Letters

To the Editor: Hereditary haemorrhagic telangiectasia (HHT) or Osler–Weber–Rendu syndrome manifests as vascular dysplasia involving the nose, skin, lung, brain and gastrointestinal tract. It is an inherited disorder manifesting as unbalanced angiogenesis.1 Bevacizumab is a recombinant, humanised monoclonal antibody that binds to and neutralises vascular endothelial growth factor (VEGF), preventing its association with endothelial receptors. VEGF binding initiates angiogenesis (endothelial proliferation and the formation of new blood vessels). VEGF and transforming growth factor β play a role in the pathogenesis of HHT, with affected patients having increased levels of these factors.2 Anecdotal reports have demonstrated the effectiveness of bevacizumab in patients with HHT. To date, good responses have been documented in patients presenting with epistaxis, haemoptysis, anaemia,3 pancreatic arteriovenous malformations4 and hepatic vascular abnormalities.5 We were referred a 71-year-old man who related a 45-year history of recurrent nose bleeds, pulmonary and gastrointestinal haemorrhage and significant facial and oral telangiectasias. He had a history of multiple hospital admissions for haemoptysis and malaena necessitating blood and iron transfusions. The patient averaged three blood transfusions and four iron infusions a year, and his haemoglobin level ranged from 90 to 120 g/L. The patient also received argon laser treatment for his gastric and duodenal telangiectasias, and was taking bovine colostrum for nosebleeds with minimal effect. Shaving resulted in regular bleeding as a result of his facial telangiectasias. Because of his significant morbidity, the patient was referred for a trial of bevacizumab therapy and underwent six cycles at 5 mg/kg by means of fortnightly intravenous infusion from March to May 2010. This treatment has resulted in an effective and tangible response. Since completing the treatment, the patient has been followed up monthly, and he reports only two nosebleeds compared with daily bouts before therapy. Further, the telangiectasias on his face and in his mouth have reduced considerably, and he has had only one gastrointestinal bleed, which occurred after heavy lifting. His haemoglobin level 2 weeks after treatment was 163 g/L and has remained stable since that time. A follow-up gastroscopy in November 2010 showed that his multiple vascular lesions had reduced to just one angiodysplastic lesion in his gastric body (Box). The only adverse effect he experienced from the bevacizumab was poor sleep with associated tiredness, but the patient was able to tolerate this in light of the amelioration of the symptoms of his HHT. Other reported side effects of bevacizumab such as hypertension, proteinuria and thrombosis did not manifest in this patient. With growing anecdotal evidence of the effectiveness of bevacizumab in treating symptomatic HHT, an argument for using bevacizumab as an adjunctive or even first-line treatment for HHT is becoming stronger. Gastroscopic images of the patient’s stomach before and after treatment with bevacizumab

Ross P Cruikshank · Boris W Chern

To the Editor: Nash and colleagues have produced another report on medicolegal matters and Australian doctors.1 This report, and one that preceded it in 2009,2 are derived from responses to a questionnaire from nearly 3000 doctors. The survey showed that 65% of respondents had been involved in “medicolegal matters”. From a mass of data, the authors conclude that medicolegal concerns impact on doctors’ practice of medicine. As potential benefits of medicolegal matters, they list improved communication of risk to patients, disclosure of diagnostic uncertainty, and better methods to track test results and non-attenders. Negative impacts included increased referral to specialists, ordering more tests, and seeing fewer patients. The authors recommend targeted training in patient safety and medicolegal aspects of practice to help doctors to be “better informed”. However, as 65% of the group had been involved in medicolegal matters, it seems unlikely they need to be better informed about them. In the title and throughout the article, there is much emphasis on the word “perceived”. With this heavy emphasis on perception, it might be thought that the key finding was that fear of a medicolegal matter was greater than the reality. In fact, the reverse was found. Of those who had experienced medicolegal matters, 46% had considered retiring early, 39% considered giving up medicine and 38% considered reducing hours of work. The respective figures for those who had not experienced medicolegal matters were 29%, 22% and 21%. The difference was highly significant. An inescapable conclusion is that medicolegal matters result in large numbers of demoralised doctors. The reality is worse than the perception. Unfortunately, the obvious question — What was the outcome of the medicolegal matter? — was not included in the survey. Given the numbers involved, it seems likely that for many doctors, although the outcome was favourable, the process had a profoundly negative effect on their work. Forty-one per cent now regard every patient as a potential litigant. A logical response to these data might have been to ask: (1) Could there be a problem with the way medicolegal matters are conducted? and (2) Is the demoralisation of a large percentage of the medical workforce good for society? Neither question was asked here. This is perhaps not surprising as, in their previous article, the authors questioned, without embarrassment and on the basis of a questionnaire, whether “psychiatric morbidity in doctors is a cause or effect of the medicolegal process”.2 This study is “one of the largest [of its kind] in the world”. Sadly, the authors’ negativity towards doctors and their unquestioning allegiance to current medicolegal practice have greatly diminished its value.

Padraic J Grattan-Smith

In reply: I agree with Grattan-Smith that current medicolegal processes have profoundly negative effects on doctors. I do not agree that my coauthors and I have “negativity” towards doctors and an allegiance to current medicolegal practice. Our aim was to investigate the impact of medicolegal matters on Australian doctors — their emotional response and their practice changes.1,2 We have shown that doctors who have a current medicolegal matter have higher levels of psychiatric morbidity,2 and that most doctors believe they change how they practise due to medicolegal concerns — more so in the case of doctors who have experienced a medicolegal matter.1 Justice Ipp and colleagues,3 when reviewing the law of negligence for the Commonwealth of Australia in 2002 with the objective of limiting liability and damages arising from personal injury or death, made note of the lack of empirical evidence in the submissions they received. We have now provided some empirical evidence of medicolegal matters from the doctors’ perspective. If such a review were conducted now, I would suggest the current medicolegal systems are not good for patients, for doctors, or for the health system in general. The evidence from our studies1,2 now allows a more informed conversation on this issue to take place.

Louise M Nash

To the Editor: The supplement of the Journal published on 16 August 2010 — “Bipolar disorder: new understandings, emerging treatments”1 — illustrates a number of features of the current implementation of the Journal’s supplement policy that are problematic. While it is clearly stated that the supplement “was supported by an unconditional grant from AstraZeneca Neuroscience”, the amount of sponsorship, to whom it was paid, and how it was used were not disclosed. Such information is particularly pertinent as evidence suggests that the pharmaceutical industry has financial motivation to see a widening of the diagnostic boundaries of bipolar disorder and a rebadging of atypical antipsychotics as “mood stabilisers”.2 The provenance of the articles is not revealed — it is not clear whether the articles were solicited, part of a symposium, or from some other source. Bipolar disorder is a controversial area in psychiatry,3 yet despite much useful information in the articles in the supplement, discussion of this controversy is a minor feature and no significant critical appraisal is offered. To give a more balanced view to readers, it would have been desirable to have included articles that highlight the controversy regarding bipolar II and bipolar spectrum diagnoses and discuss the ways in which personality disorders arising from developmental trauma and attachment problems can present with mood and behavioural disturbances that can be confused with bipolar disorder.

