Letters

To the Editor: Warfarin is an orally administered vitamin K antagonist and has many well described interactions with commonly prescribed medications.1 However, only a handful of case reports worldwide have shown that flucloxacillin, a widely used antibiotic, may affect warfarin therapy by reducing its anticoagulant effect — in one instance contributing to the development of ischaemic stroke.2,3 There are several reports describing potential mech-anisms of interaction for flucloxacillin with warfarin.4,5 We describe the case of a 64-year-old man who was diagnosed with infective endocarditis on the basis of mitral valve vegetations and blood cultures that were positive for methicillin-sensitive Staphylococcus aureus. The patient underwent mitral valve replacement with a prosthetic valve and received prolonged antibiotic therapy with intravenous flucloxacillin for 8 weeks. Initially, for nearly 4 weeks, therapeutic anticoagulation with warfarin was difficult to achieve with warfarin doses ranging between 5 and 10 mg per day (target international normalised ratio [INR], 2.5–3.5). During this time, the patient was receiving intravenous flucloxacillin at a total daily dose of 8 g (2 g every 6 h). Flucloxacillin was increased to 12 g per day (2 g every 4 h) and there was a subsequent fall in the patient’s INR, which was sustained despite increasing the dose of warfarin to 25 mg per day (Box). Completion of flucloxacillin therapy was associated with a rise in the patient’s INR and a reduction in his warfarin dose requirement. No other relevant medications were commenced during this period of observation. This case highlights the potential for a dose-related effect of intravenous high-dose flucloxacillin (up to 12 g per day) on warfarin metabolism and the need for vigilance when prescribing antibiotics in conjunction with oral vitamin K antagonists. Other penicillins such as amoxicillin can, conversely, enhance the anticoagulant effects of warfarin, so the warfarin–flucloxacillin interaction may not be intuitive for many clinicians. Doses* for oral warfarin and intravenous flucloxacillin administered to a 64-year-old man with infective endocarditis, and corresponding INR INR = international normalised ratio. * Graph shows abbreviated, not daily, data. Intervals are weekly up to Week 9, then vary according to when INR was measured.

Philip Y-I Choi · Katherine L Phillips · Ian Rae

To the Editor: We read with interest the article by Ng and colleagues on life-threatening hypokalaemia associated with ibuprofen-induced renal tubular acidosis,1 and wish to present our own experience of four patients presenting to our hospital over a year (Box). The patients all presented with biochemical signs of renal tubular acidosis with severe hypokalaemia and a normal anion gap metabolic acidosis from long-standing misuse of ibuprofen taken in combination with codeine from over-the-counter (OTC) medications. Patients 1 and 2 presented acutely with deliberate misuse that included an ibuprofen–codeine combination product. Both patients subsequently admitted to long-standing misuse of ibuprofen and codeine taken in combination. Patients 3 and 4 presented with constitutional symptoms and generalised weakness with a history of taking large amounts of an ibuprofen–codeine combination product. Both these patients required intensive care unit admission for central venous access and potassium replacement. As in the case series by Ng and colleagues, there was no history to suggest gastrointestinal loss of potassium, and medication histories were negative for drugs known to cause intracellular potassium movement or potassium wasting (eg, diuretics). Ibuprofen cessation, potassium replacement and supportive care resulted in biochemical recovery in all four patients. Opioid addiction appears to be the common thread reported by Ng et al and in our case series. Other case reports support this.2,3 Paracetamol taken in supratherapeutic doses is known to cause hepatotoxicity, and it appears that patients with opioid addiction may now be turning to ibuprofen–codeine combination products. More evidence of the danger of these products comes from a case series reporting 27 patients with ibuprofen–codeine misuse that resulted in significant morbidity, including presentations for opioid dependence, gastrointestinal haemorrhage, hypokalaemia, anaemia and/or renal failure.4 In Australia, ibuprofen–codeine combination products are available OTC, albeit in restricted amounts due to problems related to codeine misuse.1 Further restrictions may need to be considered in light of the significant morbidity related to the ibuprofen component. Baseline laboratory investigations and other characteristics of four patients with ibuprofen-induced renal tubular acidosis* RR Patient 1 Patient 2 Patient 3 Patient 4 Sex, age in years Female, 35 Male, 55 Male, 41 Female, 39 Ibuprofen dose† Unclear, years’ duration 9.0–18.0 g/day 5.0 g/day 8.0 g/day Other medications Amitriptyline 50 mg at night Esomeprazole 40 mg daily Multiple medications Nil Serum pH 7.35–7.45 7.29 7.13 7.26 7.32 Pco2, mmHg 35–45 45 42 30 28 HCO3-, mmol/L 22–32 21 13 13 14 Anion gap, mmol/L 7–17 3 9 12 11 Na+, mmol/L 136–146 137 139 142 135 Cl-, mmol/L 98–106 116 120 120 111 Urea, mmol/L 3.0–8.0 4.7 4.4 3.0 6.9 Creatinine, μmol/L 60–120 70 123 125 99 K+ on presentation, mmol/L 3.5–5.0 2.8 2.9 2.5 1.4 K+ on discharge, mmol/L 3.5–5.0 3.5 3.8 3.7 4.5 RR = reference range. Pco2 = partial pressure of carbon dioxide. HCO3- = bicarbonate ion. Na+ = sodium ion. Cl- = chloride ion. K+ = potassium ion. * Same format as used in Ng et al case series1 to allow direct comparison. † Maximum recommended: 3.2 g/day.

Colin B Page · Paul A Wilson · Aidan Foy · Michael A Downes · Ian M Whyte · Geoffrey K Isbister

To the Editor: We have previously argued that the recent rapid increase in the popularity of low-carbohydrate (“low-carb”) beers, in Australia and other countries, is more a community health risk than a healthy alternative to traditional beers.1 This contention has since been supported by a survey conducted by the Victorian Health Promotion Foundation (VicHealth), which found that “low carbohydrate beer drinkers mistakenly believe these beverages are a healthier choice than other varieties”.2 Seventy-one per cent of respondents believed that low-carbohydrate beer is healthier than full-carbohydrate beer, despite having the same alcohol content. Alarmingly, 15% of respondents indicated that they consume more beer when drinking low-carbohydrate beer because they believe it is healthier than full-carbohydrate beer. The potentially insidious marketing of health benefits for alcohol products has recently been followed by the release of lower-alcohol, lower-calorie wines such as the McWilliam’s Balance range, Cockatoo Ridge’s Low Calorie Brut Cuvée, Beringer Blass’s White Lie, and the JMB Beverages Brightlite range. These are represented as containing a “lower” rather than “low” alcohol content because, at between 6.5% and 9.5% alcohol by volume, these wines clearly contain a far higher alcohol content than the ≤ 1.15% alcohol by volume that is required by Australian food standards to be represented as a low-alcohol product.4 The health-based marketing of these wines is similar to that of low-carb beer — it implies that consuming these products is healthier than consuming traditional versions. This implied health benefit message is reinforced by endorsement of McWilliam’s Balance wines by Weight Watchers and inclusion of these wines in the Weight Watchers diet program, which is followed by over 1.8 million Australians annually.4 According to its manufacturers, “McWilliam’s Balance is destined for incredible consumer demand”.4 McWilliam’s Balance wines contain about one-third less alcohol and one-third fewer kilojoules than regular wines.4 If these wines are being consumed to replace regular wine consumption in the same quantity, they could offer a community health benefit. If they are consumed instead of soft drinks or water in the belief that they are healthier than regular wines, or consumed in larger quantities than regular wine in the belief that they are healthier, they could represent a community health threat. Presently, the Australian Government is considering making alcohol companies display nutritional information and ingredients on all beer, wine and spirits labels as a result of a submission by the Alcohol and other Drugs Council of Australia.5 Governments need to modify food regulations to help make the message more explicit: lower-alcohol, lower-calorie wines are not a licence to drink to your own health.

