Objective: To evaluate the management of cardiovascular disease (CVD) risk in Australian general practice.Design, setting and participants: National cross-sectional survey of 99 Australian general practitioners participating in the Bettering the Evaluation and Care of Health (BEACH) program. Data on 2618 consecutive adult patients presenting to the participating GPs over a 5-week period from September to October 2006 were analysed.Main outcome measures: Proportions of patients screened, treated and reaching targets according to (1) current Australian CVD risk guidelines and (2) overall or absolute CVD risk.Results: Blood pressure (BP) had not been recorded for 13% of the sample. Of 1400 patients not prescribed antihypertensive medication, treatment was indicated for 8%. Of 821 patients already prescribed antihypertensive medication, 59% were achieving target BPs. Data on low-density lipoprotein (LDL) cholesterol levels were not available for 53% of the 2175 patients who should have had lipid screening according to the guidelines. Of 624 patients not prescribed a statin, treatment was indicated for 41%. Of 368 already prescribed a statin, 62% were achieving target LDL cholesterol levels. Sufficient data for calculation of absolute risk had been recorded for 74% of the 1736 patients for whom such calculation was recommended by the guidelines. The remaining 26% either had at least one required variable unmeasured (20%) or missing from the data collection (6%). For those at high absolute CVD risk (without established disease) and those with established CVD, 23% and 53%, respectively, had been prescribed both antihypertensive medication and a statin.Conclusions: Gaps between guideline recommendations and practice in recording and managing BP were relatively low compared with gaps for lipids. When stratified by absolute risk, patients at high risk of a cardiovascular event were found to be substantially undertreated.

Ruth J Webster BMedSc(Hons), MB BS(Hons), MIPH(Hons) · Emma L Heeley BSc(Hons), MSc, PhD · David P Peiris MB BS, FRACGP, MIPH · Clare Bayram BAppSc(HIM)(Hons) · Alan Cass MB BS, FRACP, PhD · Anushka A Patel MB BS, FRACP, PhD

We have a tool for absolute risk assessment — now we need a robust implementation program In March 2009, the National Vascular Disease Prevention Alliance (NVDPA), a consortium of Diabetes Australia, Kidney Health Australia, the National Heart Foundation of Australia, and the National Stroke Foundation, released evidence-based guidelines for assessing absolute cardiovascular risk.1 The guidelines are for use by health professionals who assess patients’ cardiovascular risk, primarily general practitioners. The risk charts that accompany the guidelines differ somewhat from the New Zealand risk charts,2 which are commonly used in Australia. Both the Australian and NZ charts are based on the Framingham Heart Study.3 The Australian cardiovascular risk charts are separated at the broader level into people with and without diabetes, rather than into men and women. In addition, systolic, but not diastolic, blood pressure is included because it is the stronger determinant of future events. The charts extend to upper cut-off points of 179 mmHg for systolic blood pressure and 7.5 mmol/L for total cholesterol level, respectively. The NVDPA guidelines also have an online risk calculator (http://www.cvdcheck.org.au). The new NVDPA guidelines and charts have the advantage of taking into account other drivers of practice in Australia, such as the Royal Australian College of General Practitioners’ Guidelines for preventive activities in general practice,4 and eligibility for Pharmaceutical Benefits Scheme subsidies for statins. Absolute risk assessment maximises the effectiveness of prediction of risk of future cardiovascular disease (CVD) events in people apparently free of such disease. This is because the underlying equations acknowledge fundamental epidemiological principles: risk depends on the range of independent risk factors and, for biomedical factors, risk typically increases in a log–linear manner above ideal levels (systolic blood pressure and total cholesterol level, 115 mmHg and 3.8 mmol/L, respectively).5 The present, somewhat arbitrary, definitions of hypertension and hypercholesterolaemia as ≥ 140/90 mmHg and ≥ 5.5 mmol/L, respectively, are fundamentally flawed, and most people who have CVD events have a clustering of risk factors with only modest abnormalities. If relative risk reduction with an intervention is relatively constant (the usual case), use of the intervention in those at higher absolute risk leads to greater absolute risk reduction and net benefit, thus also maximising cost-effectiveness. All absolute risk tools share some problems. As they are derived from large population studies, they are better at rank-ordering risk in subgroups and less precise in an individual. However, individual risk assessment may be refined (particularly in those initially assessed to be at intermediate risk) by measuring biomarkers or by imaging,6 and probably more so in the future, as more evidence becomes available. Other factors that might also be added to future algorithms include anthropometric measures (of these, waist circumference or waist : hip ratio appears more predictive than body mass index), a family history of premature atherosclerotic disease, and measures of socioeconomic deprivation.7 The NVDPA guidelines acknowledge that the Framingham risk equation may underestimate risk if these factors are present. The major determinant of CVD risk is increasing age, and it is also likely that equations specific for various age groups will become available. Particularly among younger people, this will improve identification of those with greater modifiable risk. Ideally, risk equations should be developed and validated in the local population. In Australia, algorithms for the general population have been developed from the Busselton8 and Dubbo9 studies. These are important contributions, although the relatively narrow endpoint (in Busselton) and the cohort age (in Dubbo) limit their application. How best can the NVDPA tools be used by practising clinicians? The first step is to identify high-risk groups. These include people with one or more of the following: prior CVD events, peripheral arterial disease, diabetes and age ≥ 60 years, chronic kidney disease, and familial hypercholesterolaemia. Such people should be treated accordingly and do not need absolute risk assessment. In all others, absolute risk assessments should commence at age 45 years, or 35 years for Aboriginal and Torres Strait Islander people, and be repeated at intervals reflecting the initial level of risk.1 An example of how to incorporate absolute cardiovascular risk assessment into management is given in the Box. What we now need is a robust implementation program. This makes economic sense. Recently, the National Health Service Health Check program was released in the United Kingdom.10 Everyone between 40 and 74 years, not already diagnosed with heart disease, stroke or kidney disease, will be invited, once every 5 years, to have their risk assessed using an absolute risk tool, and given support and advice to help them reduce or manage their risk. Analyses showed that this program would be very cost-effective compared with other accepted health interventions. The modelled cost-effectiveness ratio of this UK program is only £2480 per quality-adjusted life-year gained. Presently, in Australia, a Medicare item number supports a single health check for those aged 45–49 years. Although cost-effectiveness analyses are sensitive to the local health care system, the UK data strongly suggest that the current Medicare item number could be expanded, and other systems-based approaches implemented, to ensure that ongoing primary care risk assessments are supported, and that people at higher risk receive lifestyle and appropriate medical management. Implementation would be most likely to be effective if decision-support tools and recall mechanisms were used and incorporated into prescribing linked to electronic health records. Accompanying materials that appropriately communicate concepts of risk to patients would also be useful. The NVDPA is now developing a single CVD risk-management guide that will integrate the various specific risk-factor guides and make it easier to manage patients according to their absolute risk status. Absolute risk assessment does not replace the need to base all approaches to CVD prevention on lifestyle change. Studies have clearly shown the value of this, whether or not individuals are receiving blood-pressure or lipid-lowering therapies.11 However, absolute risk assessment leaves behind time-hallowed approaches based on individual risk factors, treated in silos, and often “dichotomised” to be regarded as “normal” or “abnormal”. It moves us forward to a more rational and effective paradigm for preventing our major health problem. How to incorporate absolute risk assessment into management using the Australian cardiovascular risk charts (the “People without diabetes” section of the charts is reproduced below) Example: Two women with similar risk profiles, but different ages Both women are smokers, without diabetes, with systolic blood pressure, 140 mmHg; total cholesterol : high-density lipoprotein cholesterol (TC : HDL) ratio, 7.2 mmol/L; and body mass index, 27 kg/m2. A is 46 years old and estimated to have a low risk (5%–9%) of developing cardiovascular disease (CVD) within 5 years. However, if she continues to smoke and to have a high TC : HDL ratio, she will place herself at high risk of prematurely developing CVD as she gets older. The chart can be used to demonstrate this to her. The priority intervention should be lifestyle advice, including smoking cessation, physical activity and healthy eating. B is 66 years old and estimated to be at high risk (20%–24%) of having a CVD event within 5 years. As a high priority, she should receive advice about smoking cessation and other lifestyle changes, as well as statin therapy. How to use the risk chart 1. Identify the chart relating to the person’s sex, diabetes status, smoking history and age. The charts should be used for all adults aged 45–74 years (and all Aboriginal and Torres Strait Islander adults aged 35 years or older) without known history of CVD or already known to be at high risk. 2. Within the chart, choose the cell nearest to the person’s age, systolic blood pressure (SBP) and total cholesterol (TC):HDL ratio. For example, the lower left cell contains all non-smokers without diabetes who are 35–44 years and have a TC:HDL ratio of less than 4.5 and a SBP of less than 130 mm Hg. 3. The colour of the cell that the person falls into provides their 5-year absolute cardiovascular risk level (see legend above for risk category). People who fall exactly on a threshold between cells are placed in the cell indicating higher risk. Charts are based on the NVDPA’s Guidelines for the assessment of absolute cardiovascular disease risk and adapted with permission from New Zealand Guidelines Group. New Zealand Cardiovascular Guidelines Handbook: A Summary Resource for Primary Care Practitioners. Second edition. Wellington, NZ: 2009. www.nzgg.org.nz. These charts are taken from Absolute cardiovascular disease risk assessment – quick reference guide for health professionals. © 2009 National Heart Foundation of Australia. Reproduced with permission. No further reproduction is allowed.