Jon N Jureidini · Peter I Parry · Catherine M Houen · Malcolm W Battersby

In reply: Jureidini and colleagues raise legitimate issues pertinent to our Medical Journal of Australia supplement on bipolar disorders, and we are pleased to respond. First, the extent of sponsorship from AstraZeneca was for publication only. One of us (D J C) discussed the idea of the supplement with the Editor of the Journal, and AstraZeneca expressed interest in supporting the project. Neither the Journal editors nor any of the supplement authors were involved in the sponsorship negotiations between AstraZeneca and the publisher of the Journal, and neither received any financial or other assistance or reimbursement from AstraZeneca. Second, as Coordinating Editors of the supplement, we determined the content of the supplement without any input from AstraZeneca, and we directly solicited articles from leading experts of our choice in appropriate fields. All articles were subject to the usual review process accorded all publications in the Journal. Regarding the general issue of the boundaries of the bipolar concept, we are very much aware of the ongoing debate. This is a pervasive issue for a discipline devoid of biological markers that can be used to define a plane of cleavage. Indeed, we highlighted this in the second paragraph of our editorial1 as an “immediate area of controversy”. We also solicited the article by Tiller and Schweitzer specifically to address the diagnostic problems in the area of mood instability; in that article, there is specific mention of both the bipolar spectrum and mood instability in the so-called personality disorders.2 With respect, Jureidini and colleagues fall into a common trap by considering that the use of some atypical antipsychotics in bipolar disorder is a rebadging exercise. This is silliness. One could equally argue that sodium valproate, carbamazepine and lamotrigine are not legitimate mood stabilisers but, rather, rebadged anticonvulsants. Tricyclic antidepressants started life as antihistamines. What matters to us as clinicians and researchers is that people with bipolar disorder are offered the best possible care, irrespective of labels. We are also very much aware of the undeniable burden associated with mood instability and hope that the supplement we helped produce will assist general practitioners, in particular, to deliver better care to patients so afflicted.

David J Castle · Michael Berk · Barbara M Hocking

To the Editor: I found Van Der Weyden’s editorial “Whither medicine? The expansion of non-doctor practice”1 to be an unduly negative view of the emerging new clinical roles, such as nurse practitioners, in our health system. To imply, for example, that the access to prescribing rights for nurse practitioners is a significant challenge (rather than a help) to doctors is contrary to the experience of many such implementations of these roles. I have a clear view of the role of doctors. They should: be in charge and lead the decision-making process of multidisciplinary teams; be responsible for the cognitive and integrative aspects of clinical care, including the initial assessment and planning of management for undifferentiated patient presentations in all care settings; and provide high-level complex care, including procedural and diagnostic services that require their level of expertise. Doctors should not continue to provide clinical services that are not a good use of their considerable training and experience. These services, that could be provided by nurse practitioners, include routine monitoring and prescribing (under protocol and medical leadership) of maintenance treatments (such as haemodialysis treatment or routine diabetes review), and simple repetitive diagnostic or therapeutic procedures. In my experience, many doctors are bored with these intellectually limited aspects of their practice and find the quality of their clinical life substantially enhanced when given the opportunity to work in partnership with nurse practitioners. Again, in my experience, some tertiary-educated nurses are also bored with their limited clinical roles (still dominated by personal care) and can offer much more to the clinical team by focusing on the higher end of their skill base. There are clear differences between doctors and nurses in terms of selection process, education and training. However, this does not preclude both professional groups from looking at their scope of practice and focusing on the tasks that best use their expertise, rather than retaining roles based on custom and practice that are no longer relevant. If doctors embrace and lead the role redesign program, they can ensure that sensible delegations of their clinical tasks to other health practitioners can occur with benefit to all. Resistance and disengagement of doctors will not stop role redesign, as we clearly cannot sustain a health workforce in the future with a staffing model that has not changed materially for 100 years. Resistance and disengagement are more likely to lead to dysfunctional new roles being produced, without the necessary strong relationship with the medical profession required for the best patient care.

Brendan F Murphy

To the Editor: In his recent editorial,1 Van Der Weyden laments the “displacement” of doctors in modern health care by nurse practitioners and physician assistants, and bemoans the fact that discussion and debate about these matters is largely confined to medical tabloids such as Australian Doctor. In this context, the editorial cites unsubstantiated and inflammatory comments from Australian Doctor correspondents claiming that nurse practitioners place patients at risk.2,3 Remarks that nurse practitioners are “a disaster unfolding” and “people will die”3 are not only inflammatory but also inaccurate. Medical and nursing insiders have made these claims with self-appointed legitimacy and without evidence. They demonstrate a surprising level of ignorance about the role of nurse practitioners and the evidence base that supports their practice, particularly in emergency care.4 In an era where the drum of quality and safety in health care and evidence-based practice beats the loudest, where is the evidence to support such claims? Perhaps the lack of evidence is the reason why such claims implying that nurse practitioners present a risk to patients are housed in medical tabloids, where they escape the rigorous scrutiny of peer review that would otherwise expose this deficit. Van Der Weyden bewails that nurse practitioners are the only health professionals “whose skills and talents are extolled”.1 We doubt whether such trivialities are at the forefront of the minds of emergency nurse practitioners, who comprise a large proportion of nurse practitioners in Australia. As part of the broader health care team, their focus — and the focus of their physician, nurse and allied health colleagues — would be on the immediate and ongoing needs of their patients. Van Der Weyden asserts that an assumption of the equivalence of nurses and physicians underpins the political and industrial agenda for “doctor displacement” in general practice in Australia. Such an assertion is entirely moot. High-quality and safe health care cannot be realised by a monopoly of nurses, or physicians, or any other health profession. Nurses and physicians are only two of the many threads in the tapestry of high-quality, safe and evidence-based health care. Their success lies in symbiotic mutualism, not commensalism, amensalism, or parasitism. And, just like in tapestry, pulling any one thread from the fabric renders the picture incomplete.5 Unless there is substantial evidence to the contrary, bringing the safety of nurse practitioners into question is senseless, particularly given the well deserved support they have from their peers in the wider health community and their patients, both in Australia and overseas.

Ramon Z Shaban · Julie M Finucane · Dianne J Crellin

In reply: I welcome the comments of Murphy and of Shaban and colleagues on my recent editorial,1 which explored, as Shaban et al say, the “displacement of doctors in modern health care by nurse practitioners and physician assistants”. The main focus of the editorial was on the current philosophical relativism muddying the definition of what a doctor is and the academic qualifications underpinning all professional training. It calls for equally rigorous criteria to be applied to non-doctor practitioners and their scope for independent practice. Undoubtedly, the potential utility of non-doctor practice is dependent on bilateral mutualism, with a clearly defined scope of practice. However, the push for independent practice remains problematic. Whether there is a genuine commitment for bilateral mutualism to occur, beyond the usual rhetoric, is of concern — witness the recent difficult negotiations on defining the framework for cooperative practice, and the reticent views of doctors on the suitability of nurse practitioners and their scope for independent practice, as reported in Australian Doctor.2-4 The fundamental question, which must be addressed, is whether the granting of Pharmaceutical Benefits Schedule and Medicare Benefits Schedule privileges to non-doctors is simply a political strategy to create a two-tiered health system under the illusion of cost containment.

