Letters

Jonathan P Williamson,* Stan Braude† * Intensive Care and Respiratory Registrar, † Intensivist, Department of Respiratory and Critical Care, Manly District Hospital, Darcy Road, Manly, NSW 2095. JonowilliamsonATozemail.com.au In reply: We agree that our patient’s survival from the near-drowning incident was primarily attributable to the initial and subsequent supportive care. Clearly, the contribution of hypothermia to his survival cannot be quantified from one case. However, previous studies have shown that the use of controlled hypothermia in comatose survivors of out-of-hospital cardiac arrest improved survival with good outcome. 1,2 These studies did not focus on drowning victims — a study in this group would be extremely difficult — but had neurological recovery in patients with anoxic brain injury as principal outcome. In this sense, it can be argued that the aetiology of the brain anoxia is not in itself important. The Amsterdam World Congress on Drowning in 2002 recommended the use of controlled hypothermia in the comatose near-drowned patient. 3 This is a relatively simple procedure (albeit labour intensive) and is becoming the standard of care in many hospitals for out-of-hospital cardiac arrest. In these hospitals, its routine use in the near-drowned patient would not be difficult. Given the evidence so far accumulated in its favour, and the lack of adverse effects if undertaken correctly, it seems justified to seriously consider its use in the near-drowned patient. We therefore argue that the ventilation and supportive care of our patient aided his physiological recovery, while the neurological recovery was at least partly due to the hypothermia.

Jonathan P Williamson · Stan Braude

Andrew Firestone Psychiatrist, 30 Burke Road, East Malvern, VIC 3145. afireATtpg.com.au To the Editor: The drug company-funded article Diabetes, psychotic disorders and antipsychotic therapy: a consensus statement by Lambert and Chapman1 tests some ethical boundaries. Firstly, although categorised as a position statement, it does not express the position of any professional body. The cumbersome title was probably inspired by a recent landmark review of the same topic.2 But there, the American Diabetes Association (ADA), with others, recommended that prescribers bear in mind the strong association of olanzapine and clozapine with diabetes when choosing an antipsychotic drug. The MJA article does not dispute the ADA data, which rate a brief mention. But — and here is the second, more serious, ethical issue — the key ADA recommendation, that the varying diabetogenic potential of antipsychotic drugs should be a factor to consider when choosing an antipsychotic drug, is not mentioned at all. Instead, the article appears to be trying to use the weight of an impressive consultation process to influence prescribers to ignore the present state of knowledge. One cannot take issue with the Australian recommendations, which echo those of an important North American 2002 conference.3 But the funding source means that the omission of the ADA recommendations is an ethical problem: one must question why they have been omitted. To end on a positive note, the Australian recommendation for a prospective comparison trial of antipsychotic drugs for weight gain and diabetes is certainly a good one. It is high time that a university took this up —and published the results without drug company assistance.

Andrew Firestone

Timothy J R Lambert,* Leon H Chapman† * Director, OPEN (Office for Psychiatric Evaluation and Educational NewMedia), Department of Psychiatry, University of Melbourne, 7th Floor, Charles Connibere Building, Royal Melbourne Hospital, Melbourne, VIC 3050; † Diabetologist, International Diabetes Institute, Melbourne, VIC. lamberttATunimelb.edu.au In reply: Our article did not ignore the relative diabetic potential of various antipsychotic drugs. We wrote “clozapine and olanzapine are associated with greater weight gain and a higher occurrence of diabetes and dyslipidaemia than risperidone and quetiapine”, and so on.1 However, the article was not aimed to influence prescribing habits, but rather to alert health professionals to the relative metabolic risks both inherent in people with psychosis and arising from treatment with antipsychotic drugs in general, and the consequent need for constant assessment. The article tried to emphasise the need to balance risk versus benefit. We also tried to underline the need to effectively treat the illness (ie, the psychosis) with the most appropriate agent. Ignoring this would be akin to not using corticosteroids in severe asthma for fear of metabolic consequences. Finally, the article is a pointer to the full consensus statement, which is available on the Internet at www.psychiatry.unimelb.edu.au/open/diabetes_consensus/ and may be downloaded without charge.

Timothy J R Lambert · Leon H Chapman

Marc M Cohen Professor of Complementary Medicine, School of Health Sciences, RMIT University, PO Box 71, Bundoora, VIC 3083; and President, Australasian Integrative Medicine Association. marc.cohenATrmit.edu.au To the Editor: I read Constable’s article1 on age-related macular degeneration with interest, but was surprised at its somewhat guarded advice on nutritional supplementation and the fact that it gave only passing reference to uncontrolled studies of the carotenoids lutein and zeaxanthin and failed to mention a number of controlled studies that have recently shed light on the potential for these nutrients to influence the progression of age-related macular degeneration (ARMD). Lutein and its isomer, zeaxanthin, are deposited in the macula, where they make up the macular pigments and act as a blue-light filter to protect the underlying tissues from phototoxic damage, as well as providing antioxidant activity. Lutein was not available in supplement form at the time of conducting the Age-Related Eye Disease Study (AREDS).2 However, the more recent Lutein Antioxidant Supplementation Trial (LAST), a double-masked, placebo-controlled, randomised trial of lutein and antioxidant supplementation in people with ARMD, demonstrated that taking 10 mg lutein daily, with or without additional nutrients, improved visual function.3 Interestingly, lutein supplementation was also found to improve vision in a small, randomised, placebo-controlled study of people with cataracts. It was suggested that these improvements were due to improved macular function and increased macular pigment density.4 Furthermore, a recent study showed that lutein supplementation results in increased macular pigment density in both normal and ARMD patients.5 Lutein occurs naturally in foods such as eggs, spinach, romaine (cos) lettuce, broccoli, zucchini, corn, peas and Brussels sprouts. Although lutein is readily absorbed from foods and dietary supplements, surveys indicate that average lutein intake may be below levels that are associated with disease prevention.6 Toxicology studies have established that lutein is generally safe, with potential for use as a supplement in foods and beverages.6 While advice on smoking cessation and increasing fruit and vegetable intake is useful for a wide range of conditions, including ARMD, Constable’s statement that “antioxidant supplements should be recommended if a fresh diet is impractical and if retinal signs of progression are present”1 appears overly cautious. In light of recent findings on the potential benefits of antioxidants such as lutein, and the low cost and minimal risks associated with supplementation compared with the potentially devastating consequences of blindness from ARMD, it may be prudent to make more general recommendations on nutritional supplements, rather than waiting until signs of retinal progression are evident.