Andrew M Tonkin MD, FRACP, FCSANZ · Andrew N Boyden MPH, FRACGP · Stephen Colagiuri FRACP

Although glycated haemoglobin (HbA1c) has become the key biochemical marker of long-term glycaemic control, analytical method-dependent differences in results can occur when haemoglobin variants are present or HbA1c is reduced by decreased red cell survival. When the measured HbA1c level is discordant with the patient’s blood glucose measurements and clinical status, fructosamine is an alternative biochemical marker that can provide a more accurate estimate of the glycaemic control and enable clinicians to appropriately manage patients. Clinical recordA 65-year-old, centrally obese man (body mass index, 32.7 kg/m2) with a 23-year history of type 2 diabetes mellitus was referred to a diabetes clinic in January 2008 for stabilisation of his blood sugar levels. His diabetes was complicated by ischaemic heart disease, peripheral vascular disease, hypertension, dyslipidaemia, and stage 3 chronic kidney disease. His glycated haemoglobin (HbA1c) level on referral was 11.0%, measured using an ion-exchange chromatography (IEC) method on a Bio-Rad Variant II analyser (Bio-Rad Laboratories, Sydney, NSW), and the laboratory fasting glucose measurement was 19.3 mmol/L (Box 1). Both these results were consistent with the patient’s home blood glucose measurements (> 10 mmol/L). On presentation, the patient’s medication included human mixed insulin (Mixtard 30/70; Novo Nordisk, Sydney, NSW) (80 units before breakfast and 75 units before dinner), as well as simvastatin, aspirin, clopidogrel, diltiazem, ramipril, frusemide, omeprazole, bisoprolol, irbesartan and glyceryl trinitrate. The insulin regimen was changed to a basal-bolus regimen of insulin aspart and insulin glargine, which was titrated weekly on the basis of home blood glucose measurements. After 6 weeks, the patient’s HbA1c level had decreased to 5.8%, which appeared to be inconsistent with the home blood glucose measurements and the laboratory fasting glucose measurement (15.1 mmol/L). This change in HbA1c level coincided with the implementation of a modified method (“NU”) on the Bio-Rad Variant II analyser. Haemoglobin (Hb) studies (electrophoresis and chromatography) demonstrated an abnormal Hb variant interfering with the HbA1c measurement. The patient’s fructosamine level was tested and the result indicated improved glycaemic control, but not to the extent suggested by the HbA1c level. A week after the fructosamine measurement, the HbA1c measurement was repeated with a Siemens DCA 2000 analyser (Siemens, Melbourne, Vic) using an immunoassay (IA) method, which is less likely to be influenced by Hb variants. The result was congruent with the fructosamine estimation of the glycaemic control (Box 1). On subsequent visits, the patient’s HbA1c level was measured with a different IEC method on a Bio-Rad D-10 analyser (Bio-Rad Laboratories, Sydney, NSW), from which a substantially higher result was obtained (Box 1). A further fructosamine measurement (280 μmol/L) suggested the glycaemic control was better than the HbA1c results now indicated. To investigate the effect of the Hb variant on the different HbA1c assays, the patient’s 9 December 2008 sample was analysed using the different analytical systems available locally (Box 1). The highest (9.0%) and lowest (4.4%) HbA1c results were obtained from IEC methods on different analysers from the same supplier. Before the modification of the Bio-Rad Variant II method, there was incomplete separation of the Hb variant and HbA1c peaks (Box 2, A). After implementation of the modified method, the separation of the Hb variant and HbA1c peaks was much more distinct (Box 2, B and C). The instrument software integrates only the one HbA1c fraction or peak and therefore underestimates the HbA1c level by about 50%. The Bio-Rad D-10 chromatogram (Box 2, D) is similar in appearance to the chromatogram from the original Bio-Rad Variant II method (Box 2, A). The range of HbA1c values obtained with the affinity chromatography (AC) and IA methods spanned a range from 6.8% to 7.9% (Box 1); this variation is within the anticipated interlaboratory performance. To avoid such variation, one analytical method should consistently be used for monitoring longitudinal changes. The patient’s Hb variant was characterised as a heterozygote for the Hb Athens-Georgia mutation by a reference laboratory (Southern Cross Pathology Australia, Melbourne, Vic). This is a very rare and clinically silent variant detected in Caucasians where only one β-chain is affected,1,2 and, depending on the separation method, it can produce two peaks on the chromatogram, as was the case with the modified Bio-Rad Variant II NU method (Box 2, B). DiscussionThis case illustrates some of the caveats associated with measuring glycaemic control. A multifactorial approach is required to achieve optimal glycaemic control, as failure to recognise the true state of control might result in inappropriate clinical management decisions and less than optimal patient care. The rate of HbA1c formation is proportional to the average blood glucose concentration over the life span of red blood cells (about 120 days). Methods used to measure HbA1c are divided into the three categories of IEC, AC