Stephen P McKenzie · Evie R Leslie · Peter G Miller

To the Editor: I refer to the article by Cameron and Cooke,1 and the letter from Forero and colleagues.2 Cameron and Cooke correctly identified key problems associated with using a time-based process standard as a solution to poor patient outcome linked to overcrowding in emergency departments (EDs). They highlighted the need for monitoring to ensure “patient safety and quality of care are not compromised at any stage of the emergency pathway”. Forero et al challenged their assertion that the United Kingdom has replaced the 4-hour rule, and suggested there are three new time-based measures used as indicators of performance. Unfortunately, Forero et al have not noted the critical difference in new UK policies, in which no specific time cut-off is used as the benchmark for good performance.3 While acknowledging the importance of timeliness of care, “clinical outcomes and the experience of the patient” will be the focus of emergency care in the UK under the new Department of Health initiative effective April 2011.4 Surely Andrew Lansley’s (UK Secretary of State for Health) statement that “the four hour standard should be abolished”5 must mean nothing else but complete abandonment of this standard!. Concerns regarding a time-based performance indicator (and funding) were previously illustrated by Nocera in this Journal, who showed that numerical key performance has been a primary motivation for data fraud in Victoria and New South Wales, relating to ED waiting time.5 Furthermore, there is a possibility of admitting an unprepared patient to a ward at 4 hours,6 without acceptance of care by specialist team. A patient not properly worked up and sent to ward will not have the same automatic privileged access to critical care staff ratios or fast-tracked requests for pathology or radiology investigation provided in the ED. This can contribute to the excessive length of stay and, indirectly, hospital bed block. I caution against overly enthusiastic support for the 4-hour rule being instituted in Australian hospitals as a panacea to access block in the ED, and stress the need for better discharge planning, experienced patient flow and bed management, and improved hospital staff rostering for after hours. The latter include rethinking of ED doctors’ 24-hour staffing, with ED specialists attending to patients primarily,7 and junior doctors as assistants (if a 4-hour standard is to be attained), especially when facing an imminent glut of junior doctors, who will require close supervision, rotating through the ED.8

Shyan L Goh

To the Editor: We read with interest the recent cover article by Bhonagiri and colleagues detailing increased standardised mortality rates for patients admitted to Australian intensive care units (ICUs) out of hours.1 Have the authors considered a secondary analysis controlling for night-time staffing ratios? Aside from staffing levels, human factors such as the effects of fatigue and sleepiness due to circadian rhythm misalignment and sleep deprivation should be considered and further investigated. Studies have consistently shown that human cognitive and motor performance is substantially worse at night than during the day,2 due to the influence of the endogenous circadian clock. A recent study of emergency medicine registrars at an Australian tertiary hospital showed a 21% decrease in performance at night, in clinical scenarios of fellowship examination standard.3 Sleep during the day is of poorer quality and shorter duration than sleep during the night,4 resulting in chronic sleep restriction that exacerbates the impairment occurring in night work.5 Consecutive night shifts are associated with an increasing risk of accidents and injuries.6 In doctors, including consultants, inadequate sleep (fewer than 6 hours) is associated with harmful effects on patient outcomes.7 Despite our cultural beliefs, doctors are likely to suffer from the same biological effects of sleep loss and circadian rhythm disturbance as suffered by other humans. ICUs may provide one of the best hospital environments in which to study medical error, because of defined and limited personnel compared with non-ICU ward areas. ICUs also usually have better record-keeping and error-recognition systems, because of higher staff:patient ratios. Possible risk mitigation strategies include increasing the number of night staff, implementing oversight mechanisms for specified procedures and decisions, and ensuring that rosters and shift lengths are designed according to evidence linking sleep disturbance with poor patient outcomes. Such evidence should form the basis of any regulatory frameworks.

Dev A S Kevat · Andrew R Davies · Peter A Cameron · Shantha M W Rajaratnam

To the Editor: Frei and colleagues recently drew our attention to combination analgesic misuse-related morbidity.1 The same phenomenon has also been reported in New Zealand.2 About 50 years ago, analgesic misuse was widespread in Australia and commonly involved chronic, excessive use of combination analgesics (including the aspirin–phenacetin–caffeine [APC] products, Bex and Vincent’s Powders). After many years, some people who used APC developed “analgesic nephropathy”, which made up 12%–15% of dialysis cases.3 I recently performed a retrospective chart review of patients who were referred to the Drug and Alcohol Services at the Western Hospital (Melbourne) for excessive compound analgesic use between September 2005 and September 2010. There were 32 patients (18% of all referrals; median age, 38 years; 23 were women). All had some form of chronic pain, had initiated compound analgesic use for acute pain (eg, headache) and all described progressive use of analgesics because of psychogenic effects (eg, “gave me energy”, “helped me forget”). All 32 patients were diagnosed with opioid dependence and had medical and psychiatric problems correlating with their compound analgesic misuse. One patient, a 34-year-old man, reported taking more than 70 codeine–ibuprofen tablets daily and sustained recurrent gastric ulceration, which eventually required surgery. Despite this, he continued to misuse the analgesics until he undertook opioid replacement pharmacotherapy. A 24-year-old man misusing the same analgesic, despite completing a detoxification program, also relapsed and died after bleeding from gastric ulceration.4 Overall, the patient profiles were remarkably similar to those described by Frei and colleagues.1 Combination analgesic misuse appears largely correlated with products containing drugs of dependence (eg, codeine) and the phenomenon of “rebound pain” (ie, pain that recurs after a short-acting analgesic effect wanes, or “medication overuse headache”). Most morbidity and mortality risks associated with combination analgesic misuse are a consequence of chronic overdose of the non-steroidal anti-inflammatory drug and/or paracetamol components. Paracetamol (mostly when in combination with an opioid analgesic) is reported as the commonest cause of acute liver failure in the United States and United Kingdom.5 Another long-term complication can be hearing loss.6 Two patients in my clinic group had hearing loss, and the ear, nose and throat specialist’s opinion was that it was related to analgesic misuse. Dextropropoxyphene–paracetamol combination products are still available in Australia but are no longer available in the UK. I question the need for opioids in combination analgesic products and, if used, they should be restricted to prescription.

