Letters

To the Editor: My compliments on the issue of the Journal on the survival of general practice (20 July 2009). But something was missing — a patient’s perspective. I hear from fellow Sydneysiders that they cannot find a general practitioner offering continuity of care. They tell me that: All recommended GPs have “closed books”. They can’t get an appointment on the day and have to wait until a few days later, unless it’s a “real emergency”. At big, “commercial” practices, they seldom see the same GP again — and must tell their story each time. Their GP (preferably female) is there some weekdays only. They can’t find a GP who does home visits. Neither “their” GP, nor any of the others in the practice, is available after hours — they must ring an emergency doctor with no access to their records. GPs want them out quickly with a prescription or referral. GPs say that, although it’s a simple procedure, it’s better done by a specialist. GPs want to start a “care plan”, even if there’s nothing much wrong. They’re not happy with attention from the nurse — they want to see the doctor. And so it goes. Back in 2006, the Australian Consumers Association, together with advice on choosing a GP, commented: The relationship you have with your doctor can be one of the most crucial in your life ... A positive ongoing relationship with your GP is extremely valuable, making it all the more important to choose the right one.1 Shouldn’t the MJA open its pages — on an issue which matters so much to them — to patients, to air their concerns? As it would be anecdotal, we would need evidence. A recent article in the BMJ surveyed British attempts at harnessing the views of patients.2 The authors’ opening comments were: “There is now a widespread realisation that patients’ views are not optional but essential to achieving high quality care.” Similarly, Australian patients’ expectations about weight management in general practice were discussed in the Journal in 2006.3 Is general practice’s survival not about adapting to meet patients’ requirements for high quality of service? In special issues devoted to the adaptation of general practice to future change, should not bodies like the Australian Consumers Association and some of the patient support groups, such as Arthritis Australia, be asked to contribute? Perhaps the MJA’s discussion is missing the wood for the trees?

Peter C Arnold

To the Editor: Hospitalisation rates for seasonal influenza are highest among young children and people aged over 65 years.1-3 Calculation of laboratory-confirmed infection rates is difficult because influenza testing is not consistently performed. Using diagnostic codes to identify hospitalisations for acute respiratory illness provides one measure of the relative burden of pandemic (H1N1) 2009 (pH1N1) virus infection compared with influenza virus infections in previous influenza seasons. On 26 May 2009, the first pH1N1 virus human infection in New South Wales was identified, and between June and August 2009, pH1N1 was the predominant circulating influenza virus strain (found in 15%–82% of influenza A-positive specimens).4 In July 2009, the Hunter New England Area Health Service (HNEAHS) (population, 866 000) in NSW established population-based surveillance for hospitalisations for acute respiratory illness at all 35 HNE public hospitals admitting patients with respiratory illness. Data on hospitalisations coded with eight International Classification of Diseases (10th revision) codes (Box 1) were analysed by age group and year. Data for 2007 and 2008 (relatively severe and relatively mild influenza seasons, respectively)5 were used for comparison. Monthly hospitalisation rates for acute respiratory illness were calculated for 1 January 2007 to 31 August 2009. Over the period June to August in 2007 and 2008, 1736 and 1267 hospitalisations for acute respiratory illness occurred, respectively, and monthly hospitalisation rates peaked during August in both years (859 [9.7/10 000 persons] in 2007 and 517 [5.8/10 000 persons] in 2008). The highest hospitalisation rates occurred in children aged 0–4 years (113 [20.6/10 000 persons] in 2007 and 37 [8.9/10 000 persons] in 2008) and in people aged ≥ 62 years (276 [16.3/10 000 persons] in 2007 and 212 [12.1/10 000 persons] in 2008). In 2009, over the same 3-month period (June to August), there were 2378 hospitalisations for acute respiratory illness, with monthly hospitalisation rates peaking in July (1029 [11.4/10 000 persons]). Between May 2009 (before pH1N1 circulation) and July 2009, the monthly hospitalisation rate for acute respiratory illness in the HNEAHS increased by 260% (from 385 [4.3/10 000 persons] to 1029 [11.4/10 000 persons]). During the same period, age-specific hospitalisation rates increased more than threefold among children aged 0–4 years (from 31 [5.5/10 000 persons] to 101 [17.9/10 000 persons]) and 5–16 years (from 36 [2.5/10 000 persons] to 140 [9.8/10 000 persons]), and more than sixfold among people aged 17–31 years (from 43 [2.6/10 000 persons] to 281 [16.9/10 000 persons]) (Box 2). In July 2009, age-specific hospitalisation rates among people aged 5–61 years exceeded respective peak age-specific hospitalisation rates for 2007, while hospitalisation rates among children aged 0–4 years and people aged ≥ 62 years remained below 2007 peak rates for their respective age groups. Although our analysis calculated hospitalisation rates for various types of respiratory illness (including infections with non-influenza viruses) and may be affected by changes in health care-seeking behaviour and coding practices, comparison over multiple seasons suggests several unique features of the 2009 influenza season in the HNE region. Compared with 2007 and 2008, the HNEAHS experienced a rapid, early increase in hospitalisations for acute respiratory illness, coinciding with the emergence of pH1N1. Furthermore, a disproportionate burden of hospitalisations occurred among people aged 5–61 years (particularly those aged 17–31 years), with a relatively lower burden among those aged ≥ 62 years. Ongoing surveillance will determine whether these age-specific trends continue in the 2010 influenza season. 1 Emergency department ICD-10 separation codes used for acute respiratory illness hospitalisation surveillance Code Disease J11 Influenza, virus not identified J11.1 Influenza with other respiratory manifestations, virus not identified J11.8 Influenza with other manifestations, virus not identified J12.9 Viral pneumonia, unspecified J15.9 Bacterial pneumonia, unspecified J18.9 Pneumonia, unspecified J22 Unspecified acute lower respiratory infection J96.9 Respiratory failure, unspecified ICD-10 = International Classification of Diseases (10th revision). 2 Monthly hospitalisation rates for acute respiratory illness in the Hunter New England Area Health Service region, May–August 2009, compared with peak monthly rates in 2007 and 2008* * Hospitalisation rates are per 10 000 residents of the Hunter New England Area Health Service region.