and IA. In the 2008 Royal College of Pathologists of Australasia Quality Assurance Program (http://www.rcpaqap.com.au), 59% of participants used IA, 30% used IEC and 11% used AC methods, performed on 29 different commercial platforms. About 40% of all HbA1c measurements were performed with point-of-care instruments that use either IA or AC methods. Interference from abnormal Hb variants can lead to falsely elevated or lowered HbA1c results with IEC methods. AC methods are the least affected by Hb variants, as the method separates all glucose-modified Hb molecules from non-modified molecules, and calculates the HbA1c value from the total glycated Hb result.3-5 More than 1300 Hb variants have been identified,2 and about half of these are clinically silent.4 An HbA1c level < 6% or > 15% in patients with diabetes can often be due to Hb variant interference.3,6 The prevalence of Hb variants is highest in Mediterranean regions, Africa and Asia, particularly India and Pakistan. IA methods are only affected by Hb variants where the first 4–10 amino acids of the Hb β-chain are altered, and the IA antibody is unable to bind.7 Elevated levels (> 10%) of HbF falsely lower HbA1c results in IA methods.7 HbF levels are normally < 1%, but increased levels occur in hereditary conditions (β-thalassaemias, sickle cell anaemia and congenital aplastic anaemia), late pregnancy, in some patients with abnormal Hb variants, and in neonates.5 As well as recent blood transfusions and abnormal Hb variants, reduced red cell survival (as occurs in haemolytic anaemia, haemorrhage, iron deficiency anaemia, end-stage renal disease, patients on haemodialysis,3 thalassaemias or sickle cell syndromes6) is another cause of falsely low HbA1c results with all analytical methods, as a consequence of less available time for non-enzymatic glycation to occur. Fructosamine measurement is an alternative method for monitoring glycaemic control in patients with reduced red cell survival, and provides an index of glycaemia over the preceding 2–3 weeks.6 Recent studies, including a position statement from the American Diabetes Association, have suggested that simultaneous measurement of HbA1c and fructosamine might complement one another and may provide more useful clinical information than HbA1c alone.8,9 However, unlike with HbA1c, to date there are no published accepted treatment targets for fructosamine, nor are the different fructosamine measurement methods standardised. The most recent consensus statement on the standardisation of HbA1c measurement recommends that laboratories should report an HbA1c-derived average glucose or estimated average glucose (eAG) value alongside the HbA1c level.10 As the eAG is calculated from the HbA1c level, it will not assist in those patients whose HbA1c measurement is not accurate because of Hb variants or reduced red cell survival. The HbA1c result and the eAG should correlate with the patient’s glucose measurements and clinical status. If they are discordant, the HbA1c result should be rechecked using an alternative analytical method that is less susceptible to interference from Hb variants. Alternatively, fructosamine measurement might be a useful adjunct in these cases. It may be prudent to rely more on glucose tests when there is uncertainty about long-term markers of glycaemic control, although the long-term markers may still be valuable for trend analysis. Considering current migration patterns, with more than half of the nearly 150 000 settlers arriving in Australia in the 2007–08 financial year coming from Africa, the Middle East and Asia,11 patients with Hb variants and decreased red cell survival will become more prevalent in the Australian population. This case emphasises the limitations of HbA1c assays in such patients and the importance of communication between clinicians and the laboratory when unexpected results occur. 1 Results from the various glycated haemoglobin (HbA1c) analytical systems and other laboratory measurements Date Analytical system Analytical method HbA1c* eAG (mmol/L) Glucose (mmol/L) Fructosamine (μmol/L)† 29 January 2008 Bio-Rad Variant II‡ (old method) IEC 11.0% 14.9 19.3 — 11 March 2008 Bio-Rad Variant II (new method) IEC 5.8% 6.6 15.1 — 1 April 2008 Bio-Rad Variant II (new method) IEC 4.9% 4.9 — — 3 May 2008 — — — — — 271 10 May 2008 Siemens DCA 2000§ IA 7.4% — — — 28 November 2008 Bio-Rad D-10‡ IEC 9.2% 12.0 7.8 280 9 December 2008 Bio-Rad Variant II (new method) IEC 4.4% 4.4 — 234 Bio-Rad D-10 IEC 9.0% 11.7 — Siemens DCA Vantage§ IA 7.5% 9.3 — Roche Integra¶ IA 7.7% 9.7 — Primus PDQ** AC 7.9% 10.0 — Bio-Rad in2it‡ AC 6.8% 8.2 — 20 January 2009 Bio-Rad in2it AC 7.3% — — 307 eAG = estimated average glucose. IEC = ion-exchange chromatography. IA = immunoassay. AC = affinity chromatography. * All HbA1c results are aligned to the National Glycohemoglobin Standardization Program (http://www.ngsp.org). † Reference range, 190–285 μmol/L. ‡ Bio-Rad Laboratories, Sydney, NSW. § Siemens, Melbourne, Vic. DCA Vantage is an upgraded model of the DCA 2000. ¶ Roche Diagnostics, Sydney, NSW. ** Primus Diagnostics, Kansas City, Mo, USA. 2 Chromatograms from Bio-Rad ion-exchange chromatography analysers* HbA1c values: A: 11.0% B: 4.9% C: 4.4% D: 9.0%. * Bio-Rad Laboratories, Sydney, NSW.