Michael A McDonough

To the Editor: We read with interest the recent letter by He and colleagues.1 The authors described a case of ischaemic stroke in a patient with scurvy and considered whether there was a connection between the two conditions. They referred to evidence that vitamin C deficiency may be a risk factor for cerebrovascular disease, but acknowledged that a direct causal link is unlikely to be established. We propose adiponectin as the causal link between vitamin C deficiency and stroke. Adiponectin is an adipokine, secreted in multimers by adipose tissue, with insulin-sensitising, antiatherogenic and cardioprotective properties.2 A decrease in adiponectin levels — particularly the more biologically active, high molecular weight (HMW) multimers — is implicated in a number of disease states, such as obesity, type 2 diabetes, heart disease and some cancers. Adiponectin has also been reported to have cerebroprotective properties,3 and there is some evidence that levels may be reduced in patients with cerebrovascular disease.4 A recent study demonstrated that vitamin C supplementation increases the proportion of HMW adiponectin secreted from human adipocytes.5 Vitamin C levels are lower in obese and diabetic patients, and the patient reported by He et al had also been recently diagnosed with type 2 diabetes. While scurvy is admittedly rare, He and colleagues noted that subclinical vitamin C deficiency is not uncommon in the general population (about 10%). We suggest that it would be worthwhile to assay plasma vitamin C levels and total and HMW adiponectin levels in patients presenting with cerebrovascular events, and to undertake prospective studies to determine whether vitamin C supplementation improves patients’ adiponectin levels. Increased HMW adiponectin levels could be explained, at least in part, by the role of vitamin C in the multimerisation of adiponectin. Adiponectin levels are also reduced in other vascular conditions, such as ischaemic heart disease and peripheral vascular disease.4 As plasma vitamin C levels of patients with these diseases are also reduced, it is tempting to posit that vitamin C supplementation could have a role as a treatment, or even a prophylactic, in populations at risk of a range of adiponectin-related vascular diseases.

Felicity J Rose · Jonathan P Whitehead

To the Editor: The juxtaposition of articles by Braithwaite and colleagues1 and Ho and Maddern2 (a description of a trial of physician assistants [PAs] in Adelaide) provides an interesting contrast between what should be happening in health care and what is happening. While Braithwaite and colleagues argue for a value-driven change, the type of change that is occurring at the moment is that of role substitution. This is exemplified by Ho and Maddern’s assertion that “PAs ... would ... improve the quality and quantity of medical service”. The intent is to provide a substitute doctor. This is referred to as “task” substitution or transference, with the inference that those under discussion, whether PAs or nurse practitioners (NPs), will only perform a limited role — some of the tasks of a doctor. In South Australia, PAs are able to order investigations and prescribe. The former editor of this journal, Martin Van Der Weyden, discussed this issue in 2008,3 labelling it “doctor displacement”, a term that Brooks and Mitchell disputed.4 They said “[PAs] will never be able to practise independently; they will always have to practise under supervision and within the scope of practice of their supervisor”. The Health Legislation Amendment (Midwives and Nurse Practitioners) Act 2010 (Cwlth), however, provided NPs with access to the Pharmaceutical Benefits Scheme and the ability to prescribe. Any supervision by doctors seems nominal, with independent practices being set up, some attached to pharmacies. There is less supervision of NPs by the medical profession than that given to trainees in teaching hospitals, and they are effectively independent practitioners. It could be argued that United States-trained PAs are even better trained than Australian-trained NPs, and Brooks and Mitchell’s statement that they will “never” practise alone is hardly reassuring. Proponents of NPs and PAs justify their use4 by reference to a shortage of health professionals. It isn’t reasonable to take from one area of need (nursing) to bolster another area of need (medicine), and the rapid increase in medical undergraduates and increase in immigration of overseas-trained doctors renders medical workforce projections unreliable. Role substitution by PAs and NPs will only perpetuate the problems we now face, while introducing new problems related to limited training and skills and fragmentation of care. Australian GPs, traditionally well trained and highly skilled, and with the ability to manage complex problems, are the core of our health system. Proposed changes devalue their contribution by making the inevitably fatal assumption that the sick patient is easy to recognise and triage.

Patrick S Hanrahan

To the Editor: Eight Australian medical deans recently called for academic health science centres (AHSCs) — where a leading university joins with a major tertiary health care provider in a tripartite mission of excellence in clinical service, research and education.1 However, there are obstacles to their proposal due to the misalignment in purpose of universities and teaching hospitals. Why do they call for change, given that many of our public hospitals are already affiliated with universities, have academic units of the university, and are funded by governments to educate doctors? Many private hospitals are also involved in university and college education. The Garling report was commissioned in response to a crisis in the quality of acute care offered in New South Wales public hospitals.2 However, none of its 139 recommendations refer to striving to achieve excellence. While excellence must be the aim of our public hospitals, their immediate response should be patient-centred, ensuring an acceptable minimum standard of care. Other targets, such as research and concentrating limited resources on aiming for excellence in specified areas, could prove to be a distraction from this core purpose. Education was mentioned in the Garling report but in no sense was achieving excellence in clinical service or research implied to be its purpose, unless excellence is to be understood to mean the minimally acceptable level of care. Medical education and research need to fit within a public hospital system that has funding limits and is struggling to deliver its core goal of clinical care. Given the current misalignment of purpose between hospitals and universities, it is no surprise that the combined deans have expressed a tone of dissatisfaction. Mayo Clinic in the United States has a logo of three interlocking shields,3 representing a “tripartite mission of excellence in clinical service, research and education”. Mayo Clinic’s key to achieving excellence — the aspirational aim of the deans’ “world-class AHSCs” — is alignment of purpose of the hospital and the academic institution. Similarly, in Australia, the barriers highlighted by the deans1 were dealt with in the planning of Macquarie University’s medical school and hospital. A common purpose and a greenfield site, where a new culture could be introduced, were a core part of Macquarie’s approach.4 As Macquarie’s Vice Chancellor, Professor Schwartz, was reported to say in 2010: “By owning and running the hospital we can ensure that we put medical teaching and research at the forefront”.5 Macquarie knows that simply owning and running its own hospital does not necessarily assure success, but it is an important step.

Michael K Morgan · Janet D Greeley

To the Editor: The editorial on academic health science centres (AHSCs) in Australia by the deans of medicine in all eight research-intensive universities1 is an important platform for discussing fundamental issues to be considered in developing these centres. The essential basis of an AHSC is a combination of two major initiatives: Seamlessly integrating research done in laboratories and clinical trials with multidisciplinary patient care. Building a centre of innovation where questions are asked based on actual clinical problems and can be resolved by the collective efforts of on-site “knowledge workers”. It is timely and necessary to investigate this option of health care delivery, as politicians negotiate at state and federal levels on appropriate models, and is in keeping with the National Health and Medical Research Council’s objectives in its latest strategic plan for broadening and building Australia’s capacity for research.2 It is crucial that any AHSCs created justify their status. They could be national centres of excellence, funded by an agreed federal and state government contribution model, together with endowments and competitive research funds. They should not merely be cosmetic makeovers for current university hospitals, with their idiosyncratic selection of staff and clinical practice models. Their governance needs to be standardised, based on agreed principles. A competitive national selection process should include identifying submissions that define employment of specific personnel and implementation of interventions to address the challenges of health care delivery in a timely and efficient manner.3 A suggested list of required attributes of staff employed in AHSCs is shown in the Box. A single academic chief executive officer who is a proven educator and researcher and cognisant of local and regional issues of health care delivery can facilitate the development of the centre, with the assistance of similar professionals on the board of management. The knowledge workers in an AHSC should include knowledge leaders (who incorporate knowledge into clinical protocols and management plans), creators (who generate new knowledge from research data), users (clinicians and researchers who incorporate therapies and skills into the clinical arena) and learners (students training to be health professionals and researchers). Direct interaction between the financial regulators and leading researchers and clinicians in an AHSC can lead to implementation of state-of the-art clinical practice, with patient care consistently being evaluated so that clinical and financial inefficiencies can be eliminated. The interaction of knowledge workers within the AHSC can result in sharing innovative and ethical translational research with bedside clinical practice. Required attributes of academic health science centre (AHSC) staff Staff employed at AHSCs should have all these attributes: Ability — high-quality knowledge and skills Accountability — responsibility, being up to date with current evidence-based practice Availability — to the community of practice within the AHSC Accessibility — to patients and colleagues Affability — teamwork, cooperation, collaboration Affordability — social responsibility to the community and country Adaptability — dedicated to continuous professional development and ongoing research