Fatimah S Dawood · Craig B Dalton · David N Durrheim · Kirsty G Hope

To the Editor: Bronchiolitis, most often associated with respiratory syncytial virus (RSV), is a major cause of hospitalisation in young children. Those with chronic lung and congenital heart disease (the latter affecting about 192 births annually in Western Australia) are at particularly high risk.2 Immunoprophylaxis with the RSV monoclonal antibody palivizumab is effective in reducing severe RSV-related hospitalisations, and monthly immunoprophylaxis is recommended in high-risk children.2,3 Monthly immunoprophylaxis is costly; therefore, the most cost-effective schedule follows the times of peak RSV activity4 — usually the winter months, May to October. Using the Western Australian Data Linkage System,5 we investigated the seasonality of bronchiolitis hospitalisations (International Classification of Diseases-10 code J21) from 1996 to 2005 as a proxy for RSV-related illness. Data specifically for RSV-related illness were considered unreliable because some children may not have been tested for RSV, test results may not have been documented on hospital discharge notes, or RSV immunofluorescence tests may have given false negative results. Furthermore, RSV codes (B97.4, J12.1, J20.5, J21.0) were not used by hospitals in WA until July 1999. We identified 11 988 hospitalisations for bronchiolitis throughout WA among 245 249 births. Most bronchiolitis admissions (81%) were in children younger than 12 months. In the Perth metropolitan region, there was a clear winter seasonal pattern, with hospitalisations peaking in July. However, in the Kimberley region in northern WA, there was a sustained bimodal seasonality, with a peak in April and second peak in August (Box). Moreover, only 51.5% (469) of bronchiolitis admissions in the Kimberley and 61.5% (444) in the Pilbara–Gascoyne (located in mid-north WA) occurred between May and October, as opposed to 84.3% (6354) in the metropolitan region. These data support an earlier implementation and longer dosing schedule with palivizumab for high-risk children in the Kimberley and Pilbara–Gascoyne than for those in Perth. Our study has some limitations. Not all bronchiolitis hospitalisations may be caused by RSV. However, when we investigated only those hospitalisations with a specific RSV code, the monthly distribution showed a similar pattern. Additionally, timing of RSV activity, and therefore bronchiolitis, may vary from year to year. Although the numbers were too small to allow separate analysis by calendar year, bronchiolitis hospitalisations in the Kimberley showed extended seasons in 8 of the 10 years. Our findings support the need for each jurisdiction to know its seasonal pattern of bronchiolitis and RSV hospitalisations, and to implement recommended palivizumab schedules accordingly. Such use of extended prophylactic regimens may well require its cost-effectiveness to be reconsidered. Our analysis highlights the relevance of population-based data linkage studies to clinical care policy. Monthly distribution of bronchiolitis hospitalisations by region of child’s birth, 1996–2005

Hannah C Moore · Anthony D Keil · Peter C Richmond · Deborah Lehmann

To the Editor: In 2008, considerable publicity was given to the diagnosis and treatment of prostate cancer in two Australian celebrities: retired Australian Football League player Sam Newman and radio announcer Alan Jones. Newman’s cancer was reported on 5–9 March 2008, culminating in a 12-minute item on the high-rating Australian television program 60 Minutes, when Newman said, “Be tested and enjoy life”. Jones’s announcement of his forthcoming surgery was reported on 3–4 July 2008, and his recovery on 16–27 July. We investigated whether this publicity was associated with changes in the rate of prostate specific antigen (PSA) testing. We used Medicare Australia data on claims for Medicare Benefits Schedule item 66655 (which allows “one annual PSA test for an individual without prior prostate disease”) to determine the mean number of PSA tests and age-standardised testing rate between January 2002 and March 2009. We fitted a linear regression model to the log of the age-standardised rates, modelling secular trends using natural splines with two degrees of freedom (splines were piecewise cubic within the data range and otherwise linear), with indicators set for the average effect of the second, third and fourth quarters and an indicator for the second quarter of 2008. We calculated predicted values and prediction intervals (which take into account both uncertainty in the predicted mean and individual variation), excluding observed data for the second quarter of 2008 (Box). The mean monthly number of PSA tests was 72 064 in the 12 months before April 2008, increasing to 107 633 in April 2008, and 90 813 in July 2008. The seasonally adjusted age-standardised rate of PSA tests rose 17% above the secular trend in the second quarter of 2008 (95% CI, 8%–27%), with the observed data point falling outside the prediction interval (Box). This represented an additional 39 000 PSA tests during the second quarter of 2008. These data show that prostate cancer screening increased significantly in the quarter after media coverage of Newman’s prostate cancer diagnosis. Screening seemed to have returned to the expected seasonal rate by the time of Jones’s diagnosis, in the third quarter of 2008. The impact of celebrity cancer diagnoses on population screening has been demonstrated previously, most recently by an increase in breast cancer screening following news of pop singer Kylie Minogue’s breast cancer diagnosis in 2005.2 In a survey of US men, almost a third stated they would be more likely to have a PSA test after hearing celebrities endorse prostate cancer screening.3 In addition, coverage of melanoma by 60 Minutes in 1987 was followed by a 167% increase in melanoma detection in the subsequent 3 months. Whether the additional 39 000 PSA tests performed in the second quarter of 2008 result in a surge in diagnoses of prostate cancer remains to be seen. Despite continuing uncertainty about the benefits of PSA testing, but unequivocal evidence of harms,,6 Australian men’s willingness to be screened for prostate cancer appears to have been boosted by this celebrity endorsement. Age-standardised* prostate-specific antigen testing rates in Australia (assessed quarterly) Prostate-specific antigen (PSA) testing rates showed a consistent seasonal pattern, with the highest rates in the third quarter (July–September) for all years except 2008, when they were highest in the second quarter. * Standardised to Australian 2001 population.

David P Smith · Mark S Clements · Melanie A Wakefield · Simon Chapman

To the Editor: The recent article by Lowthian and colleagues raises some important concerns regarding current management of warfarin therapy in Australia, especially the provision of quality warfarin education.1 While the study focused on the uncertainty surrounding who is responsible for this task, additional barriers to providing warfarin education include limited access to suitable resources and a tendency to rely on a single verbal counselling session and/or the supply of written material, often just before discharge from hospital.2 As Lowthian et al note, it is plausible that warfarin education was provided to the patients interviewed; it may simply have been inadequate to meet their needs or delivered at the wrong time or place. It is not always feasible for health care providers to reliably provide the necessary education in busy health care settings (eg, general practitioners when prescribing warfarin, pharmacists when supplying it). The authors note a potential role for practice nurses in providing this education; we would also like to highlight the role of accredited pharmacists, who can visit patients in their homes and provide targeted medication-related education. An annual Home Medicines Review can be provided for patients taking high-risk medications such as warfarin.3 Under the Fourth Community Pharmacy Agreement Research and Development Program, the Pharmacy Guild of Australia has funded two projects that are attempting to meet the education needs of patients taking warfarin. One project is trialling a comprehensive postdischarge service involving a series of follow-up home visits by trained accredited pharmacists, to provide not only warfarin education but also point-of-care international normalised ratio monitoring, in liaison with the patients’ GPs. The other project is piloting a process whereby community pharmacists can identify potential candidates for patient self-monitoring of warfarin and, with GP collaboration, organise suitable training, with ongoing support from the pharmacist and GP. Patient self-monitoring, although not widely practised in Australia, has been shown to provide the best clinical outcomes for suitable candidates.4 An important component of these two projects is a website, launched in late 2008, containing a range of free, downloadable educational resources for both consumers taking warfarin and health care professionals responsible for its management (http://www.anticoagulation.com.au). Education is crucial in achieving optimal health outcomes for patients taking warfarin, and health care professionals should cooperate to ensure their patients are well educated. This should involve regular reinforcement of consistent messages, and can also involve better use of existing services and educational tools.