Goce Dimeski BSc · Carel J Pretorius MB ChB, FCPathChem(SA) · Anthony W Russell MB BS, FRACP, PhD · Stephen P Miller BSc · Robert J Bird MB BS, FRCP(Lon), FRCPA · Jacobus P J Ungerer MB BS, MMed(ChemPath), FRCPA

A 49-year-old man presented with verapamil toxicity complicated by hypotension and a junctional rhythm, in the context of deliberate self-poisoning with multiple drugs. The patient’s hypotension normalised following the early use of high-dose insulin euglycaemic therapy (HIET), without the need for additional vasopressors; it recurred when HIET was prematurely stopped, and again stabilised when HIET was recommenced. Consideration should be given to the early use of HIET in treating severe calcium channel blocker toxicity, rather than as a last resort after other therapies have failed. (MJA 2009; 191: 350-352) Clinical recordA 49-year-old man presented to a peripheral hospital emergency department 1–1.5 h after deliberately ingesting multiple medications: verapamil (unknown amount), controlled-release morphine sulfate (20 × 30 mg), diazepam (50 × 5 mg) and tramadol (15 × 200 mg). He was a smoker with a history of depression, ethanol misuse, chronic back pain, hypertension and a previous instance of deliberate self-poisoning with multiple drugs. At initial assessment, the patient’s vital signs were: temperature, 36.8°C; pulse, 84 beats/min; respiratory rate, 19 breaths/min; blood pressure (BP), 115/80 mmHg; oxygen saturation, 95% on room air; and Glasgow Coma Scale score, 14/15. He was drowsy, disorientated to time, and had 2 mm pupils that were equal and reactive. He had ataxia, dysarthria and was generally weak. His breath ethanol concentration was 0.172 mg%. Thirty minutes later, the patient was hypotensive (BP, 85/45 mmHg; pulse, 72 beats/min). He was treated with oxygen, 2 L intravenous (IV) 0.9% saline, a naloxone IV infusion (400 μg/h), and 10 mL IV 10% calcium gluconate. He was transferred to a tertiary referral centre and, on arrival (at 2.25 h after initial presentation), his BP was 85/45 mmHg, pulse was 64 beats/min, and an electrocardiogram (ECG) showed a junctional rhythm. Rapid sequence intubation (with propofol 40 mg + 20 mg IV and suxamethonium 100 mg IV) was performed for airway protection and ongoing management of haemodynamic instability, while metaraminol IV boluses (total, 0.7 mg) were administered. Activated charcoal (50 g) was given, and sedation was maintained with a propofol infusion. The patient remained hypotensive (BP, 75/45 mmHg; pulse, 56 beats/min) after intubation, so high-dose insulin euglycaemic therapy (HIET) was commenced at 3.5 hours after presentation. He was given dextrose (50 mL 50% glucose) and a 30 IU short-acting insulin IV bolus (~ 0.5 IU/kg), followed by a further bolus of 50 mL 50% glucose and a short-acting insulin IV infusion (30 IU/h) (Box 1). His BP improved to 110/70 mmHg at 4 hours, with a pulse of 82 beats/min and sinus rhythm on ECG, and he remained stable during transfer to the intensive care unit (ICU). The insulin infusion was abruptly stopped 5.5 hours after presentation, on arrival in the ICU. The patient’s hypotension subsequently recurred (systolic BP, 70 mmHg; pulse, 75 beats/min), prompting administration of 500 mL IV Gelofusine (a colloidal plasma volume substitute; B. Braun, Sydney, NSW) and commencement of an adrenaline IV infusion (20 μg/min). The insulin infusion (30 IU/h) was restarted at 8.5 hours, and his BP again stabilised (Box 1). The propofol IV infusion was gradually increased from 50 mg/h to 150 mg/h between 5.5 hours and 11.5 hours after presentation, and a noradrenaline IV infusion was commenced at 9.5 hours to maintain normotension. At 15.5 hours, pulmonary artery catheter measurements showed a high cardiac index (5.1 L/min/m2; reference range [RR], 2.5–4.0 L/min/m2) and a low systemic vascular resistance index (1047 dynes·s/cm5/m2; RR, 1900–2400 dynes·s/cm5/m2); the patient’s pulse was 85 beats/min and BP was 140/60 mmHg. HIET was continued and the patient remained haemodynamically stable. Adrenaline and noradrenaline were weaned off (at 17.5 hours and 23.5 hours, respectively), despite the propofol infusion rate being increased to 500 mg/h at 18.5 hours. Once sedation was withdrawn, the patient was extubated at 26.5 hours. Insulin was weaned over 5 h and discontinued at 30.5 hours; dextrose was stopped 1 h later. The patient was transferred to the observation ward and discharged well later that day, after psychiatric clearance. During treatment with HIET, the patient’s blood glucose levels were checked hourly and ranged from 6.6 mmol/L to 13.2 mmol/L (RR, 3.5–5.5 mmol/L). He received about 25 g/h of dextrose (mostly as 50% dextrose infusions). Potassium and magnesium levels were also serially monitored; the minimum potassium level was 2.7 mmol/L (RR, 3.5–5.0 mmol/L) at 8.75 hours, and the magnesium level troughed at 0.5 mmol/L (RR, 0.75–1.05 mmol/L) at 15 hours. These were corrected with a total of 200 mmol of potassium chloride and 20 mmol magnesium chloride. DiscussionHIET is an increasingly accepted therapy for calcium channel blocker (CCB) toxicity, but reports of its use are limited and it remains controversial. Indeed, the scarcity of severe CCB poisoning cases means that a randomised controlled trial of HIET may not be feasible.1 Treating clinicians who seek advice from clinical toxicologists are often hesitant about the high doses required and the potential for adverse effects. Such hesitancy is potentially harmful, as a hypotensive patient with a CCB overdose who otherwise appears well is at risk of abrupt lethal cardiovascular collapse.1 HIET is traditionally recommended after other therapies have failed.2,3 This case report aims to raise awareness of HIET for the treatment of CCB toxicity and supports its early use, rather than as a last resort.4 Verapamil binds the alpha-1 subunit of L-type calcium channels, preventing the intracellular influx of calcium.5 These channels are functionally important in cardiac myocytes, vascular smooth muscle cells, and islet beta cells.5 Verapamil’s cardiac toxicity results from excessive negative inotropy, negative chronotropy and negative dromotropy, characterised by myocardial depression, sinus bradycardia, and atrioventricular node blockade.4 Vascular smooth muscle tone is impaired, resulting in decreased afterload, systemic hypotension, and coronary vasodilation.5 Less well known are the metabolic effects of CCBs such as verapamil. Under the stress of the drug-induced shock state, the cardiac myocytes shift from using free fatty acids, their favoured “resting state” energy substrate, to carbohydrates.3,4 CCB toxicity also impairs the uptake of glucose and free fatty acids by cardiac myocytes3,4 and inhibits calcium-dependent mitochondrial activity required for glucose catabolism.3,4 Furthermore, insulin release is dependent on calcium influx into islet beta cells through L-type calcium channels.3,4 Thus, CCB