Marc M Cohen

Ian J Constable Director, Lions Eye Institute, Centre for Ophthalmology and Visual Science, University of Western Australia, 2 Verdun Street, Nedlands, WA 6009. ijcATcyllene.uwa.edu.au In reply: While the published literature on dietary supplementation with the antioxidants lutein and zeaxanthin is highly encouraging, it does not yet pass the requisite standards for public endorsement provided by large-scale, independent, evidence-based medical trials. The controlled (“LAST”) trial of lutein1 cited by Cohen consisted of just 91 patients divided into three subgroups including the placebo group, who were followed for only 1 year. The measurement of visual improvement on a Snellen chart would not be accepted as “gold standard” evidence by major granting agencies and regulatory affairs bodies, who demand the higher discrimination of a logarithmic visual acuity chart. Moreover, the data were not derived from multicentre trials and independently assessed. It is instructive to compare the methodology of the LAST trial with that of the ARED Study,2 which involved 11 centres, 3640 patients and an average follow-up of 6.3 years. For these reasons, although I mentioned lutein in an encouraging fashion, I did not endorse it to the same extent as vitamin C, vitamin E and zinc supplements. The other reasons for giving limited recommendation of antioxidant supplements at this stage relate to the fact that it is not yet clear to what extent supplements would be beneficial over and above a diet targeted to provide these antioxidants in plentiful supply. It may yet be shown that a nutritious diet — with emphasis on brightly coloured and leafy vegetables, fresh fruits, nuts and fish, coupled with reduced processed vegetable oils (except olive oil) — can, alone, provide substantial protection. While the supplements are generally deemed to be safe, they are not without occasional serious side-effects and have not been followed long term. Richer, one of the authors of the lutein study, 1 acknowledges commercial relationships with the supplement suppliers, and states that the study requires greater numbers and long-term follow-up to be confirmed. Cohen cited a second article3 that refers to a 2-year study of cataract, in which a mere 17 patients were allocated to three subgroups including the placebo group. It is not usual practice to quote conclusions from such a small, and therefore potentially unreliable, trial design. Cohen is right to point to lutein and possibly zeaxanthin supplements as an encouraging possibility for preventing blindness from macular degeneration, and I hope the evident enthusiasm and rapid marketing of lutein proves justified in the long run by forthcoming major trials.

Ian J Constable

Kenneth Wong Surgical Registrar, Gosford Hospital, Holden Street, Gosford, NSW 2250. kennethwoATyahoo.com To the Editor: I am writing to offer a registrar’s perspective on the constructive comments by Lack and Cartmill on registrar–intern interactions.1 The same comments would be equally applicable to consultant–registrar interactions. The current strict hierarchical, “militaristic” structure of the hospital system, with a “top down” approach to performance assessment (which, in turn, influences career prospects), is conducive to neglect of junior colleagues, as they are often the most expendable cogs in the wheel. In my experience, the two key selection criteria for hospital appointments and career advancement — namely, impressing senior colleagues and passing postgraduate examinations — bear little correlation to the ability to supervise or instruct junior staff. Training in human resource management is not part of any undergraduate or postgraduate medical curriculum. Yet, negative junior–senior staff interactions can potentially compromise patient safety, as junior colleagues, acting only as acolytes in the professor’s entourage, are not empowered to actively contribute to patient care. So, what are the solutions? A formal circular feedback system that has “teeth” would be a start. Incorporating regular evaluations of senior staff by junior staff as part of the hospital’s quality assurance program and as a condition of continued employment may be effective in identifying those who are unsuitable for supervising junior colleagues. Simple educational measures may alleviate some of the difficulties experienced by interns as highlighted by Lack and Cartmill.1 For example, the difficulties of contacting surgical registrars “hidden” in the operating theatre are cited as a cause of intern distress. But operating theatres are not located on a distant planet beyond feasible means of contact. Most operating theatres are equipped with telephones and are located centrally within the hospital. Educating the intern to telephone through to the operating theatre or possibly even venture inside should enable resumption of contact with even the most evasive surgical registrar. Finally, published guidelines detailing acceptable behaviours and responsibilities towards junior colleagues may benefit senior staff who may not have had appropriate senior role models themselves. Having a junior colleague attached to one’s team is not an assumed right that comes with consultant or registrar status. It is a distinct privilege that carries distinct obligations. Failure to respect these obligations should precipitate removal of this privilege.

Kenneth Wong

Jeanette I Nordon Retired, 42 Milroy Avenue, Kensington, NSW 2033. To the Editor: I spent a lot of my working life treating patients in an area with an ageing population. I am now elderly and I hear many of my peers complaining bitterly about their doctors. Even if they have a serious illness they are often told, “What can you expect at your age?”. This unhelpful attitude does nothing to alleviate the patients’ concerns. Often, after some questioning, it may be apparent that these patients have some conditions that are eminently treatable and, without this questioning, may be missed. With the advances in medicine and surgery, the proportion of elderly people in our population is increasing. “He or she has had a good innings” was a comment that I heard doctors make in the past. But, doctors change their tune as they age, and these platitudes are much less frequently used! So, in spite of the fact that we are living much longer, with new joints, new transplanted organs, new patent coronary arteries, better means of treating neoplasms, and more exotic investigations to make more exact diagnoses, we must still address our patients in a civil manner, and remember that often the older methods of diagnosis are still important. And don’t let us forget that doctors also get old.

Jeanette I Nordon

Bradley T Martin,* Pamela Palasanthiran,† Iain B Gosbell,‡ Thelma Barbagiannakos,§ Emma J Best,¶ Richard L Henry** * Respiratory Fellow (currently, Department of Respiratory Medicine, Children’s Hospital at Westmead, Locked Bag 4001, Westmead, NSW 2145), † Infectious Diseases Specialist, ¶ Infectious Diseases Fellow, Sydney Children’s Hospital, Sydney, NSW; ‡ Director, § Hospital Scientist, SWAPS Staphylococcal Reference Facility, South Western Area Pathology Service, Sydney, NSW; ** Head of School of Women’s and Children’s Health and Senior Associate Dean, Faculty of Medicine, University of New South Wales, Sydney, NSW. bradleymATchw.edu.au To the Editor: We report a case of severe pneumonia in a previously healthy 3-year-old girl of European background. Non-multiresistant methicillin-resistant Staphylococcus aureus (MRSA) was isolated from her sputum, and she was treated with intravenous vancomycin, followed by oral rifampicin and fusidic acid. After antibiotic therapy ceased, symptoms recrudesced, and computed tomography of the chest showed bronchiectasis. Sputum again grew MRSA (now also resistant to rifampicin, fusidic acid and erythromycin), as well as Pseudomonas aeruginosa. She was treated with intravenous vancomycin, ceftazidime and tobramycin. As the MRSA persisted, vancomycin was replaced with intravenous linezolid, followed by a course of oral linezolid and trimethoprim–sulfamethoxazole. More than a year after her original illness, she continues to have a productive cough and requires nebulised tobramycin to prevent exacerbations. The patient’s only risk factor was contact with her mother, who had an MRSA buttock abscess incised several months earlier. Phage typing and pulsed-field gel electrophoresis revealed that the mother’s and daughter’s isolates were identical (Box). They were found to belong to the Queensland strain of community-acquired MRSA (CA-MRSA) and to possess Panton–Valentine leukocidin, a virulence factor which is highly associated with necrotising pneumonitis and invasive primary skin infection. 1 CA-MRSA is a growing problem in Australia, and severe pneumonia due to this organism has recently been reported in adults. 2,3 The isolation of CA-MRSA before prolonged courses of antibiotics, its characterisation as a virulent strain, the response to appropriate treatment and the recrudescence of symptoms on cessation of therapy demonstrate that it was the causative organism in this case. The case is also noteworthy for the documented intrafamilial spread and the fact that the patient did not belong to the Pacific Islander community, in which CA-MRSA infections in south-western Sydney most commonly occur.4 Most S. aureus strains in the community are sensitive to flucloxacillin and dicloxacillin, so these remain the empirical treatments of choice, unless CA-MRSA is isolated or strongly suspected. CA-MRSA strains are non-multiresistant, and oral antibiotic options include clindamycin, trimethoprim–sulfamethoxazole or rifampicin and fusidic acid. 5 Intravenous vancomycin is commonly used in severe infections, but recent evidence suggests that linezolid, an oxazolidinone antibiotic with efficacy against multiply resistant bacteria, including MRSA, penicillin-resistant Streptococcus pneumoniae and vancomycin-resistant enterococci, may be more effective.6 Issues of cost, toxicity, local availability, potential development of resistance and sensitivity of isolates in vitro need to be considered before determining appropriate treatment. In conclusion, clinicians should be aware of the growing problem of CA-MRSA and the potentially devastating consequences of infection with this organism, even in otherwise healthy children. Pulsed-field gel electrophoresis (PFGE) of Staphylococcus aureus strains 1. Low-range PFGE marker. 2. Control S. aureus strain (NCTC 8325). 3. S. aureus isolate from patient. 4. S. aureus isolate from mother. 5. Queensland strain of community-acquired methicillin-resistant S. aureus (CA-MRSA).