David A Kandiah

To the Editor: A middle-aged male night-shift driver experienced dizziness, vomiting, sudden onset of limb weakness, and then collapsed and became delirious. He had no past history of renal impairment or hypertension. At presentation in an emergency department, he was hypertensive (blood pressure, 220/140 mmHg) and hyperglycaemic. An upper motor neurone pattern of persistent dysarthria and left hemiparesis was evident. An electrocardiograph and transthoracic echocardiogram confirmed sinus rhythm and left ventricular hypertrophy. Magnetic resonance angiography of the brain showed subacute basal ganglia haemorrhage (Box) and an anterior communicating artery aneurysm. Renin levels were elevated at 124.7 mU/L (reference range, 4.5–46.0 mU/L) but renal artery stenosis was absent on ultrasound. Evaluation of an elevated initial normetadrenaline level of 1610 pmol/L (reference range, < 900 pmol/L) with a diagnostic algorithm1 suggested that phaeochromocytoma was unlikely. Hypertension, proteinuria, suboptimal renal function, inactive urine sediment and normal fasting blood glucose suggested hypertensive nephropathy. Antihypertensives were initiated to mitigate the risk of further stroke, nephropathy and cardiomyopathy. Results of an electroencephalogram were normal. Further history revealed that the patient had nicotine dependence with occasional amphetamine and cannabis exposure. Before admission, he had an estimated intake of 1–2.5 bottles of cough mixture episodically (600–1500 mg of pseudoephedrine). A pattern of ingesting excessive amounts of various brands of over-the-counter combination pseudoephedrine and codeine cough mixture developed over 20 years, and he suffered cravings when abstaining. He visited various pharmacies, provided identification, was repeatedly cautioned, but rarely consulted doctors. A Naranjo score2 of 7 indicated a probable adverse drug reaction to pseudoephedrine, resulting in a disabling hypertensive haemorrhagic stroke. During 2.5 months of inpatient rehabilitation, he regained full independence in self-care and mobility. His unstable employment was interdependent with pseudoephedrine misuse. He accepted counselling regarding constructive, non-pharmacological coping strategies for social stressors. Financial, legal and housing difficulties complicated his discharge plan. He planned to return to work as a driver. Pseudoephedrine is associated with a modest elevation in blood pressure3 and hypertensive crises.4 Intracerebral haemorrhage associated with pseudoephedrine usage is anecdotally reported.5 Dependence and chronic psychoses have been reported6,7 but their prevalence is unknown. Night-shift workers, students, recreational or self-medicating users, and athletes are potentially vulnerable to misuse. Project STOP is an initiative of the Pharmacy Guild of Australia (http://www.projectstop.com.au/index.html) to curb diversion of pseudoephedrine-containing medications from retail pharmacies into illegal amphetamines. However, it is not mandatory and the National Drugs and Poisons Schedule Committee has rejected the Pharmacy Guild’s proposal to enhance Project STOP’s capabilities using an electronic messaging tool for pharmacists (NotifyRx, RelayHealth, Atlanta, Ga, USA) to regulate codeine sales (excluding cough mixtures). In contrast, New Zealand authorities now restrict the supply of pseudoephedrine to prescription only. A concerted effort from all relevant parties, including tighter regulation or legislation, is essential for harm minimisation. We urge regulatory bodies to review the effectiveness of current practice. Magnetic resonance angiogram of the patient’s brain showing likely hypertensive right basal ganglia haemorrhage

Ajay Bharatula · Peter W New

To the Editor: Laparoscopic adjustable gastric banding (LAGB) is the most common bariatric surgery performed in Australia, and diabetic patients represent an important target population.1 In one of few trials in type 2 diabetes, 73% of 30 LAGB-treated obese patients reverted to normal glucose tolerance by 2 years, compared with 13% of 30 obese patients randomly assigned to treatment with changes to their lifestyle.2 These Australian data precipitated publicity implying that many people with type 2 diabetes were cured by LAGB.3,4 However, only recently diagnosed patients were recruited. The benefits of LAGB in those with diabetes of long duration (and usually with a substantial loss of pancreatic beta-cell function5) may not be as dramatic. We reviewed the records of eight patients with insulin-treated type 2 diabetes (aged 40–65 years, with a diabetes duration of 4–39 years) referred for LAGB by one of us (T D) to two established bariatric surgical units over 4 years. All eight patients had a diabetes-specific review within 2 months of surgery and at 3 and 6 months postoperatively, and six patients had a further review at 12 months. Perioperative diabetes management was coordinated by the anaesthetist and ward staff, but patients were encouraged to contact their doctor or regional diabetes education unit for advice at any time if necessary. Patients attended the bariatric unit for saline insertion into the band once or twice before their diabetes-specific review at 3 months. No patients developed postoperative complications. The median weight loss was 14% at 6 months and 20% at 12 months (Box). By 3 months, insulin doses had been reduced in all patients and two had stopped using insulin. However, most had increased their insulin doses at 6 months (and the two who had discontinued insulin started using it again) because of unsatisfactory glycaemic control. During the 12 months’ follow-up, only one patient stopped using insulin and remained without its use without an unacceptable glycated haemoglobin (HbA1c) increase. Although our eight patients achieved the same median percentage weight loss at 1 year as trial patients with diabetes of relatively short duration achieved over 2 years,2 insulin use was still required in most cases. When asked, the patients suggested that inappropriate initial insulin reductions were not because they experienced hypoglycaemia, but rather because they expected substantial LAGB-associated metabolic improvement. Perhaps this was encouraged by media coverage3,4 and/or concerns of bariatric unit staff that continuing their insulin therapy might retard their LAGB-associated weight loss. In some cases, problems with insulin adjustment and glycaemia overshadowed the psychological benefits of progressive weight loss. These preliminary observations suggest a need for more data on diabetes management after LAGB, to inform acute treatment modification and to provide a realistic idea of the effects of LAGB on longer term disease outcomes. Changes in body weight, insulin dose and HbA1c after LAGB in eight patients with insulin-treated type 2 diabetes HbA1c = glycated haemoglobin. LAGB = laparoscopic adjustable gastric banding. Open-circle line = patients who discontinued insulin during the first 3 months of follow-up.