Luke R E Bereznicki · Leanne Stafford · Ella C Jeffrey · Gregory M Peterson · Shane L Jackson

In reply: Bereznicki and colleagues have reinforced the importance of patient education in optimising warfarin safety, while highlighting the need for role clarification in its provision. We applaud the Pharmacy Guild of Australia’s sponsorship of research projects trialling different models of service delivery, such as the coordination of postdischarge warfarin home care by pharmacists and support of patient self-monitoring programs, where appropriate. The success of such care models will be enhanced by a collaborative partnership between the patient and all members of the warfarin care team.1 In addition, appraisal of patient suitability for programs such as patient self-monitoring requires systematic and regular evaluation of cognitive function, compliance and health literacy, to reduce the likelihood of adverse events.2-4 Likewise, ongoing education with resources tailored to individual patients’ capabilities will optimise patient safety.5

Judy A Lowthian · Basia O Diug · Sue M Evans · Ellen L Maxwell · Alison M Street · Leon Piterman · John J McNeil

To the Editor: Lowthian and colleagues ask who is responsible for the care of patients treated with warfarin therapy.1 In Melbourne, it seems that this devolves mainly upon the pathology laboratory, whereas in other states, general practitioners manage care for their own patients, in my own experience. Where management of warfarin dosing, based on the international normalised ratio (INR) result, is performed by the laboratory, this is done as a courtesy to GPs. This practice possibly evolved from competition between private laboratories and, as such, may have been intended to induce other pathology requests to the service provider. Larger metropolitan private pathology services may have sufficient pathologists with haematology training to provide warfarin dosing to patients, but this may not always apply in smaller laboratories. In some laboratories, warfarin dosing may be provided to patients by scientific staff. Although warfarin therapy can sometimes be challenging, its difficulties are not usually insurmountable. Problems for pathologists arise because they are expected to give a warfarin dose by telephone to a patient they do not know and have never seen. The patient’s phone number may be not supplied or incomplete, and the call may not be answered. If answered, a brief history of previous INR results, dosages and test intervals may or may not be elicited from a person who may have poor English, who may be the patient, a relative, friend or neighbour; or a message may have to be left. If the message is received, it may not be acted on, depending on memory, understanding or level of compliance. If the message is not received, the patient and the patient’s GP may be unreasonably irate, even though multiple attempts to contact the patient may have been made. It is not hard to understand why some GPs prefer to pass this often frustrating and time-consuming aspect of treatment to pathologists — who may also be pressed for time. Problems are further compounded if warfarin dosing devolves to pathology laboratory scientists, which may be required by their employer. Scientists would be, in effect, performing drug dosing without medical training or medical registration and may be exposing themselves to litigation risk, without carrying medical indemnity. In other Australian states, it seems that GPs do provide treatment and dosing of warfarin for their own patients. In my view, this is the safest and most satisfactory outcome for patients, pathologists and scientists. With the projected advent of point-of-care testing with reliable INR results2 and new anticoagulant alternatives1 that would enable easier management of anticoagulant therapy by GPs, this whole issue could potentially be resolved.

John C Roberts

To the Editor: I appreciated Brukner’s perspective on treatment of venous thromboembolism (VTE),1 but I do feel some additional considerations and clarifications are in order. Quotes from Kearon2 and Kearon and colleagues3 about the duration of therapy are missing an important caveat. The suggestion for longer duration and possibly “indefinite” anticoagulant therapy after a first deep vein thrombosis or pulmonary embolism is in reference to unprovoked VTE. Brukner1 mentions a plane flight from China to Australia 3 days before he experienced a symptomatic pulmonary embolism. According to guidelines issued by the American College of Chest Physicians, such a flight (although I cannot comment with certainty on its duration) is likely to represent a reversible minor risk factor for VTE — “prolonged travel (eg, > 8 h)”.3 Indeed, Kearon2 and the authors of a related research article to which he refers4 make the important distinction between provoked and unprovoked VTE. Kearon comments: For patients with a minor reversible risk factor, the risk of recurrence is about 5% in the first year after stopping anticoagulant therapy. This is considered low enough to justify stopping anticoagulant therapy at the end of 3 months.2 Additional factors and preferences are also important when considering prolonged anticoagulant therapy for individual patients. For instance, I can empathise with the 25-year-old who wants to discontinue warfarin therapy after 6 months following a first unprovoked VTE — another 50 years of warfarin therapy might seem a disheartening burden. And certainly we must take into account other variables that may increase a patient’s risk of bleeding complications while receiving warfarin therapy, such as older age, the presence of other acute or chronic illnesses and the use of other medications, particularly antiplatelet therapy.3 For someone such as Brukner,1 who claims that his anxiety about a recurrence of VTE is reduced by staying on warfarin therapy, I would probably say, “That’s OK by me, as long as you are aware of the risks and implications of provoked and unprovoked VTE”. For other patients with unprovoked VTE who may not want to continue indefinite anticoagulant therapy, there are other management options worth discussing. First, there is the possibility of further risk stratification for VTE recurrence by testing D-dimer levels. This strategy is receiving considerable study and validation as a useful tool for predicting VTE recurrence.5,6 Second, for patients who refuse to continue warfarin therapy but would consider other therapies for reducing their risk of having a recurrence of VTE, I would suggest taking a daily low dose of vitamin E, which has shown some benefit in reducing VTE.7 Finally, the ASPIRE (Aspirin to Prevent Recurrent Venous Thromboembolism) Trial, which is currently underway, should provide a definitive answer as to whether aspirin is a safe and effective option for secondary VTE prevention. If the trial supports the use of aspirin for this purpose, it would offer another VTE risk-reduction option for those who prefer not to take warfarin indefinitely.8

James A Fink

To the Editor: Brukner’s personal perspective in a recent issue of the Journal highlights the inherent difficulty of managing patients taking warfarin.1 Although Brukner advocates life-long warfarin therapy for patients who have experienced a pulmonary embolism, we believe few clinicians would be willing to expose their patients to the increased risk of haemorrhage associated with long-term warfarin therapy, especially if a transient risk factor for venous thromboembolism (VTE) existed (such as frequent air travel, in Brukner’s case). There is an abundance of conjecture regarding the appropriate duration of warfarin therapy for VTE, with guidelines and clinical intuition often differing. But it is possible that, in the future, decisions about the appropriate duration of warfarin therapy may be guided by the use of pharmacogenetics. Pharmacogenetics gives clinicians an insight into how a patient’s genetic profile affects his or her ability to metabolise drugs, thereby allowing doctors to better tailor the dose and duration of the patient’s medications. In the case of warfarin, metabolism of S-warfarin (the more potent enantiomer in the racemic warfarin mixture) occurs via the cytochrome P450 system, specifically enzyme CYP2C9.2 Studies have shown that patients who metabolise warfarin normally are homozygous for the wild-type allele CYP2C9*1, whereas patients with polymorphisms in the CYP2C9 allele have reduced warfarin metabolism and increased risk of bleeding.3 The anticoagulation effect of warfarin actually occurs via inhibition of the C1 subunit of the vitamin K 2,3-epoxide reductase complex (VKORC1).4 Numerous polymorphisms have been identified in VKORC1, and it is speculated that VKORC1 polymorphisms alone may account for a significant proportion of response variability to warfarin.4 Validated algorithms have been developed to combine information on a patient’s CYP2C9 and VKORC1 genotypes with factors such as age and body surface area to identify an appropriate warfarin regimen.5 Although the pharmacogenetic information required to employ this algorithm has not been assessed for cost-effectiveness, it is quite possible that clinicians will be able to use such pharmacogenetic information to their advantage in the future. This would allow doctors to identify with greater precision which patients are likely to benefit from warfarin (and how much is required, for how long), rather than relying on equivocal evidence and clinical intuition alone.