Bradley T Martin · Pamela Palasanthiran · Iain B Gosbell · Thelma Barbagiannakos · Emma J Best · Richard L Henry

John R Gowardman,* Catherine Kelaher,† Joy Whiting,‡ Peter J Collignon§ * Intensive Care Physician (currently Launceston General Hospital, Launceston, TAS 7250), † Medical Student, ‡ Data Manager, § Director of Infectious Diseases and Microbiology, The Canberra Hospital, Canberra, ACT, and Professor, Canberra Clinical School, Australian National University, ACT, and University of Sydney, NSW. john.gowardmanATdhhs.tas.gov.au To the Editor: Bloodstream infections are frequent in healthcare settings and cause significant mortality and morbidity. 1,2 Most of these infections are caused by intravenous catheters, particularly central venous catheters (CVCs). Over 250 000 catheter-related bloodstream infections occur annually in the United States, 1 and over 3000 in Australia.2 Many CVCs are retained when no longer essential. For example, a recent one-day audit in a US teaching hospital found that 15% of CVCs (11/74) were “unjustified” most of these had been inserted in the intensive care unit but retained unecessarily after discharge from the unit.3 The risk of bloodstream infection is much higher with CVCs than with peripheral venous catheters (4.0 versus 0.2 per 1000 line-days).2,4 Such simple facts are often overlooked or inadequately emphasised in preventive programs, and CVCs may be retained for convenience. Our intensive care unit maintained an informal clinical practice of routinely removing CVCs when patients were discharged from the unit. However, an audit found that many CVCs were retained, often inappropriately, thus exposing patients to needless increased risk.5 A formal intervention policy aimed at improving CVC removal was implemented. This included a month of staff education, culminating in introduction of a formal written policy in March 2003. CVCs were to be removed when no longer clinically required or at discharge from the intensive care unit, unless the patient met predetermined retention criteria (ie, administration of vasoactive or venotoxic drugs [eg, dopamine or vancomycin] or parenteral nutrition solutions; poor peripheral venous access [after two attempts] with ongoing need for intravenous therapy; or transfer to another intensive care or coronary care unit). We undertook a prospective observational study of all patients with CVCs in the intensive care unit of our hospital in the period March to August 2003. Patients were grouped according to whether the CVC was removed per policy before or at discharge from the intensive care unit; whether it was retained per policy at discharge from the unit; or whether it was retained in breach of policy. All patients were followed up for 7 days after CVC removal. Those who died within this time were excluded from the analysis. We studied a total of 305 CVCs in 272 patients (Box). We observed: high compliance with the written policy (91%), significantly lower CVC in-situ times when policy was followed (5.1 v 8.1 days), low CVC reinsertion rates (7%), no difference in incidence of bloodstream infections between the groups. This study demonstrates that a formal policy directed at early CVC removal is effective in lowering CVC in-situ times without incurring clinical cost to the patients (eg, excessive CVC reinsertion rates). Policy breaches were infrequent (8% of all CVCs), but, when they occurred, CVC retention appeared unnecessary, and CVC in-situ times were significantly prolonged. The risk of sepsis with CVCs may be substantially lowered by policy-driven removal of CVCs, without compromising patient care. Comparison of patient characteristics and CVC outcomes when removal policy was followed versus when it was breached Policy followed Policy breached P (policy followed v breached) CVC removed CVC retained* Total CVC retained Patient characteristics Number of patients 176 71 247 25 Age (years) (SD) 60.2 (17.9) 64.9 (15.7) 61.7 (17.5) 69.0 (15.3) 0.02 ICU length of stay (days) (SD) 4.7 (8.2) 3.3 (5.2) 4.3 (7.6) 2.1 (2.0) 0.06 APACHE II score (SD) 14.7 (6.9) 14.8 (7.0) 14.6 (17.5) 14.2 (5.1) 0.31 Ventilation time (h) (SD) 51 (89) 46 (123) 51 (103) 31 (55) 0.19 CVC outcomes No. of CVCs (% of all CVCs) 202 (66%) 77 (25%) 279 (91%) 26 (8%) nt In-situ time Hours (SD) 97 (115) 202 (186) 124 (148) 197 (136) 0.009 Days 4.0 8.4 5.1 8.1 Tips cultured (% of CVCs) 136 (67%) 51 (66%) 187 (67%) 19 (73%) nt Tips infected (% of CVCs) 20 (9%) 11 (14%) 31 (11%) 4 (15%) 0.51 Catheter-related bloodstream infections Total no. 2 (1%) 0 2 (1%) 1 (4%) nt Per 1000 CVC days 2.5 0 1.4 6.0 0.33 CVC reinsertions (% of CVCs) 15 (7%) 4 (5%) 19 (7%) 0 0.38 Mean no. of ports idle (per day) na 1.5 na 1.6 nt Peripheral catheters Total no. 260 36 296 50 nt Mean no. per patient 1.5 0.5 1.2 0.5 nt Mean in-situ time (h) 63 66 64 81 nt CVC = central venous catheter. nt = not tested. na = not applicable. * Reasons for appropriate CVC retention were drug administration (32%), poor peripheral access (34%), transfer to another high dependency unit (25%) and total parenteral nutrition (9%).

John R Gowardman · Catherine Kelaher · Joy Whiting · Peter J Collignon

Vanessa M McDonald,* Peter G Gibson† * Clinical Nurse Consultant, † Professor, Department of Respiratory and Sleep Medicine, John Hunter Hospital, Locked Bag 1, Hunter Region Mail Centre, Newcastle, NSW 2310. Peter. GibsonAThunter.health.nsw.gov.au To the Editor: The delivery of asthma drugs via inhalation offers the best balance between efficacy and safety. However, poor inhalation technique limits the efficacy of this approach. In recent years, there has been a progressive increase in the types of inhalation devices used in asthma management. We questioned whether this would lead to “inhaler-device polypharmacy”, a situation in which an individual used multiple types of inhalation device to deliver his or her asthma medications. We conducted a novel investigation of this issue in 2004. We examined the computerised records of adults with asthma who had been enrolled in a standardised, evidence-based asthma management and education program1 between 2000 and 2004. We noted the number and type of inhaler devices used, as well as competence with each device (a trained asthma educator had observed and scored inhalation technique). We defined “inhaler-device polypharmacy” as the use of two or more different types of inhalation device. The devices assessed in the education program included a pressurised metered-dose inhaler (with and without a spacer), turbuhaler, accuhaler, aeroliser, autohaler, and handihaler. Nebuliser use was not included in the evaluation. We assessed a total of 511 patients: 278 (107 male; mean age, 37 years) between 1 January 2000 and 1 January 2002 (Period 1), and 233 patients (55 male; mean age, 40 years) between 2 January 2002 and 1 January 2004 (Period 2). Period 1 patients were distinct from Period 2 patients in that the latter began their treatment after the release of combination asthma therapy in a single inhaler, when polypharmacy may have been expected to diminish. Inhaler-device polypharmacy was present in 203 (73%; 95% CI, 68%–78%) patients during Period 1 and 164 (70%; 64%–75%) in Period 2 (P = 0.3) (Box). In Period 1, inhalation technique was inadequate with at least one device in 58 (29%) patients using inhaler polypharmacy and in 19 (25%) using only one device (Box). In Period 2, inhalation technique was inadequate with at least one device in 85 (52%) patients using inhaler polypharmacy and in 25 (36%) using only one device. In both Period 1 and Period 2 patients, inadequate inhaler technique with at least one device increased with the number of devices used (P values 0.02 and 0.05, respectively) (Box). We conclude that inhaler-device polypharmacy is a common problem among adults with asthma. Inadequate inhalation-device technique is also common, especially among patients using three or more delivery devices. Inhaler-device polypharmacy could lead to poor asthma control through inadequate delivery of medication. Patients with poor asthma control should be evaluated for their asthma management skills, including competency in using inhaler devices. These skills should be optimised before a new drug and/or device is added to their treatment regimen. We see no justification for the use of more than two inhalation delivery devices in asthma management. Number of asthma patients using single or multiple inhalation devices and proportion of those patients with inadequate technique, over two time periods One device Two devices Three or more devices Period 1* (n = 278) 75 (27%) 150 (54%) 53 (19%) Period 2† (n = 233) 69 (30%) 129 (55%) 35 (15%) Patients with inadequate inhalation-device technique Period 1* 19/75 (25%) 35/150 (23%) 23/53 (43%) Period 2† 25/69 (36%) 64/129 (50%) 21/35 (60%) * 1 Jan 2000–1 Jan 2002. † 2 Jan 2002–1 Jan 2004.