Martin B Van Der Weyden

To the Editor: Australia is in the process of making the most important change to its health care system since the implementation of Medicare.1 We agree with Cameron and Cooke that there are important lessons for Australia from the implementation of the 4-hour rule in the United Kingdom.2 As in Robert Zemeckis’s 1985 movie classic, Back to the future, the old question of “If I had the opportunity to do something again, what would I have done differently?” applies. We challenge the assumption that Australia is embarking on something that the UK has recently abandoned. The UK has not actually abandoned the 4-hour rule but expanded it into a suite of eight indicators that include three time-based measures, including total time in the emergency department (ED).3 Our concerns are about how the lessons learned by the UK can be applied in Australia in 2011 and beyond. Cameron and Cooke state that “Measurement systems should be in place to ensure that patient safety and quality of care are not compromised at any stage of the emergency care pathway”.2 The systems we have are neither universal nor integrated across the country. We need substantial data infrastructure, including comparable data linkage services across states. Of all the states, Western Australia has the most advanced national data linkage system. Yet even with the most sophisticated data systems in the world, proper impact assessment studies are required. Australia’s evaluation of the changes being made to rules and systems is neither systematic nor well standardised — to be safe and effective, innovation needs to be evaluated in coordinated and systematic ways.4 We also need systems-thinking approaches and simulation technologies to avoid repeating past mistakes. It is important to link theory and data to learn about the complex dynamics of ED patient flow and safety, and understand the consequences of our interventions.5 As suggested by Cameron and Cooke,2 we should focus on real-time, clinically relevant, consistent and comparable quantitative and qualitative data about patients, staff, processes, outcomes and facilities. We must learn to improve daily performance rather than sanction variable outliers. In conclusion, the lessons learned from the 4-hour target are relevant and appropriate for Australia. Cameron and Cooke have highlighted some of the dangers, including those of inadequate measurement.2 We need timely, integrated and linked data and an explicit theory of performance. We should aim to manage the risks by appropriately funded research and implementation strategies to improve this significant policy intervention while maintaining patients’ outcomes, experience and safety, and the timeliness of instigating their care.

Roberto Forero · Geoff D McDonnell · Sally M McCarthy · Peter Nugus · Jeffrey Braithwaite · Kenneth M Hillman · Daniel M Fatovich · David Mountain · Frank F Daly · Gerard J Fitzgerald · Drew B Richardson

To the Editor: The article by Nelson and colleagues1 is a welcome contribution to understanding trends in varicella zoster virus (VZV) disease epidemiology in Australia, particularly ambulatory medical attendance, for which few data sources are available. They report a decline in general practitioner encounters for varicella (chicken pox) since the introduction of varicella vaccine that is consistent with the observed 69% reduction in national hospitalisation rates in children aged 1.5 to 4 years seen from January 2006 to June 2008, 2.5 years into the National Immunisation Program (NIP).2 Nelson et al also report a trend towards higher GP encounter rates for herpes zoster (HZ [shingles]) over time. Although it may be tempting to take this rise on face value, additional analyses are required for a full understanding of patterns in HZ-related health care use, particularly accounting for age and changes in the use of prescription medications, including antivirals and opioid analgesics. Increased HZ-related health care use commencing before varicella vaccine availability has been reported in countries with universal vaccination programs, including the United States3 and Australia,4 as well as in countries where varicella vaccination is not recommended universally, including the United Kingdom.5 In Australia, prescribing of antiviral drugs for HZ increased between 1995 and 1999.6 Australia’s ageing population will contribute to the increasing prevalence of HZ over time due to the propensity of the virus to reactivate with advancing age. An analysis that we conducted shows that an increase in crude national hospitalisation rates for HZ preceded varicella vaccine availability, and that there was no increase over time in age-specific and age-standardised rates (National Centre for Immunisation Research and Surveillance, unpublished data). In addition, the suggestion from modelling studies that HZ may increase under a universal varicella vaccination program because of reduced opportunity for immune boosting in adults has yet to be observed in the US, the country with the longest-standing universal program of varicella vaccination.3 These complexities in monitoring VZV-related diseases highlight the need for very sensitive and well validated surveillance systems for both varicella and HZ in Australia. Although the authors request consideration for a universal HZ vaccination program for those over 65 years, they may not have been aware that since April 2009 The Australian immunisation handbook, ninth edition, online version has had new guidelines on HZ vaccination recommending a single dose of live attenuated VZV vaccine from the age of 60 years.7 In March 2008, the Pharmaceutical Benefits Advisory Committee recommended that this vaccine was suitable for inclusion in the NIP for those aged 60 years, with a catch-up dose for all individuals aged 61 to < 80 years. A decision regarding NIP funding has not been made, possibly because of a shortage of vaccine due to manufacturing problems.

Anita E Heywood · Kristine K Macartney

To the Editor: In Australia, addition of thiamine to bread flour (at 6.4 mg/kg) was made mandatory on 1 January 1991 in an effort to reduce the incidence of Wernicke’s encephalopathy and Korsakoff psychosis.1 Recently, an isocratic high-performance liquid chromatography (HPLC) method for the assessment of thiamine, thiamine monophosphate and thiamine diphosphate (TDP) in human erythrocytes has been described.2 This direct method of measuring thiamine in blood is superior to measuring red blood cell transketolase. We used an HPLC reagent kit (Chromsystems Instruments and Chemicals GmbH, Munich, Germany) to measure whole blood TDP concentrations in a population of 156 people who had alcohol use disorders. They were consecutive cases presenting between June and September 2010 at a driver assessment clinic in South Australia after they were convicted of two or more drink-driving offences. Thirty-two people taking a thiamine-containing medication or vitamin supplement were excluded. Based on the Diagnostic and statistical manual of mental disorders, fourth edition, text revision, of the remaining 124 people, 42 fulfilled criteria for “alcohol dependence” and 82 fulfilled criteria for “alcohol abuse” in the preceding 12 months.3 Of those tested, none had biochemical thiamine deficiency (defined as 2 standard deviations below the reference mean TDP concentration [< 66.5 nmol/L]). The lowest whole blood TDP concentration was 106 nmol/L. The highest concentration found was 362 nmol/L. The mean concentration was 217 nmol/L. This value is 2.5 standard deviations above the mean for the reference population (mean, 133 nmol/L; SD, 33 nmol/L).4,5 The reference range (66.5–200 nmol/L) was derived from a population that did not receive thiamine supplementation in foods. The characteristics of the distributions of thiamine concentrations in the Australian and reference populations are shown in the Box. The mean age of our population was 36 years, the youngest person was aged 19 years and the oldest, 73 years. The mean body mass index was 26.6 kg/m2 and the lowest was 18 kg/m2, so this group was not malnourished. The mean daily alcohol intake reported was 22 g/day but there was wide variation (range, 0–272 g/day; SD, 35 g/day). The results from the population with alcohol use disorders show remarkably elevated thiamine concentrations and no evidence of thiamine deficiency. The very high mean concentration of thiamine shows that this population is not at immediate risk of thiamine deficiency. It also suggests that mandatory supplementation of flour with thiamine has raised the baseline concentration of thiamine in Australians. Distribution of thiamine diphosphate (TDP) concentration in an Australian population with alcohol use disorders compared with a reference population4,5