Amit K Verma · Ajai K Verma

To the Editor: In their national analysis, Robson and colleagues found less favourable outcomes among term singleton babies born in public hospitals than in private hospitals.1 Most health services research is non-randomised, and it is unrealistic to expect studies such as this to be as internally valid as a randomised controlled trial.2 As noted by others,3,4 in the absence of randomisation, it is difficult to untangle the myriad differences between mothers, babies, and the care provided in private and public hospitals (ie, the results might be subject to confounding). Robson et al statistically accounted for the potential confounding effect of maternal smoking (although these data were only available for about half the mothers), age, Indigenous status, parity, diabetes, hypertension, rurality and method of birth. We replicated their analysis using the Queensland Perinatal Data Collection (July 2005 – December 2007), which included virtually complete data on maternal smoking. Our analysis of 124 300 term singleton babies gave an adjusted odds ratio (AOR) for perinatal mortality of 2.0 (95% CI, 1.4–2.7), which is similar to that reported by Robson et al. Using more detailed data from the Queensland dataset, we statistically adjusted for other potential confounders — including pre-existing and gestational diabetes, pre-existing and pregnancy-induced hypertension, pre-eclampsia, eclampsia, antepartum haemorrhage, anaemia, depression, urinary tract infection, low birthweight (< 2500 g), socioeconomic status (based on area of usual residence5), alcohol and drug misuse, and artificial reproductive technology — and obtained an AOR of 2.1 (95% CI, 1.5–2.9). We are not implying that adding more and more variables to a statistical model is an appropriate way to account for confounding. Our aim is simply to show that Robson et al’s result is robust to statistical adjustment using the available data; this is not the same as saying the analysis is robust to confounding. We found that the higher perinatal mortality in public hospitals was greater for neonatal deaths (AOR, 3.1; 95% CI, 1.8–5.6) than for stillbirths (AOR, 1.6; 95% CI, 1.0–2.4). Excluding lethal congenital anomalies4 did not materially change the result (AOR, 1.9; 95% CI, 1.3–2.8). We also stratified our analysis by level of hospital — tertiary referral (neonatal intensive care unit), base (special care nursery), and community — and obtained a similar twofold mortality excess in each stratum. Although perinatal mortality is uncommon among term singleton babies (1 in 1000 in private hospitals versus 2 in 1000 in public hospitals), any excess risk should be investigated and the reasons for it understood. The results from Robson et al’s article might be due to confounding, but they should not be dismissed and should be investigated with more detailed clinical data. Even if all the excess risk is due to confounding, explicit confirmation of this would be extremely useful. To this end, the Statewide Maternity and Neonatal Clinical Network in Queensland Health will undertake clinical review and classification of term singleton deaths according to national guidelines6 and collaborate with the Australian Maternity Outcomes Surveillance System (AMOSS)7 to enhance prospective monitoring of late gestation perinatal deaths nationally.

Michael D Coory · Guan T Koh · Vicki Flenady · Maarten Kamp

To the Editor: Robson and colleagues found higher crude odds of perinatal death in public hospitals — an unsurprising finding, given the maternal demographics in the public system.1 However, after taking into account known risk factors for poor perinatal outcome by “adjusting for the potentially confounding variables available in the NPDC [National Perinatal Data Collection]”, the authors found that the odds ratio actually went up — implying that the pregnancies of mothers in the private system are higher risk. This is implausible. There are a number of problems with the analysis. The possibility that potentially important maternal information was not included has been acknowledged.1,2 Of greater concern is the omission of a history of low birthweight from the regression model. Since intrauterine growth retardation is a very strong risk factor for perinatal death,3 and since the rate of low birthweight in the public hospitals was double that in the private hospitals, this omission is puzzling. Furthermore, while the authors’ stated aim was to assess the effect of the private model of obstetrician-led interventional care on perinatal outcomes, they included the method of birth and hospital type as independent explanatory variables. Since the interventional nature of obstetric care is, as acknowledged by the authors, a key component of the model of care provided in a private hospital, adjusting for this variable will lessen the usefulness of the study in assessing the impact of private hospital care on perinatal outcomes. Put another way, in deciding what is best for her baby, a mother who is considering giving birth in the private system cannot cherry-pick only the non-interventional side of the obstetrician-led model of care — she must adopt the entire package. Including method of birth as a separate explanatory variable artificially inflates the apparent “riskiness” of the pregnancies of mothers presenting to private hospitals to give birth. These mothers had a 75% increased incidence of caesarean section; however, most of these procedures would be elective rather than emergency. Since this distinction was not made, the women in private hospitals appear high risk despite having had a caesarean section for a low-risk pregnancy. This will have the effect of making perinatal outcomes in private hospitals appear more favourable than they actually are. As currently analysed, the data are of little value to prospective mums and dads in making the first, and one of the most emotive, of the many decisions they need to make as parents.

Daniel C Chambers

To the Editor: Of the many problems with the study by Robson and colleagues,1 the one that concerns us most is the outcome of perinatal death. The headline that this is twice as high in public hospitals has the potential to scare those who have no choice about where they give birth. Both the public and the medical community have a right to expect that this outcome is rigorously and accurately represented. We do not believe this to be the case. The perinatal death rate is made up of stillbirths and neonatal deaths in the first 28 days of life. Stillbirths will comprise 70% of all perinatal deaths, and more than 90% of stillbirths after 37 weeks’ gestation will occur before the onset of labour.2,3 It cannot be excluded that this relates to model of care but, because less than 10% of these stillbirths will have occurred during delivery, it is most certainly not related to the type of birth hospital or the interventions performed during labour. Most likely, it reflects differences in intrinsic risk that have not been controlled for by Robson et al.1 The neonatal death component of this statistic is probably confounded by ascertainment bias. Most neonatal deaths after 37 weeks’ gestation occur for two reasons: intrapartum hypoxia–ischaemia and severe congenital abnormalities. When the latter are diagnosed antenatally, the mothers will often be transferred to tertiary public hospitals for a second opinion and further management. Babies with undiagnosed lethal abnormalities or severe intrapartum hypoxia will invariably be transferred postnatally to a tertiary public hospital neonatal intensive care unit, where death often occurs after withdrawal of intensive care. The midwives data collection form is filled in at the birth hospital, and the baby is categorised as “discharged”, “transferred” or “died”. The 2006 national perinatal data collection report specifically cautions: Ascertainment of neonatal deaths within 28 days of birth is likely to be incomplete. In particular, deaths occurring among babies transferred to another hospital, readmitted to hospital or dying at home may not be known to midwives who collect these data or staff who compile state and territory data.2 Thus, it is unlikely that the difference in perinatal mortality described by Robson et al1 has anything to do with the birth hospital. To represent it as such in the public arena is irresponsible. Further, for the MJA to misrepresent “perinatal mortality” as “neonatal mortality” in the media release about this article defies belief.

