Letters

To the Editor: When discussing causes of childhood leukaemia, Ziegler et al stated, “Exposure to electromagnetic fields has been ruled out as playing any significant role”. 1 They cited one large study2 in support of this statement, but overlooked two independent pooled analyses that showed the opposite. Greenland et al analysed 12 studies involving 2656 patients and 7084 controls, 3 and Ahlbom et al analysed nine studies involving 3247 patients and 10 400 controls.4 Each analysis found an association with a doubling of risk of childhood leukaemia at levels of household exposure at and over 0.4 microtesla (4 milligauss). Confounders and sources of bias to explain these findings have been sought without success. Consequently, in 2002, the International Agency for Research on Cancer classified 50 and 60 Hz magnetic fields as a “possible carcinogen” (Group 2b)5 even though the mechanism of an effect is not clear. The role of magnetic fields in childhood leukaemia cannot be “ruled out”, given the substantial epidemiological evidence, the international classification of magnetic fields as a possible carcinogen, and the subtlety of gene–environment interactions. Moreover, although exposures to magnetic fields are low within most households, there is opportunity to easily prevent or treat the uncommon situations where household exposures exceed 0.4 microtesla by means of electrical engineering, household wiring and town planning.

Bruce Hocking

In reply: Hocking states that electromagnetic fields cannot be ruled out as a cause of childhood leukaemia. However, several large studies have all failed to find any association between childhood exposure to electromagnetic radiation and leukaemia.1-4 The two pooled meta-analyses Hocking refers to both found no increased incidence of leukaemia with exposure to electromagnetic fields of < 0.4 microtesla.5,6 Although there was an increased risk of leukaemia with exposure to ≥ 0.4 microtesla, 99.2% of children with leukaemia had not received such a high level of exposure. 5 In addition, both studies acknowledged the potential for selection bias. As such, for the overwhelming majority of children with leukaemia, exposure to electromagnetic fields does not play any significant causative role. Although we agree its effect cannot be ruled out for the remaining < 1% of patients, it should not be given undue epidemiological weight.

David S Ziegler · Luciano Dalla Pozza · Keith D Waters · Glenn M Marshall

To the Editor: The recent position statement by the Warfarin Reversal Consensus Group provides clear and concise guidelines for a number of clinical scenarios related to the use of warfarin. 1 Unfortunately, it makes the general statement about the periprocedural management of warfarin in patients with atrial fibrillation (AF), “clinical experience suggests that bridging therapy is not required” [page 496]. Clinicians caring for patients with large ischaemic stroke in these circumstances may beg to differ. Although studies of bridging therapy in patients with AF in the periprocedural period are lacking, there are data which suggest that there is a considerably higher risk of thromboembolism during this period than would be expected by simply calculating the risk for several days off anticoagulation therapy.2-4 My own study of such patients undergoing endoscopy found a stroke risk of up to 3% in those at high risk.2 Many of these strokes were severe. The prothrombotic periprocedural environment may be a factor here, although advanced age and vascular risk factors may also contribute. The outstanding risk factor, however, is a previous history of stroke,2 and this is also a major risk factor for perioperative stroke in patients without AF.5 I would suggest careful, individualised assessment of all patients, and judicious bridging therapy where possible for patients with AF who have a past history of stroke.