Philip M Crowley · Matt D Gaughwin

To the Editor: Eades and colleagues identify the scarcity of data on the health and health care needs of Aboriginal Australians.1 This is particularly so for Aboriginal children in urban settings. The Gudaga Study2 has actively worked to redress this shortcoming. The Gudaga Study (Gudaga being an Aboriginal word meaning healthy baby) is a longitudinal study of a birth cohort of Aboriginal infants born at a large outer urban hospital.2 Gudaga staff use methods that respect the values and beliefs of Aboriginal Australians3 to systematically collect information on the health, development, and service use of study participants at 6-monthly intervals. The Gudaga research team is working with the stakeholders in Aboriginal health in the region to discuss the implications of the information for policy and practice. A number of scientific articles are currently being prepared for publication. These include articles on birth outcomes, breastfeeding, universal health home visiting, health status and service use, development, and vaccination. Information collected by the Gudaga Study is contributing to the development of services for Aboriginal families in the region, and is changing the ways that service providers think about the health and service needs of Aboriginal families in the region. For example, the lack of data created difficulty in securing funding for services for pregnant Aboriginal women. Enumeration of the high rates of sudden infant death syndrome (3/149) and the removal of children by the Department of Community Services among participating infants (11/149 over 4 years) as a part of the Gudaga Study had two important effects. It influenced the public health service response to close the gap on Aboriginal disadvantage and influenced the decision to reorient child and family services and establish the Bulundidi Gudaga program with ongoing funding. The Bulundidi Gudaga program provides sustained home visiting of pregnant Aboriginal women and their infants by nurses, commencing during pregnancy and continuing until the infant is aged 2 years.4 This research developed over several years. It began during discussions with the Aboriginal community at Tharawal Aboriginal Corporation, Campbelltown, who raised concerns about the health of their children, difficulties in securing funding for an Aboriginal infant and maternal home visiting service that commenced 1999, the lack of relevant data on the needs of Aboriginal children, and receipt of National Health and Medical Research Council funding in 2003. The Gudaga Study commenced in 2005, and the first of the participating children are turning 5 years of age. The research is now part of a strong research program at the University of New South Wales into the health and development of Aboriginal children in urban settings.

Elizabeth J Comino · Lisa R Jackson Pulver · Jenny A Knight

To the Editor: Two studies in nursing homes in Sydney, New South Wales, in the 1990s1,2 showed inappropriately high use of psychotropic medications. A similar study was conducted in 2003.3 Over time, revision of management guidelines, warnings about potentially lethal side effects, and introduction of new drugs have contributed to changes in the pattern of use of psychotropic medications in aged care facilities. Following the same procedure as the earlier studies, in 2009, we examined medication use in nursing homes in half the catchment area of Sydney South West Area Health Service (SSWAHS). We obtained details of drugs prescribed for residents from medication record cards in 44 of the area’s 48 nursing homes and checked whether medications had been given as prescribed. If given regularly on at least 25 of the previous 28 days, use was recorded as regular. We noted whether medication prescribed “as required” had been taken. The SSWAHS ethics review committee approved the study. Medication cards of all 2465 residents (895 men, 1570 women; mean age, 78.7 and 84.2 years, respectively) were reviewed. The mean number of all medications charted per resident was 8.7. Data obtained from all four surveys on patients taking psychotropic medication regularly are shown in the Box. The catchment area expanded between the 1998 and 2003 surveys. However, half the nursing homes open in 1993 closed before 2009. Use of antipsychotic agents fell between 1993 and 1998. By 2003 there had been a change from conventional antipsychotics to a two-to-one preference for atypical antipsychotic medication. Since 2003, regular use of antipsychotic medication has increased by about 19%, although at a lower mean dosage than previously. The rise is mainly attributable to increased prescription of risperidone and needs continuing review to monitor for morbidity. The proportion of residents taking antipsychotic medication only as required has remained almost the same in each survey (range, 1.2%–1.4%). Regular use of anxiolytic and hypnotic medication has decreased, and of antidepressants has increased, since the 1990s. Only 3.5% of residents were regularly taking a tricyclic antidepressant in 2009. The proportions of residents prescribed anxiolytic or hypnotic medication only as required have also fallen (to 3.8% and 2.3%, respectively, in the 28 days preceding our audit). Our findings cannot be generalised. Recent evidence from Tasmania4 showed that 42% of residents were taking benzodiazepines regularly. Nevertheless, changes in medication use should provoke discussion. Number (%*) of Sydney nursing home residents taking psychotropic medication regularly Medication 19931 (n = 2414) 19982 (n = 1975) 20033 (n = 3093) 2009 (n = 2465) Any psychotropic† 1422 (58.9%) 957 (48.5%) 1461 (47.2%) 1170 (47.5%) Antipsychotics‡ 662 (27.4%) 447 (22.6%) 730 (23.6%) 690 (28.0%) Conventional‡ 662 (27.4%) 401 (20.3%) 251 (8.1%) 182 (7.4%) Haloperidol 190 (7.9%) 159 (8.1%) 167 (5.4%) 121 (4.9%) Thioridazine 354 (14.7%) 193 (9.8%) 17 (0.5%) — Chlorpromazine 53 (2.2%) 24 (1.2%) 25 (0.8%) 20 (0.8%) Trifluoperazine 57 (2.4%) 30 (1.5%) 16 (0.5%) 8 (0.3%) Pericyazine 15 (0.6%) 3 (0.2%) 10 (0.3%) 13 (0.5%) Fluphenazine 44 (1.8%) 23 (1.2%) 10 (0.3%) 11 (0.4%) Flupenthixol — 2 (0.1%) 9 (0.3%) 7 (0.3%) Zuclopenthixol — — — 9 (0.4%) Atypical‡ 48 (2.4%) 506 (16.4%) 537 (21.8%) Olanzapine — 8 (0.4%) 225 (7.3%) 180 (7.3%) Risperidone — 40 (2.0%) 219 (7.1%) 286 (11.6%) Quetiapine — — 18 (0.6%) 63 (2.6%) Amisulpride — — 4 (0.1%) 7 (0.3%) Clozapine — — 3 (0.1%) 7 (0.3%) Aripiprazole — — — 4 (0.2%) Hypnotics‡ 641 (26.6%) 335 (17.0%) 350 (11.3%) 274 (11.1%) Temazepam 530 (22.0%) 313 (15.8%) 307 (9.9%) 255 (10.3%) Nitrazepam 105 (4.3%) 17 (0.9%) 35 (1.1%) 17 (0.7%) Anxiolytics‡ 207 (8.6%) 123 (6.2%) 127 (4.1%) 117 (4.7%) Diazepam 113 (4.7%) 77 (3.9%) 92 (3.0%) 71 (2.9%) Oxazepam 72 (3.0%) 40 (2.0%) 32 (1.0%) 26 (1.1%) Antidepressants‡ 377 (15.6%) 316 (16.0%) 635 (20.5%) 630 (25.6%) Tricyclics 249 (10.3%) 120 (6.1%) 110 (3.6%) 86 (3.5%) Mianserin 87 (3.6%) 37 (1.9%) 22 (0.7%) 8 (0.3%) Moclobemide 21 (0.9%) 40 (2.0%) 20 (0.6%) 9 (0.4%) SSRIs 18 (0.7%) 103 (5.2%) 354 (11.4%) 338 (13.7%) Venlafaxine — — 81 (2.6%) 61 (2.5%) Mirtazapine — — 51 (1.6%) 126 (5.1%) Lithium 11 (0.5%) 8 (0.4%) 24 (0.8%) 17 (0.7%) — = Drug not approved for use or not prescribed in year of survey. SSRI = selective serotonin reuptake inhibitor. * All percentages are proportion of total number of residents. † Clonazepam and other anticonvulsants (apart from diazepam) were not included as psychotropic drugs. ‡ Numbers do not add to totals as some patients were prescribed more than one drug and some little-used psychotropic drugs are not listed.