Nick Evans · Girvan Malcolm · Adrienne Gordon

To the Editor: The study by Robson and colleagues1 predictably produced alarming media headlines. However, we feel the study contains potential inaccuracies that seriously undermine the conclusion that the baby toll is lower in private hospitals. Did the authors ascertain the true impact of fetal abnormality or conditions requiring transfer to tertiary care? Women with threatened preterm labour often transfer to the public system and subsequently remain under the care of public high-risk teams. Babies with a known congenital anomaly detected antenatally by private obstetricians may be similarly transferred. This highest level of care is only available in public hospitals, usually those with dedicated subspecialist services in maternal–fetal medicine, neonatology or neonatal surgery. When babies who have been transferred from private hospitals to the public neonatal intensive care system subsequently die within 28 days of birth, this may be recorded as a public hospital death. The authors stated that the “major adverse outcome associated with social disadvantage is low birthweight” but that assessment of the effect of social disadvantage was beyond the scope of their study. Not accounting for the effect of low birthweight is unacceptable. The National Perinatal Data Collection records birthweight accurately and is easily used to remove the bias of low birthweight. An internationally accepted indicator of optimal perineal outcome is the rate of intact perineum. This is known to be lower in private hospitals but was curiously not reported. Further, a prospective data audit in a tertiary hospital revealed that where episiotomy extends to third- or fourth-degree tear, this is only reported as episiotomy.2 Thus, with twice the rate of episiotomy in private hospitals,3 and its association with severe perineal trauma, this outcome could be seriously under-reported in Robson et al’s study. The authors identify the significantly higher rate of caesarean sections in private hospitals as one of the measurable benefits of this model of care and dismiss any concerns as “orthodoxy”. They have overlooked the significant morbidity and mortality among term neonates associated with the rise in caesarean rates, both elective and following labour. Research using detailed Australian and New Zealand Neonatal Network data to ascertain admission rates of babies of ‘‘low-risk’’ women to neonatal intensive care units and special care nurseries not only found higher rates of admission across each gestational age group after elective caesarean section but also reported the death of two infants.4 Such morbidity and mortality is arguably the most important differential of care experienced by women who give birth in private or public hospitals.

Sally K Tracy · Alec W Welsh · Hannah G Dahlen · Mark B Tracy

To the Editor: More than 30 years ago, I was employed by the Commonwealth Government’s Maternal Mortality Committee to identify and evaluate factors contributing to maternal and infant mortality among Aboriginal Queenslanders. At that time, government policy was to transfer all pregnant Aboriginal women from their rural communities or missions to Cairns Base Hospital at 32 weeks’ gestation until 7–10 days after birth. Findings I presented in a report to Queensland Health in 19771 and at the Australian College of Paediatrics Annual Meeting in 19792 included: Babies of women who were compulsorily transferred at 32 weeks’ gestation to Cairns Hospital had lower neonatal death rates. It was assumed that — as Aboriginal women had unreliable gestational age assessments, antenatal care was irregular, and birthweights were lower than for other races3 — the risk of premature deliveries could be avoided by early transfer. There was a lower rate of breastfeeding among mothers transferred to Cairns, largely because if they opted to bottle-feed they could return home after 3–4 days (rather than waiting 7–10 days in Cairns to ensure breastfeeding was established).1 Growth failure was common in the month after weaning.4 Bottle-fed babies experienced slower weight gain and higher rates of illness.5 Suboptimal growth in bottle-fed babies during the early postnatal months predisposed babies to poor growth patterns during infancy6 and increased death rates.7 Women returning to their communities took with them infections acquired during the hospital stay in Cairns. Separation anxiety or maternal deprivation was common among children left in their communities. There was decreased family bonding (eg, between the father and the new child) and sibling resentment at maternal separation. There was unquantifiable resentment at having babies born away from the ancestral lands. Women delayed admitting their pregnancies in an attempt to remain in their communities, resulting in fewer antenatal visits. The antenatal transfer policy has been in effect for 30 years, despite conflict between those who were predominantly concerned with maternal and perinatal mortality (who favoured compulsory delivery in Cairns Base Hospital), and those (myself included) who were concerned about the effects on children’s growth and development. During this time, I have observed weakening family and community bonds, increasing alcohol and substance misuse and sexual abuse, low school attendance, poor employment records and domestic violence. My studies of Aboriginal and non-Aboriginal children born in Cunnamulla in western Queensland followed the same cohort of children from birth8 for 20 years.9 The presence of a father who was employed at the time of the child’s birth acted as a role model for the future and was more effective than all other social interventions with respect to the child’s successful education or employment 20 years later, irrespective of race or subsequent social support or interventions offered to the child during school years.9,10 Arnold and colleagues’ recent article in the Journal records a situation almost unchanged from 30 years ago, with the exception that antenatal ultrasounds have allowed transfer to occur at 36 weeks’ instead of 32 weeks’ gestation.11 Enormous resources of goodwill, effort and money have been spent in these communities over 30 years, yet the family disruption, unemployment and abuse statistics remain at variance with the Queensland norm. Perhaps the time has come to allow low-risk births to occur in selected towns, where the mother can be surrounded by her friends and relations, and be in closer contact with her ancestral land. I endorse the article by Arnold et al and hope they are more successful in implementing change than I have been.

John W Cox

To the Editor: A letter by Scrimgeour1 in the 18 May 2009 issue of the Journal praised an earlier study by Andreasyan and Hoy2 for adding to the evidence that Indigenous people living in small communities (known as “outstations” or “homelands”) in very remote areas are healthier than those living in larger settlements. I believe this was an error. The study found that mortality was lower in both outer regional areas and very remote areas than in remote areas.2 But, unfortunately, this tells us nothing about outstations. The Accessibility/Remoteness Index of Australia (ARIA) classification used by the authors groups larger remote communities and their outstations together — categorising both as “very remote”. Scrimgeour is not alone in overstating the evidence for better health among Indigenous people living in smaller communities. The possible health benefits associated with living in outstations has become a major argument against the Australian Government’s plan to create 26 remote “hubs” that will receive improved services (to the likely detriment of smaller communities)3 and the related plan of the Northern Territory Government to develop 20 larger remote communities.4 For example, Tom Calma, Aboriginal and Torres Strait Islander Commissioner at the Australian Human Rights Commission, was reported as saying that there was “a strong body of research showing that people on homelands lived longer, healthier lives”.5 Calma seriously overstated the evidence we have to date, which consists of two studies from Utopia in central Australia and one study of land management practices in an Arnhem Land community.6-8 Although this research is encouraging, we are a long way from determining the causes of better health among sections of those two communities, and whether residence at outstations/homelands or land management practices are associated with better health in other communities as well. There are many reasons for supporting the growth of outstations, and health may be one of them, but it is crucial that those in the field of Indigenous health get this right. Rather than jumping the gun, we need more research into the effects of outstation life on health and wellbeing.