Timothy M E Davis · Catherine Coleman

To the Editor: Two key paradigm shifts are occurring with regard to diagnostic imaging services in Australia that may have far-reaching medicolegal and professional consequences for all doctors, have an impact on patient care and, ironically, increase costs to the health budget. First, the federal government announced a 3-year cost-saving trial in the 2009–10 Budget. Since 1 November 2010, the trial allows doctors to request certain “image-only” radiological investigations without an accompanying radiologist report.1 The investigations attract a lower rebate to cover only the technical component of image acquisition. The changes should not alter the cost to patients as most imaging studies, which currently include radiologist reports, are bulk billed. The trial currently involves chest x-rays and certain facial examinations. The government’s presumption is that for these investigations a radiologist’s assessment is not required and referring practitioners will assume full responsibility for the correct identification and interpretation of all primary, secondary and incidental findings. In doing so, referring doctors will also accept all liability for errors. While the incentive for referrers to request these new item numbers is unclear, the increased risk and responsibility borne by them is obvious. Second, in a measure to mimic the National Health System in the United Kingdom, there is advocacy from some levels of health administration to implement role extension for allied health professionals within diagnostic imaging. This would involve the provision of descriptive reports from non-radiologists with no conclusive interpretation, leaving referring doctors to draw their own clinical conclusions. Error rates for these types of reports are not insignificant when compared with a radiologist’s report.2,3 Disposing of a specialist’s evaluation may delay referral or management, and will again transfer responsibility for errors to the referring doctor.4 The false inference underpinning this model is that general medical and specialist training can be fast-tracked or circumvented without any detriment. The most concerning ramifications from these proposed changes are those for standards of patient care. Reduced radiologist input will result in higher error rates and inaccurate diagnoses;5 will remove the option of clinical discussion regarding difficult cases; and may compromise elements of patient care. Ironically, such medical errors often increase downstream burdens for health systems, negating any short-term cost savings. From a medicolegal perspective, undertaking independent interpretation of images and acting on descriptive reports is a high-risk activity and insurance premiums for doctors may ultimately reflect this.

Nicholas I Brown · Lawrence B Josey

To the Editor: The levels of ferritin and folate in the blood are regarded as the “gold standards” for measuring deficiencies in iron and folate, but they are complex and expensive tests. The red cell distribution width (RDW-CV%) measures variability in red blood cell (RBC) size, helps in early detection of deficiencies and is available in all automated analyses of RBCs. It is seldom listed on haematology reports, though it can be printed out at no extra cost. A raised RDW-CV% should prompt the treating doctor to consider underlying latent deficiencies and to order specific tests. Pasricha and colleagues outlined the most efficient ways of diagnosing and managing iron deficiency anaemia.1 However, they did not mention RDW-CV%. Haemoanalysers measure the haemoglobin (Hb) content and size of individual RBCs. The average RBC size is the mean cell volume (MCV), and the variation in sizes is calculated as a standard deviation (SD). The haemoanalyser converts the MCV and SD to a coefficient of variation (CV) using the formula: Normal RBCs vary slightly in size, so the normal value of the RDW-CV% is 10%–15%. Greater variability gives a higher RDW-CV%. When a person becomes iron deficient, he or she forms small RBCs. The circulation will then contain a mixture of older normal RBCs and increasing numbers of newer small cells, until all the normal cells reach the end of their 120-day lifespan. It therefore takes several weeks for the Hb level and MCV to drop low enough to diagnostic levels for iron deficiency. However, the mixture of normal and small RBCs rapidly increases the variability in the size of circulating RBCs, so the RDW-CV% reaches pathological levels before other RBC measurements do.2 A raised RDW-CV% is the first haematological sign of iron deficiency. My computer model demonstrating the mechanism and timing of changes in Hb level and RDW-CV% showed a large and early rise in the initial stages of iron deficiency before anaemia (Box).3 In the anaemia of thalassaemia, the RDW-CV% is usually normal. In combination with other parameters, the RDW-CV% helps to classify anaemias. The sensitivity and specificity for diagnoses is about 80%,4 so the RDW-CV% result should be used as a screening tool to alert the clinician to a possible disorder that can be investigated using standard tests. I recommend the RDW-CV% be included in all routine blood reports. Computer model of changes in haemoglobin (Hb) levels and red cell distribution width (RDW-CV%) in developing iron deficiency anaemia. Iron deficient red blood cells were formed from Day 0

Alan E Dugdale

To the Editor: Van Der Weyden states that “obesity” has negative connotations and the capacity to stigmatise.1 “Intending to give minimal offence and shifting the focus from the person to the condition”, people substitute politically correct terms.1 Medical practice should be scientifically, rather than politically, correct. Language aside, obesity is a blind spot in clinical practice because of the lack of any useful and accurate measure to categorise the condition. Body mass index (BMI) is the universal standard, but it is a very flawed measure. The results of epidemiological studies that support its use depend on huge population numbers, ethnic homogeneity and the exclusion of confounders including smoking and coexisting chronic disease. There is an absence of any epidemiological data showing that reducing overweight or obesity improves outcomes, despite them being frequently cited as risk factors. However, bariatric surgery has been shown to reduce cardiovascular disease, diabetes and cancer incidence.2 Central obesity is a much more powerful predictor of total mortality and cardiovascular disease mortality than BMI.3 In particular, the waist-to-hip ratio (WHR) is useful in population studies, showing precision and a lack of bias over a wide range of ethnic groups.4 Waist circumference is a better predictor than BMI but, like BMI, requires ethnic-specific criteria and is difficult to implement in today’s multiracial societies. WHR performs better as a predictor of cardiovascular disease than all lipid fractions, including total cholesterol and low-density lipoprotein cholesterol.3,5 Lowering lipid levels by drug therapy in the clinical trial setting reduces cardiovascular end points by 20% to 25%. In this context it is pertinent to note that the cost of subsidising prescriptions for lipid-lowering drugs in the financial year 2009–10 was almost $1.5 billion.6 In contrast, there is no simple prescription available to reduce levels of obesity. Healthy eating will always be important. And to make an impact on obesity, 60–90 minutes of moderate physical activity daily is required,7 but the importance of exercise is constantly overlooked and underprescribed. Studies in the United States show that physical activity, recorded daily, reduces cardiovascular disease mortality by about 37%–53%.8 Japan has undertaken an ambitious campaign to identify and counsel employees with excessive waistlines.9 This initiative will be followed with interest. A public health focus on early identification and prevention of central obesity is therefore at least as important in reducing cardiovascular disease mortality as is the measurement and treatment of lipids and hypertension. People with central or abdominal obesity have a serious health hazard and should be informed. “Political correctness” describes a practice that avoids giving offence to minorities. In view of the current epidemic of obesity, the language that we use should be explicit.