toxicity can cause hypoinsulinaemia,3,4 which, in conjunction with CCB-induced insulin resistance, may lead to hyperglycaemia and a ketoacidotic state.6 Atropine, calcium boluses and infusions, glucagon, inotropes, vasopressors, and cardiac pacing have all been advocated for managing CCB toxicity, despite questionable efficacy.3,4,7-9 For instance, the evidence for glucagon is limited to small, non-blinded animal studies where no survival benefit or improvement in mean arterial pressure was shown, although heart rate improved in some cases.7 Rarely, heroic measures such as extracorporeal circulatory support and intra-aortic balloon counterpulsation have been successfully employed.5,10 HIET was first used to treat verapamil toxicity in humans in 1993, with a favourable outcome.6 Since then, in addition to animal studies, there have been nearly 70 cases reporting the beneficial use of HIET in humans, with an overall survival rate of 85%.8 However, to our knowledge, use of HIET in humans before the administration of glucagon or vasopressors has only been reported once.6 There have been some reports of HIET failure in treating CCB toxicity, although the dosing of insulin was low or uncertain, or it was used late.6,8 Early use of HIET may be more effective than HIET rescue therapy, as CCB-induced insulin resistance is greatest in the first 24 hours2 and the maximal haemodynamic benefit of HIET may not occur immediately.6 HIET may allow the heart to overcome metabolic starvation in CCB toxicity, which compounds the direct CCB impairment of myocardial contractility.3,4 Insulin increases glucose and lactate uptake by myocardial cells and improves function without increased oxygen demand.11,12 It also induces pyruvate dehydrogenase, hastening myocardial lactate oxidation, and helps clear the cytosol of glycolytic byproducts that impair calcium handling and cause diastolic dysfunction.3 Insulin promotes excitation–contraction coupling and contractility because enhanced glycolysis promotes increased sarcoplasmic reticulum-associated calcium ATPase activity and increased cytoplasmic calcium concentrations, and promotes calcium entrance into mitochondria and sarcolemma.3 HIET may be best used adjunctively with other measures such as catecholamines, for two reasons. First, insulin-mediated inotropy is not catecholamine-mediated, and is not affected by β blockers.3 Second, although insulin appears to improve myocardial contractility, it has no chronotropic effect and may cause vasodilation.3,8 HIET is safe, and adverse events are predictable, uncommon, and easily managed.2,8 The maximum safe dose of insulin is unknown, but loading doses of 0.5–1.0 IU/kg followed by infusions of 0.1–2.5 IU/kg/h are typically used.8 Interestingly, neither the inadvertent administration of a 1000 IU insulin loading dose for verapamil toxicity13 nor treatment of toxic cardiogenic shock for 2 days with a 6 IU/kg/h insulin infusion had any adverse effects.14 Adverse effects of HIET include hypoglycaemia, hypokalaemia, hypomagnesaemia, and hypophosphataemia.2,6,8 Although these are rarely clinically significant, they necessitate careful monitoring. Hypoglycaemia (blood glucose < 3.3 mmol/L) occurred in 16% of 55 published cases,8 and no cases of hypoglycaemia within 24 hours of CCB overdose were noted in Greene and colleagues’ series of seven cases.2 Greene et al also reported a mean dextrose requirement of 0.05 g/kg/h (range, 0–0.17 g/kg/h), although the mean blood glucose level exceeded the euglycaemic range.2 Some cases of severe CCB toxicity in patients presenting with hyperglycaemia do not require any additional glucose administration despite high-dose insulin therapy,15 and hypoglycaemia may be more likely in milder cases without marked hypotension.8 In addition, hypokalaemia (potassium < 3.5 mmol/L) was noted in only two patients in Greene et al’s small series, with a minimum potassium level of 2.8 mmol/L.2 Excessive correction of hypokalaemia should be avoided, because it reflects the intracellular shift of potassium from the extracellular compartment due to the action of insulin, rather than a potassium-depleted state.4 Interestingly, hypokalaemia in HIET may augment myocardial contractility by enhancing calcium entry during systole, and increased intracellular potassium may have a membrane-stabilising effect in excitable cells.4,6 In conclusion, we advocate consideration of the early use of HIET (as detailed in Box 2) for the prevention and treatment of life-threatening complications from potentially lethal CCB overdoses. HIET is safe, inexpensive and freely available, and suitable for use even in remote settings before transfer to a referral centre. 1 Early changes in the patient’s systolic blood pressure (SBP) and heart rate, relative to treatment with high-dose insulin and adrenaline infusions Following administration of a 0.5 IU/kg short-acting insulin bolus 3.5 hours after presentation, a short-acting insulin intravenous infusion (0.5 IU/kg/h) was commenced (black line), and the patient’s blood pressure improved. The infusion was abruptly discontinued 2 hours later and the patient again became hypotensive. This resolved following commencement of an adrenaline infusion (20 μg/min) (grey arrow), and the insulin infusion (0.5 IU/kg/h) was restarted 8.5 hours after presentation (black arrow). 2 Recommended high-dose insulin euglycaemic therapy protocol,3,4,9 based on the clinical experience of the Western Australian Toxicology Service, published case reports, reviews and animal studies Commence therapy with: Glucose 25 g (50 mL of 50% solution) IV bolus, unless marked hyperglycaemia (blood glucose > 22 mmol/L) is present Short-acting insulin 1 IU/kg bolus to maximally saturate insulin receptors Continue therapy with: Short-acting insulin infusion starting at 0.5 IU/kg/h and titrated every 30 min to a maximum of 5 IU/kg/h* Dextrose 25 g/h IV infusion titrated to maintain euglycaemia (blood glucose, 5.5–14 mmol/L); central venous access may be required to allow use of concentrated solutions (eg, 50% dextrose) and limit excess volume administration Monitor: Glucose — every 20 min for first hour, then every 1 h Potassium — replace only if < 2.5 mmol/L and there is a source of potassium loss Therapeutic end points: Improvement in myocardial ejection fraction (> 50%); increased BP (systolic BP > 90 mmHg in adults) Adequate heart rate (> 60 beats/min) Resolution of acidaemia; euglycaemia; adequate urine output (1–2 mL/kg/h) Reversal of cardiac conduction abnormalities (QRS interval < 120 ms) Improved mentation Therapy is weaned after the withdrawal of other vasopressors, as cardiotoxicity resolves. Dextrose may be required after cessation of insulin. IV = intravenous. BP = blood pressure. * The maximum safe and effective rate of infusion is unknown but may be even higher than 5 IU/kg/h. In animal studies, insulin infusions as high as 10 IU/kg/h have been safely used.11