Emma E Kowal

To the Editor: In an article about Indigenous mortality in the Northern Territory, Andreasyan and Hoy1 concluded that Indigenous residents in very remote areas (VRAs) had a better health status than those in remote areas (RAs) and outer regional areas (ORAs). This result is inconsistent with previous reports and prompted us to examine the authors’ outcome. A central problem with the authors’ analysis lies in the identification of “usual residence” for death registration. The usual residence is defined by the Australian Bureau of Statistics as the dwelling at which a person spends or intends to spend 6 months or more in the year in which the question is asked.2 This definition limits its usefulness for the authors’ purpose, but is further compromised by the common practice by certifying doctors of simply using the last known address as a proxy for usual residence. In either case, the address recorded at death registration may differ from the location where a person lived for the majority of his or her life. The latter is the location more closely associated with health risks, particularly for chronic disease. As a test, we investigated changes of residence for all NT public hospital inpatients who died within a 7-year period by linking multiple hospitalisations between 1 January 2001 and 31 December 2007. We found that 26% of inpatients classified as residents of RAs at the time of death were previously usual residents of VRAs. This “unhealthy migrant” effect can be readily recognised as people relocate due to illness from VRAs, which have limited health services, to RAs or ORAs to access secondary and tertiary health care. The likelihood of inconsistent classification of usual residence in mortality data can also be tested demographically. Assuming the authors’ mortality ratios were correct for a stable population, we estimate that the Indigenous life expectancy at birth in VRAs would be 72.3 years, or 23 years longer than the life expectancy at birth in RAs (49.1 years). Such a large discrepancy is implausible. The age structure of a stable population is determined by fertility and mortality,3 and reported NT Indigenous fertility rates show a lack of substantial variation across regions.4 If the life expectancy at birth in VRAs was significantly longer than the life expectancy in RAs, VRAs would have about five times more elderly people (aged over 75 years) than the current estimates.5 The mobility of residence shown by hospital data and the absence of a substantial elderly population in VRAs suggest that the reported differential mortality rates between VRAs and RAs are the result of misidentification of “usual residence”.

Yuejen Zhao · Steve Guthridge · Shu Q Li · Christine Connors

In reply: We thank Zhao and colleagues for their interest in our study.1 The main issue they raise is misclassification of deaths by remoteness of residence. In our article, we acknowledged the role of migration to larger urban centres to access health services and raised the issue of unhealthy lifestyle and its flow-on effects on mortality. If we were to assume that 26% of deaths in hospital in remote areas were deaths of people who previously lived in very remote areas (as Zhao and colleagues suggest), regional variation in the disparity between Indigenous and total Australian all-cause mortality would narrow but would still remain. A re-analysis of our data based on this assumption1 shows that standardised mortality ratios in remote areas would drop from 875% (95% CI, 799%–956%) to 646% (95% CI, 582%–717%) in 1998–2000 and from 731% (95% CI, 665%–801%) to 540% (95% CI, 484%–601%) in 2001–2003. In very remote areas, the standardised mortality ratios would increase from 214% (95% CI, 193%–236%) to 281% (95% CI, 258%–306%) in 1998–2000 and from 208% (95% CI, 189%–228%) to 264% (95% CI, 242%–286%) in 2001–2003. Furthermore, in our article we stressed the importance of examining Indigenous migration to enable more accurate interpretation of our findings and called for future studies to “clarify the reasons for these differences in mortality by remoteness, with a particular focus on migration”. Our studies of Queensland data and national data (unpublished) have shown a similar pattern of higher Indigenous mortality in remote areas than in very remote areas, but the difference in mortality rates between these areas is highest in the Northern Territory. Thus, the phenomenon of the “methodological” error applies to all of these studies. We propose to undertake a prospective study of Indigenous mortality that will overcome some study design problems inherent in a cross-sectional study.

Karen Andreasyan · Wendy E Hoy

To the Editor: We commend the Indigenous Health issue of the Journal (18 May 2009). Its editorial emphasis — that partnerships with and continued leadership by Aboriginal and Torres Strait Islander peoples will be key to closing the gap between Indigenous and non-Indigenous Australians1 — is supported by preliminary, unpublished findings from our research into improving mainstream general practice care of Indigenous patients. Couzos and Thiele emphasised that closing the gap in health and life expectancy between Indigenous and non-Indigenous Australians depends on Aboriginal community controlled health services (ACCHSs).2 By virtue of their governance structure and focus, these services deliver culturally safe and appropriate primary health care to Indigenous Australians, while addressing issues of Indigenous autonomy and other social determinants of health.2 However, although not all general practices see Indigenous patients, 0.9% of general practice encounters (range, 0.7%–1.6%) are with Indigenous patients, equating to about one million consultations a year. Indigenous Australians present to general practitioners with essentially the same range of clinical conditions as do non-Indigenous Australians, although consultation rates for diabetes and circulatory conditions are higher for Indigenous patients.3 Most Indigenous Australians (76%) live in urban and regional areas, and are widely spread through the general population. They are likely to need mainstream services including general practice and primary care services, at least some of the time and for the foreseeable future. There is clearly a need for initiatives beyond support for ACCHSs, Indigenous workers and communities, to improve mainstream services for Indigenous Australians in a culturally sensitive and appropriate manner.4 Better sociocultural education for health care providers, trainees and students is required to close the gap that exists in mainstream understanding and acceptance of Indigenous cultures and aspirations. The Inala Indigenous Health Service in Brisbane is an example of a mainstream practice successfully developing into an accessible service.5 Our research aims to improve mainstream general practice care for Indigenous Australians with diabetes who live in urban areas of Victoria. As the following statement made by Indigenous participants in focus groups for our research indicated, health services must be patient-centred: We need to hold the health system — and that includes GPs — accountable for delivering help to Aboriginal people. The best one to do that is the consumer. Focus group participants also highlighted the importance of working together: I think we need to take some responsibility ourselves as (Indigenous) workers in organisations and go to these mainstream services. Whether it’s diabetes or drugs and alcohol, we need to say look, you get funded to look after everybody, and we want to come here and tell you how to look after our people when they come to your centres.

Siaw-Teng Liaw

In reply: It is unclear how many mainstream general practice consultations involve Aboriginal and Torres Strait Islander patients. Of 485 300 patient encounters attributed to general practices in the BEACH study (2003–2008), 7292 were with Indigenous patients, but 2906 of these encounters took place in Aboriginal community controlled health services (ACCHSs) rather than in general practices.1 If funding to close the gap in Aboriginal disadvantage is being channelled to general practice and the Divisions of General Practice (through recent measures of the Council of Australian Governments), then the Indigenous health outcomes of mainstream services must be carefully attributed.2 The ACCHS sector agrees there is a need to make general practices culturally secure for Indigenous Australians. For example, the Aboriginal Health Council of Western Australia has developed modules for cultural safety training, which are accredited by the Royal Australian College of General Practitioners for GPs’ professional development.3 The National Health and Hospitals Reform Commission report recommends that health services be required, by accreditation processes, to meet specific standards of cultural safety for Indigenous patients to ensure high-quality care.4 Within a quality assurance framework, systematic reforms such as these can potentially improve mainstream services, while supporting Indigenous workers who face unrealistic pressures to improve their local services. As Liaw points out, these initiatives are in addition to the vital role of ACCHSs in closing the health disparity gap.