Vanessa M McDonald · Peter G Gibson

Raoul A Walsh,* Judith Lumley† * Senior Research Academic, Centre for Health Research and Psycho-oncology, The Cancer Council NSW/University of Newcastle, Locked Bag 10, Wallsend, NSW 2287. † Director, Mother and Child Health Research, La Trobe University, Melbourne, VIC. Raoul. WalshATnewcastle.edu.au To the Editor: Problems with interpreting odds ratios reported in meta-analyses of smoking-cessation interventions have recently been highlighted.1 Ford and Dobson2 have erred in a different way when applying the findings of the Cochrane review on smoking cessation interventions in pregnancy3 to calculate the public health benefits of delivering such interventions to all pregnant women in Australia. When all methodologically acceptable randomised controlled trials were considered, the Cochrane review did find the prevalence of smoking at end-of-pregnancy was 6% lower in intervention than control groups.3 However, this does not equate to a 6% reduction in the population prevalence of smoking among pregnant women, as Ford and Dobson assume. A mean between-group difference reported in a meta-analysis is not equivalent to a difference of exactly the same magnitude in a population prevalence of a risk factor unless 100% of the population exhibit that risk factor. Clearly, as Ford and Dobson have reported, this is not the case with smoking in pregnancy, where they correctly note that about 20% of pregnant women report current smoking at their first antenatal visit.2 Therefore, smoking-cessation interventions would not reduce the prevalence of smoking by 6% from 20% to 14%. The expected reduction can be calculated as follows: expected reduction in prevalence of smoking in pregnant women = current smoking prevalence in pregnant women (20%) × between-group difference in smoking prevalence (0.06) = 1.2%. This calculation rests on two assumptions: namely, that all pregnant women in Australia currently receive usual smoking-cessation care equivalent to that of control group conditions in the Cochrane review3 and that, in the short term, antenatal care can be transformed to the point where all future pregnant women receive smoking-cessation care equivalent to that received by those in intervention groups in the Cochrane review. Therefore, it is obvious that the expected smoking prevalence of 18.8% (20% minus 1.2%) is considerably higher than the 14% calculated by Ford and Dobson.2 Unfortunately, this means the rates of reduced infant deaths, hospital separations and costs to the healthcare system estimated by Ford and Dobson have also been overstated. In summary, the gains to be expected by clinical interventions with pregnant smokers are modest. Furthermore, past evaluations of media campaigns directed specifically at pregnant women have not shown significant positive effects.4 This reinforces the importance of tobacco-control strategies which target the whole population in addition to those which target pregnant women.5

Raoul A Walsh · Judith Lumley

Jessica H Ford,* Annette J Dobson† * Research Assistant, † Professor of Biostatistics, School of Population Health, University of Queensland, Herston Road, Herston, Brisbane, QLD 4006. J. FordATsph.uq.edu.au In reply: We thank Walsh and Lumley for correcting the error in our letter. The 6% reduction in smoking during pregnancy referred to an absolute difference in prevalence of continued smoking in late pregnancy among women who smoked early in pregnancy, from 91% in the control groups to 85% in the treatment groups.1 We incorrectly hypothesised a reduction from 20% to 14% in prevalence of any smoking during pregnancy. In fact, there was a decline in smoking during pregnancy, from 22% in 1994 to 17% in 2001 in New South Wales.2 These figures illustrate well the final point that Walsh and Lumley make: whole-of-population approaches to smoking reduction can yield much greater benefits (a 5% reduction in 7 years in NSW) than high-risk approaches (from our data, the 1.2% calculated by Walsh and Lumley). Our estimates of the adverse effects of smoking in pregnancy are, at present, correct. Although we unfortunately overstated the possible reductions resulting from interventions targeted only at pregnant women, such reductions are plausible for whole-of-population approaches.3

Jessica H Ford · Annette J Dobson

Mark Mackay,* Peter Millard† * PhD student, Department of Psychology, Level 4, Hughes Building, University of Adelaide, Adelaide, SA 5005, and Principal Project Officer, SA Department of Health; † Emeritus Professor of Geriatric Medicine, St George’s Hospital Medical School, and Visiting Professor — Health and Social Care Modelling Group, University of Westminster, London. mmbmATiprimus.com.au To the Editor: Gray, Yeo and Duckett used the wrong basis of measure for their analysis of bed trends.1 Bed use per thousand of the population masks the trends in total bed-days or separations and does not address the issue of supply. These issues have important ramifications for policy decision-making. Using the same sources of data,2,3 we compared bed-related statistics and population changes for the periods 1993–94 and 2001–02. What should be of most interest to planners is that the number of multi-day bed-days only declined marginally (from 14 434 to 14 231; −1.4%), despite the significant increase (from 1698 to 3343; + 96.8%) in same-day activity. Although multi-day separations and bed-days did decline (separations, − 4.2%; bed-days, − 14.9%) for those aged 65–74 years, for those aged 75 years or over bed-days and separations increased significantly (separations, + 41.6%; bed-days, +27.7%). Furthermore, same-day activity increased significantly for those aged 65 or more years. Furthermore, the authors failed to highlight the implications of changes in the relative age mix of activity. For those aged 75 years or more, the increase in proportion of separations (+ 5.8 percentage points) and bed-days (+ 1.8 percentage points) was greater than the increase in this proportion of the population (+ 1.1 percentage points). For the 65–74-years age group, the proportion of same-day hospital activity increased (+ 1.3 percentage points), unlike the reduction in that proportion of the population (− 0.2 percentage points). Moreover, the question of whether an ageing population has resulted in the need for more beds can not be answered without considering the supply of beds. From our experience, the growth in same-day activity has been achieved, at least in part, by substituting same-day beds for inpatient beds. The need for increased same-day beds has been considerable. Statistics relating to same-day beds do not appear to be reported for Australia as a whole. However, the increasing implied bed occupancy (including same-day) shown in the Box supports this conclusion. We surmise that the reduction in supply of multi-day beds combined with a marginally altered demand for multi-day beds has led to increasing numbers of bed crises. Given that relative growth in same-day activity can be attributed to people aged 65 years or over, and that the number of multi-day bed-days for those aged 75 years or more has increased, it appears that the ageing of the population, combined with the manner in which the substitution of beds has occurred, has contributed to increasing bed crises. Changes in implied bed occupancy Financial year Change from 1998–99 to 2001–02 1998–99 1999–00 2000–01 2001–02 Total bed-day utilisation (000s) 22 323 22 597 22 467 23 218 + 4.0% Total available bed-days (000s) 28 868 28 540 28 675 28 787 − 0.3% Implied occupancy 77% 79% 78% 81% + 4.3%