David J Blacker

To the Editor: The recent position statement from the Warfarin Reversal Consensus Group provides a comprehensive, coherent and practical approach to warfarin reversal management. 1 In reviewing the position statement, and with particular reference to the paragraph about modifiers of warfarin response, we noted that the contribution of cytochrome P450 2C9 (CYP2C9) genotype to the response to warfarin was not addressed. There is debate in the current literature about the clinical utility of evaluating CYP 2C9 genotype in patients already taking or about to start warfarin therapy. Nonetheless, a significant body of evidence supports the contribution of CYP2C9 genetic variants as modifiers of response to warfarin therapy. CYP2C9 is the enzyme principally involved in metabolising warfarin.2 Several studies have identified the presence of single nucleotide polymorphisms in the CYP2C9 gene resulting in the expression of two allelic variants of CYP2C9 (CYP2C9*2 and CYP2C9*3) that are associated with reduced enzymatic activity, impaired metabolism of and increased sensitivity to standard warfarin doses.2,3 The allelic frequency of the mutant genotypes is in excess of 21% in the white population2 (they occur at reduced frequencies in African American populations and are rare in Asian populations4). The presence of allelic variants (CYP2C9*2 and CYP2C9*3) with reduced enzymatic activity is closely correlated with increased bleeding complications.2,3 Thus, there is potential for a considerable clinical impact given the large number of patients taking warfarin. We have identified an allelic frequency of CYP2C9*2 and CYP2C9*3 genotypes in an Australian population of patients attending an anticoagulant clinic comparable to that reported in the literature.2,3 We also identified international normalised ratios in excess of the target range in patients with the CYP2C9*2 or CYP2C9*3 genotype undergoing induction warfarin therapy with standard dosing regimens, relative to those who did not have these genotypes (personal, unpublished data, presented as: Cytochrome P450 CYP2C9 genotyping and warfarin induction therapy, presented at the 2004 Annual Scientific Meeting of the Haematology Society of Australia and New Zealand [Oct 17–20, Melbourne, Australia]). Recent reports suggest that CYP2C9 genotyping before inducing warfarin therapy may avert bleeding complications.5 However, CYP2C9 genotyping is currently only available within research institutes and larger corporations with research and development facilities and does not attract a Medicare rebate. While simple and inexpensive, genetic CYP2C9 screening has yet to be proven cost effective. However, genotyping may be of benefit in averting over-anticoagulation in certain clinical scenarios. These include commencing warfarin therapy in “high risk” elderly patients; those in whom low-dose, long-term, low-testing-frequency warfarin regimens are being contemplated; and in other “high risk” patients, such as those with conditions affecting warfarin metabolism, including liver disease, and in those taking medications known to interact with the hepatic metabolism of warfarin.

David J Blacker · Faye Gray · Keith Byron

To the Editor: The article by Baker et al was a timely review of managing anticoagulation therapy and balancing the risks of thrombosis and bleeding.1 However, in managing anticoagulation therapy before non-cardiac surgery in patients with mechanical cardiac valve prostheses, the suggested 5-day cessation of warfarin therapy, with only subcutaneous heparin cover, is not appropriate. I have had three patients with mechanical bileaflet mitral prostheses develop valve thrombosis while under this protocol, two with a fatal outcome. I have also had one patient with a mechanical bileaflet aortic valve develop a popliteal arterial embolus requiring thrombectomy, despite being treated according to the protocol. The consequences of valve thrombosis and thromboembolism far outweigh the lesser complications of increased bruising or bleeding associated with non-cardiac surgery. To avoid the potentially devastating complications of valve thromboembolism associated with the routine cessation of warfarin therapy 5 days before surgery, warfarin ought to be continued to maintain an INR (international normalised ratio) of around 2.0, supplemented with subcutaneous heparin. Alternatively, full intravenous heparinisation can be used while ceasing warfarin treatment, and continued postoperatively until the INR is restored to the therapeutic level. Warfarin should never be reversed with vitamin K, except in cases of life-threatening haemorrhage. Apropos of the therapeutic INR ranges generally recommended for mechanical cardiac valve replacements, the current generation of prostheses does not require the anticoagulation intensity of the older style prostheses.2,3 Lower intensity anticoagulation is sufficient to prevent thromboembolism at decreased risk of haemorrhagic complications.4 My personal practice for patients with bileaflet mechanical prostheses is to maintain an INR of 2.0–2.5 for aortic valves, and 2.5–3.0 for mitral valves. The higher intensity for mitral prostheses relates to potential increased thrombogenicity because of lower leaflet opening pressures, as well as the common association of left atrial dilatation and atrial fibrillation.

Serge Lubicz

To the Editor: A middle-aged woman with atrial fibrillation had her warfarin therapy stopped for 2 days before dental extraction. She had a catastrophic stroke and is now a plaintiff. I was asked if her medical management accorded with common practice. At the October 2004 Annual Conference of the Royal Australian College of General Practitioners, I conducted a straw poll of 20 experienced GPs, of whom 18 said they would stop warfarin for between 2 and 4 days before a dental extraction. Some of these GPs regarded a dental extraction as elective surgery and pointed me to authoritative (but slightly ambiguous) sources to back up their view. 1,2 However, a review of the medical and dental literature shows that this is an example of common practice lagging behind clinical evidence. The first controlled trial of dental extraction in patients on warfarin therapy was conducted in 1983.3 It showed that it was not necessary to cease warfarin prophylaxis for patients whose international normalised ratio (INR) was within the normal therapeutic range. Since then, two major literature reviews have confirmed these conclusions.4,5 A recent Australian review on warfarin reversal expresses a similar point of view.6 The incidence of a serious embolic complication from stopping therapy with warfarin is 1%, and this is three times more likely to occur than bleeding complications in patients whose warfarin therapy was continued.4 Furthermore, a stroke is a catastrophic event, while a bleeding tooth socket is simply messy and usually easily controlled. An authoritative review and position statement on warfarin therapy and dental procedures from the Australasian Society of Thrombosis and Haemostasis may be the catalyst required to align common practice with clinical evidence.