Sophie Couzos · Dea D Thiele

To the Editor: Finally! An article in the Journal about health reform that carries no spin and decries further futile experimentation in management. Lewis and Leeder are to be congratulated on their insightful review.1 As they point out, social and environmental determinants of health are far more important to a community’s well-being. This was recognised intuitively as long ago as 1986, with the promulgation of the Ottawa charter,2 and its recommendation that health services be reoriented primarily toward promoting heath rather than delivering acute care per se. As Lewis and Leeder articulate, the evidence in favour of this line of thinking is actually quite potent.1 However, as they point out, the thing that surprises students and practitioners in public health is why the “bigger picture” has been so difficult to comprehend and act on. Rather than a need for the “stars to be aligned”, perhaps this is the time for stronger advocacy? And while we’re at it, evaluation tools for health promotion programs need to become more sophisticated if we’re going to convince our colleagues, politicians and the community that we’re spending their money wisely. The transformation that Lewis and Leeder recommend is likely generational in its span, but what better time to make a start?

George Larcos

To the Editor: A previous report from our institutions identified a steady increase in the prevalence of paediatric treadmill friction burn injuries, from three in 2001 to 17 in 2006.1 We sought to determine whether there was any change in this trend during the past 2 years. Children younger than 16 years with treadmill-related injuries were identified from prospectively collected data from burns and trauma databases maintained by the trauma research nurses at two paediatric tertiary trauma centres in Sydney (the Children’s Hospital at Westmead and Sydney Children’s Hospital) between January 2007 and December 2008. Sixty-five children sustained treadmill-related injuries (17 in 2007 and 48 in 2008); 43 were boys. The mean age at the time of the injury was 3.7 years (range, 9 months to 14 years). Friction burns ranged from less than 1% to 7% of total body surface area, and most patients sustained a total body surface area burn of 1% or less (58 patients). The most common site of injury was fingers and/or hand (49), followed by forearm or upper arm (6), and torso (5). In most cases, a limb or part of a limb was trapped between the rear roller and the treadmill belt. Fourteen patients required surgery, including 13 who underwent a skin grafting procedure. Most injuries occurred while the treadmill was in use by others, with the children approaching unnoticed from behind (46). In nine cases, the injury happened when the patients themselves, at a mean age of 7.8 years (range, 2–12 years), were using the treadmill. The substantial increase in prevalence of treadmill injuries in children during the past 2 years may be related to increased sales of treadmills as the community becomes more conscious of obesity. The data also reflect other Australian studies that show that children younger than 5 years are at greatest risk, accounting for 90% of paediatric treadmill injuries during the period January 2004 to June 2007.2 Despite the risk of injury, particularly for children, there appears to be no current national regulations governing the supply of treadmills or advice that should be given to customers at the point of sale. The New South Wales Government introduced legislation in June 2009 mandating prominent permanent warning labels to be affixed to all new treadmills — the Fair Trading Amendment (Treadmills) Regulation 2008 (NSW). The NSW Office of Fair Trading, with assistance from the NSW Severe Burn Injury Service and Kidsafe NSW, has developed an alert poster (copies of which may be downloaded or ordered from their website) for display at childcare centres, playgroups and places where domestic treadmills are sold.3 The Australian Competition and Consumer Commission recently published a safety alert brochure on domestic treadmills, which contains a safety checklist.4 Although helpful, the brochure does not include previous recommendations such as caution with headset use (ie, decreased awareness of children near the treadmill), and the use of mirrors or alternative positioning to ensure children approaching the treadmill can be seen.1 As most injuries occur within the first 6 months of purchase of the treadmill,5 educating parents seems to be most important around the time of purchase. Design modifications could also reduce the risk of entrapment of a digit or hand.2 It is likely that, without better application of current injury prevention strategies, the prevalence of these injuries will continue to increase.

Lawrence H Kim · Deborah A Maze · Susan Adams · Sarah Guitonich · Siobhan Connolly · Anne Darton · Andrew J A Holland

To the Editor: Contact burns in children caused by hair-straightening devices are increasingly common. Although the dangers of hair dryers and other similar devices are well known,1 there is less awareness of the risks associated with hair straighteners. The relevant Australian Standard does not mention hair straighteners.2 Four recent studies from the United Kingdom have reported on this problem,3-6 but there is no readily identifiable published information from Australia. Hair straighteners consist of two opposing ceramic plates that are held apart when not in use. The plates are reported to reach average temperatures of 169.5°C within 4 minutes 20 seconds of being switched on. They can cause burns (temperature > 66°C) on short-term contact (10 seconds) for a period of up to 9 minutes 20 seconds after being switched off,3 and can take 30 minutes to cool to below 50°C, at which temperature they can cause superficial burns on prolonged contact. Using data collected by the Stuart Pegg Paediatric Burns Centre at the Royal Children’s Hospital, Brisbane, and the Queensland Injury Surveillance Unit, we identified 22 patients treated for hair-straightener injuries between January 2004 and June 2009. Sixteen of these were treated within the past 2 years. The median age of patients was 43.4 months (range, 9 months to 14 years). A mean of 1% of total body surface area was involved. Injuries were to the forearm and hands (16 patients) (Box), foot and lower leg (five patients), and the back (one patient). The burns were significant, with 19 partial-thickness burns, and three full-thickness burns requiring surgery. Nine of the 22 children (41%) required long-term scar management. We observed two typical patterns of injury. In toddlers (16 patients aged 9–48 months), the main mechanism of injury was grasping or pulling down a hair straightener that was either turned on or cooling, with inadequate supervision a common factor. An early-teen group (three patients) had self-inflicted burns from accidental contact or misuse, including one patient who misguidedly used the device in an attempt to remove leg hair, sustaining full-thickness burns requiring skin grafting. Increased awareness of the potential dangers of hair straighteners might help prevent burns. We suggest four precautions: Hair straighteners should be placed out of reach of children during use and storage; Children should be supervised while the device is warming or cooling; Manufacturers should label the device to warn of potential dangers; and Manufacturers should either redesign the device so that plates are not exposed, or provide a cool-touch cover. Burns to a toddler’s hand caused by contact with a hair-straightening device

