust that we need to restore. Breen’s analysis, an important step in the needed debate on medical professionalism, should account for not merely shifts in the ethical balance, but also the incremental erosion of trust. As it stands, he expressed our very Australian attitude “she’ll be right”. Our overseas colleagues, as well as locals, have suggested that “she won’t be right, mate” when it comes to managerialism eroding the ethical foundations of medicine.4

George Halasz

In reply: My recent article was submitted under the category of “For Debate”, so it is pleasing that Halasz has joined the debate. I am disappointed that he interprets my view as “she’ll be right”. My point is that revising or repackaging existing ethical codes will not, on its own, fix any of the perceived problems of “managerialism eroding the ethical foundations of medicine”. Working constructively, consistent with existing ethical codes, within our health care system, as is also suggested by Green and Bloch,1 is more likely to achieve better outcomes for our community. As I stated and as Green and Bloch imply, this will not always be a simple matter. I am in fierce agreement with Halasz over steps to reduce erosion of trust,2 but that was not the focus of my article.

Kerry J Breen

To the Editor: Clark et al have claimed to map the distribution of services for people with chronic heart failure (CHF) against the distribution of these people.1 An examination will show that they have mapped the distribution of people likely to have CHF, using age and Aboriginality as surrogate markers. The stated mapping of the services shows the services probably available to these people. A map is drawn to show us what the cartographer wants us to see.2 The authors note that high prevalence in remote regions has been shown on the maps, but they have not considered different mapping methods to provide a better representation of their results.3 This has led to an anomaly so that, when calculating numbers of people with CHF, the maps show remote areas with giant households containing between 24 and 300 people. CHF programs were located by a snowball sampling technique, which by its nature will miss isolated examples. Isolation is a feature of rural and remote practice, so this method is biased to finding metropolitan examples. In my own rural practice in Griffith, I found a local program that had been operating in 2004 and a distance program run by a health fund, neither of which had been identified by Clark et al. On the medical front, the authors asserted that access to a CHF management program is a mark of equity in health services. This is based on a metro-centric model looking at admission with CHF to a major teaching hospital, and showing that rates of readmission and death were reduced where a nurse and a pharmacist made a single visit to someone with CHF in their home after hospital discharge. The relevance of this activity to a rural person with a single community pharmacist who may make a home visit, a single point of contact with medical services in their general practitioner, and the possible availability of a community nurse to visit them regularly is unproven. Perhaps the city folk were copying the principles of the services we already had?

Elizabeth A Dodd

In reply: We thank Dodd for her commentary on our article.1 We concur with many of the highlighted issues relating to our suboptimal response to the burden and management of chronic heart failure (CHF) in rural and remote Australia. These include the lack of rigorous epidemiological data and lack of specialist services “beyond city limits”. Unfortunately, we have limited space to respond fully. However, we re-emphasise that, although our previous estimates2 complement that of the Canberra Study,3 neither can replace an Australia-wide study of CHF that samples metropolitan, regional, rural and Indigenous communities. We also stand by (within the context of the stated limitations) the accuracy of our mapping of the CHF programs and the location of general practice services in Australia for the study period. Our geo-mapping approach and data have been well validated by the National Centre for Social Applications of Geographic Information Systems (GISCA).4 For example, Jenks’ (natural breaks) classification is used for all sociodemographic thematic mapping at GISCA. Overall, we identified only four CHF programs which were located in regional areas. Other rural programs were excluded as they did not meet our prespecified definition of a CHF program. In summary, we acknowledge the need for better data to describe the burden of CHF throughout Australia. We also explicitly acknowledge the need for a less “metro-centric” approach to CHF service: perhaps by using remote monitoring techniques.5

Robyn A Clark · Andrea Driscoll · Justin Nottage · Skye McLennan · David M Coombe · Errol J Bamford · David Wilkinson · Simon Stewart