Christopher P Nickson MB ChB, DTMH, GCertClinTox · Mark Little FACEM, DTMH, MPHTM

Objective: To provide an estimate of the morbidity and mortality resulting from abdominal overweight and obesity in the Australian population.Design and setting: Prospective, national, population-based study (the Australian Diabetes, Obesity and Lifestyle [AusDiab] study).Participants: 6072 men and women aged ≥ 25 years at study entry between May 1999 and December 2000, and aged ≤ 75 years, not pregnant and for whom there were waist circumference data at the follow-up survey between June 2004 and December 2005.Main outcome measures: Incident health outcomes (type 2 diabetes, hypertension, dyslipidaemia, the metabolic syndrome and cardiovascular diseases) at 5 years and mortality at 8 years. Comparison of outcome measures between those classified as abdominally overweight or obese and those with a normal waist circumference at baseline, and across quintiles of waist circumference, and (for mortality only) waist-to-hip ratio.Results: Abdominal obesity was associated with odds ratios of between 2 and 5 for incident type 2 diabetes, dyslipidaemia, hypertension and the metabolic syndrome. The risk of myocardial infarction among obese participants was similarly increased in men (hazard ratio [HR], 2.75; 95% CI, 1.08–7.03), but not women (HR, 1.43; 95% CI, 0.37–5.50). Abdominal obesity-related population attributable fractions for these outcomes ranged from 13% to 47%, and were highest for type 2 diabetes. No significant associations were observed between all-cause mortality and increasing quintiles of abdominal obesity.Conclusions: Our findings confirm that abdominal obesity confers a considerably heightened risk for type 2 diabetes, the metabolic syndrome (as well as its components) and cardiovascular disease, and they provide important information that enables a more precise estimate of the burden of disease attributable to obesity in Australia.

Adrian J Cameron MPH · David W Dunstan PhD · Neville Owen PhD · Paul Z Zimmet MD, PhD · Elizabeth L M Barr MPH · Andrew M Tonkin MD · Dianna J Magliano PhD · Shirley G Murray GradDipPractMan · Timothy A Welborn PhD · Jonathan E Shaw MD

A 71-year-old man who presented to hospital with chest pain and a history of cardiovascular disease was repeatedly hospitalised over the course of a month for care that included multiple investigations, intensive care, transfer to and from a metropolitan hospital, discharge, and readmissions for collapse, hemiparesis, and vision change. The medical team excluded underlying disease related to his initial chest pain and subsequent neurological symptoms. A search for (undisclosed) prior hospitalisations revealed multiple previous admissions and invasive investigations at hospitals across Australia, resulting in a diagnosis of Munchausen syndrome. Assuming that, despite interventions, patients with Munchausen syndrome or somatoform disorders often continue to seek care at other hospitals, we discuss the implications of this patient’s behaviour for the health care system, society, and the risk to his own health. In our view, this case highlights conflicts between privacy legislation and doctors’ mandates to protect the patient from harm, as well as their duty to attend to the financial viability of health services by communicating with other potential health care providers. The health care system and similar patients may benefit from efforts to educate doctors about this spectrum of disorders and from considering the implementation of a highly confidential, structured notification system.

Dawn E DeWitt MD, FACP, FRACP · Stephanie A Ward MB BS · Sandeep Prabhu MB BS(Hons), LLB(Hons) · Bruce Warton MB BS, GradDipHealth

Extracorporeal membrane oxygenation (ECMO) is a technique that involves oxygenation of blood outside the body, and provides support to selected patients with severe respiratory or cardiac failure. The two major ECMO modalities are venoarterial and venovenous. Data from several randomised trials support the use of ECMO in neonatal respiratory failure, and a recent randomised controlled trial of ECMO in adults has produced encouraging results. The evidence base for ECMO use in cardiac disease is developing, but progress has been slowed by considerations of clinical equipoise and evolving indications for ECMO. Advancing ECMO technology and increasing experience with ECMO techniques have improved patient outcomes, reduced complications and expanded the potential applications of ECMO. Awareness of the indications and implications of ECMO among doctors managing patients with severe but potentially reversible respiratory or cardiac failure may help facilitate better communication between health care teams and improve patient recovery.

Steven J Lindstrom MB BS(Hons), BMedSc(Hons) · Vincent A Pellegrino MB BS, FRACP, FJFICM · W Warwick Butt MB BS, FRACP, FJFICM