John Snowdon · Daniel Galanos · Divya Vaswani

To the Editor: While clinicians often communicate with patients and families, documentation of these conversations is inconsistent. Documentation is critical for continuity of patient care, medicolegal reasons and research,1 and is particularly important in the intensive care unit (ICU), where discussions regarding prognosis and withdrawal of care occur frequently. There are scant published data on documentation of conversations with patients in ICUs and their families. We conducted a retrospective audit of patients admitted to the ICU of Wesley Hospital (a 500-bed private teaching hospital in Brisbane) between 1 January and 31 August 2009 to: determine levels of documentation of communication with patients and their families by the ICU medical staff; and compare this with documentation of communication by the primary physician before and after admission to the ICU. After obtaining Wesley Hospital ethics committee approval, all patients who were cared for in the general ICU for more than 5 days were studied. During the study period, there were 862 ICU admissions, 100 of which met our inclusion criteria. The charts of only 82 patients could be successfully retrieved and these were used for final analysis. These patients had a mean age of 64 years (SD, 14 years), and a mean Acute Physiology and Chronic Health Evaluation II (APACHE II) score of 17 (SD, 7). Sixty patients (73.1%) survived to hospital discharge. In the ICU, there were 39 family conferences at any stage between an ICU clinician and the families documented for 24 patients (29% of patients; 1.6 conferences per patient). Eleven of these conferences took place in the first 48 hours, eight between 2 and 4 days, and 20 beyond 96 hours of ICU admission. The Box shows that there was a greater proportion of documented family conferences for patients who died compared with those who survived at both 2–4 days (27% v 3%; P < 0.01) and beyond 96 hours (86% v 1.5%; P < 0.001). Of note, there was no documented communication between the hospital’s admitting physician and patients or families before ICU admission or after discharge from the ICU. Intensivists use any prior discussions to make decisions about continuing or withdrawing care.2 The absence of documentation before ICU admission is clinically relevant in this context. Potential reasons for inadequate documentation include (i) discussions occurring informally at the bedside or outside of the ICU (corridor conversations) and (ii) nurses providing updates in the clinician’s absence. Better documentation in the charts of dying patients may reflect their longer ICU stays, which provide more opportunity for communication. Moreover, discussions on treatment withdrawal are more likely to be documented as they are often a shared decision-making process. Globally, levels of documentation vary (10%–90%).3,4 Potential strategies to improve documentation include: bedside reminders (such as “have you documented family conferences?”); availability of a communications officer; an internal appointments system for formal discussions; and the use of communication kits.5 Despite being a retrospective study, our findings suggest a need to improve levels of documentation, and may prompt clinicians to examine their documentation practices and develop protocols to improve record keeping. Comparison of the documented communication rates for intensive care unit (ICU) patients who died and those who survived

Riad L Silcock · Bala Venkatesh · Ranald L Pascoe · Dianne K Fisher

To the Editor: Before and since 1 July 2010, when the National Registration and Accreditation Scheme for health practitioners commenced, the claim that mandatory reporting laws will deter impaired doctors from seeking help has frequently been made. It was on the basis of this claim that Western Australia legislated to exempt health professionals from reporting impaired practitioners they are treating. At a recent conference of the Royal Australian College of General Practitioners, a representative of a medical indemnity organisation labelled the mandatory reporting laws a disgrace because the health of impaired doctors who are deterred from seeking help for this reason would be put at risk. However, she also indicated that the problem was more one of perception than reality because doctors feared triggering a mandatory report automatically if they sought help from another doctor for a perceived impairment.1 It is a problem of perception because, under the laws, only doctors whose impairment places the public at risk of “substantial” harm are required to be reported.2 If doctors have an unreasonable fear of mandatory reporting, we can infer that many are unaware of the details of the laws, in particular the reporting thresholds. Yet an argument against introducing the laws was that doctors were already under an ethical obligation to report, to the relevant authority, unprofessional conduct, impairment or performance that would put patients at risk.3 For this argument to be valid, doctors would need to be aware of the details of mandatory reporting because the Medical Board of Australia’s code of conduct for doctors states, in its list of ethical obligations, that doctors should be aware of their reporting obligations.4 So this particular argument does not appear to be valid. Because medical professionalism puts the wellbeing of the patient first; because psychological or physical health status may affect professional performance; and because the Board, like the state boards that preceded it, has a primary duty to the safety of the public — any doctor whose impairment poses a substantial risk or, in the absence of that doctor’s insight, any treating doctor who considers that a substantial risk exists should surely feel ethically compelled to report the matter to the Board. No doctor whose impairment does not pose a substantial risk should feel deterred from seeking medical help. The consequences for impaired doctors who are reported under the new legislation are no different from those of reporting a doctor when it was “merely” an ethical requirement — being placed on an impaired practitioners’ register and supported, managed and monitored, while, in most cases, continuing to practise. If impaired doctors and their treating doctors feel deterred by mandatory reporting laws, we are entitled to conclude that there was, and continues to be, significant non-compliance with the ethical obligations that arguments against mandatory reporting depend on.

Malcolm H Parker

To the Editor: A 28-year-old man presented to his general practitioner with a history of epigastric pain and constipation over 1 month. In addition, he had a history of chronic low back pain. Findings on physical examination were unremarkable. Laboratory investigations showed normo-chromic, normocytic anaemia with basophilic stippling (Box 1). His whole-blood lead level was subsequently estimated to be 4.12 μmol/L (level recommended by the National Health and Medical Research Centre for all Australians, < 0.48 μmol/L). The patient was referred for toxicological review. Further questioning revealed he had used three Ayurvedic medicines (Vatyog [Arya Aushadhi Pharmaceutical Works, Indore, India], Sahacharadi [Arya Vaidya Nilayam, Madurai, India] and Gandharvahastadi [Arya Vaidya Nilayam, Madurai, India]) for back pain, dispensed to him 3 months earlier during a trip to India. He ceased taking the medications, and a 19-day course of oral chelation with succimer was administered. His blood lead concentration fell rapidly, with a moderate rebound 6 weeks after the completion of chelation therapy. A negative blood lead result for the patient’s pregnant partner excluded environmental exposure in the patient’s home. Vatyog and Sahacharadi were analysed for heavy metals (Gandharvahastadi was not available for analysis). Sahacharadi was lead-free, but the Vatyog tablet tested contained 448 μg of lead. The patient had potentially ingested 896 μg of lead daily for 3 months. World Health Organization guidelines recommend daily lead intake should not exceed 3.5 μg/kg/day.1 Dietary intake of lead in developed nations has been reported to be about 0.1–0.7 μg/kg/day.1 Ayurvedic medicine originated in India more than 2000 years ago and relies heavily on herbal products.2 Many people take Ayurvedic medicine without any problems. In some traditional remedies, salts of heavy metals are included as active ingredients.3 A study in the United States found that one-fifth of Ayurvedic herbal products manufactured in South India and sold in Boston contained potentially harmful concentrations of lead, mercury or arsenic, or combinations of these.2 In Australia, traditional Indian and Chinese medicines authorised for supply are regulated as complementary medicines and must meet manufacturing and quality standards that ensure the absence of contaminants.3 However, there is no quality control of medications imported for personal use or purchased over the internet. Importantly, this case involved tablets prepared by a registered pharmaceutical manufacturer and presented in sophisticated packaging (Box 2). Reports of lead contamination from traditional Indian and Chinese medicines have been intermittently publicised4,5 and include recent warnings from the New South Wales Health Department concerning Ayurvedic medicines. Patients with lead toxicity commonly present with non-specific clinical features, and lead poisoning might only be suspected when a blood film shows anaemia with basophilic stippling. While enquiring about a patient’s environmental, occupational and social history is important for determining possible sources of lead exposure, clinicians should also ask patients if they have used alternative and complementary medicines and whether these were obtained in Australia or from overseas. 1 Blood film from the patient showing coarse basophilic stippling 2 Packaging from the lead-containing Ayurvedic medicine