To the Editor: With the ski season in Australia drawing to a close for another year, it is a good time to reflect on the injury prevention benefits of wearing helmets when skiing or snowboarding. Skiing falls can be fatal. Two people have died from head injuries on Australian skifields in recent years: a skier died after colliding with a tree branch on an intermediate run at Mt Buller, Victoria, in 2003; and in 2006, a novice snowboarder died after falls sustained while snowboarding at Thredbo, New South Wales.1 Neither person was wearing a helmet. In Australia in 2002–03, 3.5% of skiing-related hospital admissions and 6.2% of snowboarding-related admissions were due to intracranial injuries.2 During the 2004 and 2005 ski seasons we collected data on the use of helmets in snowboarders presenting to the Mt Buller Medical Centre. Of 494 snowboarders, 17.6% had been wearing helmets, and none had sustained a head injury. Of the nine patients with head injuries, none had been wearing helmets. These figures are similar to those reported in overseas studies, which have shown that wearing a helmet can reduce the snow-sport head injury rate by up to 60%.3,4 The use of helmets for snow sports makes intuitive and biological sense, as it does for cyclists, but, unfortunately, Australia is yet to issue a snow-sport helmet performance standard, as it does for bicycle helmets. Helmet use should be strongly recommended for all snowboarders and skiers. In particular, helmets should be made compulsory for children, who are more susceptible to head injury4 and who are often present at ski resorts in large organised school groups that could readily be made to comply. At present in Australia, helmet use is not compulsory for children attending skiing or snowboarding lessons, as it is in North America. This is in spite of the fact that helmet use is compulsory in Australia for school skiing and snowboarding competition events. Some skiers and snowboarders are gradually getting the message about helmets, and a recent informal survey at Mt Buller (Buller Ski Lifts personnel, personal communication) estimated the rate of helmet use to be 20% among adults and 68% among children — but this still leaves over 30% of children vulnerable. Snow-sports helmets now come in many colours, shapes and sizes, and are increasingly acceptable to young people. A helmet is probably the cheapest individual item of clothing for a ski holiday. And it may save your life.

Graham M Slaney · Judith Finn · Angus Cook · Philip Weinstein

To the Editor: It was interesting to read of the trial conducted by Manley et al1 using yoghurt containing Lactobacillus rhamnosus to clear vancomycin-resistant enterococci. I would like to add an historical note. The use of yoghurt in restoring bowel flora was practised by Dr J H Kellogg (of Corn Flakes fame) around the end of the 19th century. Kellogg was the chief physician at the Battle Creek Sanitarium in Michigan and was an advocate of high colonic irrigation, for he believed the colon was a sewer of toxic materials that were the causal factor in many diseases. Following this procedure, the patient was given a pint of yoghurt — half to be taken orally, and the remainder given by enema.2,3 By these measures, Kellogg claimed to have cured many conditions, from cancer of the stomach to psychiatric problems.

H Reginald Magee

To the Editor: Security requirements for air travel have recently become very strict and include limitations on the carriage of medication and medical equipment. International flights to and from Australia are often lengthy, and patients needing regular medication can suffer serious complications without it. Diabetic patients are particularly vulnerable, as illustrated by this case. A 54-year-old engineer was returning to Australia after a 4-month placement in Norway. He had a history of type 2 diabetes, which had become insulin dependent 5 years previously. His diabetes was well controlled with 40 units of insulin twice daily, and he had no other major medical problems. At a Norwegian airport, his insulin, needles and syringes were detected on security screening of his cabin baggage. Security staff told him that he was not permitted to carry his insulin or equipment in the cabin without a letter from his doctor and a current valid prescription. The man’s protests were to no avail, and he boarded without his insulin. During the 25-hour journey to Sydney, he developed vomiting, polyuria, sweating and dyspnoea. Despite making cabin staff aware of the underlying problem, he was offered no assistance apart from a steady supply of airsickness bags. On arrival in Sydney, he was very ill and was taken by ambulance to St George Hospital, where he required admission to the intensive care unit. His pulse rate was 130 beats/min and respiratory rate 30 breaths/min. His urine was strongly positive for ketones and his blood glucose level was 51 mmol/L. Arterial blood gas analysis showed very severe metabolic acidosis with a pH of 6.9, Pco2 18 mmHg, and Hco3 4 mmol/L. His diabetic ketoacidosis was treated conventionally, with aggressive extracellular volume and electrolyte replacement, and insulin by infusion. His condition improved rapidly, and he was discharged home the next day. Australian doctors and their diabetic patients should be reminded that airline security requirements are now very strict in most countries, and that life-threatening ketoacidosis can readily develop over the course of a flight between Australia and the northern hemisphere. Insulin-dependent patients must continue to take their insulin during these flights and should not board without their supplies. In Australia, the Department of Transport and Regional Services stipulates that people with medical requirements may carry “prohibited items” such as hypodermic needles, but must also carry a doctor’s letter, a medical certificate, or a current National Diabetes Services Scheme card.1 Supplies should be clearly labelled, carried in a clear plastic bag and declared to security staff before being screened. The United Kingdom Department of Transport2 and the United States Transportation Security Administration3 have broadly similar requirements.

George Skowronski