How you can use the evidence to improve your patients’ outcomes The most recent edition of Heart Foundation guidelines for the management of hypertension is an evidence-based and practical guide for doctors.1 It is self-evident that clinical guidelines need to be used by doctors if they are to improve population health outcomes. Despite publication of multiple editions of the hypertension guidelines, blood pressure (BP) control in Australia is less than ideal.2 The reasons for this are varied, and include health system, doctor and patient factors.3 Here, I outline simple but effective strategies for addressing some of the doctor factors associated with lack of BP control (Box), based on the Heart Foundation guidelines and supplemented by research conducted in Australian general practice. These strategies should help protect patients from stroke, myocardial infarction and other major organ damage, and are all practical in the general practice setting. Although they will not lead to universal control (because other factors are at play), they should help protect against therapeutic inertia and doctors’ doubts about their own self-efficacy — issues that may adversely affect patient health. Get blood pressure measurements from a variety of sources. When doctors measure BP, the measurements they record may differ from the true values, because of measurement error, “white coat effect”, poor technique, single measurements, observer error, and data misinterpretation.4 These problems can be addressed, to some degree, in a variety of ways. One approach is to have someone else, or something else, record BP for adult patients. In clinical practice, BP should be measured repeatedly (and preferably by a nurse) — three times, 5 minutes apart, and the last two measurements averaged. The process can be automated with some oscillometric devices, which further reduces bias.4 Away from the practice, the patient can record their BP on a validated,5 regularly serviced machine that they have been taught to use, or they can have their BP recorded by an ambulatory BP monitor. The latter are superior predictors of hard clinical endpoints compared with clinical measurements.6 Specific advice about technique for patients (as well as clinicians) is covered in the chapter of the Heart Foundation guidelines entitled “Measuring blood pressure”.1 Repeated measurements help reduce measurement error and variability, but they need to be interpreted logically. Suitable home BP monitoring can be achieved by asking the patient to measure BP in the morning and evening, to do so twice on each occasion (2 minutes apart after sitting quietly for 5 minutes), and to record the second measurement in a spreadsheet or diary for use at their next appointment. Interpreting the data can be as simple as highlighting elevated measurements, calculating the percentage of elevated systolic and diastolic measurements, or averaging the measurements. The goal is all or nearly all measurements (or average BP) at or below target levels. When interpreting the data, remember that cut-points are lower for recordings made away from the practice; for example, 135/85 mmHg is the cut-point for BP measured away from the practice in patients with uncomplicated hypertension. Act on absolute risk. In cases where repeated measurements of elevated BP are recorded in at-risk individuals, general practitioners may still not initiate or intensify BP management. Barriers to initiation or adjustment of drug therapy include: clinical uncertainty about underlying true BP and distrust of the technology used to measure BP; distrust of the evidence underpinning the recommendations for management of hypertension; a perceived increased rate of adverse events associated with drug therapy among older patients; perceived patient attitudes towards drug therapy or the need for it; a lack of internal motivation on the part of the practitioner; and health system issues such as lack of time in consultations. The decision to initiate treatment of elevated BP should not be based on BP alone (unless it is very high). An absolute cardiovascular disease risk score should be used, such as the recently released Australian cardiovascular risk charts, that now include risk for Aboriginal and Torres Strait Islander peoples.7,8 This is a more holistic approach than use of a single risk factor — it integrates all risk factors and thus more accurately identifies at-risk individuals. In primary prevention, population risk calculators are required as doctors cannot reliably estimate absolute risk.9 Patients with mildly elevated BP, who are at low absolute risk, do not require drug therapy but still need action on lifestyle factors that affect BP (eg, alcohol intake, diet, overweight/obesity, and physical inactivity). Don’t neglect behavioural factors. GPs recognise that behavioural factors underlie elevated BP and mitigate against effective BP control, but may feel that they have limited influence on their patients’ lifestyle. However, brief advice from a GP is the most cost-effective intervention for smoking cessation.10 Also, walking is a simple, free, all-year activity that GPs can recommend. For overweight patients, caloric restriction can be recommended and, for all patients, recommendations that can be considered include moderation of alcohol intake (do not recommend alcohol to non-drinkers), restriction of salt intake (by reading and interpreting processed food labels), and consumption of fruit and vegetables (two serves of fruit and five serves of vegetables per day). Advice should be supplemented with appropriate referrals (eg, to a dietitian). Accept that most patients will need more than one drug. Most patients will need more than one drug to control their BP.11 This is exacerbated by the need to manage the clustering of risk factors and multiple morbidity, which is common among patients, and especially older patients, with high blood pressure. These factors drive a high evidence-based pill count, which should be distinguished from unnecessary polypharmacy. Thus, the need for two or more drugs to effectively manage hypertension should be communicated to patients from the outset. Follow the guideline recommendations for combinations of drugs. Ways to deal with the necessary polypharmacy in managing high BP in at-risk individuals include: minimising side effects by starting with low doses (especially in older patients and patients with renal impairment), using low-dose combinations, discontinuing ineffective drugs, avoiding agents contraindicated for other conditions that are present, and monitoring for adverse outcomes such as renal impairment; minimising cost by using fixed-dose combinations, generics, agents with a larger number of daily doses dispensed, and drugs listed on the Pharmaceutical Benefits Scheme (avoiding “brand premiums”); increasing adherence by using combination therapies (especially those that allow within-combination dose adjustments); and reducing polypharmacy across morbidities by choosing antihypertensive agents that are indicated for other diseases that are present. Treat to goal. Once treatment of high BP has been moved to an absolute risk basis, the goals are logically reduced to lower levels for those individuals who are at high absolute risk. For example, the guidelines recommend lower BP targets for increasing levels of proteinuria in patients with chronic kidney disease.1 These patients will require greater individual risk factor reduction to reach low risk than patients who are at intermediate risk. This means more drugs, higher doses, higher costs, and greater difficulty in reaching therapeutic targets. In cases where the goal is not being reached, assessing for adherence to drug therapy is important — especially during the initiation of drug therapy. Participants in the Second Australian National Blood Pressure Study who answered yes to the question “Did you ever forget to take your medication?” were significantly more likely to experience a cardiovascular event or death than those who answered no.12 Strategies for dealing with necessary polypharmacy will also help reach the goals of target BP and adherence to drug therapy. The five ways together. Combining these strategies will help to improve BP control via an evidence-based chain of action: obtaining BP measurements systematically, in and away from the general practice setting; stratifying patients according to absolute risk, and acting on risk; considering behavioural measures for all patients; and utilising drugs (usually two or more) for patients who are at high risk, to reach recommended, targeted goals. Simple evidence-based strategies for managing high blood pressure in general practice Get blood pressure measurements from a variety of sources Act on absolute risk Don’t neglect behavioural factors Accept that most patients will need more than one drug Treat to goal