Nilika G Wijeratne · James C G Doery · Andis Graudins

To the Editor: I describe two episodes of transient recurrence of psychosis temporally related to ingestion of an “energy drink” in an obese (125 kg) 27-year-old New Zealand Maori man who had been diagnosed with schizophrenia 8 years earlier. The patient had found that risperidone 6 mg/day effectively relieved persecutory ideas and auditory hallucinations. He had stopped using cannabis and alcohol to excess, but continued to drink up to 10 cups of instant coffee throughout the day for a “lift”, apparently without insomnia or other complications. In July 2009, he consumed a 60 mL Demon Shot energy drink and enjoyed an hour-long “buzz”. Repeating the dose did not re-create the desired effect, and instead made him uneasy, irritable and paranoid; for the first time in many months, he had recurrent thoughts, lasting several hours, of people wanting to harm him. One week later, he drank three shots over 15 minutes. He again experienced a buzz and was observed to be emotionally labile — initially laughing and talkative, and later, restless, withdrawn and argumentative. He had a rapid pulse and insomnia. These symptoms subsided over the next day, and when he was back to his usual self after a further 2 days, he described having had paranoid ideas (“gangsters after me ... scared to leave the house”) over several hours after consuming the drinks. His family also associated these symptoms with the drinks, noting a striking similarity to his illness before commencing antipsychotic treatment. He has since avoided energy drinks and continued risperidone monotherapy, remaining stable for 15 months. Demon Shot is a concentrated energy drink, widely available in Australia and New Zealand. The product’s web page describes each “insanely intense” shot as containing 200 mg caffeine, plus taurine, guarana, and B vitamins (http://www.demonenergy.com.au/products/demon-shots). As a regular smoker, the patient does have increased caffeine metabolism, and his response to consuming large amounts of coffee suggests he is not particularly sensitive to caffeine. Nevertheless, he did exceed the maximum recommended dose (two shots per day) on the second occasion, consuming at least 600 mg of caffeine (4.8 mg/kg) virtually as a single dose. The additional presence of guarana extract (48 mg per shot in Australia; unspecified in New Zealand) is probably relevant, as guarana is a further source of caffeine and may have other stimulant properties. Caffeinated drinks are popular among patients being treated for schizophrenia,1 possibly due to partial reversal of the unpleasant effects of dopamine blockade.2 Although case reports3 and a later controlled study4 suggest that high doses of caffeine may exacerbate psychosis, this has only recently been described for energy drinks.5 This case provides naturalistic challenge–dechallenge–rechallenge evidence that some patients with treated schizophrenia may be vulnerable to exacerbation of their illness by such products.

David B Menkes

To the Editor: At budget estimates hearings of the Senate Community Affairs Committee in June 2010, answers were provided to questions on notice asked by Senator Guy Barnett to the Therapeutic Goods Administration (TGA) about the use of mifepristone for medical abortion in Australia since 2006.1 The answers are of interest as they include the number of practitioners who have become authorised prescribers of mifepristone in Australia since the “Harradine Amendment” was overturned in federal parliament in February 2006, as well as details of their practice. Nationally, 81 medical practitioners now have TGA authorised prescriber approval for mifepristone: 33 in New South Wales and 18 in Victoria (several large private clinics have gained approval in these states); 15 in South Australia, six in the Australian Capital Territory, five in Western Australia, and four in Queensland. There are none in Tasmania or the Northern Territory, so women in these two regions have no access to mifepristone abortion. There is very accurate documentation of all adverse effects of mifepristone–misoprostol medical abortion, which must be reported 6-monthly to the TGA. This information is then available to the general public through Senate estimates questioning. To 31 December 2009, 2926 medical abortions using mifepristone and misoprostol were performed in Australia by authorised prescribers. These include early and late procedures. The following adverse events were reported in that period: significant haemorrhage (7; 0.24%); retained products of conception requiring dilatation and curettage (D&C) or dilatation and extraction (84; 2.9%); ongoing pregnancy requiring surgical evacuation (14; 0.48%); and nausea and vomiting (10; 0.34%). These results are all well within the parameters expected from Australian and overseas studies of mifepristone–misoprostol use,2-5especially as a high proportion of the 2926 abortions would have been performed in the second trimester, as reported in a recent WA study.2 Large overseas studies on the use of mifepristone–misoprostol for early medical abortion (to 63 days of pregnancy) show a continuing pregnancy rate of around 1%, the need for D&C in 2%–3% of cases, and heavy vaginal bleeding requiring transfusion among 1 : 500 to 1 : 1000 women.3-5 These complications are more common in second-trimester procedures than in early medical abortions.2-5 Use of mifepristone in Australia is still restricted to authorised prescribers, and it is therefore not accessible to many women who might wish to use it. However, the number of cases performed in Australia is now large enough to conclude that mifepristone is safe and effective for the Australian women able to access it.