Timothy A Welborn · Satvinder S Dhaliwal

To the Editor: We read with interest the recent editorial by Nordin,1 which makes several imprecise observations on our recent position statement in the Journal.2 Here, we analyse some of his statements, as we believe that they are misleading to your readers and hazardous to institutionalised older persons. The Consensus Conference on Treatment of Osteoporosis in Residential Aged Care Facilities (RACFs) was organised as a unique type of meeting in which Australian experts in osteoporosis and geriatric medicine, including representatives from the Australian and New Zealand Bone and Mineral Society (ANZBMS) and Osteoporosis Australia, participated in multiple interactive sessions with 50 geriatricians and general practitioners who practise in RACFs. The goals were to appraise current evidence in the field of falls and fracture prevention in RACFs and to define practical, evidence-based recommendations. A similar meeting took place in 2004 in Canada,3 where conclusions played a pivotal role in optimising osteoporosis care in RACFs. Conclusions of the Australian meeting and recommendations subsequently published in the Journal are products of both the general consensus of the participants in the final plenary session and contributions of all the coauthors.2 Our article states, “In adults with a baseline calcium intake of 500–900 mg/day, increasing or supplementing this intake by a further 500–1000 mg/day has a beneficial effect on BMD [bone mineral density]”.2 In light of the evidence that we cited4 and more recent evidence,5,6 it is Nordin’s responsibility to highlight the potential risks of excessive calcium intake, from dietary sources plus supplements, in a population that is at high risk of cardiovascular disease.7 Moreover, we are not alone in raising this concern — a recent statement from the American Society for Bone and Mineral Research has expressed similar concern.8 In addition, Nordin cites the seminal work of Chapuy and colleagues; although this study was carried out in nursing homes and apartments for older people, it only looked at independent, ambulatory older people.9 Furthermore, the statement regarding calcium compliance is again supported by a study performed in ambulatory populations, in which compliance is likely to differ from that in our population of interest. Finally, Nordin asserts that our article promotes the use of bisphosphonates, particularly the intravenous variety, and makes the unfounded suggestion that the recommendation of bisphosphonates was due to the relationship between the sponsor and some of the coauthors. This is inaccurate. The University of Sydney, funded by a medical education grant, organised the Consensus Conference. Also, both the ANZBMS and Osteoporosis Australia endorsed the meeting and the integrity of the funding process. Indeed, maintaining independence from the sponsor was a major goal of the Consensus Conference, which was attested to by the feedback from participants. In conclusion, a basic knowledge of geriatric pharmacology and a good understanding of the current literature on geriatric medicine are enough to value the recommendations presented in our article.

on behalf of Jacqueline J Close, Julien P de Jager, Peter R Ebeling, Charles Inderjeeth, Stephen Lord, Andrew J McLachlan, Ian R Reid, Bruce R Troen and Philip N Sambrook

To the Editor: The report by Leyden and colleagues highlights the value of examining the total experience of stroke thrombolysis in one population.1 The results are devastating: protocol violations in more than a third of cases (consistent with other reports of up to 50%2), and a 10% symptomatic intracranial haemorrhage (ICH) rate (representing a number needed to harm [NNH] of 10). As a clinician, I would be “gutted” if my treatment harmed every 10th patient. The 22% mortality at 3 months is consistent with real-world evidence that stroke thrombolysis increases mortality.3 Although the authors state that the rate of symptomatic ICH was not statistically significantly different to that in the National Institute of Neurological Disorders and Stroke (NINDS) study, an absolute increase of 3.6% (10% versus 6.4%) is clinically important to patients and their families. Presumably, this is largely related to the age protocol violations: 10 of 53 resulted in symptomatic haemorrhage (19%; NNH = 5), including seven cases of intracerebral haemorrhage and five deaths. In all, there were 39 cases of any ICH (25%; NNH = 4). The article highlights that 54% of thrombolysis cases were not on the Safe Implementation of Thrombolysis in Stroke (SITS) registry. This result adds to the concerns of a selection bias in the SITS registry. As the authors point out, the sample size is small — too small, in my opinion, to draw any rigorous conclusions. This highlights that registry results should, at best, be hypothesis generating. However, it has also been highlighted that patients in the SITS International Stroke Thrombolysis Register do worse than those in the placebo group of the European Cooperative Acute Stroke Study III (ECASS III).4 The authors also refer to the ECASS III results, which contend that the time window for stroke thrombolysis should be extended to 4.5 hours. However, methodological and analytical flaws in this study, as well as the NINDS study, cast doubt on this statement.5 A recently published independent review of evidence on stroke thrombolysis concluded, “There is no consistent or proven benefit to thrombolytics”; it included all 11 clinical trials, of which nine had no benefit (with four of these causing harm).6 There are multiple examples in medicine where small studies suggest a benefit, but larger more definitive studies confirm otherwise. Hence, it is very important to look at the totality of the evidence.7 While I agree with the authors that poor access to acute stroke units is deplorable, the real challenge is to define the role, if any, for thrombolysis in acute stroke. Pronouncements that we need to be thrombolysing more are a disservice to those who seek the truth.

Daniel M Fatovich

In reply: To a carpenter, everything looks like a nail, and to a stroke thrombolysis sceptic, every study seems to confirm their opinion. A result cannot be “clinically important” yet statistically not so. We found no difference in symptomatic intracranial haemorrhage rates between our study and others using the same definition. The most widely accepted estimates of the true number needed to harm (for functional outcome at 3 months, following treatment within 3 hours) is about 30, as opposed to a number needed to benefit of around three.1 Our study does not suggest that thrombolysis increases mortality. Mortality cannot be compared between different populations, with different aetiology and severity. We have demonstrated a large number of relative “protocol violations” according to 2007 guidelines, the most common of which was that the patient was older than 80 years, but there is robust evidence that thrombolysis is safe and effective in this cohort.2 The benefit of a therapy cannot be assessed by a tally of “positive” and “negative” trials. A recent meta-analysis of all tissue plasminogen activator trials (seven trials, 2199 patients),3 and the relevant Cochrane review,4 confirm benefit in appropriate patients treated with tissue plasminogen activator within 4.5 hours. Stroke thrombolysis is effective. We must overcome the barriers to administering it frequently, safely and rapidly.

Tim Kleinig · James M Leyden · Andrew Lee · Jim Jannes

To the Editor: A 61-year-old man presented to the emergency department (ED) of a tertiary hospital seeking treatment for alcohol withdrawal after 36 hours of abstinence. He reported central chest pain radiating to the jaw and left arm that had been present for 2 hours before his arrival at the hospital. He had no history of cardiac disease and no known risk factors for coronary artery disease. An electrocardiogram (ECG) showed sinus tachycardia with T-wave inversion in leads V1, V2 and V3. Two hours after the patient’s arrival at the ED, he tested positive for troponin-T. Over the next hour, his ECG showed development of ST elevation of 1–2 mm in leads V3, V4 and V5. Because of severe alcohol withdrawal, his clinical status precluded urgent coronary angiography; and after treatment with diazepam was commenced, the ST elevation that was evident no longer met criteria for urgent angiography. The patient was given standard medical therapy for acute coronary syndrome, including aspirin, clopidogrel and intravenous heparin, while in the ED, along with ongoing diazepam for alcohol withdrawal. He was later admitted to the coronary care unit with a diagnosis of acute coronary syndrome. The next day, an ECG showed development of widespread T-wave inversion in leads V1 to V5. The dynamic ECG changes were not associated with ongoing chest pain. On Day 3 of the patient’s admission, coronary angiography showed normal coronary arteries, and ventriculography showed apical ballooning of the left ventricle, consistent with a diagnosis of takotsubo cardiomyopathy (Box). Treatment with an angiotensin-converting enzyme inhibitor and a β-blocker was commenced. Three months later, follow-up echocardiography showed a return to normal regional and global left ventricular function. Takotsubo cardiomyopathy takes its name from a traditional Japanese octopus trap that has a similar shape to the abnormally contracting left ventricle seen with this condition.1 Typical findings in a patient with takotsubo cardiomyopathy are chest pain associated with emotional or physical stress, with ST segment changes on electrocardiography and apical ballooning on ventriculography, which is generally expected to resolve within weeks to months; troponin level may or may not be positive. The mechanism of this condition has not yet been determined, but it appears likely that it is due to hyperadrenergic-hypercatecholaminergic states (such as alcohol withdrawal) resulting in localised or diffuse coronary vasospasm.2 Takotsubo cardiomyopathy has only rarely been associated with alcohol withdrawal, and has once been reported in a patient with alcohol withdrawal associated with seizures.3,4 Coronary ventriculography image showing apical ballooning of the left ventricle