Mark R Nelson MB BS(Hons), FRACGP, PhD

The global financial crisis teaches us that systems like Medicare may have hidden long-term costs if they are based on short-term gains Dear Nic, Forgive my informality, but I have noticed that Australians like to shorten things — this even applies to Medicare. As a former TeRD (temporary resident doctor), I dreamed of being able to access Medicare for my own chronic diseases. Now I am a proud Australian citizen and grateful for the care my general practitioner gives me courtesy of Medicare. He could view me as a cash cow because my ailments make me eligible for more care plans than I’d like. Instead, he sees me and addresses my concerns when needed, and I have never felt processed or tick-boxed. Likewise, I want to give my patients quality, evidence-based and compassionate care. I love my job. I am at my best when trying to sort out what needs to be worried about and what does not. But although the Medicare system seems to be working for me as a patient, it does not work for me as a doctor. Medicare does not reward doctors who remain working in the “swampy lowland [of] messy, confusing problems [that] defy technical solution”.1 Generalists like me can ensure appropriate investigation and referral, and thus reduce costs of health care.2 GPs provide accessible and comprehensive care for common problems and provide continuity and team coordination for complex care.3 But we seem to have created an inverse care law in Australia, where specialists and GP subspecialists gain more income, and managing undifferentiated illness — often the hardest to sort out — is not rewarded. We pay premiums to people who cut out the known, not to those who draw out the unknown. To maximise this lower generalist income I am entitled to as a GP, I should conduct many consultations that last just over 5 minutes. However, taking a longer history and performing a focused physical examination (neither possible within 6 minutes) significantly increase my chances of weighing the multitude of factors that might contribute to a diagnosis or problem identification without recourse to expensive investigations (Box 1). Also, I am reminded that giving insufficient time or care to establishing a sound doctor–patient relationship and rushing consultations are two of the 10 “deadly sins” that will increase my risk of litigation.5 But this safer and, in the long term, cheaper care for my patients and my country generates less income for me in the short term. General practice grew up when most illness was acute and there were limited therapeutic options; the funding arrangements reflected the style of practice. Now, these arrangements put us in a quandary — the way to make the most money is to see people for a short time and deal with only one problem at a time. Telling people to come back for another visit seems grossly inefficient to me but is, admittedly, one way of earning a crust. Many patients want to save my and their time and bring in a list, little knowing that this will cost me income. I’ll use the example cited by the Professional Services Review (PSR), in which the clinical problems are more easily defined (a rare treat in my practice), to illustrate my less well defined billing problem. The PSR’s advice that a patient seen for a repeat script for a stable condition, an ear syringe and a blood pressure measurement would not qualify as a level C consultation even if the consultation lasted more than 20 minutes6 means that a level C consultation cannot be billed.6 However, the evidence shows that to do all three tasks well and safely is neither quick nor uncomplicated. Issuing a repeat script for a stable condition requires a check of the condition and its current impact on function, the medication, its known side effects, and potential interactions with other medications.7 The consultation should include questions about over-the-counter medications and complementary and alternative medicines (CAMs) taken, given that CAMs were reported to be used by 52.2% of 3015 people surveyed in South Australia, of whom 49.7% used conventional medicines on the same day and 57.2% did not report the use of CAMs to their doctor.8 According to medicolegal advice, before removing ear wax GPs should take a full history, asking specifically about ear discharge, previous perforation of the eardrum or ear infection carefully examine the external auditory canal recommend the use of wax softening agents explain the potential complications of the procedure ensure the person performing the ear syringing is fully trained ensure the equipment is correctly assembled. If the nozzle of the syringe is not properly secured, it may become detached and cause damage to the external auditory canal and/or tympanic membrane.9 The Heart Foundation’s Guide to management of hypertension 2008 recommends that doctors should “Manage identified lifestyle risk factors in all patients, whether or not BP [blood pressure] is elevated”.10 This cardiovascular risk assessment includes: personal and family history, smoking assessment, risk of diabetes, body mass index calculation, waist circumference measurement, exercise assessment, lipid assessment, and nutrition.10 Time and skills in motivational interviewing are needed to encourage change to reduce the risks identified.11 Once these simple, uncomplicated6 tasks are done, the GP should make clear, comprehensive and contemporaneous notes12 at a standard that enables another practitioner to take over care. Notes should include demographic and contact details, known allergies and a summary. Once the patient leaves, I begin my unpaid administrative work — reading letters from hospitals and emails from my Division of General Practice and practice manager; checking results; responding to patients’ queries; checking recall lists; and planning follow-up. Do you see my dilemma? Each task can be done quickly, yes, but only with potential longer-term safety risks and costs. If I do one thing per consultation, it would take three visits to deal with the problems. This has a higher overall cost in terms of making appointments for both patients and staff, patient time out of work and in travel — and what of the environmental costs of all this travel (unless I have persuaded them to cycle to the practice, thanks to my motivational interview about cardiovascular risk)? I would argue it is reasonable and good practice to do all this in one half-hour appointment and claim a Medicare Benefits Schedule item 36 long consultation. Medicare policy does not! Tell me, why not? Medicare and those practising medicine must learn the hard-hitting lesson from the current global financial crisis — that systems based on short-term gains have hidden long-term costs.13 You say you want GPs to provide quality care and include health promotion.14 Yet the announcement of increased audits of GPs’ billing practices coincides with a reduction in longer consultations of nearly a million from 5.53 million to 4.55 million between corresponding 6-month intervals in 2007–2008 and 2008–2009.15 I ask you, which do you want — short-term lower costs or longer-term better health for the people of Australia? Please value the role of the generalist; reconsider advice that “implementation of a 7 tier item structure in place of the current 4 tier item structure would improve the quality of health care in Australia” (Box 2);16 and use holistic cost–benefit analysis to inform health policy.13 Thanks for listening. Oh, and can I ask one final question? When you next need milk, will you implement the same system we apply to Medicare and just get the milk, and nothing else, on that visit to the shops? Or will you be reckless and go in with a list — wanting multiple things? Doesn’t it make much more sense to buy everything you need at once? Yours sincerely, Susan PS: please refrain from calling me Sue — I hate to be cut short. 1 A teenage girl presents to a general practitioner with recurrent headaches Option 1: brief history, referral for a computed tomography (CT) scan Time taken by GP: 6-minute consultation, 2 minutes to read report as normal, 6-minute review consultation. Income for the GP: two level-B consultations. Holistic cost–benefit analysis: cost of CT scan, radioactivity exposure for teenager, time off school and work for teenager and parent, anxiety about result, transport to and from x-ray department, return visit to the GP for brief review, but no engagement of teenager with GP to discuss emotional wellbeing, preventive or sexual health. Teenager has no understanding of tension headache. High chance of further consultations with other practitioners to establish cause for headaches. Option 2: comprehensive history and examination, no referral for CT scan Time taken by GP: 19-minute consultation giving teenager space to talk about home, education and employment, activities, drugs, depression, sexuality or suicide (HEADSS assessment tool).4 GP conducts a brief examination, then negotiates the management of tension headaches relating to upcoming school examinations and a boyfriend who will finish with her unless she agrees to start a sexual relationship. Nineteen-minute review consultation and discussion about contraception. Income for the GP: two level-B consultations. Holistic cost–benefit analysis: no expensive investigations, no exposure to radioactivity and no time off school or work or transport to attend x-ray department. Teenager understands nature of tension headaches and is able to take simple analgesics when needed. Teenager relieved to have talked about concerns and comfortable to access contraception when she is ready. 2 The Attendance Item Restructure Working Group seven-tier rebate system* The seven-tier rebate system creates a more consistent rebate per minute. At 2003 rates, this ranged from $2.00 to $2.50, whereas for the current structure, the rebate per minute ranges from $2.00 to $4.00 for consultations less than 10 minutes, but only $1.00 to $2.00 for consultations greater than 10 minutes. The proposed structure removes incentives towards consultations of just over 5 minutes. * Figure adapted from the Final report of the Attendance Item Restructure Working Group.16

Susan M Wearne MMedSc, FRACGP, FACRRM

To the Editor: One of the most talked about solutions to some of the problems of our health care system is “preventive health”. The rationale appears to be that “an ounce of prevention is better (and presumably cheaper) than a pound of cure”. Perhaps this is the reasoning behind the ever-increasing Medicare Benefits Schedule item numbers, inducing general practitioners to do more and more preventive health checks. This is expected of GPs, conditional on the services being “cost neutral” to the government.1 Reasonable as it sounds on the face of it, this may be neither efficient nor cost-effective, given that: most preventive health issues (such as asthma, diabetes, obesity, hypertension and stroke) can not be covered reasonably well in less than several hours or several long consultations, depending on the educational level of the target audience; Medicare Australia appears reluctant to pay a fair fee for these long consultations without imposing a lot of red tape; and the average patient seeking such preventive health advice is usually middle-aged or older, and the opportunities for true prevention (rather than risk factor management) may have long passed. A better solution to this predicament may lie in changes to school curricula. Any time spent on general common-sense health and hygiene topics in high schools would be cheaper to provide (costing only tens of dollars per hour if provided by teachers versus hundreds of dollars if provided by GPs). Health education in schools may also help students establish a healthy lifestyle from a young age, benefits of which could be reaped for decades. In other words, health education may have to become a compulsory part of the curriculum for prospective teachers. Local GPs could give lectures on health education to aspiring teachers. Topics could include the importance of adequate sleep, adequate exercise and an adequate intake of fresh fruit and vegetables on a daily basis; the hazards of smoking and drinking; and mundane but important areas such as simple hygiene practices, skin care and even dental care. If more patients had some basic knowledge of these and many other common topics, such as the differences in symptoms and natural history between viral and bacterial respiratory infections, the number and length of GP consultations could potentially be reduced. This, in turn, would have a direct flow-on effect on the overall efficiency of the primary health care system and, undoubtedly, the tertiary health care system as well.

Tony A Marshal