Zoe M Poiner · Michael D Kerr · Belinda A Wallis · Roy M Kimble

To the Editor: The current pandemic influenza A (H1N1) strain first caused infections in Mexico in April 2009 and rapidly spread to over 160 countries. Confirmed laboratory infections now number over 160 000, with millions of people probably already infected and further spread inevitable.1 Fears have been expressed that the enormous death toll seen with the H1N1 “Spanish ’flu” pandemic of 1918–1919 might be repeated. Although many deaths during that pandemic were caused by the direct effects of the influenza virus, over 95% of deaths were due to secondary bacterial pneumonias.2,3 If, as in 1918, most people with the current H1N1 strain have a mild illness from which they fully recover, this raises the important question of how we can readily identify patients co-infected with bacterial pathogens who may need antibiotic treatment for pneumonia. This is important in a situation where large numbers of people may need to be assessed, and demand for both antiviral and antibacterial agents may be high. Certain clinical features, such as the presence of a biphasic illness or the late development of purulent sputum, may suggest bacterial infection, but we do not know how reliable these features will be.4 The Australian Community-Acquired Pneumonia (CAP) Study was the largest ever prospective aetiological study of CAP.5 All patients were assessed for both bacterial and viral pathogens, including seasonal influenza.5 Using data from that study, easily measured clinical markers in patients infected with both influenza virus and a bacterium were compared with markers in patients with only an influenza virus identified. Patients with both influenza virus and a bacterial pathogen tended to be younger and appeared to have poorer outcomes.6 The most notable clinical differences between the two groups at presentation were the higher mean respiratory rate and faster heart rate in those with influenza virus plus a bacterial pathogen (Box). However, there were major overlaps between the groups in these parameters, so they were not very discriminatory if used alone. Taken with other clinical features,4 our data suggest that the presence of a respiratory rate of ≥ 25 breaths/min and a heart rate of ≥ 100 beats/min may help identify people who are more likely to need prompt clinical assessment and a chest x-ray. While these features may help identify patients more likely to benefit from antibacterial therapy, we would also argue that the small proportion of patients whose influenza is serious enough for them to be admitted to hospital should probably be treated with empirical antibiotics as well as antivirals. Patients with influenza plus a bacterial pathogen compared with patients with influenza alone or a bacterial pathogen alone Influenza plus bacterial pathogen (n = 17) Influenza alone (n = 51) P Bacterial pathogen without influenza (n = 293) Mean age (years) (SD) 55.2 (26.1) 66.7 (20.0) 0.046 62.9 (20.9) Male sex (%) 52.9% 54.9% 0.89 62.1% Mean RR (breaths/min) (range) 28.6 (16–48) 24.6 (16–48) 0.14 24.9 (12–60) Age-adjusted tachypnoea (%)* 47.1% 25.5% 0.10 28.0% Mean systolic BP (mmHg) (range) 137.4 (107–215) 137.1 (65–196) 0.97 128.3 (60–215) Mean diastolic BP (mmHg) (range) 68.2 (45–116) 69.5 (25–103) 0.81 67.1 (29–116) Mean temperature (°C) (range) 37.8 (36.2–40.6) 37.8 (35.5–39.6) 1.0 37.9 (33.5–40.8) Mean pulse rate (beats/min) (range) 113.4 (75–145) 96.3 (56–152) 0.01 104.5 (43–175) Mean Spo2 (range) 92.4 (81–99) 91.8 (44–100) 0.79 92.6 (50–100) Mean SMART-COP score† (range) 2.7 (0–7) 2.2 (0–9) 0.49 2.5 (0–9) Need for intensive care (%)‡ 29.4% 13.7% 0.14 13.0% 30-day mortality (%) 5.9% 0 0.08 6.5% BP = blood pressure. RR = respiratory rate. Spo2 = oxygen saturation (as measured by pulse oximetry). * Age-adjusted tachypnoea was defined as RR ≥ 25 breaths/min in patients aged ≤ 50 years or RR ≥ 30 breaths/min in patients aged > 50 years.6 † A tool for determining severity of community-acquired pneumonia (for details, see Charles et al6). ‡ All patients required either mechanical ventilation or vasopressor support.

Patrick G P Charles · Paul D R Johnson · Peter J Collignon

To the Editor: A recent article in the Journal describes, again, barriers to implementation of cardiometabolic monitoring among patients prescribed antipsychotic drugs.1 The cardiac health of patients with psychosis is not routinely assessed at first presentation for mental health services, adverse side effects of antipsychotic drugs are not systematically monitored, and patients with treatable risk factors for heart disease are not identified.2 We propose a practical solution to the seemingly intractable problem of implementing guidelines for cardiometabolic monitoring — change the delivery system. We have employed a general nurse to conduct cardiometabolic monitoring in a pilot study at the Recovery And Prevention of Psychosis Service (RAPPS), a first-episode psychosis service in Melbourne. All 15 eligible patients had their height, weight, blood pressure, waist circumference, fasting total cholesterol, high- and low-density lipoprotein cholesterol, triglycerides and glucose assessed according to national guidelines3 within 1 month of entry to the service, in the hospital, as an outpatient, or in the patient’s home; 14/15 blood samples were taken while the patient was fasting. Very early monitoring (within 7 days of first exposure to antipsychotics) was not implemented for four patients because they were inpatients and judged by ward staff as too unwell to be approached by a general nurse. Future follow-ups will be conducted at 3, 6, 12 and 18 months. Abnormal findings are referred to the treating psychiatrist, who is responsible for ensuring the patient receives appropriate follow-up. A general nurse can implement clinical guidelines, but this initiative requires substantial planning and ongoing management. Systematic identification of all patients eligible for monitoring requires identification of all pathways into the relevant mental health service, so as to begin monitoring at, or very close to, the point of first exposure to antipsychotics; management tools to track patients over time; and a clinical pathway to track test results and ensure appropriate medical interventions occur when required. Failure to implement prescribed monitoring guidelines is important because individuals with schizophrenia have a 20% shorter life expectancy than individuals in the general community.4 Side effects of antipsychotic drugs may include dramatic weight gain and elevations in serum cholesterol and glucose levels, which exacerbate the risk for cardiovascular disease. Most early deaths among individuals with schizophrenia are due to cardiovascular disease.5 Failure to monitor cardiovascular health and the adverse side effects of antipsychotic drugs is an important, life-shortening, failure of care. A simple solution to a complex problem exists if an effective delivery system is used.

Debra L Foley · Katherine I Morley · Karyn E Carroll · John Moran · Patrick D McGorry · Brendan P Murphy

In reply: Foley and colleagues rightly point out that a way to improve the cardiometabolic health of patients with psychosis is to change the way that mental health services are delivered. Although barriers to monitoring exist at the level of the patient, the illness, and the service,1 by focusing too narrowly on the barriers presented by patients, a blaming culture can be perpetuated. If blame is to be attributed, it should be directed towards inflexible services with a medieval belief in separating mental and physical health care. A number of centres in Australia have started to innovate in service delivery, with structured physical health clinics running in parallel to, and integrated with, mental health clinical programs. Our own centre, the Concord Centre for Cardiometabolic Health in Psychosis (ccCHIP), has been developed to take the notion of integrated care a step further — to actually treat the cardiometabolic abnormalities present. Our model involves a multidisciplinary team comprising psychiatrists, endocrinologists, and dietitians. However, we believe the potential for broader multidisciplinary input exists, including nurses, pharmacists, psychologists, occupational therapists, social workers and the patient’s general practitioner. It is our philosophy that although detection is the first step to improving the parlous outcomes for our patients, without active intervention, these poor outcomes are unlikely to improve. Recently, we received funding from the New South Wales Department of Health to develop a more comprehensive plan for education and training, including the production of a manual, to help psychiatric services in NSW develop their own monitoring and intervention services, using ccCHIP as their resource base. This initiative points to the need for government involvement to support these initiatives. Finally, it is apposite that Foley and colleagues write from the perspective of an early psychosis service — we believe that early detection and intervention for psychosis should be for physical as well as mental health issues.2

Timothy J R Lambert