Angus G Thompson · Joseph Hung

To the Editor: We would like to congratulate Gandy and colleagues on their recent article in which they assess outcomes and patient flow in an acute care surgery (ACS) model.1 We have also performed a retrospective historical control study that examined the effect of an ACS model on assessment time and time to operation for acute appendicitis. Our findings were presented in poster format at the Royal Australasian College of Surgeons Annual Scientific Congress in Perth in May 2010.2 We introduced an ACS model in 2007 at Nambour General Hospital, a 350-bed regional hospital on Queensland’s Sunshine Coast. Our model differs in certain details from the model used by Gandy and colleagues at Prince of Wales Hospital, but is similar in principle. The aim of the ACS model was to provide an in-house consultant surgeon to be more available and more directly involved in the care of emergency surgical patients. In our study, the outcome measures included time to assessment of the patient in the emergency department by the surgical registrar, and time to operation after this assessment. We performed a retrospective chart audit of 569 patients who underwent emergency appendicectomy in the calendar years 2006 and 2008. The ACS model resulted in an increase in both time to assessment (198 minutes in 2006 compared with 263 minutes in 2008; P < 0.0001 [t test]) and time to operation (597 minutes in 2006 compared with 793 minutes in 2008; P < 0.0001 [t test]). These results surprised us. Various explanations were postulated, including the trend of an expanding local and regional population on the Sunshine Coast placing a greater demand on the emergency theatre through the study period. Like us, Gandy and colleagues did not see a reduction in time to theatre and in fact “observed no significant change in time from presentation to arrival in theatre”. This was explained on the basis of “an increase in the number of patients treated conservatively overnight”. We have reviewed our data and found a similar trend, with 35% of patients in 2006 and 54% in 2008 managed conservatively overnight. This may, to some extent, explain our surprising results. Our appendicectomies in both historical control patients and those treated in the ACS model were all performed laparoscopically, thus removing one of the confounders experienced in the Prince of Wales Hospital data. A comparison of these two sets of data emphasises the fact that to measure time to assessment and time to operation in isolation misses the important concept of reduction in complication rates, as successfully demonstrated by Gandy and colleagues1 (we did not record complication rates in our study). This process of assessment could be taken a step further with a cost–benefit analysis looking at the presumed reduction in costs associated with the anticipated lower rate of complications resulting from the involvement of the consultant surgeon.

Simone L Geere · Ratna Aseervatham · David Grieve

To the Editor: Further to the recent article by Anstey and colleagues on community-acquired Klebsiella pneumoniae liver abscesses,1 we report two similar cases at our hospital in late 2010. Case 1: A 55-year-old Indonesian-born man was referred from general practice in October 2010 with a 5-day history of fever and progressive epigastric pain. He did not have diabetes, but did have dyslipidaemia. He had migrated from Indonesia in the 1980s; his most recent visit to Indonesia was in January 2010, for 3 weeks. As he had mildly deranged liver function test results, he was investigated with abdominal ultrasound and computed tomography (CT). Both showed a large multiseptate collection in the left lobe of the liver (Box, A). The liver collection was drained under radiological guidance, yielding a pure growth of K. pneumoniae. Urine culture was also positive for an identical isolate of K. pneumoniae. This man had a rapid clinical response to percutaneous drainage and was discharged on oral ciprofloxacin therapy. Case 2: A 25-year-old Indonesian-born man presented to our emergency department in early November 2010 after 2 days of headache, high fever and abdominal cramps, culminating in an acute confusional state. He had no significant medical or surgical history and had last visited Indonesia in March 2010, for 2 weeks. Initial therapy and investigations were aimed at excluding a diagnosis of meningitis. Results of a CT scan of the brain and of cerebrospinal fluid analysis were unremarkable. The patient remained acutely unwell and developed diarrhoea and right upper quadrant abdominal pain. Blood cultures were positive for K. pneumoniae within 48 hours of admission. Abdominal CT showed a large multiloculated abscess in the right lobe of the liver (Box, B). The liver abscess aspirate grew a pure culture of K. pneumoniae. The patient responded to treatment with ceftriaxone and large-volume percutaneous drainage. In both these cases, an antibiotic sensitive mucoid strain of K. pneumoniae was cultured. These cases add weight to the possibility raised by Anstey and colleagues that community-acquired K. pneumoniae liver abscess is indeed an emerging phenomenon in Australia. Further, the extended length of time between our patients’ travel to Indonesia and the clinical presentation (9 and 8 months, respectively) is suggestive of local (Australian) acquisition of the disease. Clinicians should consider abdominal imaging in cases of bacteraemia due to K. pneumoniae. Abdominal computed tomography scans showing Klebsiella pneumoniae liver abscesses

Kudzai N Kanhutu · Jeffrey J Post · Kate R Clezy · Hong Y L Foo

To the Editor: Interest in alternative therapies for Clostridium difficile infections (CDIs) is increasing as these infections become important causes of patient morbidity and mortality. Recurrent CDIs can be severe and difficult to treat. In-vitro data,1 followed by reports of the efficacy of tigecycline in the treatment of severe refractory cases of CDI,2 suggest that tigecycline should be considered as an alternative or adjunctive antimicrobial agent in these situations. To date, it has been used mostly as a “salvage” strategy in combination with other antibiotics in the face of clinical deterioration.2,3 We report the successful use of tigecycline monotherapy in the treatment of a patient with recurrent C. difficile colitis. An 83-year-old woman was admitted to hospital in July 2009 with acute diverticulitis. She was treated with intravenous cefotaxime (1 g three times daily for 6 days): her presenting fever and abdominal pain resolved but she developed watery diarrhoea. Despite positive stool cultures for toxigenic C. difficile, initial toxin testing by enzyme immunoassay (EIA [TechLab C. Difficile Tox A/B II]) of stool specimens was negative. After a 7-day course of oral metronidazole 200 mg three times daily, the diarrhoea abated. One month after discharge, our patient re-presented with anorexia, severe abdominal pain and diarrhoea. Six days of oral metronidazole, prescribed by her local doctor, had little effect. A computed tomography scan of the abdomen revealed diffuse thickening of the colon from the ileocaecal junction to the rectum, consistent with a pancolitis. Sigmoidoscopy showed grossly abnormal mucosa with pseudomembranes present. A diagnosis of C. difficile pseudomembranous colitis was made. After 10 days of oral vancomycin 250 mg, four times daily, her symptoms had resolved, and repeat sigmoidoscopy showed reversal of the mucosal changes. Six days later, the pseudomembranous colitis recurred. She rapidly responded to the recommencement of oral vancomycin, given as a tapering course over 6 weeks. Twelve days after completing the 6-week course of vancomycin, the patient presented with her third episode of colitis. Most reported strategies for recurrent CDI, such as faecal transplantation, probiotics or novel antimicrobials,4 were not practicable or available for timely use for our patient. Tigecycline, a broad-spectrum glycylcycline antibiotic, is available as part of the hospital formulary for the treatment of complicated skin and soft-tissue infections and complicated intra-abdominal infections. Encouraged by recent reports of success using tigecycline as adjunctive therapy for severe cases of CDI,2 we prescribed, as monotherapy, intravenous tigecycline 50 mg twice daily for 2 weeks. Our patient’s condition improved over 1 week. At 3-month follow-up, she remained asymptomatic, with repeat stool cultures and polymerase chain reaction (PCR) testing for C. difficile toxin negative at Days 75 and 107 following the last episode of colitis. Our case also highlights a diagnostic matter. In general, use of EIA to detect C. difficile toxin A or B is highly specific. However, in clinical settings where the prevalence of CDI is low, the positive predictive values for these assays are inadequate to rule in the diagnosis of CDI. Confirmatory laboratory testing using an alternative method (in this case, PCR) proved more reliable in the diagnosis of our patient’s recurrent CDI. Typing showed that our patient’s isolate was not PCR ribotype 027, a hypervirulent strain in Europe and North America associated with high mortality.5 We recommend consideration of tigecycline as a useful antimicrobial agent in the management of both recurrent and severe CDI.