Caroline M de Costa

To the Editor: Following the 1918 influenza pandemic, during which an estimated 50 million people died,1 the relationship between influenza and secondary bacterial infections such as Streptococcus pneumoniae (pneumococcus) became recognised as an area of considerable scientific importance. It has been shown that influenza infection results in epithelial damage, up-regulation and exposure of respiratory tract receptors, alterations in the immune response and increased adherence of pneumococcus.2 The most severe form of pneumococcal infection, invasive pneumococcal disease (IPD), has a mortality of 7%–9%.3 It occurs frequently in the Indigenous population of the Northern Territory, with an incidence of 70.5 per 100 000, compared with 7 per 100 000 in Australia overall.3 In population studies, 11%–20% of seasonal increases in IPD have been attributed to influenza.4,5 During the increase in influenza notifications in 2009 in the NT, as a result of pandemic H1N1 (2009) influenza, a concurrent increase in IPD notifications was also recorded. Our study aimed to investigate whether there was a relationship between influenza and subsequent IPD. We calculated the relative risk of IPD in the 4 weeks after laboratory-confirmed influenza compared with the background risk. Cases were defined as patients who were diagnosed with IPD within 4 weeks of laboratory-confirmed influenza being diagnosed. Data concerning cases of influenza and IPD between 2005 and 2009 were extracted from the NT Notifiable Diseases System and merged by date of birth using Stata, version 11 (StataCorp, College Station, Texas, USA), leading to 75 matches. The 75 matched records were checked individually to determine whether they met the case definition, resulting in eight potential cases. Demographic characteristics (name, sex, Indigenous status and address) were then checked to confirm the match. One case was excluded, leaving seven cases eligible for analysis. We identified 2567 cases of influenza and 346 cases of IPD in the study period. The risk of IPD within 4 weeks of influenza was calculated as 7/2567 (2.7 × 10-3). To calculate the background risk of IPD in a 4-week period, we first calculated the annual risk of IPD occurring without previous influenza (339/1 076 470 person-years) and divided this by the number of 4-week periods in a year (13). This gave a background risk of 2.42 × 10-5 and a relative risk of 112.5 (95% CI, 48.9–224.8; χ2 = 758.3; P < 0.001). This analysis is based on population surveillance data, and is therefore limited by the possibility of ascertainment bias due to variations in influenza testing. Nevertheless, our study provides additional evidence that IPD is an important complication of influenza, and reinforces the need for clinicians to promote influenza vaccination in high-risk individuals and to be aware of complications which may occur in the weeks after the initial viral infection. Additionally, achieving high coverage of pneumococcal vaccination in at-risk groups will reduce the impact of influenza.

Laura J Edwards · Peter G Markey · Heather M Cook · James M Trauer · Vicki L Krause

To the Editor: Resistant gram-negative bacteria (especially Escherichia coli) are a major and growing problem worldwide.1 Some strains are resistant to all available antibiotics.2 We report a patient with relapsing multi-resistant E. coli bacteraemia from a prostate infection. Relapses occurred despite treatment with numerous parenteral antibiotics that should have been effective. His infection was cured using azithromycin. A 69-year-old man developed dysuria and fever 2 days after a transrectal prostate biopsy; he had received ciprofloxacin for prophylaxis. He had travelled to Morocco 15 months before this episode and to Vietnam 1 year earlier. Blood and urine cultures grew E. coli that showed sensitivity to ceftriaxone, gentamicin and nitrofurantoin; intermediate sensitivity to ampicillin; and was resistant to ciprofloxacin, cotrimoxazole, tetracycline, doxycycline and cephazolin. He was treated with intravenous ceftriaxone for 2 weeks, followed by oral amoxycillin/clavulanate with a good clinical response. The patient relapsed 1 week after completion of this treatment, with dysuria and fever. E. coli was cultured from his urine, with the same sensitivities as before. He was treated for 4 days with ceftriaxone and 2 weeks with amoxycillin/clavulanate. One week after his second course of therapy, he re-presented with dysuria and fever. Urine and blood cultures grew E. coli with the same sensitivities as the previous cultures. A prostate ultrasound showed no focal abscesses. He received ceftriaxone 2 g and gentamicin 7 mg/kg, yet remained febrile. After 2 days, gentamicin was discontinued and azithromycin 500 mg orally daily was added. He became afebrile within 24 hours and his C-reactive protein level fell. Azithromycin was selected because its minimum inhibitory concentration was 4 μg/mL, and because of its efficacy against multiresistant salmonella.3 The patient was treated for 1 week with ceftriaxone and for 3 weeks with azithromycin. He remained asymptomatic and his C-reactive protein normalised. There were no further relapses. He underwent prostatectomy for confirmed prostate cancer 2 months after discontinuing azithromycin. There was no histological evidence of prostate infection. We believe that while travelling in Morocco or Vietnam, he acquired multiresistant E. coli, which was carried in his bowel and inoculated during transrectal prostate biopsy, a common infective risk of this procedure. We believe the initial treatment failure was due to poor antibiotic penetration of the acidic prostate environment, and azithromycin was responsible for the eventual cure. Case reports and clinical trials have shown successful use of azithromycin in treatment of chronic prostatitis due to Chlamydia trachomatis,4 and that azithromycin is active against E. coli.5 This case report demonstrates successful use of azithromycin for treatment of E. coli prostatitis resistant to ciprofloxacin.

Simon H T Jiang · Peter J Collignon

To the Editor: As a family history of cystic fibrosis (CF) is uncommon among children diagnosed by newborn screening, offering carrier testing in the general population is warranted Cystic fibrosis is the most common severe autosomal recessive genetic condition in children. The carrier frequency in populations of Northern European ancestry is one in 25 and the incidence of CF in Victoria, Australia is 1 in 2874.1 There is no cure for CF, but advances in management have improved life expectancy. A question about a family history of CF is often asked as part of preconception or prenatal care in populations in which CF is more prevalent. However, anecdotally, most parents of a baby with CF do not report a family history and the diagnosis is unexpected. Carrier testing would provide information that may be used by couples to make reproductive decisions, such as prenatal and preimplantation genetic diagnosis of a fetus or embryo, respectively. Australia, the United Kingdom, other European countries, and all states in the United States now offer newborn screening for CF. Apart from records of affected older siblings,1 there are no clinical data for the existence of a family history of CF among children diagnosed with CF through newborn screening. We audited the family pedigrees, collected soon after diagnosis, of all children born in Victoria in 2000–2004 who were diagnosed with CF through newborn screening. From the extended pedigrees of 82 children, we identified five families with a family history of CF. In two pedigrees, the children were first cousins; in another two pedigrees, the children were first cousins once removed; and in one pedigree, the children were second cousins. There were no families in which older siblings had been previously diagnosed with CF, but in two families the diagnosis triggered further examination of older siblings who were subsequently diagnosed. These empirical findings that most babies with CF (77/82; 94%) are born to families with no family history of CF support clinical observations. Although inquiry about a family history of CF is necessary as part of prenatal or preconception care, this is not sufficient. Even when a family history is known, most relatives do not undertake carrier testing. For example, in an audit of cascade carrier testing after a diagnosis of CF through newborn screening, only 11.8% of eligible (non-parent) relatives were tested.2 Not surprisingly, a family history-based approach to offering carrier testing will not provide the vast majority of couples with the opportunity to learn their carrier status and make informed reproductive decisions. Therefore, in addition to newborn screening to diagnose affected babies, CF carrier screening in the general population (of individuals with a risk of one in 25)3 is needed.