Max Kamien

In reply: We thank Blacker for his constructive and helpful comments. Our recommendations on bridging therapy in patients with atrial fibrillation were for patients with chronic atrial fibrillation who had not previously had a thromboembolic event.1 We do agree with Blacker that extreme care needs to be exercised in patients with atrial fibrillation and a previous thromboembolism. These patients should be managed along the same lines as patients who are at relatively high risk of recurrent thromboembolism. We also wish to emphasise that it is extremely important to assess each individual patient carefully, and to use the consensus guidelines as guiding principles, and not apply them blindly. Dear and his colleagues correctly point out that there are several published studies that have confirmed increased warfarin sensitivity in allelic variants of the cytochrome P450 2C9 (CYP2C9) enzyme. Polymorphisms associated with reduced enzymatic activity have been reported to be associated with increased warfarin sensitivity. They suggest that determining the genotype of individuals before commencing warfarin therapy may be of benefit in reducing the incidence of over-anticoagulation in a select group of patients. We do not believe that this approach is currently practical or possible. From a practical point of view we recognise several reasons why patients become over-anticoagulated when treated with warfarin. In our article we discussed several important modifiers that contribute to an individual’s sensitivity to warfarin. While we agree that polymorphisms of the CYP2C9 gene on its own have been linked with increased sensitivity to warfarin, we are not aware of any studies showing a synergistic interaction of the polymorphism with other clinically recognised causes of increased warfarin sensitivity. Furthermore, we are not aware of any properly conducted studies that have attempted to address the clinical or economic viability of screening for CYP2C9 polymorphisms in patients for whom warfarin therapy is planned. Finally, the time required to obtain the results of this investigation would preclude its application in the routine management of patients who require warfarin therapy. The letter by Lubicz highlights the difficulties encountered in bridging anticoagulant therapy in patients with prosthetic valves. As pointed out in our article, the management of these patients is controversial and mostly anecdotal.1 We believe that the recommendations in our article are useful for most patients, but would like to emphasise the need to consult with the relevant experts in order to avoid bleeding or thrombosis. We would not recommend routine full therapeutic anticoagulation therapy with heparin immediately after surgery, or the combined use of warfarin at any international normalised ratio (INR) with subcutaneous heparin before surgery. Such approaches are more likely to cause confusion and predispose the patients to either bleeding or the risk of thrombosis. Patients with prosthetic valves require careful handling, and involving experts in their management is critical. Kamien’s comments are important and illustrate the difficulties in changing entrenched practices. We hope that our recommendations will go some way to improving the way we manage patients on warfarin therapy who are about to undergo surgery.

on behalf of the Warfarin Reversal Consensus Group

To the Editor: Incidents involving assaults on staff by medical equipment are uncommon, but have been reported in this Journal before. 1 We report another “attack”, involving an x-ray machine and an anaesthetist. A woman was scheduled for endoscopic retrograde cholangiopancreatography in the radiology suite. During induction of general anaesthesia, the patient’s foot moved against an x-ray table control knob (Box). This triggered slow, downward movement of an x-ray “C-arm”, which was positioned above the head of the unsuspecting anaesthetist. Tracheal intubation was rudely interrupted when the C-arm met the anaesthetist’s head and pushed it towards the patient’s face. However, the radiographer in attendance quickly reversed the movement just before the anaesthetist and patient collided. The radiology suite is often regarded as an unfriendly environment for anaesthetists.2 This incident reminds us that, in some cases, it may be frankly hostile! A patient’s foot activates a control knob on an x-ray table