Elaine Y L Cheong · Thomas Gottlieb

To the Editor: In their editorial, Terpening, Hodges and Cordato argue for routine screening for dementia in Australia.1 Most of the editorial is devoted to discussing which test should be used, and the authors contend that the most-used test — the mini-mental state examination — has such poor test characteristics that it would be a very poor basis for routine screening. However, the discussion about which test to use ignores the elephant in the room — should we screen for dementia in the first place? In their 1968 World Health Organization public health paper on screening for disease, Wilson and Jungner stipulate that “There should be an accepted treatment for patients with recognized disease”.2 There is no evidence whatsoever that this is the case with dementia. Terpening and colleagues cite an article in their editorial in support of their assertion that “development of effective dementia treatments depends on earlier and more accurate identification of disease”.3 However, that article only states that early intervention might help to slow some forms of cognitive decline or progression to dementia. This is a very slim evidence base for routine mass screening. The development of effective treatments can never be a justification for routine population-wide screening. Even in a study environment, screening the study population with a view to developing treatments rather than testing them, would struggle to find ethics approval. The evidence is clear — there is no basis for screening for dementia. It would produce many false positives and false negatives, and would cause much anxiety without any benefit from early treatment. As long as no effective treatments are available, the case for screening for dementia is void.

Jan J Barendregt

To the Editor: Roberts-Thomson and colleagues1 raise important questions about the implications of introducing masters-level medical degrees with doctorate-level nomenclature (ie, Doctor of Medicine [MD]) to Australia. In particular, the potential consequences for postgraduate training deserve further attention. As graduate numbers rapidly increase,2 competition for training positions will further intensify. At the prevocational level, perceptions of enhanced work-readiness could favour applicants with masters-level MD qualifications, such that other graduates might be displaced from popular, metropolitan teaching hospitals. At the vocational level, rigorous college selection processes (which typically include assessing a candidate’s interview performance, curriculum vitae and academic achievements) could favour graduates of new-age MD programs if they specifically reward the attainment of postgraduate qualifications (as is currently the case for some specialties3). Graduates might also lay claim to advanced standing and additional recognition of prior learning on the basis of their academic status. The extent to which these situations materialise will depend on whether masters-level medical programs claim, and deliver, a superior quality in education. For example, the University of Melbourne has committed to producing “outstanding graduates with advanced clinical skills”4 through its new model.5 In the short term, there is unlikely to be any objective evidence of difference in outcomes between the pathways, and demonstrating this would be both complex and contentious. At present, Australian Medical Council standards do not differentiate between qualifications, and new programs will continue to be accredited according to the same rigorous process. Alternatively, if masters-level MD programs lay no claim to enhanced quality over their undergraduate cousins, then the rationale for change should be examined. A purely market-driven deviation from recognised nomenclature could have important unintended consequences, and would be out of step with international efforts to standardise nomenclature (such as the Bologna Process in Europe). An important aspect of the University of Melbourne graduate-school model is the reintroduction of full-fee-paying places for professional-entry degrees. This brings with it significant implications for student debt, both for the trainee (in terms of debt accumulation, career choice and wellbeing) and the community (in terms of workforce distribution).6 Some commentators have suggested that the principle of merit-based entry is compromised by the presence of full-fee-paying places.7 It is unknown exactly how masters-level MD courses will differentiate themselves from undergraduate programs, and what their impact will be. The divide between so-called academic and vocational programs will probably be exaggerated,8 with potential implications for postgraduate training and workforce development. Whatever eventuates, the call for national consistency in higher education nomenclature deserves serious consideration, and the drivers behind any such process must be enhanced quality and equity of access at all stages of training.

Rob D Mitchell · Michael A Bonning · Alex L Markwell

To the Editor: The recent article by Lewis and colleagues highlights the important role of long-acting reversible contraceptives (LARCs) in reducing unintended pregnancy in Australian teenagers.1 LARCs are defined as contraceptives that are administered less than monthly and include hormonal implants and injections, and intrauterine devices (IUDs).2 The critical importance of improving access to LARC methods has been recognised in the United Kingdom by the National Institute of Health and Clinical Excellence, which produced guidelines for implementing this policy in 2005.2 The United States has recently followed this lead. In 2009, expanding access to intrauterine devices and other LARCs, particularly for younger women, was declared a national public health priority by the US Institute of Medicine.3 Our particular interest is to expand Australian women’s access to intrauterine contraception, including the copper devices and the levonorgestrel-releasing device (LNG-IUD). IUDs provide highly effective long-term contraception, and the LNG-IUD offers additional benefits for women with heavy menstrual bleeding.2 Although IUDs are the most widely used reversible contraceptives in the world, they are underused in Australia; the most recent available data suggest use by about 1.2% of women using contrceptives,4 compared with 17% in France and 21% in Sweden.5 The reasons for the low uptake of IUDs are undoubtedly complex, but appear to include lack of information, and misinformation in relation to infection risk and their unsuitability for younger women. There is now good evidence that modern devices present minimal risk of infection and no increased risk of subsequent infertility. There is increasing experience of their use in younger women, and nulliparity is not considered a contraindication.6 To investigate barriers to acquiring an IUD, we surveyed 334 of the 366 women who attended for IUD insertion over 3 months in 2009 at family planning clinics in New South Wales and Queensland. Excluding the 16 women (5%) for whom there were missing data, 16% of respondents (51 of 318) had not found it easy to obtain IUD-related information and almost a fifth (58; 18%) had been told it was not a suitable method for them by either a health professional or a friend or family member (or both), despite these women meeting appropriate medical eligibility criteria at the family planning clinic. Although family planning organisations are currently engaged nationally in developing and delivering IUD-insertion training for general practitioners, we suggest that increasing appropriate use of IUDs in line with other countries will only be achieved if the misperceptions of the risks relating to modern IUDs among consumers and health professionals are addressed. This is crucial to reducing the burden of unintended pregnancy, particularly in young women.

Deborah Bateson · Caroline Harvey · Julia Williams · Kirsten I Black