Belinda J McClaren · Sylvia A Metcalfe · David J Amor · MaryAnne Aitken · John Massie

To the Editor: Rahman and colleagues suggest that iodine deficiency in Victoria increased between 2001 and 2006, based on the findings of thyroid-stimulating hormone (TSH) levels in neonates at routine newborn screening.1 Indeed, their data as presented suggest a doubling of the percentage of mothers with iodine deficiency to over 9% during that period. This could be correct. Certainly, as they state, there is much evidence to suggest that there is mild iodine deficiency in Australia. However, there are caveats about the data they report which are not mentioned. Data from New South Wales do not show this trend. While they do suggest a degree of mild iodine deficiency, there was no increase in the percentage of neonates with TSH levels > 5 mIU/L of whole blood from 2002 to 2009 (Box), although the average age at sampling falls slightly (from 2.96 to 2.32 days) over this period. The World Health Organization has defined iodine sufficiency as being indicated, inter alia, when more than 3% of newborns aged 3–4 days have a TSH level > 5 mIU/L of whole blood.2 Factors that affect the TSH level in a newborn screening program include the precise age at sampling, and any changes to the method of TSH analysis used. In a Swiss study assessing the efficacy of iodine supplementation, there was a small but significant decrease in the TSH level from Day 3 to Day 4 of age.3 This is unsurprising: following the TSH surge in the first hours after birth, TSH levels decline gradually to a steady level at about Day 7.4 There could well have been a trend to earlier sampling in Victoria, within the bounds of the 2–4 days of age assay that Rahman and colleagues mention, over the period studied, but these crucial data are not given. The dried blood spot TSH assay method is not described either. A change in any aspect of the methodology; for example, if the manufacturer modified the antibody used, may produce a small, clinically insignificant but numerically significant, change in results. If the data presented by Rahman and colleagues for Victoria do not have these biases, then the situation warrants further investigation, but whatever is happening in Victoria seems not to be replicated over the border. Percentage of newborns with thyroid-stimulating hormone (TSH) level > 5 mIU/L of whole blood, detected by routine newborn screening in New South Wales, by year Year Newborns with TSH level > 5 mIU/L 2002 3.80% 2003 3.68% 2004 3.87% 2005 5.02% 2006 4.48% 2007 3.56% 2008 3.92% 2009 4.00%

Bridget M Wilcken · Veronica C Wiley

In reply: The methods used for blood sample collection and analysis remained unchanged during our data collection period. One source of thyroid-stimulating hormone (TSH) calibrators and reagents was used over the study period by a single laboratory covering all of Victoria. Material from the United States Centers for Disease Control and Prevention was used for external quality assurance, ensuring that the results were in agreement with those of other laboratories. The per cent coefficient of variation over the period ranged from 10% to 20%. The table of neonatal TSH values for New South Wales provided by Wilcken and Wiley further demonstrates the value of using TSH levels as a screening tool for population iodine status, even with a decreasing mean age of sample collection. While we dealt with the effect of sample collection time in our published article,1 here we present a table illustrating analysis of the Victorian neonatal TSH values for samples collected at 48, 72 and 96 hours after birth (Box). The percentage of elevated TSH values increased from 2001 to 2006 at each collection time and, although the percentage of elevated TSH values decreased with increasing age, these values were still indicative of iodine deficiency. Iodine status varies between regions. The National Iodine Nutrition Study (NINS) found both South Australia and Queensland iodine sufficient, while the neighbouring states of NSW and Victoria were iodine deficient.2 The results also indicated that iodine status was worse in Victoria than in NSW; therefore, we might expect similar differences in TSH values. We are now in the process of analysing Victorian TSH values for 2007 to 2010. Percentage of newborns with thyroid-stimulating hormone (TSH) level > 5 mIU/L for blood samples collected at 48, 72 and 96 hours after birth, Victoria, 2001–2006 Sample collection time (h) Percentage of neonates with TSH > 5 mIU/L according to birth year 2001 2002 2003 2004 2005 2006 48 5.73% 6.83% 8.47% 10.58% 11.86% 13.53% 72 4.20% 5.15% 6.87% 7.01% 9.13% 9.38% 96 2.49% 3.21% 4.37% 3.78% 5.98% 5.34%

Ashequr Rahman · Gayle S Savige · Nicholas J Deacon · Ivan Francis · Janice E Chesters

To the Editor: O’Leary and Major1 have opened debate on the issues raised by the New South Wales-wide introduction of the Clinical Excellence Commission Between the Flags (BTF) observation charts, which incorporate escalation thresholds for vital signs and other criteria. In the BTF charts, “yellow” zone criteria trigger a clinical review and “red” zone criteria, a rapid response.2 Evidence shows that deterioration can be recognised early, reducing serious consequences.3,4 O’Leary and Major trialled a subset of the draft BTF paediatric calling criteria in the context of triage in an emergency department, applying them retrospectively and comparing the actual triage decision with the one that would have been made using the BTF criteria alone. They also examined patient disposition for patients falling within the yellow and red zones. They concluded that “the physiological parameters ... are not suitable as a triage tool in the paediatric emergency department, do not replace an experienced triage nurse, and are a poor predictor of disposition”.1 We are not surprised by this conclusion. The Australasian Triage Scale is designed to assess a patient’s urgency based on presenting problem and general appearance, possibly combined with physiological observations.5 Trialling a subset of vital signs, on their own, against the triage process, although interesting, is unlikely to demonstrate a strong correlation in decision making for the following reasons. The BTF vital signs observations are designed for use in the context of a “track and trigger system” in a general ward, to monitor trends, not as a substitute for the triage process. Vital sign observations on their own contribute little to triage decisions. Triage decisions are poor predictors of disposition (eg, up to 67% of triage Category 2 patients are discharged home from the emergency department) (Sydney South West Area Health Service emergency department data for July 2010, for Campbelltown, Liverpool and Royal Prince Alfred hospitals). On their own, we would expect vital signs to be poorer predictors of disposition outcome than triage decisions, which have the benefit of information on presenting problem and general appearance. Context for vital sign observations has a major influence on their interpretation. We recommend that more work be done on the value of the BTF vital signs criteria as a complement, not alternative, to triage processes.

Charles H Pain · Clifford F Hughes · Marino Festa · Jodie Ekholm · Matthew O’Meara

To the Editor: Pearce and Haikerwal state that “legislation to introduce health identifiers [was] recently passed by Parliament” and that e-health “can ease the patient journey, improve quality of care and reduce costs”.1 It is critically important to comprehend the purpose of the unique health identifier. Its primary function is to be the “key” to a patient’s clinical data and information. It is not a clinical decision-support tool that will improve care. There are many systems that require multiple identifiers for a given patient. However, the success of these systems is dependent on their ability to provide information management tools.2-5 The authors correctly state that “Australia’s health care system lags behind all other sectors of our economy in the use of computerised systems”. What must be debated is their statement that, although “general practice and community pharmacy are highly computerised, the hospital sector is not”. The debate should move from the uptake numbers for computerisation to the evidence of whether these implementations have improved care — for example, through fewer adverse drug events, decreased resource use, improved quality of care and better patient outcomes. I suspect the evidence is very thin in the Australian context. The authors observe: “Uncoordinated implementation of differing, incompatible systems within and between hospitals compounds a dire lack of national coordination of effort.” This is not a new phenomenon. We actually know what works and, in some advanced systems, what does not work.6 This evidence base should provide the stimulus for pursuing the changes necessary to implement effective health information technologies. These changes are more social, professional and cultural than technical.7 In their final comments on the National E-Health Transition Authority, Pearce and Haikerwal maintain their focus on the technologies. Can we wait 5–10 years for the e-health system to be connected via the National Broadband Network? The necessary information management tools can be implemented now. Care must be a priority. It would help if the focus was on successful implementation and a willingness to listen to those who have some degree of success in this field. A review of the National E-Health Transition Authority’s website list of clinical leaders suggests that there are few clinical informaticians currently involved.

Terry J Hannan