Mark Mackay · Peter Millard

Len C Gray,* Stephen J Duckett† * Professor in Geriatric Medicine, University of Queensland, Princess Alexandra Hospital, Ipswich Road, Woolloongabba, QLD 4102; † Professor of Health Policy, Latrobe University, Melbourne, VIC lgrayATsoms.uq.edu.au In reply: Mackay and Millard have raised some important issues in relation to our analysis. Our article was developed to encourage wider reflection and their response is thus welcomed. The primary criticism levelled by Mackay and Millard was that we underplayed the importance of supply of beds in our interpretation of the trends. We agree that bed supply is an important driver of utilisation patterns. We acknowledged this, in part, in the discussion as a possible explanation for rising separation and declining bed-utilisation rates in the older patient population. We are also sympathetic to the hypothesis that there may be a process of substitution of same-day separations for multi-day separations. However, data relating to bed availability are not readily available, and thus could not be included in our study. Our article was designed to highlight different trends between age groups, which have not previously been reported. Now that these trends have been identified, further research and analysis is required to fully explain them, with a view to supporting an intelligent strategy to prepare for future population ageing.

Len C Gray · Stephen J Duckett

Paddy A Dewan Head of Paediatric Surgery, Sunshine Hospital, PO Box 152, Parkville, VIC 3052. Paddy.dewanATwh.org.au To the Editor: Three recent articles in the MJA about complaints by patients attending hospital, 1 attitudes of hospital staff toward incident reporting2 and whistleblowing3 show that complaints are common, that cultural change is needed to allow staff to understand that a complaint from a patient or staff member should be viewed as an opportunity for change, and that quality assurance sometimes relies on whistleblowers but does not always appreciate their efforts. Faunce and Bolsin report on three whistleblower incidents,3 but fail to mention one at the Royal Children’s Hospital, Melbourne, in which I was involved. Attempts to highlight deficiencies in delivery of paediatric surgical care and concerns about the response to adverse events were managed with threatening tactics (of dismissal) by the division of surgery. This was followed by a hospital board investigation that, in my opinion, had neither the skill mix nor the terms of reference to adequately investigate the quality of care or the bullying. The subsequent investigation by the Department of Human Services involved narrowly focused terms of reference and failed to consider outcomes in some circumstances, thereby facilitating the “shooting of the messenger”. Current legislation does not effectively allow for dealing with threatening behaviour in the workplace, particularly when the refusal to look at complaints and adverse events in a productive manner goes well beyond the confines of the hospital involved. The Community Advisory Committee parliamentary enquiry was held in camera, with evidence being kept from the public. Worksafe legislation on bullying does not deal well with the complex situations that arise in the healthcare industry.4 The Colleges and other professional bodies, such as the AMA and the Medical Boards, need to take a proactive rather than a reactive role if further whistleblower incidents are to be avoided. I concur with the statement of Faunce and Bolsin that: “Even after substantiation of their allegations, the whistleblowers . . . received little respect and support from their institutions or professions”.3 From personal experience, I am very aware of the lack of support that stems from an ethos wary of public criticism, and the reactive bullying to which the whistleblower is often subjected. Until the culture of healthcare focuses on quality and caring, whistleblower sagas will continue to occur.

Paddy A Dewan

Luke R Bereznicki,* Shane L Jackson,† Gregory M Peterson‡ * PhD Candidate, † Research Fellow, ‡ Professor of Pharmacy, Unit for Medication Outcomes Research and Education, University of Tasmania, Private Bag 26, Hobart, Tasmania 7001. lberezniATutas.edu.au To the Editor: If a new drug such as ximelagatran is to be considered as a replacement for warfarin in preventing the thromboembolic complications associated with atrial fibrillation (AF), drug cost becomes an important issue. Brighton’s recent article in the Journal, 1 while comprehensive, does not discuss the cost-effectiveness of ximelagatran treatment. Ximelagatran was approved in several European countries for the prevention of venous thromboembolism associated with orthopaedic surgery. The cost of the drug for this indication (24 mg given twice daily) is 4.5 euros (A$7.7) per day.2 This represents the best available estimate of the cost of using ximelagatran for AF, although the dose is higher in AF (36 mg twice daily), and there are limitations in applying the drug cost in one country to another country. Routine monitoring of the antithrombotic effect of ximelagatran (ie, international normalised ratio [INR] testing) was not conducted in clinical trials. While this is potentially advantageous, frequent testing of alanine aminotransferase (ALT) levels is recommended at baseline and monthly for the first 6 months of therapy, every second month for the remainder of the first year, and every third month thereafter, for safety reasons.3 This is because some patients taking ximelagatran will develop elevated ALT levels (about 6.1% of patients to greater than threefold normal, and 3.4% to greater than fivefold normal) when ximelagatran therapy is commenced.3 The costs of INR and ALT tests are very similar (about $25 and $22, respectively). Although INR monitoring may be more frequent with warfarin than ALT testing with ximelagatran, the cost difference associated with therapeutic monitoring would remain far less than the likely cost of ximelagatran. We estimate the cost associated with treating 1000 patients with AF with ximelagatran instead of warfarin for 1 year, taking into account drug costs, monitoring costs and the slight difference in major bleeding rates, to be about $2.4 million (Box). A United States Food and Drug Administration advisory committee has recently raised concerns about the safety of ximelagatran (after episodes of severe liver damage), and has recommended that it not be granted any indication for use without further safety data. In particular, ALT monitoring did not prevent 3 deaths attributable to ximelagatran-associated hepatocellular necrosis.3 In light of the recent withdrawal of rofecoxib (Vioxx; Merck Sharp & Dohme), warfarin carries the intangible benefits of a long and proven track record. It certainly requires careful management and ongoing monitoring, but healthcare resources might be better spent on improving the use of warfarin rather than paying substantially increased costs for a drug with similar efficacy and an uncertain safety profile. Estimated costs of treating 1000 patients with atrial fibrillation (AF) with ximelagatran or warfarin for the first year of therapy. Ximelagatran* Warfarin† Total cost $2 803 821.00 $106 800.00 Cost per patient $2 803.82 $106.80 Monitoring Test (frequency/year) ALT (10)‡ INR (20)§ Total cost $217 000.00 $507 000.00 Cost per patient $217.00 $507.00 Major bleeding¶ Annual incidence** 1.6% 2.2% No. of expected events 16 22 Total cost $38 730.00 $53 253.00 Ischaemic stroke†† Annual incidence‡‡ 1.6% 1.6% No. of expected events 16 16 Total cost $101 936.00 $101 936.00 Overall cost Total $3 161 487.00 $768 989.00 Per patient $3 161.49 $768.99 Cost difference compared with warfarin Total $2 392 498.00 — Per patient $2 392.50 — ALT = Alanine aminotransferase. INR = International normalised ratio. * Cost of giving ximelagatran (24 mg twice-daily) to prevent venous thromboembolism post-surgery (German data; the dose for prevention of thromboembolism in AF is 36 mg twice-daily).3† Cost of warfarin taken from the Australian Pharmaceutical Benefits Scheme, December 2004. ‡ Monitoring cost derived from the cost of conducting ALT testing (Medicare Benefits Schedule, December 2004) according to the manufacturer’s directions (tests at baseline, monthly for the first 6 months, 2-monthly for remainder of the first year). § Cost derived from Medicare Benefits Schedule (December 2004) based on a frequency of 20 tests per annum. ¶ The cost of a hospital admission caused by a major bleed was $2420.60 in Australia for the years 2002–2003 (estimate based on 2002–2003 public hospital data).4 Intracranial haemorrhage may be associated with significant ongoing costs, but a smaller proportion of major bleeding incidents. ** No significant difference between warfarin and ximelagatran in either SPORTIF III5 or V;6 statistically significant when data from both trials were combined at P < 0.05. †† Cost ($6371) taken from the NEMESIS study7 and covers acute admission to an Australian hospital with ischaemic stroke only; this is an underestimate of the ongoing costs associated with ischaemic stroke. ‡‡ No significant difference between warfarin and ximelagatran in SPORTIF III5 and V;6 no significant difference when data from both trials were combined at P < 0.05.