Richard H Riley · Leigh J Coombs

Robert J Menz General Practitioner, East Adelaide Healthcare, 296 Payneham Road, Payneham, SA 5070. robert.menzATeahc.com.au To the Editor: “Texting” tendinitis (resulting from excessive sending of text messages via mobile phone) has not been reported in Australia, although a recent article in the Adelaide Advertiser reported a case in Italy. 1 A 13-year-old girl presented to me in mid-January with an acutely tender swelling in the mid-radial aspect of her right forearm. It had been present for about 2 days. There was no history of trauma, or recalled change of activity. Further enquiry revealed that she had been given a mobile phone in December and that the associated plan allowed $100 credit that had to be used between 5 January and 4 February. This equates to nearly 300 SMS messages, or 10 a day, if all available credit were used for sending text messages (although, in this case, some of the credit had been used in making calls). The phone and plan also allowed up to 760 characters per message, instead of the usual 160. The patient had been using only her right thumb to press the keypad, and was using “traditional” rather than “predictive” text input (ie, creating the message one letter at a time, rather than using the mobile’s interpretative software to reduce the number of keystrokes). Examination of the patient’s forearm revealed a firm, tender swelling in the dorsi-radial aspect of the mid-forearm (presumably involving the abductor or extensor pollicis longus muscle). There was pain with resisted thumb and wrist dorsiflexion. A presumptive diagnosis of “texting” tendinitis was made. The condition settled rapidly with explanation and reassurance, rest, application of naproxen gel twice daily for 2 days, and use of both hands to operate the keypad. To my knowledge, this is the first report of this condition in Australia, although other unusual overuse injuries of the hand have been described with Nintendo playing. 2 Perhaps the manufacturers of mobile phones should include health warnings of the risk of overuse injury as part of product labelling.

Robert J Menz

Lourdes I St George,* Daniel Lin† * Obstetrician and Gynaecologist, Suite 4, 36 Belmore Street, Burwood, NSW 2134. † Paediatrician, Westmead Private Hospital, Westmead, NSW. lourdesstgeorgeATbigpond.com To the Editor: A 33-year-old woman, who had borne five children and had had previous caesarean sections, presented in her eighth pregnancy with worsening malabsorption after biliopancreatic diversion for morbid obesity, performed 3 years earlier. Before surgery, she had weighed about 130 kg (height,161 cm; body mass index [BMI], 46 kg/m2); she had gradually reduced her weight to 67 kg. Her surgery had created intestinal malabsorption resulting from the intestinal bypass and from dietary restriction because of gastroplasty. The physiological stress associated with pregnancy worsened her anaemia from protein and vitamin deficiencies, especially fat-soluble vitamins and calcium. She required frequent hospitalisation for intravenous fluids to compensate for dehydration from vomiting and diarrhoea. She was taking oral iron, folate, vitamin D, a calcium supplement, vitamin B12, and having vitamin K injections. Her total weight gain in pregnancy was poor (from 71 kg to 74 kg). At 32 weeks she presented with premature labour and a persistent low fetal baseline heart rate of 90 beats per minute and an unstable lie. She had an emergency caesarean section and delivered a baby boy with a birth weight of 2095 g (average for gestational age). Apgar scores were 7 and 8 at 1 and 5 minutes, respectively; the baby required ventilation for hyaline membrane disease and phototherapy for jaundice, although his blood profile was normal. His clinical course thereafter was uneventful. Obesity (BMI > 30 kg/m2), has become the epidemic of the 21st century, with one in two Australian women being overweight or obese. 1 Morbid obesity (BMI > 40kg/m2) is associated with a 6–12-fold increase in mortality.2 A multifaceted approach is essential for treatment in all patients with obesity, but unfortunately, medical treatment mostly produces short-term weight loss. Thus, bariatric surgery is being performed more frequently. Biliopancreatic diversion has two components: a limited gastrectomy results in reduction of oral intake, inducing weight loss, especially during the first postoperative year; and the construction of a long limb Roux-en-Y anastomosis with a short common “alimentary” channel of 50 cm length, which maintains weight loss long term. Scopinaro, who pioneered this technique, has published long-term results reporting 72% excess body weight loss maintained for 18 years.3 He documented 239 pregnancies in 1136 patients who had undergone biliopancreatic diversion, 25% of whom had been infertile before the operation. During pregnancy, 20% required parenteral nutrition and had fetuses that were small for gestation age. The women had a mean weight gain of 6 kg during their pregnancies, and 80 % delivered babies at term with a mean birth weight of 2.8 kg. 4 From the patient’s perspective, the great advantage of biliopancreatic diversion is the ability to eat a normal diet and still achieve excellent, long-term weight loss. The most serious potential complication is protein malnutrition, with a need to take supplemental calcium and vitamins, particularly vitamin D, lifelong. Because of this potential for significant complications, patients who have had biliopancreatic diversion require lifelong follow-up and pregnancy should be avoided. Ideally this operation should be performed in women who have completed their childbearing.