Luke R Bereznicki · Shane L Jackson · Gregory M Peterson

Donald B Reid Co-convenor, Colleague of First Contact PO Box 896, Bridgetown, WA 6255 dbreidAThotlinks.net.au To the Editor: Thank you for your in-depth look at some of the concerns in doctors’ health in the October 2004 issue of the MJA. 1 I believe it would have been useful to include in the issue some practical information for doctors wanting to seek help, either for themselves or for a colleague. The attached table of contact phone numbers does not cover every state and territory, but it is a starting point. The services offered are confidential, and can be anonymous if desired. In Western Australia, the contact can include access to a list of doctors willing and able to be GPs for their colleagues. Further information is available on the Doctors’ Health Advisory Service website <www.doctorshealth.org.au>. Editor’s note: The AMA website also has a very useful “Doctors’ Health Database” at <www.ama.com.au/web.nsf/tag/doctors-health-database>. Australasian Association of Doctors’ Health Advisory Services (DHASs): helplines for doctors Victorian Doctors’ Health Programme (VIC) (03) 9495 6011 DHAS (SA) (08) 8273 4111 Colleague of First Contact (WA) (08) 9321 3098 DHAS (NSW) (02) 9437 6552 DHAS (New Zealand) (04) 471 2654 DHAS (QLD) (07) 3833 4352 DHAS (TAS) (03) 6223 2047 (in hours) (03) 6235 4165 (after hours)

Donald B Reid

Max Kamien Emeritus Professor, Senior Research Fellow, Discipline of General Practice, University of Western Australia, Perth, WA mkamienATcyllene.uwa.edu.au To the Editor: Over the past two years, the Journal has pointed out the health hazards and the lack of logic in the Health Insurance Commission’s closure of its previously cost-effective and successful “Doctor Shopping Hotline”.1-4 But it has taken the death of a 25-year-old “prescription shopper” in Cairns, his crusading mother, a scathing report by the Queensland Coroner5 and public exposure of these problems by Mark Bannerman on ABC TV (The 7.30 Report, 22 Dec 2004) for discernible action to occur. On that program, the Federal Minister of Health and Ageing promised that a “Prescription Shopper Line” would be up and running by the end of January 2005, and indeed it was activated on 31 January. This leaves two outstanding issues. The first is for the Health Insurance Commission to engage in an open exercise of mutual education by clearly reviewing its process of thinking in closing the previously successful Doctor Shopping Hotline and its lack of urgency in reinstituting its proposed better and broader successor.6 The second, and more important, issue is in understanding the underlying factors and thought processes of those doctors whom prescription shoppers describe as an “easy touch”. 7,8

Max Kamien

Ursula Bayliss,* Christopher Cowell,† James Hong,‡ Veronica Wiley,§ Bridget Wicken¶ * Clinical Nurse Consultant, §Principal Scientist, ¶ Clinical Director, NSW Newborn Screening Programme, † Head, Institute of Endocrinology & Diabetes, The Children's Hospital at Westmead, Westmead, NSW 2145; ‡ Paediatrician, North Gosford Medical Centre, North Gosford, NSW. bridgetwATchw.edu.au To the Editor: We report an acute presentation of congenital hypothyroidism in a child almost 6 years old. The condition was not detected by newborn screening. Screening of all neonates started in New South Wales in July 1977, with thyroid stimulating hormone (TSH) being measured in dried blood spots taken from a heel-prick blood sample (currently at 2–3 days of age). A whole-blood TSH level of 40 mIU/L or above triggers a request for full thyroid function testing, whereas with a level of 20–39 mIU/L a second sample is requested. We have screened over 2.3 million babies and detected 690 babies with congenital hypothyroidism. Ten babies with dyshormonogenesis or ectopic thyroid tissue had normal results and were missed by the screening test. Since screening started, “juvenile hypothyroidism” not associated with thyroid antibodies has all but disappeared. A healthy girl aged 5 years 11 months presented with acute dysphagia and drooling. There were no previous dysphagic symptoms. Initially, epiglottitis was suspected; however, at endoscopy a lingual thyroid was visualised at the base of her tongue, and this was confirmed by a technetium scan. She had normal growth and development, with both height and weight at the 50th centiles, a pulse rate of 90 beats/min, and normal deep tendon reflexes. The whole-blood TSH level at newborn screening on Day 3 was 40 mIU/L (reference range [RR], < 20 mIU/L). Thyroid function testing at another hospital on Day 10 showed a serum TSH level of 16.6 mIU/L and a serum free thyroxine (FT4) level within the normal range (12 pmol/L; RR, 11–30 pmol/L). These results were interpreted as normal, whereas, in fact, the TSH level was above the reference range for 10 days of age (< 10 mIU/L), although within the reference range for 2–7 days. On the patient’s admission for treatment of acute dysphagia, the TSH level was 10.9 mIU/L and the FT4 level was 18 pmol/L. A diagnosis was made of compensated hypothyroidism secondary to the ectopically placed lingual thyroid. Thyroxine treatment was commenced on diagnosis, and regular follow-up arranged. Three months after the start of treatment, the results of thyroid function tests (FT4, 17 pmol/L; TSH, 2.7 mIU/L) were within the normal range. Acute presentation of a lingual thyroid is most unusual.1 This case emphasises that further investigations must be performed when thyroid function test results are equivocal. Unfortunately, the thyroid status was considered normal because the FT4 value was within the normal range. All babies whose TSH results remain elevated while the FT4 levels are normal should have a thyroid scan, as we recommend when reporting results.

Ursula Bayliss · Christopher Cowell · James Hong · Veronica Wiley · Bridget Wicken