Lourdes I St George · Daniel Lin

Alexandra A Bennett,* Jo-anne E Brien,† Peter S Macdonald‡ * PhD Candidate, † Professor of Clinical Pharmacy, University of Sydney, Sydney, NSW (address for correspondence: Therapeutics Centre, St Vincent's Hospital, Darlinghurst, NSW 2010); ‡ Associate Professor of Medicine, and Cardiologist, St Vincent's Hospital, Sydney, NSW. sashabATpharm.usyd.edu.au To the Editor: We wish to add our perspective to the article by Phillips et al. 1 Needs identified by GPs included education about the effectiveness and target dosing of angiotensin-converting enzyme (ACE) inhibitors and β-blockers, and improved communication. We wish to highlight the potential roles hospital and community pharmacists have in supporting GPs caring for patients with heart failure. It is expected that by 2010 there will be at least 25 patients with heart failure per GP and 100 per community pharmacy in Australia. A recent review of 100 patients with heart failure discharged from St Vincent’s Hospital (SVH) in New South Wales showed they were taking an average of 9.5 regular medications, two-thirds of which were cardiac medications. 2 Their average age was 70.5 years. They had an average of 7.3 diagnoses, including ischaemic heart disease, atrial fibrillation and osteoarthritis. They were commonly taking amiodarone, warfarin and digoxin. Six per cent of patients had taken cyclooxygenase-2 (COX-2) inhibitors before they were admitted to hospital. 2 While rates of ACE inhibitor (or angiotensin-II-receptor antagonist) and β-blocker use at discharge were high in patients with systolic dysfunction (84% and 65%, respectively), only a minority of patients were taking target doses (27% and 15%, respectively). This highlights the need for good communication between healthcare providers. Discharge letters are often illegible and do not necessarily prioritise issues or detail future management, such as stating whose responsibility it is to up-titrate the dose of ACE inhibitor or β-blocker. Electronic entry of medical information, including e-prescribing (currently being trialled in some hospitals), may assist. Some patients have typed medication cards from a pharmacist on discharge. However, this is not routine practice. Ideally, all patients should receive such cards with supporting information. Copies of this information should be provided for the GP and pharmacist. Such a system would support Australian Pharmaceutical Advisory Council guidelines for continuity of care. Since 2002, a pharmacist has consulted with patients in the SVH Heart Failure Clinic regarding medication and lifestyle issues. Problems identified are referred to the treating cardiologist. A pilot study of this service showed high patient satisfaction (T Hargraves, Pharmacist, St Vincent’s Hospital, personal communication). Such a service could also be provided by community pharmacists, perhaps linked to home medicines review. A pharmacist is also employed by the community multidisciplinary heart failure service based at SVH. These positions support patients and their carers as well as healthcare providers, including GPs, community and hospital pharmacists and nurses. Evidence for such roles for pharmacists is supported by US and UK data. 3 We propose that designs for future models of care for patients with heart failure should incorporate pharmacists.

Alexandra A Bennett · Jo-anne E Brien · Peter S Macdonald

Matthew J Bragg,* Paul Middleton* * Emergency Physician, Prince of Wales Hospital, Barker St, Randwick, NSW 2031. braggmATsesahs.nsw.gov.au To the Editor: We read with interest the case reported by Williamson and colleagues of an adult survivor of near-drowning complicated by cardiorespiratory arrest. 1 This is a remarkable account of survival with near-intact neurological recovery from what was a very bleak initial clinical scenario, and the pre-hospital and hospital personnel responsible for his resuscitation should be congratulated for their efforts. However, the authors’ use of therapeutic hypothermia in this case does not necessarily support their contention that “controlled hypothermia . . . should be used in near-drowned patients who have spontaneous circulation but remain comatose”. As presented, the case illustrates the benefit of supportive care in general, and the use of appropriate controlled ventilation in particular. As the authors noted, “gentle hyperventilation to ‘blow off’ excess CO2” corrected the hypercapnia and acidosis. The graphs of arterial pH, lactate level and Pco2 presented in the report show a linear improvement in all three indices after controlled ventilation, before hypothermia measures were begun. Indeed, the commencement of hypothermia had no discernible impact on these trends. While there is some evidence in the literature for the use of controlled hypothermia after cardiac arrest,2 there is no direct evidence of its benefit for victims of near-drowning. We do not feel that controlled hypothermia can currently be recommended as standard of care for near-drowning on the basis of this single case report.

Matthew J Bragg · Paul Middleton

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

Jonathan P Williamson · Stan Braude

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

Andrew Firestone

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

Timothy J R Lambert · Leon H Chapman

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

Marc M Cohen

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

Ian J Constable

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

Kenneth Wong

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

Jeanette I Nordon

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

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

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

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

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

Vanessa M McDonald · Peter G Gibson

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

Raoul A Walsh · Judith Lumley

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

Jessica H Ford · Annette J Dobson

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

Mark Mackay · Peter Millard