Emma J Best,* Monica M Lahra,† Pam Palasanthiran‡ * Paediatric Infectious Diseases Fellow, † Microbiology Registrar, Neonatal Medicine, Royal Prince Alfred Hospital, Sydney, NSW. ‡ Infectious Diseases Physician, Sydney Children’s Hospital, Level 4, High Street, Randwick, NSW 2031; PalasanthiranpATsesahs.nsw.gov.au To the Editor: Pasteurella multocida is an oral commensal of domestic pets known to be an opportunistic human pathogen after traumatic animal contact. The most common infections in humans are skin and pulmonary infections. This report outlines a case of P. multocida meningitis, which has not previously been reported in Australia. A 19-day-old girl presented with a 12-hour history of fever and poor feeding. Her temperature was 39.5°C, and she was irritable, with no localising signs or skin lesions. A full septic screen was performed. Cerebrospinal fluid (CSF) showed a neutrophilic pleocytosis and gram-negative coccobacilli. She was treated with intravenous cefotaxime and gentamicin. Within 24 hours both CSF and blood cultures showed growth of gram-negative bacilli. The initial Gram stain, growth on chocolate agar and positive oxidase and catalase tests were suggestive of a Haemophilus species. However, further biochemical tests revealed the organism to be P. multocida. The infant made an excellent clinical recovery, with normal neurological and growth assessments at 6 and 12 months. The family owned two cats but reported no contact between their baby and the pets. A single tonsillar swab performed on each cat by a veterinarian 10 days after the baby’s presentation failed to isolate Pasteurella species. The family elected to keep the pets. Pasteurella meningitis occurs at extremes of age, in the immunocompromised (associated with liver cirrhosis, renal disease and haematological malignancies) and after traumatic head injury.1 Infants aged under 1 year account for almost half the cases of P. multocida meningitis. On review of the literature, we found 37 reported cases of P. multocida infection in infants (Box).1-5 In more than three-quarters of these cases, there was known contact with household animals — in more than half of these contact was non-traumatic (licking or presumed handling of the pet). Molecular studies in one of the cases with no history of traumatic contact confirmed that P. multocida isolates from pet and infected child were indistinguishable.2 This infection is unusual, and, given the popularity of household pets, the risk appears low. However, this case highlights the relative immunocompromise of newborn infants, and is a reminder of the importance of hand hygiene and preventing contact between newborn infants and pets. Details of 38 case reports of invasive Pasteurella multocida infection in infants (including current case)1-5 Mean age (range) 2.6 months (1 day– 11 months) Type of infection Meningitis 30 (79%) Puerperal sepsis, chorioamnionitis 7 (18%) Bacteraemia (postnatal) 1 (3%) Nature of animal contact Traumatic (scratch, bite) 9 (24%) Non-traumatic 22 (58%) Unknown 7 (18%) Type of animal (n = 31) Cat 16 (52%) Dog 11 (35%) Both 4 (13%)

Emma J Best · Monica M Lahra · Pam Palasanthiran

Megan L Counahan,* Ross M Andrews,† Rick Speare‡ * Surveillance Manager, Communicable Diseases Section, Department of Human Services, Level 17/120 Spencer Street, Melbourne, VIC 3000; † Senior Research Fellow, Centre for International Child Health and Clinical Epidemiology and Biostatistics Unit, Murdoch Children’s Research Institute, Melbourne, VIC; ‡ Professor, School of Public Health and Tropical Medicine, James Cook University, Townsville, QLD. megan.counahanATdhs.vic.gov.au To the Editor: For parents to treat head lice (pediculosis) effectively in their children, it is necessary for them first to recognise it is present. We conducted a school-based screening program involving 1838 children from 16 randomly selected primary schools in Victoria between May and October 2001 (participation rate, 55.2%).1 As part of this program, we compared a written report from parents on their child’s pediculosis status against results of our examination (7–10 days later). We examined the scalp and hair of each child for lice (“crawlers”) or viable louse eggs (“active infestation”) and dead or hatched louse eggs (“inactive infestation”) using white hair conditioner, which makes lice and eggs easier to see with the naked eye, and a fine-toothed head lice comb. This is a validated, accurate and sensitive diagnostic technique.2 Parents were unaware of the proposed screening date, and the study team was unaware of the parents’ reports. We compared parental report about pediculosis against results of our screening for 1179 children who could be matched with completed questionnaires. Overall, 149 children (12.6%) had active pediculosis, but parents reported head lice in only 36 children (3.0%) (Box 1 and Box 2). These comprised 24 of the 149 children with confirmed pediculosis (16%), and another 12 children who did not have pediculosis when examined. The positive predictive value (PPV) of parental report was 66.6%, indicating that parental reporting was not a reliable indicator of pediculosis. An implication of the low PPV is that some children may have been unnecessarily treated with insecticide for an infestation they did not have. On the other hand, a substantial proportion of children with head lice had not been identified by their parents and could contribute to ongoing transmission within schools. While it was possible they were infected subsequent to completion of the questionnaire, this seemed unlikely, as 72% were found to have multiple louse eggs, indicating a longer duration of infestation than the 7–10 days since the questionnaire was completed. Our study clearly demonstrates that parental reporting of head lice in their children is unreliable. We suggest several possible reasons: parents did not see the head lice, did not recognise them, or used a diagnostic technique with a lower sensitivity than the method we chose, such as examining dry hair. It is also possible that parents were inhibited from reporting pediculosis by the possible repercussions, such as exclusion of the child from school. Indeed, children whose parents failed to answer the question about pediculosis had a higher prevalence of head lice than those whose parents answered. Nevertheless, parents’ management of pediculosis is likely to improve if a sensitive detection method is used. To improve the sensitivity of parental diagnosis and control of head lice we recommend that parents be instructed to screen their children weekly using hair conditioner and combing. 1 Screening results compared with parental report Pediculosis by parent report Pediculosis on examination Yes No Total Yes 24 12 36 No 99 969 1068 Unsure 26 49 75 Total 149 1030 1179 2 Sensitivity and specificity of parental report versus screening Pediculosis prevalence By parental report 3.0% (36/1179) By screening 12.6% (149/1179) Sensitivity 16.1% (24/149) Specificity* 98.8% (1018/1030) Positive predictive value 66.6% (24/36) Negative predictive value* 89.0% (1018/1143) * Specificity and negative predictive value were calculated after grouping “unsure” and “no” responses.

Megan L Counahan · Ross M Andrews · Rick Speare

Fiona M Wood,* Bess V Fowler,† Daniel McAullay,‡ Jocelyn R Jones§ * Plastic Surgeon and Director, † Epidemiologist, Burns Service of Western Australia, Royal Perth Hospital, GPO Box X2213, Perth, WA 6847; ‡ Senior Policy Officer, § Manager, Office of Aboriginal Health, Health Department of Western Australia, Perth, WA. FionawATmccomb.org.au To the Editor: People with major burn injuries (50% total body surface area or more) now have an improved likelihood of survival with the implementation of aggressive treatment regimens, including supportive therapy, nutrition, and advances in the control of sepsis. Technological developments and treatments, particularly expedient wound closure, early surgical debridement, covering of large burn wounds, early skin repair,1 use of cultured epithelial autograft2 and ventilation,3 have also contributed to improved outcomes for people with these injuries. In Australia, there are inequities in access to health services which may particularly affect Aboriginal people.4 We therefore undertook a retrospective, observational study to compare the incidence of major burn injuries, clinical and demographic characteristics of patients with burns, as well as treatment and outcomes between Aboriginal and non-Aboriginal children and adults in Western Australia between 1992 and 2002. Potential cases were identified using data linkage from the Western Australian Department of Health. Raw data came from clinical records. Of the 84 people identified with major burn injuries, nine were Aboriginal (11%) and 75 were non-Aboriginal (89%). The incidence of major burn injury among Aboriginal people is greater than expected, as data from 2001 show that 3.5% of the WA population are Aboriginal. Aboriginal people with major burn injuries were younger than non-Aboriginal people with those injuries (mean, 21 v 35 years). Eight of the nine Aboriginal people (89%) had flame-only burns, compared with 33 of 75 non-Aboriginal people (44%). No statistically significant difference was seen between the groups in the percentage of total body surface area affected, provision of treatment (including number of operative procedures, applications of cultured epithelial autografts, units of blood products used, nasogastric feeds, and antibiotic doses) or length of hospital stay. We found that, although a greater percentage of Aboriginal people sustained major burn injuries, after this group entered the hospital system they experienced comparable levels of service and outcomes to non-Aboriginal people. Further research into burn care is warranted, from culturally and environmentally appropriate prevention through to critical appraisal of outcomes.

Fiona M Wood · Bess V Fowler · Daniel McAullay · Jocelyn R Jones

Huy A Tran Director, Department of Clinical Chemistry, Hunter Area Pathology Service, John Hunter Hospital, Locked Bag No. 1, Hunter Region Mail Centre, New Lambton Heights, NSW 2310. huy.tranAThunter.health.nsw.gov.au To the Editor: I read with interest the recent review of Paget’s disease by Walsh.1 I would recommend that calcium and phosphate levels should be included in the initial biochemical assessment, as both tests are cheap and readily available. As Paget’s disease predominantly afflicts the older population, coexisting vitamin D deficiency is likely. Low (but within the normal range) calcium and phosphate levels may support this diagnosis. Conversely, hypercalcaemia, a rare event in Paget’s disease except in prolonged immobilisation,2 may indicate primary hyperparathyroidism, which is significantly associated with Paget’s disease,3 or, less commonly, metastatic bone disease. Both these conditions have prognoses and management distinctly different from those of Paget’s disease. Serum total alkaline phosphatase levels may not be elevated in 15% of active Paget’s disease.4 While bone-specific alkaline phosphatase level is more useful in these situations, this test is not readily available in some laboratories and, even among those in which it is available, some only provide qualitative results, making it less useful for monitoring Paget’s disease and the response to therapy. A suitable alternative test is urinary deoxypyridinoline/creatinine ratio, which can be done either on a random urine sample or a 24-hour urine collection. In addition, the serum total alkaline phosphatase level can be spuriously low in malnourishment, and specifically in zinc deficiency,5 a frequent occurrence in elderly people. I describe here a case highlighting such a problem. A 72-year-old socially isolated widower of 8 years presented with progressively worsening pain in his right hip in the preceding 3 months. He had poor appetite and had lost 6 kg in weight, but had no symptoms of malignancy. Clinical examination showed a thin man (body mass index, 20 kg/m2), who was otherwise normal with no features of zinc deficiency. A plain x-ray of the pelvis showed bilateral osteosclerosis. His total alkaline phosphatase level was 28 U/L (reference range, 35–110 U/L). Other investigations for metabolic bone disease gave normal results, including one for vitamin D level. Among other nutritional parameters, his zinc level was 5.2 mol/L (reference range, 10.0–18.0 mol/L). A computed tomography scan of the thorax and abdomen showed no evidence of malignancy, and a bone scan was consistent with Paget’s disease. A zinc supplement was prescribed and his diet optimised. At 6-week review, the serum zinc level had improved to 12.5 mol/L, but the serum total alkaline phosphatase level was 250 U/L. This confirmed that the patient’s acquired hypophosphatasia was secondary to zinc deficiency, with zinc being a critical cofactor for alkaline phosphatase activity.4 In light of the “correct” total alkaline phosphatase level, the patient was given intravenous pamidronate, with resulting marked resolution of his symptoms, including a 5-kg weight gain and normalisation of total alkaline phosphatase level. Although this case is unusual, it nevertheless highlights the need to consider occult and coexisting nutritional morbidities in an elderly population.

Huy A Tran

Stephen N Bolsin Director, Division of Perioperative Medicine, Anaesthesia and Pain Management, Geelong Hospital, Ryrie Street, Geelong, VIC 3220. stevebATbarwonhealth.org.au To the Editor: Two recent articles in the Journal highlight the need to re-evaluate the collection of performance data in Australian healthcare, as well as the uses and analysis of these data.1,2 Individual report cards are an extremely good and ethically mandated means of monitoring performance, especially when the information is given to patients as part of an informed-consent process.2 However, it is possible to provide more valuable analyses than simple crude complication or mortality rates. Cusum (cumulative summation) analysis was developed for industrial quality assurance to monitor production processes and detect subtle deviations from a preset, defined level of achievement. It can be applied to clinical practice to identify statistically significant improvements (or decrements) in performance, using agreed definitions of “acceptable” and “unacceptable” performance levels.3,4 It can be risk-adjusted if necessary. Cusum analyses are routinely undertaken by the Geelong Hospital Department of Anaesthesia for monitoring performance of College-accredited trainee anaesthetists, and have been suggested by surgeons as a method for monitoring performance of a series of procedures.5 Although cusum analysis may seem highly threatening to many senior professionals, the support it provides and the cultural change it achieves in trainee anaesthetists have already been well documented in a unique Australian initiative.4 Modern regulatory theory describes three levels of regulation: the individual (micro), organisational (meso), and state or national (macro) levels. The personal professional monitoring program based on personal digital assistants (PDAs) and cusum analysis that was introduced for accredited trainee anaesthetists by Geelong Hospital operates at all these levels. It encourages reflection on individual performance by accredited trainees in a supported environment; organisational review by the supervisor of training within a clinical governance framework; and College supervision, collation and endorsement as part of a national training program. The fact that the reporting structures inherent in this PDA-based model conform to these highest standards of regulatory theory and clinical governance confirms that the required professional change recommended by Irvine1 can be easily achieved through mechanisms already operating in Australian hospitals. The model also achieves cultural change in the trainees and the highest incident reporting rate in modern healthcare (96.7%–100% voluntary reporting of critical incidents occurring in their practice). 6 These two factors should mandate the wider introduction of the PDA-based program in Australian hospitals if the profession and the industry are to be taken seriously on this issue.

Stephen N Bolsin

David G E Caldicott,* Cameron Duff† * Convener, Royal Adelaide Designer Drug Academic Research (RADAR) Unit, Emergency and Trauma Department, Royal Adelaide Hospital, Adelaide, SA; † Director, Centre for Youth Drug Studies, Australian Drug Foundation, Melbourne, VIC. dcaldicoATmail.rah.sa.gov.au To the Editor: Threatened with a surge of Athenian, one-eyed jingoism regarding Australian drug policy that the recent conference report by Ritter et al1 might have elicited, we offer a warning. Australia has achieved much to be proud of with its harm-reduction policies in recent decades. As Ritter et al attest, Australian researchers and practitioners are “leading the way” in generating political and community support for greater harm-reduction efforts. However, the implementation of real harm-reduction measures can hardly be described as “Olympian” under the current administration. Real Australian successes in the area of harm reduction have arguably occurred despite federal and state policy rather than because of it. Individual positions taken by clinicians such as Dr Alex Wodak, in the face of severe opposition and at times intimidation, account for much of this success. The sad reality is that the “Tough on drugs” approach currently pursued in Australia seems doomed to soon fuse with the Americans’ globally denounced “War on drugs”. Real harm reduction can hardly be said to have been given a “fair go” in the past decade, with 85% of the total drugs budget in Australia committed to law enforcement — the paltry remainder split between research and treatment.2 While harm reduction strategies have been widely implemented in response to the problems associated with injecting drug use, such strategies have not been nearly as popular in our responses to other types of drug use. Harm reduction is yet to be embraced as an effective response to the problems associated with the so-called “party drugs”, despite mounting evidence of its efficacy in Europe. Any premature triumphalism on the subject of harm reduction ought to be eschewed. Australia’s recent heritage is quietly being betrayed at a federal level. A little-publicised federal report recently called for a move away from harm minimisation and harm reduction.3 This is despite evidence indicating that functional drug use is emerging as “normal” rather than deviant behaviour among many Australians. 4 Clearly, we must redouble our efforts to ensure that harm reduction becomes a central part of Australia’s public policy stance. In an era in which it often seems easier to succumb to the whims of our larger neighbours than to resist them, it becomes even more important that doctors and health professionals, and particularly the younger generation of researchers, stand firm. We are, after all, standing on the shoulders of giants.

David G E Caldicott · Cameron Duff